tag:blogger.com,1999:blog-593052633314060792024-03-05T22:46:52.676+05:30Dr Satyajit Mohanty blogssatyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.comBlogger596125tag:blogger.com,1999:blog-59305263331406079.post-35720384728448232462013-12-24T21:54:00.006+05:302023-01-03T17:52:17.925+05:30Pulled elbow & dislocation of radial head at elbow<div dir="ltr" style="text-align: left;" trbidi="on">
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Traumatic disruption of radio-humeral architecture may take many forms & a cause of lateral elbow pain with elbow stiffness. Subluxation & dislocation occur at this joint without fracture. We are herewith presenting a small review of pulled elbow in children & radial dislocation in adults. The purpose of doing so is to present the clinician to better identify these seemingly equal entities. <br />
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<b>Pulled elbow: </b><br />
It is also known as nursemaid's elbow. It is a common injury in young children. It is considered a minor condition in medicine but cause mush distress to parents of a child. <br />
It results from a sudden longitudinal traumatic pull on pronated and extended forearm, usually by an adult or taller person. This sudden pull pulls the radius through the annular ligament, resulting in subluxation (partial dislocation) of the radial head. <br />
The child experiences sudden acute pain and loss of function in the affected arm.<br />
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<b>DD:</b> <br />
It appears to be infrequently recognized or diagnosed. Differential diagnosis of traumatic radial head subluxation from traumatic radial head dislocation, congenital radial head dislocation, brachial plexus palsy and "invisible" elbow fractures should be considered. Congenital radial head dislocation is the most common congenital elbow abnormality. Patients generally remain asymptomatic until adolescence and, at that time, may benefit from radial head resection. Open reduction and ligament reconstruction may offer advantages over late radial head resection if performed before the age of 2 years.<br />
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<b>Variants of pulled elbow:</b><br />
It is postulated here that there are two types of traumatic rotary radial head subluxation in pronation, the simple type and the lateral type. Careful analysis of AP view of elbow reveals the change of the shape and position of the radial tuberosity indicating the simple type, or concommitant with lateral displacement of the radial head on the ulna indicating the lateral type. <br />
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<b>Treatment procedure:</b><br />
Pulled elbow is usually treated by manual reduction of the subluxed radial head. Various manoeuvres can be applied. Flexion & supination is believed to be common method employed however few authorities recommend hyperpronation. Most textbooks recommend supination of the forearm, as opposed to pronation and other approaches. It is unclear which manoeuvre is most successful. <br />
According to a Cochrane reviw (2009) pronation method might be more effective and less painful than the supination method for manipulating pulled elbow in young children. <br />
However premanipulative roentgenograms are compared with postmanipulative roentgenograms in such cases to check repositioning. <br />
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<b>Dislocation cases: </b><br />
In closed reduction followed by plaster cast immobilisation for 4 weeks give a good result. In neglected cases where reduction is delayed neocapsule is believed to form hence even arthrography is therefore of little help to differentiate a long standing traumatic dislocation from a congenital dislocation. Various authors prefer & avoid open reduction, which carries a risk of joint stiffness, it is unnecessary to mention old unreduced dislocations cannot be reduced by manipulation. <br />
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<b>Adult cases of dislocation of radial head: </b><br />
<b><br /></b>In adults, isolated radial head dislocation is an extremely rare injury. Isolated traumatic dislocation can be either anterior or posterior. The mechanism leading to an isolated radial dislocation has been variously described. Most authors describe an indirect mechanism. The proximal radioulnar joint is most stable in supination: in this position, the contact between radius and ulna is maximal and the interosseous membrane, the annular ligament, and the anterior fibres of the quadrate ligament are all taut, thus drawing the radial head snugly against its notch in the ulna. Cadaveric studies have shown that posterior dislocation of the radial head cannot occur without the rupture of the annular ligament; in addition, partial tear of the quadrate ligament and the proximal interosseous membrane takes place. <br />
The speculated the mechanism to be a hyperextension of the elbow with forearm in prone position leads to a posterior dislocation of the radial head.<br />
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Posterior dislocation of radial head: only few more than 20 cases are described in medical literature but there are no guidelines for treatment. An inability to pronate/supinate while able to flex the elbow should suggest posterior radial head dislocation. There is swelling obvious on the lateral and posterior aspect of the elbow. The elbow is held in flexion and partial supination. Tenderness is present laterally at the elbow, and the radial head is palpable posteriorly. There is no swelling or tenderness over the ulna.<br />
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<b>Treatment approach in posterior dislocation:</b> Under general anesthesia, gentle traction, pronation, and direct pressure over the radial head is used to reduce the dislocation. Postreduction, the elbow is generally stable. Immobilization is done in a long-arm cast for 4 weeks in either flexion (110 degres) & supination or uncommonly flexion & pronation. Patient generally recovers complete range of motion.<br />
The diagnosis may be easily missed on radiographs and, therefore, require a high index of suspicion. Authors have reported isolated anterior dislocation of the radial head in young woman without functional disorders. Early reduction is important in order to avoid the necessity for excision of the head of radius and its attendant complications.<br />
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If missed or neglected, an open reduction must to be done with either an annular ligament reconstruction or a radial head excision; in these conditions, the results were poor with a restriction of forearm supination and pronation and significant risk of degenerative arthritis of the elbow and the distal radioulnar joints. Closed reduction of an elbow dislocation is unlikely to be successful if attempted later than 21 days after the injury. The results are acceptable if open reduction is undertaken within 3 months of the injury, but after 6 months the results are disappointing and arthroplasty is an alternative.</div><div dir="ltr" style="text-align: left;" trbidi="on"><b style="color: blue;"><br /></b></div><div dir="ltr" style="text-align: left;" trbidi="on"><b style="color: blue;">References:</b></div><div dir="ltr" style="text-align: left;" trbidi="on"><span style="color: blue;"><span style="background-color: white;">1. Krul M et al Cochrane Database Syst Rev. 2012 Jan 18;1:CD007759. doi: 10.1002/14651858.CD007759.pub3. (Manipulative interventions for reducing pulled elbow in young children.)<br />2. Woo CC; J Manipulative Physiol Ther. 1987 Aug;10(4):191-200. (Traumatic radial head subluxation in young children: a case report and literature review.)<br />.3. Obert L et al; Chir Main. 2003 Aug;22(4):216-9. (Isolated traumatic luxation of the radial head in adults: report of a case and review of the literature.)<br />4. Damak B et al; Acta Orthop Belg. 1998 Dec;64(4):413-7. (Isolated traumatic anterior dislocation of the radial head).<br />5. Bruce C et al; J Trauma. 1993 Dec;35(6):962-5. (Unreduced dislocation of the elbow: case report and review of the literature.)<br />6. Sachar K et al; Hand Clin. 1998 Feb;14(1):39-47. (Congenital radial head dislocations.)<br />7. Koulali-Idrissi K et al; Chir Main. 2005 Apr;24(2):103-5. [Isolated dislocation of the radial head in an adult (case report and literature review)].<br />8. J Emerg Trauma Shock. 2010 Oct;3(4):422-4. doi: 10.4103/0974-2700.70767. Isolated, traumatic posterior dislocation of the radial head in an adult: A new case treated conservatively.</span></span></div>
satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0Lane 3, Tankapani Rd, Badagada Brit Colony, RP-81, Pandav Nagar, Bhubaneswar, Odisha 751018, India20.2468263 85.8485876-12.491387687847915 50.6923376 52.985040287847909 121.0048376tag:blogger.com,1999:blog-59305263331406079.post-3451087785362564002013-10-25T21:56:00.001+05:302013-10-25T21:56:47.959+05:30Manage LBA & SIJ pain by Hip intervention<div dir="ltr" style="text-align: left;" trbidi="on">
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<br /><b>Crucial role of hip in Hip-spine syndrome </b><br /><br />Cervical & dorsal spine can produce lumbar spine pain along with lower extremity pain that may mimic sciatica. Similarly muscle imbalances & hip capsular problems may produce SI joint & lumbar spine pain with radiating symptoms in the lower extremity.<br /><br />In the following article we are trying to focus on hip producing spine & SI joint problems producing radiating & non-radiating symptoms. <br /><br />
Concomitant presence of hip & spine problem named hip-spine syndrome is reported in medical literature but amount of research in this area is scanty. As relates to physiotherapy it becomes difficult to chuck out action plan as every bit of physical intervention must be directed to exact tissue at fault. What causes what, hip gives rise to spine fault or vice versa is yet to be concretely ascertained. Burns SA et al (2) found joint mobilization/manipulation and strengthening exercises directed at the hip alleviates both hip & lumbar spine pain. They have concluded patients with lumbopelvic-hip pain respond favorably to manual therapy and exercise targeting regions adjacent to the lumbar spine and further individuals with a primary complaint of LBP with hip impairments may benefit from interventions to reduce hip impairments. <br /><br />
Many crucial hip joint functions are maintained by pelvifemoral muscles during static & dynamic functions. Hip also has a strong capsule that may suffer from tightness & contracture which may further affect muscle function of hip leading to altered biomechanics of pelvic & lumbar spine producing pain in the mentioned areas. As mentioned above hip mobilization may not only alleviate lumbar spine pain it may also improve muscle function & capsular flexibility. According to Howard M et al (3) use of grade IV non-thrust mobilization improves hip abductor strength immediately post-intervention in healthy individuals assumed to be because of stimulation of mechanoreceptors. In a study by Yerys et al (4) it is revealed that a significant increase in gluteus maximus strength in response to Grade IV P-A mobilizations performed on the anterior hip capsule. Clinicians can utilize these findings in everyday practice to improve muscle strength by integrating manual therapy with therapeutic exercises.<br /><br />
<b>A review of biomechanical prospective of spino-pelvic organization & lumbo-coxa chain in sagital plane:</b><br />
i. Standing & static posture & lumbar spine curvature to pelvis: Standing in an erect position is a human property (5). According to Mehta VA et al (8) relation of the pelvis to the spine is overlooked as a contributor to sagittal balance. However, it is now recognized that spinopelvic alignment is important to maintain an energy-efficient posture in normal and disease states. Sagital pelvic alignment is very much dependant on the hip joints. Similarly pelvis anatomy and position, defined by the pelvis incidence, interact with the spinal organization in shape and position to regulate the sagittal balance between both the spine and pelvis. Sagittal balance of the human body may be defined by a setting of different parameters such as (a) pelvic parameters: pelvic incidence (PI), pelvic tilt (PT) and sacral slope (SS); (b) C7 positioning: spino-pelvic angle (SSA) and C7 plumb line; (c) shape of the spine: lumbar lordosis. The genuine shape of the spine is probably one of the main mechanical factors of degenerative evolution. This shape is oriented by a shape pelvis parameter, the pelvis incidence. In case of pathology, this constant parameter is the only signature to determine the original spine shape we have to restore the balance of the patient.<br /><br />
ii. Bending & lifting: Bending and lifting activities are associated with injury to the lumbar discs and ligaments, and cadaveric experiments suggest that this damage is most attributable to a high bending moment (bending stress) acting on the osteoligamentous spine. Dolan P et al (6) examined the hypothesis that people with poor sagittal mobility in the lumbar spine and hips apply higher bending stresses to their spines during everyday lifting activities. They found all subjects flattened or reversed their lumbar lordosis when lifting, and most came close to or exceeded their static in vivo limit of lumbar flexion in many of the activities. The bending moment acting on the lumbosacral junction rose to about 30 Nm, which is about 50% of that required to cause injury in a single lift. Bending moments were significantly lower in subjects who had good sagittal mobility in the lumbar spine. Good hip mobility was similarly associated with a reduction in bending moment, but this reached significance only in subjects who reported a history of low back pain.<br /><br />
iii. Hip Lateral Rotation (HLR) test: Pattern of hip lateral rotation vary in different back pain suffers i.e. they move their hip differently (9). Linda R et al (7) examined whether lumbopelvic motion associated with a clinical test of active hip lateral rotation (HLR) systematically varied between people classified into 1 of 2 low back pain (LBP) subgroups: lumbar rotation (Rot) or lumbar rotation with extension (RotExt). And they further examined whether the timing of hip and lumbopelvic rotation with HLR would be more symmetric, right versus left, in people in the Rot subgroup compared with the RotExt subgroup.<br /><br />
They found People in the Rot and RotExt subgroups displayed systematic differences in how they moved the hip and lumbopelvic region with the clinical test of active HLR. These findings are potentially important because such differences in movement patterns between subgroups of people with LBP suggest different contributing factors and may require different treatments to affect the movement patterns. Here normalizing faulty movement i.e. hip lateral rotation may lead to alleviation of LBA. <br /><br />
<b>Patterns of hip contracture & it’s genesis: </b><br />
<b> </b>Analysis of patterns in poliomyelitis reveals that fibrosis of gluteus maximus muscle may lead to limited flexion of the hips and various degrees of contracture of the abductor and external rotator muscles (1). In such cases affected hip could not be flexed in the usual sagittal plane, but had to be flexed in abduction. If gluteus maximus tightness & contracture is addressed excellent correction of the other hip contractures are achieved.<br /><br />Sitting posture: In relaxed sitting posture hip rolls in to abduction & external rotation being flexed. This may lead to contracture of hip external rotators & abductors. That may also lead to tightness of posterior hip capsule. <br /><br />If hip remains or maintains an abduction, external rotation position then there is compensatory pelvic posture for example iliac out-flare. Hence all of this may lead to altered dynamic sagital balance of the whole lumbopelvocoxa region which may further lead to a degenerative pathogenesis in any of the above.<br /><br />Examples:<br />1. Patients with lower back or buttock pain that radiates into the posterior or lateral leg are often referred to physical therapy with a diagnosis of sciatica. Often the physical exam does not reveal neurologic findings indicative of radiculopathy. Instead, there is hip abductor muscle pain and weakness. This syndrome involves muscle imbalances that result in overuse strain of the gluteus medius and gluteus minimus muscles, Myofascial trigger points, and trochanteric bursitis. This paper describes hip abductor pain syndrome and provides a rationale for the diagnosis and treatment. Treatment salient points are discussed above (9). <br />2. According to a case study by Boyle KL interventions to restore and maintain the optimal position of pelvis and hip (femoral head in the acetabulum) may be beneficial for treating patients with chronic LBP/SIJP. The patient’s pain may be alleviated in just a few days performing exercises to reposition the pelvis and restore posterior hip capsule extensibility and internal rotation (11) anterior interior chain pattern of postural asymmetry. <br /><b><br />References: </b><br />
<br />1. YS Hang; J Bone Joint Surg Am, 1979 Jan 01;61(1):52-55. Contracture of the hip secondary to fibrosis of the gluteus maximus muscle. <br />2. Burns SA et al Physiother Theory Pract. 2011 Jul;27(5):384-97. doi: 10.3109/09593985.2010.509382. Epub 2010 Aug 26. Clinical decision making in a patient with secondary hip-spine syndrome.<br />3. Howard Makofsky et al, J Man Manip Ther. 2007; 15(2): 103–110. Immediate Effect of Grade IV Inferior Hip Joint Mobilization on Hip Abductor Torque: A Pilot Study. <br />4. Yerys et al; Journal of Manual & Manipulative Therapy, Volume 10, Number 4, 2002 , pp. 218-224(7). Effect of Mobilization of the Anterior Hip Capsule on Gluteus Maximus Strength.<br />5. Roussouly P et al; Eur Spine J. 2011 Sep;20 Suppl 5:609-18. doi: 10.1007/s00586-011-1928-x. Epub 2011 Aug 2. Biomechanical analysis of the spino-pelvic organization and adaptation in pathology.<br />6. Dolan P et al; Clinical Biomechanics, Volume 8, Issue 4, July 1993, Pages 185–192. Influence of lumbar and hip mobility on the bending stresses acting on the lumbar spine.<br />7. Linda R. Van Dillen et al; Archives of Physical Medicine and Rehabilitation, Volume 88, Issue 3, March 2007, Pages 351–360. Symmetry of Timing of Hip and Lumbopelvic Rotation Motion in 2 Different Subgroups of People With Low Back Pain.<br />8. Mehta VA et al; Neurosurgery. 2012 Mar;70(3):707-21. Implications of spinopelvic alignment for the spine surgeon.<br />9. Dennis C et al; The Iowa Orthopaedic Journal, Volume 23 57. RATIONALE FOR TREATMENT OF HIP ABDUCTOR PAIN SYNDROME. <br />10. Barbee E et al; phys ther.1990,70:537-541. Patters of hip rotation range of motion: A comparison between healthy subjects & patients with low back pain.<br />11. Boyle KL. Physiother Can. 2010;preprint. doi:10.3138/ptc.2009-37. Managing a female patient with left low back pain and sacroiliac joint pain with therapeutic exercise: a case report.<br /> <br /><br /></div>
satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-69662462603834792262013-09-30T21:13:00.001+05:302013-09-30T21:13:23.821+05:30Chronic fatigue syndrome<div dir="ltr" style="text-align: left;" trbidi="on">
<b>Introduction:</b><br />
Severe fatigue is a common complaint among patients. Often, the fatigue is transient or can be attributed to a definable organic illness. Some patients present with persistent and disabling fatigue, but show no abnormalities on physical examination or screening laboratory tests. In these cases, the diagnosis of chronic fatigue syndrome (CFS) should be considered. <br /><br />
According to Centers for Disease Control and Prevention (CDC, USA) Chronic fatigue syndrome (CFS) currently is defined as:<br />(1) fatigue of at least 6 months' duration, seriously interfering with the patient's life; and (2) without evidence of various organic or psychiatric illnesses that can produce chronic fatigue.<br /><br />The World Health Organization classifies myalgic encephalomyelitis/chronic fatigue syndrome (ME/cfs) as a nervous system disease. Together with other diseases under the G93 heading, ME/cfs shares a triad of abnormalities involving elevated oxidative and nitrosative stress (O&NS), activation of immuno-inflammatory pathways, and mitochondrial dysfunctions with depleted levels of adenosine triphosphate (ATP) synthesis.<br /><br /><b>Clinical features:</b><br />Elaborately CFS is characterized by debilitating fatigue with associated myalgias, tender lymph nodes, arthralgias, chills, feverish feelings, and postexertional malaise. According to Komaroff there may be abrupt onset with an 'infectious-like' illness, intermittent unexplained fevers, arthralgias and 'gelling' (stiffness), sore throats, cough, photophobia, night sweats, and post-exertional malaise with systemic symptoms. <br />According to Clauw 4 of the following criteria need to be present: sore throat, impaired memory or cognition, unrefreshing sleep, postexertional fatigue, tender glands, aching stiff muscles, joint pain, and headaches.<br /><br />
<b>Prevalence: </b><br />
While chronic, debilitating fatigue is common in medical outpatients, CFS is relatively uncommon. Prevalence depends substantially on the case definition used.<br />Etiology: <br />It is known that CFS is a heterogeneous disorder possibly involving an interaction of biologic systems. Medical research continues to examine the many possible etiologic agents for CFS (infectious, immunologic, neurologic, and psychiatric), but the answer remains elusive. <br /><br />
<b>Diagnosis:</b><br />
Diagnosis of CFS is primarily by exclusion with no definitive laboratory test or physical findings. <br />Differential diagnosis should be considered carefully as similarities with fibromyalgia & teperomadibular joint disorder exist and concomitant illnesses include irritable bowel syndrome, depression, and headaches.<br />Course of CFS: <br />According to Komaroff the illness can last for years and is associated with marked impairment of functional health status.<br /><br />
<b>Treatment:</b><br />
Therefore, treatment of CFS may be variable and should be tailored to each patient. Therapy should include graded exercise (SF-36 is useful in assessing functional status), diet, good sleep hygiene, antidepressants, and other medications, depending on the patient's presentation.<br />It is note worthy that for graded exercises to be implemented one need to assess the exercise capacity of the individual. <br /><br />
<span style="background-color: blue;"><b>References:</b></span>1. Komaroff AL et al, Am J Med. 1996 Jan;100(1):56-64. An examination of the working case definition of chronic fatigue syndrome.<br />2. Craig T et al Am Fam Physician. 2002 Mar 15;65(6):1083-90. Chronic fatigue syndrome: evaluation and treatment.<br />3. Komaroff AL, Ciba Found Symp. 1993;173:43-54; discussion 54-61.Clinical presentation of chronic fatigue syndrome.<br />4. Buchwald D Am J Med. 1996 Oct;101(4):364-70. Functional status in patients with chronic fatigue syndrome, other fatiguing illnesses, and healthy individuals.<br />5. Bates DW et al Arch Intern Med. 1993 Dec 27;153(24):2759-65. Prevalence of fatigue and chronic fatigue syndrome in a primary care practice.<br />6. Clauw DJ, PM R. 2010 May;2(5):414-30. doi: 10.1016/j.pmrj.2010.04.010. Perspectives on fatigue from the study of chronic fatigue syndrome and related conditions.<br />7. Aaron LA et al Best Pract Res Clin Rheumatol. 2003 Aug;17(4):563-74. Chronic diffuse musculoskeletal pain, fibromyalgia and co-morbid unexplained clinical conditions.<br />8. Morris G et al; Mol Neurobiol. (2013).The Emerging Role of Autoimmunity in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/cfs).<br /><br /></div>
satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-13809895860152751702013-01-05T21:03:00.002+05:302013-01-07T11:30:57.640+05:30 Diagnosis of Posterior heel pain & role of eccentric exercise in mid-portion Achilles tendinopathy<div class="separator" style="clear: both; text-align: center;">
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<b>Introduction: </b><br />
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Degenerative disorders of tendons present an enormous clinical challenge. They are extremely common, prone to recur and existing medical and surgical treatments are generally unsatisfactory. Posterior heel pain is a common complaint in both athlete and non-athlete. Posterior heel pain is multifactorial and includes paratenonitis, tendinosis, tendinosis with partial rupture, insertional tendinitis, retrocalcaneal bursitis, and subcutaneous tendo-Achilles bursitis. Each of these entities is distinct, but they often occur in combination.<br />
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To avoid stereotyped treatment programs and there by failure of treatment, we need to know & classify homogenous appearing clinical entities into it’s own due place. With respect to posterior heel pain we encounter similar appearing entities in the Achilles tendon itself. Hence Van dijk et al in 2011 has sought clear terminology to delineate each of pain syndromes arising out of posterior heel. Following is an outline of new terminology they proposed; the definitions hereof encompass the anatomic location, symptoms, clinical findings and histopathology. <br />
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<b>1. Mid-portion Achilles tendinopathy:</b> a clinical syndrome characterized by a combination of pain, swelling and impaired performance. It includes, but is not limited to, the histopathological diagnosis of tendinosis.<br />
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Anatomic location: 2–7 cm from the insertion onto the calcaneus.<br />
Symptoms: A combination of pain, swelling and impaired performance. <br />
Signs: Diffuse or localized swelling<br />
Histopathology: Includes, but is not limited to, the histopathological diagnosis of tendinosis: implies histopathological diagnosis of tendon degeneration without clinical or histological signs of intratendinous inflammation, not necessarily symptomatic<br />
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<b>2. Achilles paratendinopathy:</b> Achilles tendon is a weight-bearing tendon that lack a true tendon sheath but ia surrounded by paratenon. There is an acute or chronic inflammation and/or degeneration of the thin membrane around the Achilles tendon in this entity. There are clear distinctions between acute paratendinopathy and chronic paratendinopathy, both in symptoms as in histopathology. <br />
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<i><b>Acute Achilles paratendinopathy: </b></i><br />
Anatomic location: Around the mid-portion Achilles tendon<br />
Symptoms: Edema and hyperaemia<br />
Signs: Palpable crepitations, swelling<br />
Histopathology: Edema and hyperaemia of paratenon, with infiltration of inflammatory cells, possibly with production of a fibrinous exudate that fills the space between tendon sheath and tendon<br />
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<i><b>Chronic Achilles paratendinopathy: </b></i><br />
Anatomic location: Around the mid-portion Achilles tendon<br />
Symptoms: Exercise induced pain<br />
Signs: Crepitations & swelling less pronounced than it’s acute counterpart<br />
Histopathology: Paratenon thickened as a result of fibrinous exudate, prominent and widespread proliferation of (myo)fibroblasts, formation of new connective tissue and adhesions between tendon, paratenon, and crural fascia<br />
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<b>3. Insertional Achilles tendinopathy:</b> located at the insertion of the Achilles tendon onto the calcaneus, bone spurs and calcifications in the tendon proper at the insertion site may exist. <br />
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Anatomic location: Insertion of Achilles tendon onto calcaneus, most often with formation of bone spurs and calcifications in tendon proper at insertion site<br />
Symptoms: Pain, stiffness, sometimes a (solid) swelling<br />
Signs: Painful tendon insertion at the mid-portion of the posterior aspect of the calcaneus, swelling may be visible and a bony spur may be palpable<br />
Histopathology: Ossification of enthesial fibrocartilage, and sometimes small tendon tears occurring at tendon-bone junction<br />
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<b>4. Retrocalcaneal bursitis:</b> an inflammation of the bursa in the recess between the anterior inferior side of the Achilles tendon and the posterosuperior aspect of the calcaneus (retrocalcaneal recess). <br />
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Anatomic location: Bursa in the recess between the anterior inferior side of the Achilles tendon and the posterosuperior aspect of the calcaneus (Retrocalcaneal recess)<br />
Symptoms: Painful swelling superior to calcaneus<br />
Signs: Painful soft tissue swelling, medial and lateral to the Achilles tendon at the level of the posterosuperior calcaneus<br />
Histopathology: Fibro-cartilaginous bursal walls show degeneration and/or calcification, with hypertrophy of the synovial infoldings and accumulation of fluid in the bursa. Alternatively, the bursa may be primarily involved by inflammatory or infectious bursitis due to an inflammatory arthropathy<br />
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<b>5. Superficial calcaneal bursitis:</b> inflammation of the bursa located between a calcaneal prominence or the Achilles tendon and the skin.<br />
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Anatomic location: Bursa located between calcaneal prominence or the Achilles tendon and the skin<br />
Symptoms: Visible, painful, solid swelling postero-lateral calcaneus (often associated with shoes with rigid posterior portion) <br />
Signs: Visible, painful, solid swelling and discoloration of skin. Most often located at posterolateral calcaneus; sometimes posterior or posteromedial<br />
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Histopathology: An acquired adventitious bursa, developing in response to friction. When inflamed, lined by hypertrophic synovial tissue and fluid.<br />
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Finally, they suggested that previous terms as Haglund's disease; Haglund's syndrome; Haglund's deformity; pump bump (calcaneus altus; high prow heels; knobbly heels; cucumber heel), are no longer used.<br />
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<b>Pathology of Achilles tendon disorders:</b><br />
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Tendinopathy is essentially an 'overuse', degenerative condition. Histopathology studies indicate intratendinous failed healing response and neoangiogenesis in achilles tendinopathy. Neovascularisation evident on Doppler ultrasound correlates well with pain and poor function. Power Doppler study shows microvessels arise on the ventral side of the TA tendon. However according to Richards PJ (2005) there is non-linear relationship between tendonopathy, TA size and the amount of microvascularity. <br />
Mid portion achilles tendionopathy: Tendinopathy of the main body of tendo Achillis affects athletic and sedentary patients. Mechanical loading is thought to be a major causative factor. However, the exact mechanical loading conditions which cause tendinopathy are poorly defined. Repetitive mechanical loading induces a non-inflammatory pathology, and repetitive microtrauma ultimately exceeds the healing response. <br />
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<b>Diagnostic clues: </b><br />
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A Haglund's deformity or precisely RCB (Retrocalcaneal bursitis) is present in asymptomatic patients & more to that it does not indicate presence of insertional Achilles tendinitis. A vast majority of the insertional Achilles tendinitis patients have calcification at the tendon insertion (Kang , 2012). <br />
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On the basis of X-ray Singh R(2008) for diagnosis of etiology of posterior heel pain described certain angles, lines and soft tissue parameters that focus to describe the calcaneal prominence and its relationship to Achilles tendon and its bursae. Following are the points of diagnosis: <br />
Parallel pitch lines, Chauveaux-Liet angle, ill-defined retrocalcaneal recess, superficial tendo-Achilles bursa and anteroposterior diameter of Achilles tendon more than 9 mm about 2 cm above insertion are reliable objective diagnostic indicators of bony deformity of calcaneus and soft tissue affection in patients with posterior heel pain. <br />
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<i><b>Skeletal US imaging:</b></i><br />
A study by Richards PJ (2005) reveal that power doppler is more sensitive to reveal tendon microvascularity than colour doppler in TA tendonopathy. Morphologically abnormal adult TAs were larger than 5.9 mm but power doppler flow is only seen in TAs above 6.5 mm.<br />
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<b>Treatment of posterior heel pain: </b><br />
<br />
Although most cases of this disorder are successfully treated nonoperatively, a small subgroup of recalcitrant cases may benefit from surgical intervention. (Impact of conservative treatment is discussed below.) <br />
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If paratenonitis is present, the paratenon is partially excised, and adhesions are released. Areas of symptomatic tendinosis are excised with repair of the residual defect in the Achilles tendon. An alternative for patients with tendinosis who are at increased risk for wound problems or who do not want a large open incision is percutaneous or endoscopic tenotomy. A symptomatic Haglund's deformity or inflamed retrocalcaneal bursa is excised. Augmentation of the Achilles tendon may be considered if debridement threatens the structural integrity of the tendon, in older patients, and in revision surgery (6).<br />
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Complete ruptures in active, athletic persons should be treated operatively in most cases and result in predictably good outcomes. There may be some cases that escape early recognition and require a reconstructive procedure to salvage a potentially severe functional deficit.<br />
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Extracorporeal shock wave therapy, Peritendinous injections and eccentric training decrease neovascularity, relieve pain and improve outcome. Although surgery is the last resort in those patients failing conservative management, it is still unclear how the removal of adhesions and excision of affected tendinopathic areas affects healing and vascularity, or resolves pain.<br />
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<i>Other options commonly taken:</i><br />
US therapy with or without phonophoresis, shoe modification (heel raise) & biomechanical correction through shoe, contrast heat, night splintage in TA stretched position. <br />
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<b>Impact of conservative treatment:</b><br />
<br />
According to Richard PJ (2005) in patient with conservatively managed tendinopathy of the mid-Achilles tendon over 1 year there was a reduction of MRI enhancement and number of vessels on power Doppler, followed by morphological improvements and a reduction in size. Vessels per se related to the abnormal morphology and size of the tendon rather than symptoms. Symptoms improve before the Achilles size reduces and the restoration of normal imaging over time.<br />
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<b>Role of Eccentric exercise</b> in management of posterior heel pain arising out of achilles tendinopathy:<br />
Recently eccentric, but not concentric, exercises have been shown to be highly effective in managing tendinopathy of the Achilles (and other) tendons. The mechanism for the efficacy of these exercises is unknown although it has been speculated that forces generated during eccentric loading are of a greater magnitude. <br />
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All portions of TA suffering achilles tendinopathy do not respond equally to eccentric exercises. Eccentric exercises for the calf muscles have been shown to be effective for chronic non-insertional Achilles tendinopathy (AT). However, the relative effectiveness of various dosages is unknown. Study by Rompe JD et al (2008) found eccentric loading show inferior results to low-energy shock wave therapy in chronic recalcitrant insertional tendinopathy assessed at four months of follow-up. Hence the location of the lesion has a profound effect on efficacy of eccentric exercises. <br />
<i><b><br /></b></i>
<i><b>Dose:</b></i> Relative effectiveness of various dosages of eccentric exercises for AT is still unclear. However, it appears that highly variable compliance rates result in similar positive outcomes (14). <br />
Possible explanation: According to Rees JD et al; oscillations (while eccentrically loaded) provide a mechanism to explain the therapeutic benefit of eccentric loading in Achilles tendinopathy and parallels recent evidence from bone remodelling, where the frequency of the loading cycles is of more significance than the absolute magnitude of the force.<br />
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<b>References: </b></div>
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1. van Dijk CN et al; Knee Surg Sports Traumatol Arthrosc. 2011 May;19(5):835-41. Epub 2011 Jan 11. (Terminology for Achilles tendon related disorders.)<br />
2. Kang S et al; Foot Ankle Int. 2012 Jun;33(6):487-91. (Insertional Achilles tendinitis and Haglund's deformity.)<br />
3. Singh R et al; Foot (Edinb). 2008 Jun;18(2):91-8. Epub 2008 Mar 19. (Diagnostic significance of radiologic measurements in posterior heel pain.)<br />
4. Schepsis AA et al; Am J Sports Med. 2002 Mar-Apr;30(2):287-305. (Achilles tendon disorders in athletes.)<br />
5. Tan SC et al; Disabil Rehabil. 2008;30(20-22):1608-15. doi:10.1080/09638280701792268. (Achilles and patellar tendinopathy: current understanding of pathophysiology and management.)<br />
6. Aronow MS; Clin Podiatr Med Surg. 2005 Jan;22(1):19-43. (Posterior heel pain -retrocalcaneal bursitis, insertional and noninsertional Achilles tendinopathy).<br />
7. Rompe JD et al; Disabil Rehabil. 2008;30(20-22):1666-76. doi: 10.1080/09638280701785825. (Mid-portion Achilles tendinopathy--current options for treatment)<br />
8. McShane JM et al; urr Sports Med Rep. 2007 Oct;6(5):288-92. (Noninsertional Achilles tendinopathy: pathology and management.)<br />
9. Solan M et al; Foot Ankle Clin. 2007 Dec;12(4):597-615, vi. (Management of insertional tendinopathy of the Achilles tendon.)<br />
10. Meyer A et al; Scand J Med Sci Sports. 2009 Oct;19(5):609-15. doi: 10.1111/j.1600-0838.2009.00981.x. Epub 2009 Jul 6. (Eccentric exercise protocols for chronic non-insertional Achilles tendinopathy: how much is enough?)<br />
11. Richards PJ et al; Skeletal Radiol. 2010 Jun;39(6):509-21. doi: 10.1007/s00256-009-0772-0. Epub 2009 Aug 27. (Longitudinal microvascularity in Achilles tendinopathy (power Doppler ultrasound, magnetic resonance imaging time-intensity curves and the Victorian Institute of Sport Assessment-Achilles questionnaire): a pilot study.)<br />
12. Rees JD et al; Br J Sports Med. 2009 Apr;43(4):242-6. doi: 10.1136/bjsm.2008.052910. Epub 2008 Nov 3. (Eccentric exercises; why do they work, what are the problems and how can we improve them?)<br />
13. Rees JD et al; Rheumatology (Oxford). 2008 Oct;47(10):1493-7. doi: 10.1093/rheumatology/ken262. Epub 2008 Jul 22. (The mechanism for efficacy of eccentric loading in Achilles tendon injury; an in vivo study in humans.)<br />
14. Meyer A et al; Scand J Med Sci Sports. 2009 Oct;19(5):609-15. doi: 10.1111/j.1600-0838.2009.00981.x. Epub 2009 Jul 6. (Eccentric exercise protocols for chronic non-insertional Achilles tendinopathy: how much is enough?)<br />
<br />satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-27714139402274363532012-07-18T21:21:00.003+05:302012-07-18T21:21:41.899+05:30Entrapment of medial calcaneal nerve (MCN)<div dir="ltr" style="text-align: left;" trbidi="on">
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<br />Peripheral nerve entrapment is a rare, but important, cause of foot and ankle pain that often is underdiagnosed and mistreated. A peripheral nerve may become entrapped anywhere along its course, but certain anatomic locations are characteristic (2). <br /><br />The medial calcaneal nerve (MCN)<br /><br />The Tibial nerve is called the planter nerve in the sole. The tibial nerve passes to the sole of the foot takes a turn on the medial side of the calcaneum is called MCN. The medial calcaneal nerve arises from tibial nerve of the inner side of the ankle, perforates the laciniate ligament, travels downwards passing below the bony projection on the inner side of the ankle, and supplies the skin over the medial aspect of the heel. Hence it is the most important nerve for heel sensations. MCN have 2 branches. The anterior branch dominate the cutaneous sensation of the anterior part of the medial calcaneal and heel weight loading field, while the posterior branch dominate the sensation of the posterior and median part.<br /><br />How entrapment occurs?<br /><br />
A nerve can become entrapped on its way through the tissue planes. Usually in case of entrapment, the nerve gets compressed between a static and a mobile surface. As the body moves, the nerve is subjected to repeated sliding or friction, leading to compression and trauma. This trauma may damage the outer sheath of the nerve that helps with signal transmission and cause other structural alterations that eventually lead to pain and loss of function.<br /><br />
<i>Causes of MCN entrapment:</i> The medial calcaneal nerve may become entrapped between the tight fascia at the origin of the abductor hallucis muscle and the heel bone (calcaneus). An excessive pronation of the foot may lead to medial calcaneal nerve entrapment. This can occur as a postoperative complication during the release of the lateral plantar nerve branch (4).<br /><br />
S/S of MCN entrapment:<br /><i> </i><br />
<i>Stages of nerve entrapment (2):</i>Clinically, any nerve entrapment is divided into three stages. <br />Stage I: patients feel rest pain and intermittent paresthesias which are worse at night.<br />Stage II: continued nerve compression leads to paresthesias, numbness, and, occasionally, muscle weakness that does not disappear during the day. <br />Stage III: patients describe constant pain, muscle atrophy, and permanent sensory loss. <br /><br />
There is pain and parasthesia (burning or tingling) in the areas supplied by the nerve, that is below the inner bony projection of the ankle and under the heel. The pain usually initiates on the inside of the heel and travels towards the center. Any activity may further aggravate the pain.<br />When the medial calcaneal nerve is trapped the Tinel’s sign is positive. This test is performed by lightly tapping the skin over the nerve, which leads to tingling in the area supplied by the nerve.<br />Medial calcaneal nerve entrapment should not be confused with other causes of heel pain, such as plantar fasciitis and tarsal tunnel syndrome. Accurate diagnosis is important to achieve the desired results.<br /><br />
Palpation of MCN:<br />A thorough understanding of the causes of peripheral nerve entrapment, the anatomic course and variation of the peripheral nerves, the diagnostic modalities, and the treatment options can simplify this complex problem (2).<br />According to Tang et al anatomical position of MCN is relatively constant with 95% accuracy, MCN can be palpated at the following site:<br /><br />MCNs arises from the tibial nerve at 3.3 cm up the horizontal plane of the tip of medial malleolus. They sent out anterior branches and posterior branches from 0.3 cm below the horizontal plane of the tip of medial malleolus on average. <br /><br />
Physical Testing:<br /><br />
Although diagnostic confusion abounds because of the multiple etiologies of peripheral nerve entrapments and their complex physical and temporal relation David Butler’s neural tension testing is very important to assess the reduced mobility of the nerve within the tissue plane. <br /><br />
Electrophysiological testing:<br /><br />Electrodiagnosis is a powerful tool for evaluating lower extremity disorders that stem from the peripheral nervous system. Electrodiagnostic testing can help differentiate neurogenic versus non-neurogenic causes of complaints such as pain, weakness, and paresthesias. It can help practitioners pinpoint the anatomic location and reveal the underlying pathology in peripheral nerve lesions. <br /><br />Treatment:<br /><br />
The first line of treatment includes rest and supportive therapies. Avoid activities that lead to pain; immobilization may also help. Use cold compresses and anti-inflammatory painkillers to reduce the symptoms. Massage or ultrasound therapy is also useful.<br />If rest and conservative treatment fail to eradicate the symptoms, surgical decompression of the nerve may be required. Surgical treatment usually produces good results.<br /><br />
Author’s comment:<br /><br />Try Butler’s nerve gliding exercises & Neurodynamic techniques. I have personally tried alternative digital compression-relaxation at the site where the nerve takes a sharp angulation at heel with varied success rates but it is worth trying. <br /><br /><b style="color: blue;">References:</b><br style="color: blue;" /><span style="color: blue;">1. Tang J et al; Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2010 Apr;35(4):386-9. (Anatomic characteristics and clinic significance of the medial calcaneal nerve).</span><br style="color: blue;" /><span style="color: blue;">[Article in Chinese]</span><br style="color: blue;" /><span style="color: blue;">2. Hirose CB et al; Foot Ankle Clin. 2004 Jun;9(2):255-69. (Peripheral nerve entrapments).</span><br style="color: blue;" /><span style="color: blue;">3. Roy PC; Foot Ankle Clin. 2011 Jun;16(2):225-42. (Electrodiagnostic evaluation of lower extremity neurogenic problems).</span><br style="color: blue;" /><span style="color: blue;">4. http://docpods.com/medial-calcaneal-nerve-entrapment</span><br style="color: blue;" /><br /><br /><br /><br /><br />
</div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-68384317287105542102012-07-05T20:43:00.000+05:302012-07-05T20:43:07.772+05:30Planter heel pain: planter fascitis, Fat pad atrophy, combined PF & FPA.<div dir="ltr" style="text-align: left;" trbidi="on">
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<i style="color: blue;">What the following article is on?</i>Discussion on 3 conditions with mostly similar symptom of planter heel pain.<br /><br />Synonyms of planter heel pain: Subcalcaneal heal pain, calcaneodynia etc. <br />Synonyms of Planter fascitis: Planter fasciosis, Planter fasciopathy etc. <br /><br />
Planter foot pain is seemingly the most innocuous yet significant morbid condition affecting the adults hampering their ADLs & QOL. According to a recent research paper (1) Plantar heel pain can be provoked by PF (Planter fascitis), FPA (Fat pad atrophy), combination of PF + FPA and other causes. Patients with PF or FPA typically show different characteristics in clinical features but overall may look quite similar. Plantar heel pain requires differential diagnosis for appropriate treatment.<br />DD of planter foot pain includes following:<br /><br /><i>Planter heel pain can be sub-divided in to neural & non-neural pain. The non-neural pain can again be sub-divided into 2 bony & soft tissue pains.</i><br /><b>Bony pathology: </b>Calcaneal stress fracture, apophysitis of the calcaneus (Sever's disease), osteomyelitis, or inflammatory arthropathy. <br /><br /><b>Soft tissue pathology:</b> Fat pad atrophy (FPA) or contusion, plantar fascia rupture and plantar fasciitis (PF). <br /><br /><b>Neural pathology:</b> Entrapment or compression of the first branch of the lateral plantar nerve (Baxter's nerve), medial calcaneal branch of posterior tibial nerve, or nerve to abductor digiti quinti muscle. <br /><br />Other neural causes include S1 radiculopathy, tarsal tunnel syndrome, and peripheral neuropathy.<br /><br />Many times planter foot pain is due to combination of different pathologies coexisting together. For example it is reported that Planter fascitis & fat pad atrophy coexist to produce planter foot pain. Similarly Labib et al described the heel pain triad (HPT). HPT is a combination of plantar fasciitis, posterior tibial tendon dysfunction and tarsal tunnel syndrome.<br /><br />We are going to discuss S/S of 2 different pathologies with similar presentation and they often coexists. <br /><br /><b>A. Planter fascitis (PF):</b>According to Buchbinder (5) PF is reported to be the most common cause of plantar heel pain. The peak age is between (40-60) years. <br /><br />Pathology of PF(6): <br />The pathology is still unknown.<br />Histopathologic examination of biopsy specimens from patients undergoing excessive extension or microinjuries of the plantar fascia shows secondary degenerative changes in the plantar fascia, with or without fibroblastic proliferation, and without acute inflammation.<br />However there is aging caused physiological changes are thought leading to PF. There is increased stress on the calcaneus and plantar fascia due to of loss of buffering tissue such as water and collagen of the fat pad.<br /><br />Risk factors for PF:<br />1. running excessively (or suddenly increasing running distance) <br />2. occupations that involve long periods of standing <br />3. pes planus <br />4. limited ankle dorsiflexion<br />5. obesity<br /><br /><i>Basis of clinical diagnosis:</i>1. Pain characteristics: first-step morning pain and relief of pain after walking (most significant finding). Medial calcaneal tuberosity pain must be view is association with morning 1st step pain to diagnose PF. Unilateral pain is more common than bilateral.<br />2. Association with abnormal foot biomechanics: TA tightness & Limited ankle DF is most commonly associated with PF. Both pes planus & Cavus are associated with PF however Pes palnus is more associated with PF than pes cavus.<br />Explanation of association of pes planus & TA tightness with PF:<br />Limited ankle dorsiflexion on the involved side significantly increased the risk of PF. According to Inman et al (7) approximately 10 degrees of ankle dorsiflexion with the knee extended is required during a normal gait. If the Achilles tendon is shortened, limiting ankle dorsiflexion, excessive pronation of the foot may occur to compensate for this limitation. Greater the limitation in ankle dorsiflexion, the more load on the plantar fascia. Excessive pronation of the foot increases tensile loads on the plantar aponeurosis.<br />Hence repetitive pronatory stress that increases tensile force on the plantar fascia causing the plantar arch to lower is the cause of PF. The pronatory effect increases with age, and is related to limited ankle dorsiflexion caused by decreased elasticity of the tendons, and the reduced range of motion that occurs with age.<br />Digiovanni et al (8) reported relief or absence of plantar heel pain in 52% of patients participating in exercises to stretch the plantar fascia, and 22% after stretching the Achilles tendon. This provides a good target for treatment. <br />3. Heel spur: Heel spur is a common incidental finding in PF than FPA. <br />Diagnosis on the basis of US scanning:<br />Hypoechoic fusiform-shaped swelling more than 4 mm in thickness at the origin of the plantar fascia.<br /><br /><b>B. Fat pad atrophy (FPA):</b>There is loss of buffering tissue such as water and collagen of the fat pad under the heel mostly due to age. The fat pad atrophies and shock absorbency diminishes in subjects that were older than 40 years. Yi et al (1) used the following criteria to diagnose FPA. FPA is said to the causing planter heel pain if more than 3 of the following criteria are present:<br />1. pain at heel center or margin <br />2. worsening pain when barefoot <br />3. worsening pain after a long period of standing <br />4. palpable calcaneus <br />In addition to the above following US scan finding: when the patient had a fat pad that was less than 3 mm in thickness.<br /><br />S/S: <br />1. B/L pain is common than U/L.<br />2. Pain characteristics: <br />a. aching pain (commonest) but also tingling, cold (5.4%) and burning sensations. (highest to lowest in that order)<br />b. pain after a long walk, pain at night and resting pain (highest to lowest in that order).<br />3. Both pes planus & cavus are associated with FPA. <br />4. Risk factors of FPA: B/L pain which get more severe with prolonged standing is likely to be caused by FPA.<br /><br /><b>C. PF+FPA (PFFPA): </b> PF and FPA may share very similar symptoms and are difficult to distinguish from one another further it has been seen. PF can be co-morbid with FPA. PFFPA shares features common to both PF & FPA. In case of mixed characteristics of PF and FPA, PFFPA should be considered first and ultrasonography should be used as an key diagnostic tool.<br /><br /><b>Treatment options:</b><br />
It is imperative to diagnose correctly among seemingly similar S/S in planter foot pain. Many FPA & PFFPA cases are misdiagnosed as having PF and treated with conservative therapy including local steroid injection. In cases treated with steroid to PF there are reports of planter fascia rapture in running, hence it is cautioned to diagnose correctly & treat aptly. <br />Though many surgical options are available including minimal invasive techniques, there are myriad non-surgical techniques available. Nevertheless, nonsurgical management of plantar fascitis (a predominate cause of planter heel pain) is successful in approximately 90% of patients (2). The options in physical medicinesfor planter heel pain includes: rest, massage, nonsteroidal anti-inflammatory drugs, night splints, heel cups/pads, custom and off-the-shelf orthoses, injections, casts, and physical therapy measures such as shock wave therapy (2). Stretching exercises of the plantar fascia and Achilles tendon can also relieved pain (1). In many studies standing TA stretching is compared with stretching through a prefabricated night splint. Findings suggest that stretching through a prefabricated night splint is a very good option in managing planter foot pain from PF that also is claimed to speeding up the time to recover (4). Heel cushions, heel cups, or low-dye taping can be applied to relieve the pressure on the calcaneus of FPA patients. In those involved in sports correction of training errors and orthotics are essential components in any treatment program (3).<br />Surgical treatment should be considered in only a small subset of patients with persistent, severe symptoms refractory to nonsurgical intervention for at least 6 to 12 months (2).<br /><br />
<b style="color: blue;">References:</b><br style="color: blue;" /><span style="color: blue;">1. Yi TI et al; Ann Rehabil Med. 2011 Aug;35(4):507-13. Epub 2011 Aug 31. Clinical characteristics of the causes of plantar heel pain.</span><br style="color: blue;" /><span style="color: blue;">2. Neufeld SK et al; J Am Acad Orthop Surg. 2008 Jun;16(6):338-46. Plantar fasciitis: evaluation and treatment.</span><br style="color: blue;" /><span style="color: blue;">3. Ryan J; Am Fam Physician. 1995 Sep 1;52(3):891-8, 901-2. Use of posterior night splints in the treatment of plantar fasciitis.</span><br style="color: blue;" /><span style="color: blue;">4. Barry LD et al; J Foot Ankle Surg. 2002 Jul-Aug;41(4):221-7. (A retrospective study of standing gastrocnemius-soleus stretching versus night splinting in the treatment of plantar fasciitis.</span><br style="color: blue;" /><span style="color: blue;">5. Buchbinder R. Clinical practice. Plantar fasciitis. N Engl J Med. 2004;350:2159–2166. </span><br style="color: blue;" /><span style="color: blue;">6. Lemont H, Ammirati KM, Usen N. Plantar fasciitis: a degenerative process (fasciosis) without inflammation. J Am Podiatr Med Assoc. 2003;93:234–237.</span><br style="color: blue;" /><span style="color: blue;">7. Inman VT, Ralston HJ, Todd F. Human walking. 2nd ed. Baltimore: Williams & Wilkins; 1994. pp. 45–72.</span><br style="color: blue;" /><span style="color: blue;">8. Digiovanni BF, Nawoczenski DA, Malay DP, Graci PA, Williams TT, Wilding GE, Baumhauer JF. Plantar fascia-specific stretching exercise improves outcomes in patients with chronic plantar fasciitis. A prospective clinical trial with two-year follow-up. J Bone Joint Surg. 2006;88:1775–1781. [PubMed]</span><br style="color: blue;" /><br /></div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-75675426111108771622012-05-26T13:01:00.004+05:302012-05-26T13:01:49.459+05:30Ulnar wrist pain: TFCC injury & DD of Ulnar sided wrist pain<div dir="ltr" style="text-align: left;" trbidi="on">
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<br /><br />Many ulnar wrist pains are obscure & according to Bottke both surgical exploration and nonoperative treatment have been less than satisfying. Most of the times specific physical examination and standard radiographs were unrevealing in these cases. Even with specific diagnostics test such as arthroscopy, treatment results could not be correlated with arthrographic findings (1). <br /><br /><b>Ulnar wrist pain,Distal RUJ & TFCC: </b><br />
The distal radioulnar joint (DRUJ) acts in concert with the proximal radioulnar joint to control forearm rotation. The DRUJ is stabilized by the triangular fibrocartilage complex (TFCC). This complex of fibrocartilage and ligaments support the joint through its arc of rotation, as well as provide a smooth surface for the ulnar side of the carpus. TFCC and DRUJ injuries are part of the common pattern of injuries we see with distal radius fractures. While much attention has been paid to the treatment of the distal radius fractures, many of the poor outcomes are due to untreated or unrecognized injuries to the DRUJ and its components (2).<br />Triangular fibrocartilage complex (TFCC) tears are a common source of ulnar sided wrist pain. Originally described by Palmer, in 1981, as a complex of several structures, our understanding of the anatomy and the function of the TFCC has been refined by histologic studies. The TFCC plays an important role in load bearing across the wrist as well as in distal radioulnar joint (DRUJ) stabilization. A thorough knowledge of the anatomy as well as the Palmer classification system helps to guide treatment options (3).<br /><br />
<b>Palmer’s Classifications of TFCC Lesions (4)</b><br />
Class 1: Traumatic<br />A. Central perforation<br /><br />B. Ulnar avulsion <br /><br />- With styloid fracture<br />- Without styloid fracture<br /><br />C. Distal Avulsion (from carpus)<br /><br />D. Radial avulsion <br /><br />- With sigmoid notch fracture<br />- Without sigmoid notch fracture<br /><br />Class 2: Degenerative (Ulnar Impaction Syndrome)<br />A. TFCC wear<br /><br />B. TFCC wear <br /><br />+ lunate and/or ulnar head chondromalacia<br /><br />C. TFCC perforation <br /><br />+ lunate and/or ulnar head chondromalacia<br /><br />D. TFCC perforation <br /><br />+ lunate and/or ulnar head chondromalacia<br />+ lunotriquetral ligament perforation<br /><br />E. TFCC perforation <br /><br />+ lunate and/or ulnar head chondromalacia<br />+ lunotriquetral ligament perforation<br />+ Ulnocarpal arthritis<br /><br />
For further reading on TFCC readers are directed to: (5)<br />http://en.wikipedia.org/wiki/Triangular_fibrocartilage. <br /><br />
<b>Differential diagnosis of Ulnar sided wrist pain (6):</b><br />
1. TFCC injury: <br />S/S: 1. Ulnar wrist pain 2. Snapping or clicking <br />Physical Tests: 1. TFCC compression test 2. Piano key sign 3. Supination lift test 4. Palpation <br /><br />
2. Lunotriquetral Interosseous Ligament (LTIL) Injury:<br />S/S: 1. Joint tenderness 2. Decreased ROM 3. Decreased grip strength 4. Painful clunk with radial & ulnar deviation <br />Physical Tests: 1. Ballottement test 2. Shuck test 3. Shear test 4. Ulnar snuffbox test<br /><br />
3. Arthritis (DRUJ /Pisotriquetral): <br />S/S: 1. Pain & crepitus with loading 2. Decreased ROM 3. Decreased grip strength 4. Localized pain <br />Physical Tests: 1. Grind tests 2. Palpation of joint lines 3. Ballottement tests 4. ROM<br /><br />
4. DRUJ Instability: <br />S/S: 1. Pain with forearm rotation <br />Physical Tests: 1. Grind tests 2. Palpation <br /><br />
5. ECU Pathology: <br />S/S: 1. Pain specific to ECU tendon 2. ECU subluxation <br />Physical Tests: 1. Palpation of ECU tendon over ulnar head 2. Resisted wrist extension & ulnar deviation 3. Active forearm supination & ulnar deviation<br /><br />
6. Fracture (Ulnar styloid, Triquetrum, Hamate): <br />S/S: 1. Tenderness & edema 2. Decreased ROM 3. Decreased wrist strength 4. Pain with motion <br /><br />Physical Tests: 1. Palpation of bony landmarks 2. DRUJ stability (ulnar styloid) 3. Resisted 5th digit flexion (hamate)<br /><br />7. Midcarpal Instability: <br /><br />S/S: 1. Midcarpal clunk with ulnar deviation & pronation 2. Volar sag at ulnar wrist 3. Often bilateral <br /><br />Physical Tests: 1. Mid carpal shift test<br /><br />8. Kienbock's Disease: <br /><br />S/S: 1. Chronic wrist pain without trauma 2. Tender dorsal lunate 3. Decrease ROM 4. Decreased grip strength 5. Arthritis (late stage) <br /><br />Physical Tests: 1. Palpation of Lunate<br /><br />9. Ulnar Nerve Entrapment: <br /><br />S/S: 1. Paresthesia to 4th & 5th digits 2. Hand intrinsic weakness <br /><br />Physical Tests: 1. Tinel's to Guyon's Canal 2. History/pattern of symptoms <br /><br /><br />10. Ulnar Artery Thrombosis: <br /><br />S/S: 1. Night pain 2. Pain with repetitive activity 3. Cold intolerance 4. Exquisite tenderness at site of pathology 5. Dependent rubor or ulceration or 4th or 5th fingertips 6. Sympathetic fiber excitation of ulnar proper digital nerves <br /><br />Physical Tests: 1. Allen test.<br /><br />11. Dorsal Ulnar Cutaneous Nerve Neuritis <br /><br />S/S: 1. Sensory changes to 4th & 5th digits 2. Pain or sensory changes at elbow and/or hand weakness, indicative of more proximal ulnar nerve pathology . <br />Physical Tests: 1. Sensory exam 2. Palpation 3. Wartenburg sign (motor pathology) 4. Froment sign (motor pathology) <br /><br /><b>Comments on DD of TFCC:</b><br />
N.B. Acute trauma to the triangular fibrocartilage complex includes tears of the fibrocartilage articular disk substance and meniscal homolog as well as radioulnar ligament avulsions, with or without an associated fracture (7).<br />The critical distinction is in differentiating injuries that produce instability of the distal radioulnar joint from those that do not. Also important is the recognition of acute injuries in the context of an ongoing degenerative pattern (ie, Palmer class 2 lesions) (7). Subluxation of the ulnar head relative to the sigmoid notch of the radius, as assessed by MRI with the wrist in pronation, is a predictor of tears of the foveal attachment of the TFCC (8). Horizontal tear and fibrillation of TFCC disk without TFCC tear at the radiocarpal joint present with ulnar-sided wrist pain due to isolated triangular fibrocartilage complex. Arthroscopic debridement only relieves pain after surgery and helps in achieving good functional recovery (9).<br /><br /><b>Evaluation: </b><br />
Patient evaluation includes clinical examination, imaging studies, and wrist arthroscopy (diagnostic). The Palmer classification is typically used to define injuries to the triangular fibrocartilage complex (10). <br /><br />
<b>TFCC management outline: </b><br />
Both surgical & Non-surgical therapies have claimed success. Nonsurgical management includes temporary splint immobilization of the wrist and forearm, oral nonsteroidal anti-inflammatory medication, corticosteroid joint injection, and physical therapy. Surgical strategies include débridement, acute repair, and subacute repair. Most surgical procedures can be performed arthroscopically. However, open ligament repair may be needed in the setting of distal radioulnar joint instability.<br /><br />
<b>Comments of the author: </b>Manual therapy: Many cases of mild-moderate ulnar sided wrist pain can be helped by MWM technique of Mulligan i.e. Medial glide to intercalar segment with wrist F/E. <br /><br />
<b style="color: blue;">References:</b><span style="color: blue;"> </span><br style="color: blue;" /><span style="color: blue;">1. Bottke CA et al; Orthopedics. 1989 Aug;12(8):1075-9. Diagnosis and treatment of obscure ulnar-sided wrist pain.</span><br style="color: blue;" /><br style="color: blue;" /><span style="color: blue;">2. Tsai PC et al; Bull NYU Hosp Jt Dis. 2009;67(1):90-6. The distal radioulnar joint.</span><br style="color: blue;" /><br style="color: blue;" /><span style="color: blue;">3. Ahn AK et al;Bull NYU Hosp Jt Dis. 2006;64(3-4):114-8. Triangular fibrocartilage complex tears: a review.</span><br style="color: blue;" /><br style="color: blue;" /><span style="color: blue;">4. Green’s operative hand surgery, fifth edition, Distal radioulnar joint instability, blz: 613-616 </span><br style="color: blue;" /><br style="color: blue;" /><span style="color: blue;">5. http://en.wikipedia.org/wiki/Triangular_fibrocartilage</span><br style="color: blue;" /><br style="color: blue;" /><span style="color: blue;">6. http://www.physio-pedia.com/Ulnar_Impaction_Syndrome</span><br style="color: blue;" /><br style="color: blue;" /><br style="color: blue;" /><span style="color: blue;">7. Henry MH; J Am Acad Orthop Surg. 2008 Jun;16(6):320-9. Management of acute triangular fibrocartilage complex injury of the wrist.</span><br style="color: blue;" /><br style="color: blue;" /><span style="color: blue;">8. Ehman EC et al; J Hand Surg Am. 2011 Nov;36(11):1780-4. Subluxation of the distal radioulnar joint as a predictor of foveal triangular fibrocartilage complex tears.</span><br style="color: blue;" /><br style="color: blue;" /><span style="color: blue;">9. Abe Y et al; Hand Surg. 2011;16(2):177-80. Ulnar-sided wrist pain due to isolated disk tear of triangular fibrocartilage complex within the distal radioulnar joint: two case reports.</span><br style="color: blue;" /><br style="color: blue;" /><span style="color: blue;">10. Henry MH; J Am Acad Orthop Surg. 2008 Jun;16(6):320-9. Management of acute triangular fibrocartilage complex injury of the wrist.</span><br style="color: blue;" /><br style="color: blue;" /><br style="color: blue;" /></div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com1tag:blogger.com,1999:blog-59305263331406079.post-1296305071728448882012-05-10T17:27:00.005+05:302012-05-10T17:31:20.521+05:30Differential diagnosis of Anatomic (Radial) snuffbox pain: It is not always DeQuervain’s tenosynovitis.<div dir="ltr" style="text-align: left;" trbidi="on">
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<b>Tendon, Bone & Ligament causes: </b><br />
1. DeQuervain’s tenosynovitis:<br />
Swelling of tendon of APL (Abductor pollicis longus) & extensor pollicis brevis at lateral wrist near anatomic snuff box. The primary complaint is radial sided wrist pain that radiates up the forearm with grasping or extension of the thumb. The pain has been described as a “constant aching, burning, pulling sensation." Pain is often aggravated by repetitive lifting, gripping, or twisting motions of the hand. Swelling in the anatomical snuff box, tenderness at the radial styloid process, decreased CMC abduction ROM of the 1st digit, palpable thickening of the extensor sheaths of the 1st dorsal compartment and crepitus of the tendons moving from the extensor sheath may be found upon examination. Other possible findings include weakness and paresthesia in the hand. Finkelstein’s diagnostic test will present positive provoking the patient’s symptoms.<br />
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If left untreated, the inflammation and progressive narrowing (stenosis) can cause scarring that further limits thumb motion. <br />
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2. Carpal Instabilities:<br />
Altered biomechanics of the wrist may produce pain. Scapholunate disassociation, scapho-trapezio-trapezoidal joint degeneratioin, and lunatotriquetral dissociation could all present with radial sided wrist pain.<br />
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3. Scaphoid Fracture<br />
A scaphoid fracture commonly present with radial sided wrist pain, tenderness and possible swelling in the anatomical snuff box, and limited ROM with pain especially at end ranges. <br />
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4. Osteoarthritis of the 1st CMC<br />
Osteoarthritis of the 1st CMC typically occurs in individuals greater than 50 years old, and will most frequently present with morning stiffness of the 1st CMC joint, a general decrease in ROM of the joint, tenderness along the joint line, and a positive grind test.<br />
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<b>Neural Causes: </b><br />
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1. Cheiralgia paresthetica:<br />
Cheiralgia paresthetica is commonly referred to as handcuff neuropathy. It is a neuropathy of the hand generally caused by compression or trauma to the superficial branch of the radial nerve.<br />
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The area affected is typically on the back or side of the hand at the base of the thumb, near the anatomical snuffbox, but may extend up the back of the thumb and index finger and across the back of the hand. /S includesnumbness, tingling, burning or pain. Since the nerve branch is sensory there is no motor impairment.<br />
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Differentiating point: It may be distinguished from de Quervain syndrome because it is not dependent on motion of the hand or fingers. <br />
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2. C6 Cervical Radiculopahy:<br />
Compression on a spinal nerve root can cause sensory disturbances, myotomal weakness, and diminished reflexes throughout the root's distribution. The dermatomal key point for the C6 nerve root is the radial aspect of the 2nd metacarpal and index finger which is close to the area of pain experienced with De Quervain’s. Since a radiculopathy can present much like De Quervain’s a thorough screen of the cervical spine is necessary.<br />
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<br /></div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-90066732070757011462012-04-28T20:43:00.003+05:302012-04-28T20:48:24.780+05:30Carpal instability: Types, Place of VISI & DISI<div dir="ltr" style="text-align: left;" trbidi="on">
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<b><i>Key word: Carpal instability, Data base: Pubmed</i></b><br />
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<b>Wrist anatomy- extrinsic & and intrinsic ligaments</b><br />
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The extrinsic (radiocarpal) and intrinsic (intercarpal) ligaments maintain carpal stability. The major extrinsic ligaments are the radioscaphocapitate, radiolunotriquetral, short radiolunate, and dorsal radiocarpal ligaments. The scapholunate and lunotriquetral ligaments are the most important intrinsic ligaments and the primary wrist stabilizers. The most common causes of carpal instability are unstable fracture of the scaphoid, scapholunate dissociation, and lunotriquetral dissociation (7). <br />
Let us discuss the causes of carpal instability. Classification of carpal instability is presented below is based on anatomic and kinematic characteristics of the wrist. A classification of the subtle patterns of carpal instability is presented below. </div>
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<b>Navarro's concept of the carpus (1921): </b><br />
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Carpals of wrist are arranged in 3 vertical longitudinal columns: lateral (scaphoid); central (lunate and distal carpal row); medial (triquetrum).</div>
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<i>Carpal dislocation occurs between:</i><br />
1. lateral and central columns- called lateral instability <br />
2. within the central column- called central instability <br />
3. central column and the triquetrum- called medial instability and <br />
4. between the entire carpus and the distal radioulnar articular surface- is called proximal instability</div>
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<b>Classification of lateral instability: </b>Lateral carpal instabilities are further subdivided according to the different components of the central column that articulate with the scaphoid. Therefore, 3 main lateral patterns may be identified:<br />
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1. scaphoid-trapezium-trapezoid subluxation <br />
2. scaphoid-capitate diastasis<br />
3. scaphoid-lunate dissociation (rotatory subluxation of the scaphoid)</div>
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<b>Classification of medial instability: </b>Medical carpal instability may take place between the triquetrum and the lunate, or the triquetrum and the hamate. Dissociation between lunate and triquetrum results in static forms of instability, while disruption of triquetrohamate support leads to dynamic forms of instability.</div>
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<b>VISI (volar-flexed intercalated segment instability):</b> It is example of medial instability. In lunate-triquetrum instability, is believed responsible for VISI in which the lunate collapses into a volar-flexed position and there is longitudinal "crumpling" of the radiocarpal link.</div>
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<b>Proximal instability:</b><br />
Proximal carpal instability may lead to disruption at the level of the radiocarpal joint or at the level of the midcarpal joint. Proximal carpal or radiocarpal instability may occur in an ulnar (ulnar translocation), dorsal (dorsal subluxation), or volar direction (volar subluxation). It is usually associated with loss of the anatomic alignment of the distal radius.</div>
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<b><br />Exclusive discussions on VISI & DISI:</b><br />
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Navarro’s carpus concept can be called column concept. But "The row concept best explains the behaviour of the carpal bones. 8 carpals comprising of 2 row of 4 carpals each. The proximal row acts as an intercalated segment- there is no direct control of this row. It is controlled by the bones surrounding it via the short interosseous ligaments. It has a natural tendency if isolated to 'pop out' and tilt dorsally."<br />
Intercalated segment: The intercalated segment is the proximal carpal row identified by the lunate. The term 'intercalated segment' refers to it being the part in between the proximal segment of the wrist consisting of the radius and the ulna and the distal segment, represented by the distal carpal row and the metacarpals.</div>
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<b>DISI:</b> DISI, or dorsiflexion instability, the lunate is angulated dorsally. It is the most frequent mid carpal instability. It occurs due to complete tear of scapho-lunate ligament. </div>
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DISI pattern:<br />
1. when the scapholunate joint is dissociated, the scaphoid is palmar flexed and the lunate is dorsiflexed<br />
2. Scapho-lunate angle usually 30- 60degrees (average 46 degrees) and with DISI it is greater than 70degrees </div>
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What you look in lateral wrist X-ray if you suspect DISI: If you think the lunate is tilted, measure the scapholunate angle ( 30-60°is normal, 60-80°is questionably abnormal, >80° is abnormal) and the capitolunate angle (<30° is normal).</div>
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<i>What you look in AP wrist X-ray if you suspect DISI:</i> Guilula’ arc.</div>
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<b>VISI:</b> It is a palmar flexion instability where the lunate is tilted palmarly too much. While most DISI is abnormal, in many cases VISI is a normal variant, especially if the wrist is very lax. It occurs due to complete tear of lunotriquetral ligament. There is posterior subluxation of both lunate & scaphoid due to lack of union with triquetrum. Scaphoid & Lunate remain interdependent hence the scapho-lunate angle is normal. </div>
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VISI pattern:<br />
1. lunate palmar flexed<br />
2. if the lunate and triquetrum can be seen, the normal lunotriquetral angle of approximately -16 degrees becomes neutral or positive</div>
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<i>Note:</i> in conventional radiography: According to Toms et al (8) Conventional radiographic abnormalities are usually limited to volar intercalated segment instability (VISI) patterns of carpal alignment and are not specific.</div>
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<b>Mid carpal instability:</b><br />
Midcarpal instability (MCI) is the result of complex abnormal carpal motion at the midcarpal joint of the wrist. <br />
Palmar, dorsal, ulnar midcarpal instability, and capitolunate or chronic capitolunate instability are all descriptions of types of MCI with often overlapping features.<br />
It is a form of non-dissociative carpal instability (CIND) (see below for dissociative & non- dissociative carpal instability) and can be caused by various combinations of extrinsic ligament injuries that then result in one of several subtypes of MCI.<br />
Palmar midcarpal instability (PMCI) is the most commonly reported type of MCI. It has been described as resulting from deficiencies in the ulna limb of the palmar arcuate ligament (triquetrohamate-capitate) or the dorsal radiotriquetral ligaments, or both.</div>
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<b>Another broad classification of carpal instability:</b>Dissociative & non- dissociative carpal instability. </div>
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The causes of carpal instability are dissociation of the intercarpal ligaments on either side of the lunate, are so-called scapholunate dissociation or a luno-triquetral dissociation. Carpal instability non-dissociative is generally due to a laxity or attenuation of the intrinsic ligaments of the carpus and are associated with deformity of the distal radius (6).<br />
Ulnar translation of the carpus on the distal radioulnar articular surfaces occurs with shear stretching of the origins of the radiocarpal ligaments. The radial styloid attenuation of the ligaments may result in abnormal motions of the carpal bones going from ulnar to radial deviation at which time a catch-up click may occur (6).</div>
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<b>Radiography choices in carpal instability (8):</b><br />
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1. Stress view radiographs (To demonstrate carpal instability) <br />
2. Videofluoroscopy (To demonstrate abnormal carpal kinematics) <br />
3. Dynamic US can be also used to demonstrate midcarpal dyskinesia including the characteristic triquetral "catch-up" clunk. <br />
4. Tears of the extrinsic ligaments can be demonstrated with MR arthrography, and probably with CT arthrography.</div>
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<b>Treatment approach:</b><br />
Plan of management for carpal dislocations are based upon the following basic criteria: whether the dislocation is perilunate or lunate dislocation. In most cases they are managed identically (5).<br />
Step 1: In all cases anatomic restoration of the 3 key elements (scaphoid, lunate, and capitate) is essential. <br />
Step 2: Following initial closed reduction, rotary subluxation of the scaphoid and intercalary segment instability must be specifically looked for and corrected in the patient with perilunate or lunate dislocation without fracture of the scaphoid. <br />
Failure to obtain or maintain anatomic position by closed methods is an indication for open reduction and internal fixation.<br />
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<b><i>Operative methods & choices:</i></b><br />
1. Unstable carpal articulations can be treated with limited carpal arthrodesis.<br />
2. Ligamentous defects can be treated with capsulorrhaphy or ligament reconstruction.</div>
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<b>Complications:</b>As with all ligamentous injuries, early diagnosis and treatment are essential. Missing the concomitant injuries include median nerve damage, osteochondral fractures of the carpal bones, and fracture of the radial styloid. Pain & Post-op stiffness are a usual complications. </div>
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<b style="color: blue;">References:</b><span style="color: blue;"> </span><br />
<span style="color: blue;">1. Taleisnik J; Clin Orthop Relat Res. 1980 Jun;(149):73-82. (Post-traumatic carpal instability).</span><br />
<span style="color: blue;">2. http://www.wikiradiography.com</span><br />
<span style="color: blue;">3. LK Ruby; The Journal of Hand Surgery. Volume 13, Issue 1, January 1988, Pages 1–10 (Relative motion of selected carpal bones: A kinematic analysis of the normal wrist)</span><br />
<span style="color: blue;">4. Taleisnik J; Bull Hosp Jt Dis Orthop Inst. 1984 Fall;44(2):511-31.</span><br />
<span style="color: blue;">5. Green DP; Clin Orthop Relat Res. 1980 Jun;(149):55-72. (Classification and management of carpal dislocations).</span><br />
<span style="color: blue;">6. Linscheid RL et al;Orthopade. 1993 Feb;22(1):72-8. (Carpal instability).</span><br />
<span style="color: blue;">7. Timins ME et al; Radiographics. 1995 May;15(3):575-87. (MR imaging of the major carpal stabilizing ligaments: normal anatomy and clinical examples).</span><br />
<span style="color: blue;">8. Toms AP; Skeletal Radiol. 2011 May;40(5):533-41. Epub 2010 May 14. (Midcarpal instability: a radiological perspective).</span><br />
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</div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-10519085151203043632012-03-12T12:14:00.004+05:302012-03-12T12:14:58.060+05:30LASER therapy in physiotherapy<div dir="ltr" style="text-align: left;" trbidi="on">
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<b>Synonyms:</b> <br />• Therapeutic Laser<br />• Low Level Laser Therapy<br />• Low Power Laser Therapy<br />• Low Level Laser<br />• Low Power Laser<br />• Low-energy Laser<br />• Soft Laser<br />• Low-reactive-level Laser <br />• Low-intensity-level Laser<br />• Photobiostimulation Laser<br />• Photobiomodulation Laser<br />• Mid-Laser<br />• Medical Laser<br />• Biostimulating Laser<br />• Bioregulating Laser<br /><br /><b>4 categories of lasers</b><br />– Crystal & Glass (solid - rod)<br />• Synthetic ruby & others (synthetic ensures purity)<br /><br />– Gas (chamber) – 1961<br />• HeNe, argon, CO2, & others <br /><br />– Semiconductor (diode - channel) - 1962<br />• Gallium Arsenide (GaAs under investigation)<br /><br />– Liquid (Dye) - Organic dyes as lasing medium<br /><br />– Chemical – extremely high powered, frequently used for military purposes<br /><br /><b>Types of laser:</b><br /><br />Lasers are of 3 different type soft laser, mid laser, power laser. Soft lasers are used for dermatological purposes where depth of penetration is only superficial, Physiotherapy lasers are mid lasers where depth of penetration is from .5-2cm for class III lasers up to 10 cm in type IV lasers. Power lasers are destructive lasers used in different medical & dental surgery. <br />There are 4 different classes of laser i.e. Class I-IV. All 4 class are used in physiotherapy. However class I-III lasers are commonly used. Class IV physiotherapy & surgical lasers are not to be confused with each other.<br /><br /><b>Class of lasers:</b><br /><br />Class I: Low power lasers<br />Class II: Power out put up to 1mW (400-700 nm wavelength).<br />Class IIIa: Power out put up to 5mW.<br />Class IIIb: Power out put up to 5-500mW.<br />Class IV: Power out put up to 500-7500mW.<br /><br />* All lasers can cause eye damage except Class I laser. As the power increases the potential of causing eye damage is more. <br /><br />* Class III lasers are also known as LLLT i.e. low level laser therapy.<br /><br />* Class IV lasers are also known as high power laser therapy. <br /><br />* High-power lasers (class IV) have power output of up to 7,500 mW; and supposedly offer more power, deeper penetration (can penetrate up to 10 cm instead of 0.5 to 2.0 cm for class III lasers) and a larger surface treatment area (cover up to 77 cm2 instead of 0.3 to 5.0 cm2 for class III lasers) <br /><br /><b>Modes of Laser:</b><br /><br />Either it is continuous or Pulsed. In pulsed laser frequency is a key area for therapeutic efficiency.<br /><br /><i>Why red or IR lasers are used?</i><br />• Red light affects all cell types<br />– Absorbed by the mitochondrial present in all cells<br />– Cytochromes (respiratory chain enzymes) within the mitochondria have been identified as the primary biostimulation chromophores (primary light-absorbing molecules). <br />– Since enzymes are catalysts with the capability of processing thousands of substrate molecules, they provide amplification of initiation of a biological response with light. <br /><br />• <i> Infrared light </i>is more selective absorbed by specific proteins in the cell membrane & affects permeability directly<br /><br /><b>Tissue response:</b><br /><br />• Magnitude of tissue’s reaction are based on physical characteristics of:<br />– Output wavelength/frequency<br />– Density of power<br />– Duration of treatment<br />– Vascularity of target tissues<br /><br />• <i>Direct effect -</i> occurs from absorption of photons <br />• <i>Indirect effect – </i>produced by chemical events caused by interaction of photons emitted from laser & the tissues<br /><br /><b>Patient & Laser parameters:</b><br /><br />• Patient parameters<br />– Need medical history & proper diagnosis<br />• Diabetes – may alter clinical efficacy<br />– Medications <br />• Photosensitivity (antibiotics)<br />– Pigmentation<br />• Dark skin absorbs light energy better<br />
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<b> Laser Parameters</b><br />
<br />– Wavelength<br />– Output power<br />– Average power <br />– Intensity<br />– Dosage<br /><b><br />Laser Wavelength:</b> This is measured in Nanometers (nm). Longer wavelength (lower frequency) imparts greater penetration. Wavelength is affected by power.<br /><b><br />Laser output:</b> It is measured in Watts or milliwatts (W or mW). It is important in categorizing laser for safety. It is not adjustable. <br /><b><br />Power Density or Laser intensity:</b> Beam diameter determines power density. Units of measurement is W or mW/cm2.It takes into consideration actual beam diameter. If light spread over lager area then there is there is lower power density. <br /><b><br />Average Power:</b> It is dependant on the mode of laser beam delivery i.e. Continuous or pulse-train (burst) frequency mode. Knowing average power is important in determining dosage with pulsed laser. If laser is continuous laser then avg. power = peak output power. If laser is pulsed (burst) then avg. power is = to peak output power multiplied by duty cycle (frequency). <br /><br /><b>DOSAGE: </b>Laser dosage is amount of energy applied per unit area. It is measured in Joules/square cm (J/cm2). Joule is unit of energy &1 Joule = 1 W/sec. Dosage is dependent on:<br />– Output of laser in mW<br />– Time of exposure in seconds<br />– Beam surface area of laser in cm2<br />Various dosage ranges per site (1-9 J/cm2). <br /><br /><b>Recommended Dosage Range</b><br />– Therapeutic response = 0.001-10 J/cm2<br />– Minimal window threshold to elicit response<br />– Too much – suppressive effect<br />– Open wounds – 0.5-1.0 J/cm2<br />– Intact skin – 2.0-4.0 J/cm2 <br />– Average treatment – 6 J /cm2<br /><br /><b>Different common lasers in physiotherapy:</b><br /><br />1. Helium-Neon Lasers <br /><br />• Uses a gas mixture in a pressurized tube<br />• Now available in semiconductor laser<br />• Emits red light<br />• Wavelength: 632.8 nm<br />• Power output: 1.0-25.0 mW <br />• Energy depth: 6-10 mm<br />• The higher the output of the lasers (even though they are still low power) lower the delivery time<br /><br />2. Indium-Gallium-Aluminum-Phosphide Lasers<br /><br />• InGaAip<br />• Replacing HeNe lasers<br />• Semiconductor <br />• Wavelength: 630-700 nm<br />• Power output: same as HeNe<br />• Energy depth: superficial wound care<br /><br />3. Gallium ArsenideLasers<br /><br />• Semiconductor - produces an infrared (invisible) laser<br />• Wavelength: 904–910 nm <br />• Power output: may produce up to 100 mW<br />• Energy depth: 30-50 mm<br />• Short pulse-train (burst) duration (100-200 ns)<br /><br />4. Gallium Aluminum ArsenideLasers<br /><br />• GaAIAs<br />• Semiconductor<br />• Wavelength: 780-890 nm<br />• Power Output: 30-100 mW (up to 1000 mW)<br />• Energy Depth: Very high more than the above said laser<br /><br /><b>Laser Application techniques:</b><br /><br />• Gridding Technique <br />• Divide treatment areas into grids of square centimeters<br />• Scanning Technique<br />• No contact between laser tip in skin; tip is held 5-10 mm from wound<br />• Wanding Technique <br />• A grid area is bathed with the laser in an oscillating fashion; distance should be no farther than 1 cm from skin<br />• Point Application (On acupuncture point)<br /><br /><b>Treatment techniques for contact treatment:</b><br /><br />Dosage is the most important variable in laser therapy & may be difficult to determine. However it may be simplified i.e. for general application, only treatment time & pulse rate vary. Usually there is a handheld applicator & tip should be in light contact with skin while laser is engaged for pre-calculated time. Maintain laser perpendicular to treatment surface. Put firm contact unless open wound. Clean area prior to treatment. <br /><br />Always begin with minimal treatment and gradually increase (Better to underexpose than to overexpose). Check for pre/post-treatment changes. Ask the patient how they are doing prior to next treatment because you may have to adjust dosage. <br /><br />Avoid direct exposure into eyes (If lasing for extended periods of time, safety glasses are recommended). May experience a syncope episode during treatment during chronic pain, but it is very rarely reported. <br /><b><br />Application of heat & cold with LASER:</b> If icing – use BEFORE phototherapy because it enhances light penetration. If using heat therapy – use AFTER phototherapy because it decreases light penetration. <br /><br /><br /><br /><b>Use of Laser therapy in different field of medicine</b><br /><br />1. Vascular condition: Venous ulcer (Ref: M.E. Sugrue et al; Annals of Vascular Surgery, Volume 4, Issue 2 , Pages 179-181, March 1990). Results of this pilot study are encouraging. Raynaud's phenomenon is also treated by Laser therapy (Hirschl et al, 2004). Popularly pressure ulcers are treated by laser therapy in neurorehab words. <br /><br />2. Neurological condition: Stroke (Ref: Int J Stroke. 2012 Feb 2. doi: 10.1111/j.1747-4949.2011.00754.x.). This study named transcranial laser therapy for acute ischemic stroke: a pooled analysis of NEST-1 and NEST-2, support the likelihood that transcranial laser therapy is effective for the treatment of acute ischemic stroke when initiated within 24 h of stroke onset. If ultimately confirmed, transcranial laser therapy will change management and improve outcomes of far more patients with acute ischemic stroke. <br /><br />Similarly laser therapy is also reported to be beneficial in number of other neurological conditions both in animal & human subjects. Examples are closed-head traumatic brain injury (mice)( In mice it is reported that there is less neurological deficits in post-traumatic brain injury treated with laser for traumatic brain injury.), neurodegenerative diseases (humans) example Alzheimer’s disease. <br /><br />3. ENT conditions: Tonsillitis (Vestn Otorinolaringol. 2006;(3):19-22. Russian.), Tinnitus (FrankW et al; GMS Health Technol Assess. 2006 Aug 30;2:Doc17). <br /><br />
4. Surgical conditions: Chronic wound healing, Kaviani and colleagues (2006) examined the effects of low level laser therapy (LLLT) in the treatment of post-mastectomy lymphedema & concluded that LLLT has encouraging results on this condition. LLLT can be used as a conservative therapy for arm lymphoedema secondary to breast cancer treatment (BC Cancer Agency; 2007). Mastodynia is also treated successfully. Lymphangitis is also reported to be treated successfully<br /><br />
5. Dental conditions: post-operative pain after endodontic surgery (Kreisler et al; 2004). Markovic and Todorovic (2007) found after lower third molar surgery laser therapy can be recommended to minimize swelling & oedema. TMJ conditions also show encouraging results. <br /><br />
6. Musculoskeletal conditions: Bursitis, Tendinitis, Ligament injuries, CTS, Neck pain, LBA, myofascial pain syndrome (MPS), Post exercise pain (to treat plyometric induced pain), planter heel pain(Crawford and Thomson, 2003; Landorf and Menz, 2007). <br /><br />
7. Rheumatological conditions: RA (most studied) other rheumatologic pain<br /><br />
8. Other conditions: After effects of tuberculosis, Smoking cessation, Dysmenorrhea etc. <br /><br /><br /><br /><br /><br /><br /><br /><br /> <br /></div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-71851342461226952192012-03-01T12:44:00.000+05:302012-03-01T12:44:09.619+05:30Classification of spondyloarthritides (SpA) & USpA<div dir="ltr" style="text-align: left;" trbidi="on">
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<br /><b>Classification of spondyloarthritides (SpA) & USpA</b><br />Definition: The spondyloarthritides (SpA) are an interrelated group of rheumatic diseases that are characterized by common clinical symptoms and genetic similarities.<br /><br />For clinical purposes, 5 subgroups are differentiated: <br />1. AS (ankylosing spondylitis) <br />2. Psoriatic SpA (PsSpA)<br />3. Reactive SpA (ReSpA) <br />4. SpA associated with inflammatory bowel disease (SpAIBD) and <br />5. Undifferentiated SpA (uSpA)<br /><br /><b>Features of SpA:</b><br />
<br />Important clinical features of the SpA are <br />1. inflammatory back pain (IBP)<br />2. asymmetric peripheral oligoarthritis predominantly of the lower limbs <br />3. enthesitis <br />4. specific organ involvement such as anterior uveitis (eye) , psoriasis (skin) and chronic inflammatory bowel disease<br /><br />
The most important subtype of SpA is ankylosing spondylitis (AS), which is now considered part of axial spondyloarthritis. <br />ASAS Classification: ASAS stands for Assessment of SpondyloArthritis International Society. <br />ASAS group has recently developed criteria to classify patients with axial SpA with or without radiographic sacroiliitis, and criteria to classify patients with peripheral SpA.<br /><br />
<b>Axial SpA:</b><br />
1. LBA (>3 months almost every day)<br />2. Radiographs and magnetic resonance imaging (MRI can detect active inflammation and structural damage associated with SpA.)<br />3. HLA-B27 (Leucocyte antigen): SpA are genetically linked (90% of cases), the strongest contributing factor being HLA B27. <br />According to the ASAS axial SpA criteria, patients with chronic back pain aged less than 45 years at onset can be classified as having axial SpA if sacroiliitis on imaging (radiographs or MRI) plus 1 further SpA feature are present, or if HLA-B27 plus 2 further SpA features are present.<br /><br />
<b>Peripheral SpA: </b><br />
1. Patients with peripheral arthritis (usually asymmetric arthritis predominantly involving the lower limbs) enthesitis, or dactylitis.<br />2. Patients can be classified as having peripheral SpA if 1 of the following features is present: uveitis, HLA-B27, preceding genitourinary or gastrointestinal infection, psoriasis, inflammatory bowel disease, sacroiliitis on imaging (radiographs or MRI) in addition to point no 1.<br />3. Or if 2 of the following features besides the entry feature are present: arthritis, enthesitis, dactylitis, inflammatory back pain, or a positive family history of SpA.<br /><br />
<b>USpA </b><br />
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Clinical features of USpA: <br />Vast majority of USpA have IBP (Inflammatory back pain) & asymmetrical peripheral arthritis predominately of lower limbs.<br /><br />
HLA B27 is more helpful uSpA diagnosis: Liao et al analysed the clinical features of Chinese undifferentiated spondyloarthritis (USpA) patients with predominantly axial involvement. They found in Chinese population Both HLA-B27 status and SIJ MRI findings influence the classification of Chinese axial USpA patients, but HLA-B27 seems of more value.<br /><br />
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<b>References:</b><br />1. Braun J & Sieper J; Z Rheumatol. 2010 Jul;69(5):425-32; quiz 433-4. Spondyloarthritides.<br />2. van den Berg R & van der Heijde DM; Pol Arch Med Wewn. 2010 Nov;120(11):452-7. How should we diagnose spondyloarthritis according to the ASAS classification criteria: a guide for practicing physicians.<br />3. Liao Z et al; Scand J Rheumatol. 2011 Nov;40(6):439-43. Epub 2011 Jul 4. Clinical features of axial undifferentiated spondyloarthritis (USpA) in China: HLA-B27 is more useful for classification than MRI of the sacroiliac joint.</div>
<span style="color: blue;">4. http://www.medscape.org/viewarticle/545412_2</span><br style="color: blue;" /><br /></div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-19682593125074355092012-02-16T19:36:00.000+05:302012-02-16T19:36:15.766+05:30Eosinophilic Fascitis: 300 cases in 35 years<div dir="ltr" style="text-align: left;" trbidi="on">
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All people dealing with soft tissue pain & dysfunction "Eosinophilic Fascitis" is rearrest of the rare condition to encounter.<br />
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Take a note of it. It is a matter of debate for all fascia researchers & people involved in "Fascia research congress"<br />
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Pubmed link to "Eosinophilic Fascitis": <br />
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http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001483/<br />
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<br /></div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-34299720427849006692012-02-02T18:05:00.000+05:302012-02-03T11:02:51.335+05:30Lumbar Retrolisthesis: Introduction, types, physiotherapy treatment<div dir="ltr" style="text-align: left;" trbidi="on">
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A retrolisthesis is a posterior displacement of one vertebral body with respect to the adjacent vertebrae to a degree less than a luxation (dislocation). Retrolisthesis is relatively rare but when present has been associated with increased back pain and impaired back function. Clinically speaking, retrolisthesis is the opposite of spondylolisthesis (anterior displacement of one vertebral body on the subjacent vertebral body). Retrolistheses are most easily diagnosed on lateral x-ray views of the spine. Views, where care has been taken to expose for a true lateral view without any rotation, offer the best diagnostic quality.<br />
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Retrolisthesis may occur more commonly than initially believed. However retrolisthesis (backwards slippage of one vertebral body on another) has historically been regarded as an incidental finding, one which doesn’t cause any symptoms, and is considered to be of little or no clinical significance. But there is a possible association between retrolisthesis and increased back pain and impaired back function.<br />
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Retrolisthesis may be present in up to 30% of extension radiographs of patients complaining of chronic low back pain. Retrolisthesis has been found to be associated with disc degeneration, decrease in lumbar lordosis, and decrease in vertebral endplate angle.<br />
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According to Shen et al (Shen M et al; Spine J. 2007; 7(4): 406–413) it is possible that the contribution of pain or dysfunction related to retrolisthesis was far overshadowed by the presence of symptoms due to the concomitant disc herniation.<br />
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<b>Crucial questions in musculoskeletal medicine in retrolysthesis:</b><br />
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1. Do individuals with lumbar disc herniations have increased levels of back pain, back dysfunction, and decreased quality of life pre-operatively if they have concomitant retrolisthesis at the involved herniated disc level? <br />
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2. Does the presence of degenerative changes (disc degeneration, degenerative endplate changes, posterior element degenerative changes) along with retrolisthesis worsen the symptoms and / or possibly the prognosis in these operative cases? <br />
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<b>Grading & Classification:</b><br />
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<b>Classification system:</b><br />
<b><i>Complete Retrolisthesis -</i></b> The body of one vertebra is posterior to both the vertebral body of the segment of the spine above as well as below.<br />
<i><b>Stairstepped Retrolisthesis -</b></i> The body of one vertebra is posterior to the body of the spinal segment above, but is anterior to the one below.<br />
<i><b>Partial Retrolisthesis -</b></i> The body of one vertebra is posterior to the body of the spinal segment either above or below. <br />
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Since the vertebral body in a retrolisthesis moves in a posterior direction, the grading used for spondylolistheses is of little use. Clinicians & researchers use the following grading systems after following X ray reading:<br />
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There are always 2 vertebrae involved in measuring the magnitude of a retrolisthesis for translation (slippage). The lower segment is considered the position of stability. The upper segment rests on it. The upper segment is considered the segment of mobility and is the one being determined for retrolisthesis.<br />
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1) A line is drawn along the top of the vertebral body of the lower spinal segment.<br />
2) Then at the top-back most portion of the lower vertebral body, draw line at 90 degrees to line, till it projects well into the body of the vertebra above. <br />
3) Then draw another line parallel to the line just drawn this time at the posterior most lower portion of the upper vertebral body. <br />
4) The distance between the upright lines and is measured. Any distance of 3mm or greater is a retrolisthesis. This measurement represents the degree of translation (slippage) of the upper of the two segments.<br />
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<b>1. Few clinicians follow the following criteria:</b><br />
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Percent subluxation can be calculated for any individual with greater than or equal to 3 mm of posterior displacement. A cut-off point of 3 mm has been used previously both in orthopaedic research and clinical practice. This 3mm cut-off corresponds to a slip of 8% which is used as the lower limit to define retrolisthesis. <br />
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<b>2. Other few follow the following criteria:</b><br />
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In this grading system anterior to posterior dimension of the intervertebral foramina (IVF) is divided into four equal units. A posterior displacement of up to ¼ of the IVF is graded as Grade 1, ¼ to ½ as Grade 2, ½ to ¾ as Grade 3, ¾ to total occlusion of the IVF as Grade 4.<br />
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<b>Joint stability & retrolisthesis: </b><br />
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Joint stability is easily evaluated by the use of flexion and extension lateral x-ray views of the spine. If vertebral translation present on standing (stressed by gravity) lateral view x-rays then it indicates that the spinal joints at those levels are already in a "significantly stressed" state. It further means that if this is the condition then there may be degree of soft tissue looseness at best and soft tissue tearing at worst otherwise a positional translation of this magnitude could not be present.<br />
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Implications of joint instability are derived from DRE (Diagnosis related estimates) tables. If translation of 4.5mm & angular change of 15 degree or more at L1, L2 or L 3, 20 degree or more at L4 and 25 degree or more at L5 is found then Category IV instability is present. This would mean that 20% to 23% “whole person impairment” is present at each level where this if found. <br />
Pathology & structures involved:<br />
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Retrolysthesis is caused in lumbar by flexion injury or by prolonged & continual use of lumber spine flexion over a period of time. <br />
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Spine instability causes damage to of the connecting soft tissues especially juxtaposed ligaments, discs, muscles, tendons and fascia. Muscle spasm may also be present. Nerve compression may be present at intervertebral foramen (IVF). The compression of the IVF’s contents include spinal (sensory and motor) nerves, arteries, veins and lymphatic vessels which cater to the nutritional and waste removal needs of the spinal cord.<br />
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Degenerative spinal changes are often seen at the levels where a retrolisthesis is found. These changes are more pronounced as time progresses evidenced by end plate osteophytosis, disc damage, disc narrowing, tearing failure and eventually results in disc bulging.<br />
“A retrolisthesis hyper loads at least one disc and puts shearing forces on the anterior longitudinal ligament, the annular rings, nucleus pulposis, cartilage end plates and capsular ligaments. The bulging, twisting and straining tissues attached to the endplates pull, push and stretch it. It is worsened with time, gradually<br />
becoming irreversible. This is the aetiology of degenerative joint disease in retrolysthesis.<br />
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<b>X-ray & radiological findings:</b><br />
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• Vacuum phenomenon (in the nucleus pulposis of the intervertebral disc below the retrolisthesis), <br />
• Reduction of disc height with corresponding loss of the disc space, <br />
• Marginal sclerosis (more dense due to stress) of the adjacent vertebral bodies, <br />
• Osteophyte (spur) formation and <br />
• Apophyseal (guiding) joint instability. <br />
• With a retrolisthesis there is always a less than ideal positioning of spinal segments. (subluxation)<br />
• There is also always a reduced anterior to posterior dimension of the spinal canal compared to the way it is supposed to be. This leads to nerve signal alteration.<br />
• The greater the posterior displacement, the more significant it is for producing nerve root impingement and irritation, a dysfunctional spinal cord even to the point of a cauda equina compression syndrome if present in the lower lumbar spine.<br />
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<b>Patient clinical presentation:</b><br />
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Patients present with varied S/S with retrolysthesis from little pain to severe disabling pain. Patient may also present with sciatica with or without neurological deficits. In patients with neural claudication lumbar canal stenosis due to lysthesis is also seen. <br />
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<b>Physiotherapy:</b><br />
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Both IV joints & facet joints may produce pain & radiation. <br />
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Maitland transverse glides/ lateral PA glides on to the side of pain can be administered in cases associated mostly with facet restrictions. Central PA is also administered in appropriate cases with mutifidus & other spinal exercises. LS belt in majority cases may aid relief from pain. <br />
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McKenzie’s exercises to stretch the anterior spinal structures both with mobilization & manipulation in McKenzie style along with home exercises in McKenzie is highly advisable.<br />
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Spine muscle atrophy is seen in many cases of long standing retrolythesis. Spine stabilization exercises are sought in most cases and appropriate home exercises must be advised with follow ups with the physiotherapist. <br />
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Electrotherapy is directed to reduce pain. Few clinicians also believe that modalities like SWD or MWD can reduce the rate of degeneration hence also used in degenerative retrolysthesis. </div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-10366782312807162752012-01-13T17:35:00.000+05:302012-01-13T17:46:28.773+05:30Sitting ergonomics: Different sitting postures & analysis of chair sitting muscle work<div dir="ltr" style="text-align: left;" trbidi="on">
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<b>Different varieties sitting postures:</b><br />
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A. Common sitting postures:<br />
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1. Chair sitting <br />
2. Crossed sitting<br />
3. Crossed sitting with arms wrapped around both knees & locked in front <br />
4. Half crossed sitting<br />
5. Crook sitting <br />
6. Inclined sitting (to back)<br />
7. Inclined sitting (to sides)<br />
8. Inclined long sitting<br />
9. Side sitting<br />
10. Stoop sitting<br />
11. Fall out sitting<br />
12. Ride sitting<br />
13. Kneel sitting<br />
14. Crouch sitting <br />
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B. Activities in sitting:<br />
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1. Twisting in sitting<br />
2. Bending & reaching in sitting (sidewise- office works & in front- driving)<br />
3. Hitching & Hiking (to relieve pressure on buttocks in prolonged sitting)<br />
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C. Co-existing unavoidable stress factors in sitting:<br />
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1. Whole body vibration (driving)<br />
2. Noise stress<br />
3. Visual stress<br />
4. Psychological stress<br />
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<b>Analysis of muscle work in sitting posture:</b><br />
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Ideal sitting posture: The following discussion is in the context of a quiet ideal chair sitting posture without any upper limb activity. The position is taken on a flat base chair or stool, the height & width of the sitting area allow the thighs to supported & hips and knees is flexed to 900 . In ideal sitting femora are parallel to each other & feet rest on the floor with ankle at 900 where as hells are vertically below the knees. <br />
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<b>Muscle work in ideal sitting posture:</b><br />
<br />
a. Joints of lower extremity have no muscle work except at hip. Flexors of hip work in reverse origin insertion fashion to prevent slumping of the lumbar spine. <br />
<br />
b. Joints of spine: <br />
i. Global extensor muscles of the spine (Ex-Multifidus): these postural muscles keep the trunk upright. Action of these muscles may be counterproductive at lumbar & cervical spine where it’s action produces a bow string effect & increases the lordotic curvature leading to reduction in the over all height of the spine at these places. Therefore at the lumbar & cervical spine this action must be counteracted by the local flexors (lumbar & cervical spine flexors) to ensure local spine lengthening and maintain the correct & ideal local spine posture. <br />
ii. Flexors of the lumbar spine (Abdominals): In sitting they must work to prevent the bow string effect produced by the global extensor muscle. Scientific literature indicates they contract in an in to out fashion. Hence transverse abdominis is of prime importance in maintaining the core stability & correct spinal alignment. Where as the straight abdominals (rectus abdominis) maintain the correct pelvic tilt matching the spine alignment so that correct contact points are maintained at the chair base- body interface.<br />
iii. Flexors of the cervical spine (pre-vertebral neck muscles) act to prevent the bow string effect produced by the global extensor muscle.<br />
iv. Posture of the head on the cervical spine is finely controlled at the CVJ & at atlanto-axial joint by own set of flexors-extensors to maintain this sagittal posture. <br />
<br />
c. Other joints in sitting: <br />
i. TMJ: elevators of the mandible close the mouth against the pull of the gravity.<br />
ii. Thoraco-scapular junction: Thoraco scapular muscle (rhomboids) retracts the scapula so that the glenoid cavity faces laterally. Cervico scapular muscles (levator scapulae) work to elevate a depress scapula due to the pull of the gravity.<br />
<br />
d. Joints of upper extremity: No muscle work is required for quite sitting but sitting with occupational arm demands may leads to more activation of the external rotators of the arm, abductors, elbow flexors, forearm pronators, wrist extensors & finger flexors. <br />
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<br /></div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-86957848714188307312011-12-06T19:46:00.001+05:302011-12-07T11:02:49.606+05:30Baastrup disease: Lumbar interspinous bursitis<div dir="ltr" style="text-align: left;" trbidi="on">
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<br />
This disease is named after Danish radiologist (1855 - 1950) Christian Ingerslev Baastrup. <br />
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<b>Introduction & Epidemiology: </b><br />
It is claimed that Baastrup disease is responsible for intractable LBA (1). Though it is reported in mostly lumbar spine it’s cervical spine variant is also reported (2). Gardella called Baastrup disease as spinous process syndrome (3). It is reported in many occupational areas such as miners (4) & heavy vehicle drivers (8). Among of much debate now it is considered mostly a case of aging related problem. Let us discuss in little more detail:<br />
<br />
The Baastrup disease is characterized by the development of abnormal contact between adjacent spinous processes of the lumbar spine that results in rubbing against each other producing a bursitis which further result in focal midline pain and tenderness relieved by flexion and aggravated by extension. <br />
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<b>Epidemiology: </b><br />
It tends to be more common in the elderly. According to Maes et al (5) the prevalence of Baastrup disease is 8.2% (44 of 539) of the study population. In this study the lumbar spine was studied. This study also revealed that Baastrup disease is associated with age (P = 0.001), central canal stenosis (P = 0.0013), disc bulging (P = 0.0341), and anterolisthesis (P = 0.0429). There were no associations between Baastrup disease and disc degeneration, disc herniation, endplate findings, retrolisthesis, scoliosis, lordosis, or gender. <br />
According to Kwong et al (6); Baastrup disease occurs with high frequency among the elderly. This study suggests that Baastrup disease develops with increasing age and is part of the expected degenerative changes in the aging spine. According to these researchers (6) in their CT scan based study of 1008 patients evidence of Baastrup disease was found in 413 patients (41.0%). A decade-on-decade increase in frequency was found with a peak of 81.3% among patients older than 80 years. As many as five spinal levels were found to be affected in some patients (4.1% of 413), but in most patients (35.4%), one level was affected. Baastrup disease was most common at L4-L5. Associated degenerative changes were found at almost all affected levels (899/901). Hence Kwong et al urged the clinicians that because of the nearly universal association with other degenerative changes, caution must be taken before diagnosing Baastrup disease as the cause of back pain.<br />
According to Hanger (8) prevalence rate of this disease in a group of heavy automotive vehicles drivers is 13% of the test population.<br />
<br />
<b>Pathology</b><br />
Patients with Baastrup disease may experience pain owing to irritation of the periosteum or adventitial bursae between abutting spinous processes. This process can result in a degenerative hypertrophy, inflammatory change and even a pseudarthrosis with bursa formation. This interspinous bursa may extend between the ligamentum flavae in the midline forming an epidural cyst and further contributing to the already existing canal stenosis. <br />
This condition is usually seen patients with excessive lordosis of the lumbar spine. Often Baastrup lesions of the lumbar spine are located at L3-L4 and L4-L5 segments (8).<br />
<br />
<b>Palpation </b><br />
I myself employ the following technique to find a Interspinous bursa is swollen or not.<br />
First the spinous processes are palpated. The gap between the spinous process (Interspinous area) is located and palpating finger (usually the thumb) is slided on the slope following a parallel path way to that of laminas. Reaching on to the area between the spinous process from the side is easy & if Baastrup disease is present then obviously high degree of tenderness is elicited.This palpation also gives us the idea if the crowding of (kissing of ) spinous process as compared with other interspinous spaces & further it may reveal the tissue texture of the local tissue. Inflammed bursa with cyst may impart a "bouggy" feeling to the palpating hand. <br />
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<b>Radiographic features (9)</b><br />
<i>Plain film and CT</i><br />
<i> </i>• often shows close approximation and contact of adjacent spinous processes (kissing spines) <br />
• there is resultant enlargement, flattening and reactive sclerosis of apposing interspinous surfaces.<br />
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<i>MRI</i><br />
May demonstrate interspinous bursal fluid and a postero-central epidural cyst(s). MRI can be very helpful in determining whether there is resulting posterior compression of the thecal sac. <br />
<br />
<i>Baastrup's sign:</i> Also known as kissing spine, is an radiographic sign. It is characterized by posterior spinous processes 'kissing' and touching one another on sagittal plane. <br />
<br />
<b>Treatment (9)</b><br />
Both conservative and surgical options are available for treatment. Local steroid injection into the interspinous processes will often ease the back pain. Surgical options include interspinous process decompression devices (e.g, Wallis system, X STOP), and steroid / local anaesthetic injection into the bursa.<br />
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<b>Physiotherapy: </b><br />
<br />
No references are there about physiotherapy. However electro-analgesia & thermo-analgesia are quite effective. SWD, PSWD, MWD & FIR exert powerful anti-inflammatory effect with thermo-analgesia. IFT gives anti-inflammatory effect with electro-analgesia. UST in pulsed mode directed appropriately to the focal tissue is both anti-inflammatory & analgesic. <br />
Manual mobilization techniques are tried once the local tenderness is less. Contrast heat in acute inflammation & Hot fomentation thrice a day is also very effective in long standing cases which should be used as a home remedy. Egronomic corrective methods & postural awareness are of utmost importance as they may be primary factor that produced such a disorder. Manual therapists well versed with soft tissue & fascial techniques should try out techniques that may lengthen the thoracolumbar fascia. <br />
The outcome of physiotherapy is so satisfactory that author opine on his clinical experience, steroid infiltration & surgery are rarest of rare probabilities to be employed. <br />
<br />
<b>References:</b><br />
1. FERNANDEZ DE LA MELA I; Medicamenta (Madr). 1951 Dec 10;9(210):404-5.[Lumbar interspinal nearthrosis (Baastrup disease) as responsible for some intractable backaches].<br />
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2. VIALLET P J Radiol Electrol Arch Electr Medicale. 1950;31(3-4):206-7. [Two cases of cervical localization of Baastrup disease].<br />
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3. GARDELLA G; Ann Radiol Diagn (Bologna). 1952;24(4):260-74.[Spinous process syndrome (Baastrup disease)].<br />
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4. Gajdek D; Chir Narzadow Ruchu Ortop Pol. 1976;41(2):171-4. Polish. No abstract available. [Baastrup syndrome of the lumbar spine in miners].<br />
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5. Maes R et al; Spine (Phila Pa 1976). 2008 Apr 1;33(7):E211-5. [Lumbar interspinous bursitis (Baastrup disease) in a symptomatic population: prevalence on magnetic resonance imaging.]<br />
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6. Kwong Y et al AJR Am J Roentgenol. 2011 May;196(5):1156-9. MDCT findings in Baastrup disease: disease or normal feature of the aging spine?<br />
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7. Pinto PS et al Clin Imaging. 2004 May-Jun;28(3):219-22. [Spinous process fractures associated with Baastrup disease.]<br />
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8. Hagner W; Med Pr. 1988;39(1):65-70. [Baastrup's disease of the lumbar segment of the spine among drivers of heavy motor vehicles].<br />
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9. http://radiopaedia.org/articles/baastrup_syndrome</div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-80030180743843687872011-12-05T20:03:00.001+05:302011-12-05T20:05:41.180+05:30Classification of spinal cord injury: ASIA classification Vs Frankel classification<div dir="ltr" style="text-align: left;" trbidi="on">
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<br />Clinicians have long used a clinical scale to grade severity of neurological loss in SCI. First devised at Stokes Manville before World War II and popularized by Frankel in the 1970's, the original scoring approach segregated patients into five categories.<br /><br />
<b>Frankel classification:</b>Grade A: no function<br />Grade B: sensory only<br />Grade C: some sensory and motor preservation<br />Grade D: useful motor function<br />Grade E: normal function <br /><br />
<b>ASIA classification:</b>Grade A: Complete. No motor or sensory function preserved in the sacral segments (S4-S5)<br />Grade B: Incomplete. Sensory function is preserved but motor function is affected below the neurological level & includes the sacral segments (S4-S5)<br />Grade C: Incomplete. Motor function is preserved below the neurological level, and more than half of the key muscles below the neurological level have a muscle grade less than 3. <br />Grade D: Incomplete. Motor function is preserved below the neurological level, and more than half of the key muscles below the neurological level have a muscle more than 3. <br />Grade E: Normal. Motor & sensory functions are normal. <br /><br />
<b>5-Clinical syndromes in incomplete SCI by ASIA classification:</b>1. Central cord syndrome 2. Brown-Sequard syndrome 3. Anterior cord syndrome 4. Conus medullaris syndrome 5. Cauda equina syndrome <br />The ASIA committee also classified incomplete spinal cord injuries into five types. A central cord syndrome is associated with greater loss of upper limb function compared to the lower limbs. The Brown-Sequard syndrome results from a hemisection lesion of the spinal cord. Anterior cord syndrome occurs when the injury affects the anterior spinal tracts, including the vestibulospnal tract. Conus medullaris and cauda equina syndromes occur with damage to the conus or spinal roots of the cord.<br /><br />
<b>Advantages of ASIA impairment scale:</b><br />
1. First, instead of no function below the injury level, ASIA A is defined as a person with no motor or sensory function preserved in the sacral segments S4-S5. This definition is clear and unambiguous. <br />The new ASIA A categorization turns out to be more predictive of prognosis than the previous definition where the presence of function several segments below the injury site but the absence of function below a given level could be interpreted as an "incomplete" spinal cord injury.<br />2. ASIA B is essentially identical to Frankel B but adds the requirement of preserved sacral S4-S5 function. It should be noted that ASIA A and B classification depend entirely on a single observation, i.e. the preservation of motor and sensory function of S4-5.<br />3. The ASIA scale also added quantitative criteria for C and D. The original Frankel scale asked clinicians to evaluate the usefulness of lower limb function. This not only introduced a subjective element to the scale but ignored arm and hand function in patients with cervical spinal cord injury. To get around this problem, ASIA stipulated that a patient would be an ASIA C if more than half of the muscles evaluated had a grade of less than 3/5. If not, the person was assigned to ASIA D.<br />4. ASIA E is of interest because it implies that somebody can have spinal cord injury without having any neurological deficits at least detectable on a neurological examination of this type. Also, the ASIA motor and sensory scoring may not be sensitive to subtle weakness, presence of spasticity, pain, and certain forms of dyesthesia that could be a result of spinal cord injury. Note that such a person would be categorized as an ASIA E.<br /><br />
These changes in the ASIA scale significantly improved the reliability and consistency of the classification. Although it was more logical, the new definition of "complete" injury does not necessarily mean that it better reflects injury severity.<br /><br /><br /><br /></div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-53035968225414636422011-12-02T17:12:00.001+05:302011-12-02T17:18:13.972+05:30Shoulder: Bankart surgery rehabilitation<div dir="ltr" style="text-align: left;" trbidi="on">
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Bankart surgery:<br />
Bankart lesion is an injury of the anterior (inferior) glenoid labrum due to repeated (anterior) shoulder dislocation. Repeated dislocation forms a pocket at the front of the glenoid that allows the humeral head to dislocate into it. It is often accompanied by a Hill-Sachs lesion (damage to the posterior humeral head seen as a depression on X-ray). A bony bankart is a Bankart lesion that includes a fracture in of the anterior-inferior glenoid cavity. <br />
Bankart lesion warrants surgery. In Bankart surgery the anterior (inferior) glenoid labrum is reattached to the glenoid. Generally there is a anterior approach to this shoulder operation. Rehabilitation is the key to successful reinstitution of functional activities. As it is a very common injury in sports like javelin throwing return to sports is heavily dependant on post operation physiotherapy. The following is an sample schema of physiotherapy & rehabilitation approach to the Bankart surgery. <br />
<br />
Don’ts:<br />
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Restrictions up to 4 weeks: (To protect the reattached anterior capsule & labrum)<br />
<br />
1. Shoulder extension (backwards) past the plane of the body<br />
2. Shoulder external rotation (arm rotation outwards) greater than 0° (straight in front); extensive repairs may require more restrictions<br />
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For posterior repairs (To protect the reattached posterior capsule & labrum)<br />
<br />
1. Avoid any shoulder internal rotation (turning in) past the body i.e. hand behind back. <br />
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Restrictions up to 3 months:<br />
No passive forceful stretching into external rotation/extension following an anterior repair and into internal rotation for a posterior repair.<br />
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Dos: <br />
<br />
- Good posture is critical throughout the rehabilitation process to improve healing and decrease the risk of developing poor mechanics<br />
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- Aerobic conditioning throughout the rehabilitation process<br />
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- MD follow-ups Day 1, Day 8 - 10, 1 month, 4 months, 6 months and 1 year post-op<br />
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- All active exercises should be carefully monitored to minimize substitution or compensation<br />
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1 - 5 Days Post-op<br />
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1. Use of arm sling <br />
2. Ice pack for first 3 - 5 days. (Apply over the dressing but should not sip into the dressing)<br />
3. Postural education & sleeping posture advice (semi-reclined is most comfortable) <br />
4. Other general exercises: Stationary bike, stair machine etc<br />
5. Codmann’s Pendulum exercise to reduce muscular spasms, Scapulothoracic stabilizer training, elbow flexion/extension, wrist and forearm strengthening, gentle passive/active assistive exercises of the arm in flexion (front) keeping below the level of the shoulder & finally cervical muscle stretching. <br />
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* Surgeon’s check up to change dressing etc. <br />
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5 - 14 Days Post-op<br />
<br />
1. To reduce pain: IFT or TENS/ massage / contrast heat etc <br />
2. Russian current for strengthening <br />
3. Increase PROM and active assistive (AAROM) exercises as tolerated (from flexion out into the scapular plane) up to 90° unless otherwise indicated<br />
4. Soft tissue therapy to developing scar as appropriate.<br />
5. Scapulothoracic mobilization <br />
6. General conditioning as tolerated (include trunk flexion & extension exercises)<br />
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2 - 4 Weeks Post-op<br />
<br />
1. Now at this stage passive and active assisted flexion out to scaption (plane of the scapula) as tolerated.<br />
2. Sub-maximal isometrics (as dictated by pain) & Isotonic wrist, forearm.<br />
3. Resisted exercises using theraband are started from this phase onwards. <br />
a. Theraband resisted pull-downs from the front and the scapular plane<br />
b. Theraband resisted elbow flexion (high reps and low resistance)<br />
4. Active scapular elevation, depression, and retraction exercises <br />
5. Light weight bearing exercises<br />
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4 - 6 Weeks Post-op<br />
<br />
1. By 4-6 weeks resting pain is substantially less. <br />
2. Continue with passive and AAROM exercises (cane exercises, wall walking, table slide) from flexion & scaption out to abduction as tolerated<br />
3. Maximal isometrics<br />
4. Active exercises from flexion into the scapular plane against gravity as tolerated<br />
5. No resistance until able to perform 30 reps at limb weight with perfect mechanics<br />
6. Rested internal rotation 0° to the body. (Only light resistance)<br />
7. Add proprioceptive training exercises. (Alphabet writing, fine motor skills, work/sport specific exercises)<br />
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6 - 8 Weeks Post-op<br />
<br />
1. Increase AROM exercises as tolerated (serratus anterior, upper, and lower trapezius).<br />
2. Eccentrics exercises are added into protected ranges <br />
3. From this phase onwards begin LIGHT stretching into external rotation<br />
4. GHJ joints play + mobilizations as tolerated <br />
5. Increase proprioceptive training (prone on elbows, quadruped position ("on all four's") for rhythmic stabilization<br />
6. Okay to begin jogging, road cycling, and standing arm resistance exercises in the pool<br />
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8 - 12 Weeks Post-op<br />
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Emphasis on regaining strength and endurance <br />
<br />
1. PNF patterns (proprioceptive neuromuscular facilitation) can be started safely <br />
2. AROM exercises: internal rotation and external rotation as motion allows<br />
3. AROM exercises: lateral raises and supraspinatus isolation <br />
4. Rower with a high seat, decline bench press, military press in front of body<br />
5. Running, road or mountain biking, no activities with forceful, ballistic arm movement<br />
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3 - 6 Months Post-op<br />
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1. Aggressive stretching. <br />
2. Start strenuous resistive exercises<br />
3. Add light throwing exercises with attention to proper mechanics<br />
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6 Months Post-op<br />
<br />
1. Increase throwing program with focus on return-to-throwing sports as mechanics<br />
2. Sports conditioning with all of the normal shoulder movements<br />
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NB: Progression is based on individual patient presentation, which is assessed throughout the treatment process. People well versed with soft tissue & fascial tissue manipulations can appropriately employ them from 2nd week onwards. <br />
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<br /></div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-9941667637498223522011-11-22T12:06:00.001+05:302011-11-22T12:11:44.266+05:30Diagnosis of knee instability<div dir="ltr" style="text-align: left;" trbidi="on">
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<br /><br />According to Rossi et al, for knee; clinicians should have own series of exams with whom he is more confident and on whom he relies on for diagnosis. Usually, three sets of series are used: <br /><br />1. One for patello-femoral/extensor mechanism pathologies <br />2. Another for meniscal and chondral (articular) lesions <br />3. The other one for instability evaluation<br /><br />Among the above said to assess the 3rd category is difficult to diagnose. Often the diagnosis becomes more difficult because there are more than one tissue involved. <br /><br />Following are clues to diagnose them:<br /><br />1. Anerior medial instability (AMI):<br /><br />AMI occurs due to: ACL + MCL + medial meniscus injury. <br /><br />Test series to diagnose it are: valgus stress, anterior drawer, Lachman tests<br /><br />2. Anterior lateral instability (ALI): <br /><br />ALI occurs due to: ACL + lateral capsule + lateral meniscus injury. <br /><br />Test series to diagnose it are: valgus stress, anterior drawer, Lachman, pivot shift tests<br /><br />3. Posterior lateral instability (PLI): <br /><br />PLI occurs due to: Injury to posterior lateral corner of the knee. <br /><br />Test series to diagnose it are: external rotation, dial, recurvatum, posterolateral drawer tests <br /><br />4. Posterior medial instability (PMI): <br /><br />PMI occurs due to: MCL + ACL + Posterior medial corner. <br /><br />Test series to diagnose it are: valgus stress, posterior drawer, Lachman tests<br /><br />5. AMI + ALI instability:<br /><br />Occurs due to: ACL + MCL + lateral capsule ( But PCL is intact)<br /><br />Test series to diagnose it are: anterior drawer, Lachman, pivot shift, valgus stress<br />6. PMI + PLI instability:<br /><br />Occurs due to: ACL + MCL + lateral capsule (But PCL is intact)<br /><br />Test series to diagnose it are: anterior drawer, Lachman, pivot shift, valgus stress, varus stress tests <br /><br />Reference:<br /><br />Rossi et al. Sports Medicine, Arthroscopy, Rehabilitation, Therapy & Technology 2011, 3:25 (http://www.smarttjournal.com/content/3/1/25)<br /></div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-30340686272066243012011-11-20T17:53:00.001+05:302011-11-20T18:20:53.661+05:30Type of SLAP lesions & The dead arm syndrome<div dir="ltr" style="text-align: left;" trbidi="on">
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The SLAP lesions:<br />
Superior labrum tears were first described by Andrews. Further SLAP lesions as described by Snyder are subdivided into 4 types (I-IV) & this classification is according to their severity of tear. For best diagrams of the SLAP lesions refer to the following site:<br />
<br />
http://www.shoulderdoc.co.uk/article.asp?article=1027<br />
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Type I SLAP lesion:</div>
<div style="text-align: justify;">
This is a partial tear and degeneration to the superior labrum, where the edges are rough and fray along the free margin, but the labrum is not completely detached. </div>
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Type II lesion: </div>
<div style="text-align: justify;">
Type II is the comonest type of SLAP tear. The superior labrum is completely torn off the glenoid, due to an injury (often a shoulder dislocation). This type leaves a gap between the articular cartilage and the labral attachment to the bone. Type 2 SLAP tears can be further subdivided into (a) anterior (b) posterior, and (c) combined anterior-posterior lesions.</div>
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Type III lesion: </div>
<div style="text-align: justify;">
A Type III tear is a 'bucket-handle' tear of the labrum, where the torn labrum hangs into the joint and causes symptoms of 'locking' and 'popping' or 'clunking'. </div>
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Type IV lesion:</div>
<div style="text-align: justify;">
The Type IV SLAP tear is one where the tear of the labrum (bucket handle tear) extends into the long head of biceps tendon.</div>
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<span style="font-size: large;"><b>Dead arm syndrome (DAS) &; Type II SLAP lesion: </b></span></div>
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<br />
Now the most important part of the article is which of the SLAP lesion presents with “Dead arm syndrome”.<br />
Dead arm syndrome is clearly a subjective phenomenon (see the definitions below). The sufferer is mostly an athlete whose work involves lot of throwing for example base ball or cricket. The athlete will often say "I just can't throw anymore, and / or the shoulder just doesn't feel right". This type of injury tends to progress gradually over time, slowly creeping up on the overhead athlete until severe pain and subjective instability limits his or her ability to perform.</div>
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<br />
Dead arm syndrome: Definition <br />
<br />
1. Sensory diminution or loss in the arm after anterior shoulder dislocation or subluxation. (Stedman's medical dictionary)<br />
<br />
2. The Dead Arm Syndrome has been defined as the inability to throw, spike or serve at pre-injury level secondary to subjective pain and instability.</div>
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<br />
<i><b>Description & progression of DAS:</b></i></div>
<div style="text-align: justify;">
<br />
Dead arm syndrome starts with repetitive motion and thus force exerted on the posterior capsule of the shoulder. Overuse can lead to posterior capsule hypertrophy. The next step is tightness of the posterior capsule called posterior capsular contracture. This reduces the shoulder internal rotation. If shoulder activities are still continued then over time, with enough force, a tear may develop in the labrum. The shoulder is unstable and dislocation may come next. Dead arm syndrome won't go away on its own with rest—it must be treated. If there's a SLAP lesion, then surgery is needed to repair the problem. If the injury is caught before a SLAP tear, then physical therapy with stretching and exercise can restore it. Before hand how to know then a SLAP lesion or a dead am syndrome may occur? The answer is shoulders at risk for the dead arm syndrome have a marked loss of internal rotation caused by contracture of the posteroinferior capsule such that less than a 180 degrees arc of rotation is achieved with the arm abducted 90 degrees (the 180 degrees rule).</div>
<div style="text-align: justify;">
<br />
<b>What is the cause of DAS?</b><br />
According to Buckhart et al root cause of the dead arm syndrome is the Type II SLAP lesion.<br />
Type 2 SLAP lesions that cause the dead arm syndrome in overhead-throwing athletes are most likely acceleration injuries that occur in late cocking rather than deceleration injuries in follow-through.</div>
<div style="text-align: justify;">
<br />
More about Type II SLAP lesions form Buckhart et al’s article: </div>
<div style="text-align: justify;">
<br />
Clinical presentations of all 3 types of Type II SLAP lesion are different. Following are few points to remember about them.<br />
1. Posterior and combined Type 2 SLAP lesions can be disabling to overhead-throwing athletes because of posterosuperior instability and anteroinferior pseudolaxity.<br />
2. The Jobe relocation test is positive with posterosuperior pain in patients with posterior or combined anterior-posterior Type 2 SLAP lesions and is negative in patients with anterior Type 2 SLAP lesions.<br />
3. Rotator cuff tears are frequently associated with posterior or combined anterior-posterior SLAP lesions, are lesion-location specific, and typically begin from inside the joint as undersurface tears.<br />
4. The peel-back mechanism is a likely cause of posterior Type 2 SLAP lesions.</div>
<div style="text-align: justify;">
<br />
<i><b>Classification</b></i><br />
• Two categories <br />
o Aware of subluxation<br />
o Unaware of subluxation<br />
• Often misdiagnosed as other shoulder pathology or cervical lesion</div>
<div style="text-align: justify;">
<br />
<i><b>Associations with other diseases</b></i><br />
• Thoracic Outlet Syndrome <br />
o 30% of patients had coexistent TOS<br />
o Due to altered kinetics of the Scapulothoracic Joint<br />
o Resultant neurovascular compromise </div>
<div style="text-align: justify;">
<br />
Treatment of DAS:</div>
<div style="text-align: justify;">
<br />
A. Surgical: <br />
1. Repair of posterior SLAP lesions can return overhead-throwing athletes to full overhead athletic functioning. <br />
2. To securely repair the posterosuperior labrum to resist torsional peel-back, suture anchors must be placed posterior to the biceps at the corner of the glenoid. The repair must be protected against external rotation past 0 degree for 3 weeks to avoid undue premature torsional stresses on the repair from the peel-back mechanism. </div>
<div style="text-align: justify;">
<br />
B. Physiotherapy:<br />
Rehabilitation of athletes with the dead arm syndrome must include the entire kinetic chain. </div>
<div style="text-align: justify;">
<br />
<b style="color: blue;">Reference:</b><br />
<span style="color: blue;">1. Burkhart SS et al; Clin Sports Med. 2000 Jan;19(1):125-58.</span><br />
<span style="color: blue;">2. Wikipedia</span><br />
<span style="color: blue;">3. http://www.shoulderdoc.co.uk/article.asp?article=1027</span><br />
<span style="color: blue;">4. http://www.orthofracs.com/adult/elective/shoulder/dead-arm-syndrome.html</span><br />
<br /></div>
</div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-36527320309935632572011-11-18T18:19:00.001+05:302011-11-19T11:52:41.094+05:30What is metabolic fitness (MF)?<div dir="ltr" style="text-align: left;" trbidi="on">
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<a href="http://www.little-black-dress-fitness-tips.com/images/Benefits-of-Physical-Fitness.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="http://www.little-black-dress-fitness-tips.com/images/Benefits-of-Physical-Fitness.jpg" /><span style="background-color: #cccccc;"></span></a></div>
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<br />
In previous years, fitness was commonly defined as the capacity to carry out the day’s activities without undue fatigue. These days, physical fitness (PF) is considered a measure of the body’s ability to function efficiently and effectively in work and leisure activities, to be healthy, to resist hypokinetic diseases, and to meet emergency situations.</div>
<div style="text-align: justify;">
<br />
Physical fitness comprises two related concepts: general fitness (for the purpose of health), and specific fitness (a task-oriented definition based on the ability to perform specific aspects of sports or occupations). Physical fitness is generally achieved through correct nutrition, exercise, and enough rest.</div>
<div style="text-align: justify;">
<br />
PF can be measured as an out come of physical activity and also as a moderator on morbidity and mortality. Physical fitness for purposes of health, is best defined by the specific components that relate to improved health or reduced disease. The components of Health-Related Fitness are:<br />
– Morphological<br />
– Muscular<br />
– Motor<br />
– Cardiorespiratory<br />
– Metabolic<br />
For the discussion of our topic metabolic fitness is more important. Metabolic fitness is the newest component if fitness. </div>
<div style="text-align: justify;">
<br />
Metabolic fitness:<br />
<br />
Physical inactivity is strongly associated with an increased risk of premature disease and death, and the falling level of physical activity. Both aerobic fitness (maximum oxygen uptake) and metabolic capacity of the muscles are important in this matter. The role of the metabolic capacity/fitness of muscle, appears to be especially critical for the development of metabolic-related diseases and thus for the health of the individual. </div>
<div style="text-align: justify;">
<br />
Definition: A definition of metabolic fitness is proposed as the ratio between mitochondrial capacity for substrate utilisation and maximum oxygen uptake of the muscle. <br />
Indirect means of determining metabolic fitness is Glucose tolerance, blood lipid & cholesterol profiles (especially HDL & triglyerisdes) & finally lipid oxidation. </div>
<div style="text-align: justify;">
<br />
Skeletal muscle is an extraordinarily plastic tissue and metabolic capacity/fitness changes quickly when the level of physical activity is altered. High metabolic fitness includes an elevated use of fat at rest and during exercise. The capacity for glucose metabolism is also enhanced in trained muscle. </div>
<div style="text-align: justify;">
<br />
There are many adaptations to physical activity. Exercise-induced activation of genes coding for proteins involved in metabolism is described as an underlying mechanism for some of these adaptations. The increased gene expression is of relatively short duration, which implies that a certain regularity of physical activity is required to maintain high metabolic fitness. Thus, metabolic fitness is directly related to how much the muscle is used, but even low levels of physical activity have a beneficial effect on metabolic fitness and the overall health of the individual.<br />
Subcomponents of metabolic fitness include:<br />
– Glucose Tolerance<br />
– Blood Lipid and Cholesterol Profiles<br />
– Lipid Oxidation</div>
<div style="text-align: justify;">
<br />
Glucose Tolerance<br />
1. Regular exercise can be used to treat glucose intolerance in Type II diabetics.<br />
2. Effects of exercise include normalizing insulin and glucagon production by the liver, increasing insulin sensitivity by the exercising muscle, thus enhancing glucose uptake.</div>
<div style="text-align: justify;">
<br />
Blood Lipid and Cholesterol Profiles<br />
1. Exercise decreases total blood cholesterol, increases HDL-Cholesterol, and decreases blood triglycerides.</div>
<div style="text-align: justify;">
<br />
Lipid Oxidation<br />
1. High lipid oxidation alters cholesterol metabolism and reduces body f<span style="background-color: white;"></span>at to reduce risk of cardiovascular disease. Thus, chronic aerobic exercise spares glucose stores and uses more fat oxidation for fuel.</div>
<div style="text-align: justify;">
<br />
Assessment of metabolic fitness:<br />
The direct measurement of metabolic fitness and/or aerobic demand is the means that can be used as an index of the efficacy of an exercise training program or other therapeutic intervention; as medical risk factor for predicting the risk of cardiovascular disease, diabetes, death or other health outcome; or as an aid to pharmaceutical companies for drug discovery in the area of metabolic fitness, deconditioning, and oxidative biology.<br />
<br />
<div style="color: blue;">
References:</div>
<span style="color: blue;">1. Ugeskr Laeger. 2002 Apr 15;164(16):2156-62.</span><br />
<span style="color: blue;">2. Kennedy RA et al; Journal of Sports Science and Medicine (2007) 6, 448-454</span></div>
</div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-39838573970377805612011-11-12T21:00:00.000+05:302011-11-20T18:38:50.976+05:30Clinical classification of Erb’s palsy & it’s physiotherapy<div dir="ltr" style="text-align: left;" trbidi="on">
<a href="http://orthoinfo.aaos.org/figures/A00077F01.jpg"><img alt="" border="0" src="http://orthoinfo.aaos.org/figures/A00077F01.jpg" style="cursor: hand; cursor: pointer; display: block; height: 243px; margin: 0px auto 10px; text-align: center; width: 200px;" /></a><br />
<br />
<div style="text-align: justify;">
<br />
<br />
Narakas classified babies with obstetric palsy into four groups<br />
I. Upper Erb's palsy (C5, C6 injury)<br />
II. Extended Erb's (C5, C6, C7 injury)<br />
III. Total palsy (C5, C6, C7, C8 & T1 injury)<br />
IV. Total palsy with Horner’s syndrome (C5, C6, C7,C8 & T1 injury)<br />
<br />
Clinically however Narakas Group II can be sub-classified into two groups according to this 'early recovery of wrist extension.'<br />
<br />
II a. recovery of Gr 3 wrist extension before 2 months of age.<br />
II.b. recovery of Gr 3 wrist extension after 2 months of age.<br />
<br />
II a recovers the UL function much faster than the II b group.<br />
<br />
Muscles paralysed in Group I are: Biceps, Deltoid, Brachialis, Brachioradialis, partly supraspinatus, infraspinatus, Supinator.<br />
<br />
Extended erbs palsy involves the elbow & wrist<br />
<br />
Intrinsic muscles of hand & ulnar flexors are paalysed in total palsy<br />
<br />
Horner’s syndrome comprise of: Ptosis, Miosis, Anhydrosis, Enopthalmus, Loss of ciliospinal reflex.<br />
<br />
Sensory loss in Gr I & II may be in little area over deltoid.<br />
<br />
<b>Physical therapy approach in nut shell:</b><br />
<br />
Therapy is the cornerstone in the management of the symptoms of a child with BPP brachial plexus palsy. Popular or conventional physiotherapy approaches include exercise therapy, tactile stimulation, soft tissue manipulation techniques and functional splinting. Recently functional stimulation is found better than common electrical stimulation (2).<br />
<br />
Eectrotherapy:<br />
Galvanic stimulation to the paralysed muscles. Libile method is used with faradic stimulation.<br />
<br />
Exercise therapy:<br />
A comprehensive program that includes stretching exercises, safe handling and early positioning techniques, developmental and strengthening activities, and sensory awareness should be developed and updated as needed.<br />
For the first 2 weeks, the child may have some pain in the affected shoulder and limb, either from the injury or from an associated clavicular or humeral fracture. The arm can be fixed across the child's chest by pinning of his/her clothing to provide more comfort. However, some authors have discouraged this pinning in favor of immediate institution of gentle ROM exercises. Parents should be instructed in techniques for dressing the child to avoid further traction on the arm.<br />
A comprehensive therapy program should consist of ROM exercises, facilitation of active movement, strengthening, promotion of sensory awareness, and provision of instructions for home activities. Overall goals should focus on minimizing bony deformities and joint contractures associated with BPP, while optimizing functional outcomes.<br />
<br />
Splinting & taping:<br />
Often a wrist extension splint is necessary to maintain proper wrist alignment and reduce the risk of progressive contractures even at 2 weeks period.<br />
Static and dynamic splinting of the arm is useful to reduce contractures, prevent further deformity, and in some cases, assist movement. Commonly prescribed splints include resting hand and wrist splints, elbow extension splints, dynamic elbow flexion and supinator splints. Careful selection and timing of splint use is essential to optimization of the desired effect.<br />
<br />
Taping techniques may be used by the therapist to control scapular instability and hence to promote improved shoulder mobility.<br />
<br />
<b>Contractures &stretching:</b><br />
Severe contractures should be avoidable with consistent therapeutic exercises, including passive and active stretching, flexibility activities, myofascial release techniques, and joint mobilization.<br />
<br />
Stretching:<br />
Over time, these contractures can lead to progressive bony deformity and shoulder dislocation. Early and consistent stretching of internal rotators should minimize the risk of this problem. External rotation, performed with the shoulder adducted alongside the chest and with the elbow flexed to 90°, provides maximum stretch of internal rotators (specifically, the subscapularis) and the anterior shoulder capsule.<br />
The scapula should be stabilized while stretching shoulder girdle muscles to maintain mobility and preserve some scapulohumeral rhythm. Early development of flexion contractures at the elbow is common and can be exacerbated by radial head dislocation caused by forced supination. Aggressive forearm supination, therefore, should be avoided.<br />
<br />
Sensory awareness:<br />
Sensory awareness activities are useful for enhancing active motor performance, as well as for minimizing neglect of the affected limb. Use of infant massage and drawing visual attention to the affected arm can be incorporated easily into play and daily activities. Weight-bearing activities with the affected arm in all positions not only provide necessary proprioceptive input but also can contribute to skeletal growth.<br />
<br />
<div style="color: blue;">
<b>References:</b></div>
<div style="color: blue;">
<br /></div>
<div style="color: blue;">
1. Al-Qattan MM et al; J Hand Surg Eur Vol. 2009 Dec;34(6):788-91. Epub 2009 Sep 28.</div>
<div style="color: blue;">
2. Okafor UA et al; Nig Q J Hosp Med. 2008 Oct-Dec;18(4):202-5.</div>
<div style="color: blue;">
3. http://emedicine.medscape.com/article/317057-treatment</div>
<div style="color: blue;">
<br /></div>
<br />
<br /></div>
</div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-77958168658503194812011-10-28T21:00:00.000+05:302012-02-03T18:25:29.603+05:30Implications of Physiotherapists as indipendent mecine prescriber<div dir="ltr" style="text-align: left;" trbidi="on">
Hi all physiotherapists. Time is changing rapidly for us. Our services at different areas of medicine has brought credit to us. As a result of that<br />
<br />
In USA: We are trying to get into 1st hand practice where clinical entry level DPT and many such advancements are noted.<br />
Link: <br />
<br />
In UK: Recently in BBC news it was flashed that "Physiotherapists may get independent medicine prescription rites". Already physios have injection rights in UK. <br />
Link:
<br />
<div class="MsoNormal" style="text-align: justify;">
<a href="http://www.bbc.co.uk/news/health-15037491">http://www.bbc.co.uk/news/health-15037491</a></div>
<div class="MsoNormal" style="text-align: justify;">
</div>
<div class="MsoNormal" style="text-align: justify;">
<a href="http://www.somed.org/">http://www.somed.org/</a></div>
<div class="MsoNormal" style="text-align: justify;">
<br /></div>
<br />
In AUS: Physiotherapists are trying to persuade legislators to allow physiotherapists for minor surgeries "wound suturing", injection rights, independent prescription writes. <br />
Link:<br />
<br />
<cite><span style="font-size: 12pt; font-style: normal; font-weight: normal;">9thnrhc.ruralhealth.org.au/program/docs/papers/moore_D3.pdf (Download)</span></cite><br />
<cite><span style="font-size: 12pt; font-style: normal; font-weight: normal;"><br /></span></cite><br />
<cite><span style="font-size: 12pt; font-style: normal; font-weight: normal;">2008 WHO classification of "Health workers" </span></cite><br />
<br />
<div class="MsoNormal" style="text-align: justify;">
Please refer to the WHO (World
health organization) classification (2008) of health workers which is an
international standard classification where there are separate ISCO codes to
physiotherapists & physiotherapy technician. Thankfully the classification is far more indicative this time. </div>
<div class="MsoNormal" style="text-align: justify;">
<br /></div>
<div class="MsoNormal" style="text-align: justify;">
Physiotherapist: ISCO code-
2264 </div>
<div class="MsoNormal" style="text-align: justify;">
<br /></div>
<div class="MsoNormal" style="text-align: justify;">
Physiotherapy technician: ISCO
code- 3255</div>
<div class="MsoNormal" style="text-align: justify;">
<br /></div>
<div class="MsoNormal" style="text-align: justify;">
</div>
<div class="MsoNormal" style="text-align: justify;">
Link: <a href="http://www.who.int/hrh/statistics/Health_workers_classification.pdf">http://www.who.int/hrh/statistics/Health_workers_classification.pdf</a></div>
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<br /></div>
<div class="MsoNormal" style="text-align: justify;">
Thanks </div>
<div class="MsoNormal" style="text-align: justify;">
<br /></div>
<cite><span style="font-size: 12pt; font-style: normal; font-weight: normal;"></span></cite></div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-82594676500794829482011-09-24T19:28:00.000+05:302011-09-28T19:09:30.315+05:30Implication of anterior drawer test, Lachman’s test, Pivot shift test to that of knee Instability<div dir="ltr" style="text-align: left;" trbidi="on">
<br />
<br />
<br />
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<br />
<b>Lachman's vs. Anterior Draw Test</b><br />
<br />
• Lachman's test may be more difficult for clinicians to perform but tends to be more sensitive<br />
• In the anterior draw test knee is positioned so that the hamstrings have a mechanical advantage. Increased hamstring activity can inhibit tibial translation, causing a false negative test<br />
• A torn meniscus can act as a block to tibial motion, again causing a false negative while doing the anterior draw test<br />
<br />
<b>Anterior drawer test with tibia external rotation:</b><br />
<br />
Anterior drawer test with tibia in neutral rotation demonstrates equal displacement of both condyles & this displacement is eliminated by internal rotation of the tibia, then both anteromedial and anterolateral rotary instability may be present. <br />
<br />
Similarly positive anterior drawer test in neutral tibial rotation, that is accentuated when the test is repeated in 30 deg of external rotation and reduced when performed with the tibia in 15 deg of internal rotation indicates anteromedial rotary instability. <br />
<br />
<b><i>Pivot shift test is the test which indicates antrolateral instability (ALI) of the knee. </i></b><br />
<br />
Research indicates antrolateral instability further increase with injury to LCL (lateral collateral ligament) & PCL (Posterior Cruciate ligament). Broadly speaking ALI is also associated with injury to accuate complex that includes posterior 1/3 of lateral supporting structures i.e. LCL, arcuate ligament, & exension of popliteus.<br />
<br />
It is also reminded to the reader that posterior 1/3 of the lateral ligamentous complex is reinforced by biceps, popliteus, & lateral head of gastrocnemius. </div>
satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-5777396951108823672011-08-17T20:43:00.000+05:302011-08-17T20:54:49.847+05:30C6-C7 syndrome: My clinical experience & suggestions
<br /><div style="text-align: justify;"><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://mcr.coreconcepts.com.sg/wp-content/uploads/2011/06/side-sleeper.jpg"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 274px; height: 184px;" src="http://mcr.coreconcepts.com.sg/wp-content/uploads/2011/06/side-sleeper.jpg" alt="" border="0" /></a>
<br />
<br />Many confuse marked tenderness at the coracoid tip, lateral pectoral and medial elbow sites to be a variant of fibromyalgia however usually it comes along with tenderness at the C6-7 level in the cervical spine. A close look in to the history reveals in this group of patients lose tenderness at C5-6 and standard upper body sites with proper neck support during sleep, but remained symptomatic at coracoid tip, lateral pectoral, medial elbow and C6-C7.
<br />
<br />Smythe HA (1994) have supported that mechanical factors determine patterns of symptoms and tenderness in this group. This implies that we are talking of segmental referred pain or referred tenderness rather than a pathologically ill-defined spectrum called “fibromyalgia”. If we differ on this front our treatment strategy is mislead. That’s why centrally acting medications or behavioral modifications are equally disappointing outcomes. To add to that tricyclic medications, stretch and spray or trigger point injections may be simply out of wrong terminology assigned to such a clinical entity.
<br />
<br />Cyriax in his classical text book of orthopaedic medicine has elaborated how we get pain out of C6-C7 region & wry neck which is clinically better defined than the C6-C7 syndrome as we are talking of. We sleep 70% of our night in side lying positions. Most of the neck supports reach maximum up to caudal surface of vertebral body however with most we can reach adequately C5. Because of this C6-C7 segments sags towards the side on which we sleep with side flexion we also get a coupled rotation at the same site. That’s why people with Discogenic wry neck there is side-bend to the opposite side (same side bending is difficult) & restriction of the rotation to the painful side. However if there is strain to the facet joint structures we may get a pattern side-bend to the same side (opposite side bending is difficult) & restriction of the rotation to the non-painful side.
<br />
<br />Physical strategies that have been helpful in such cases as far as my experience go is as follows:
<br />1. Electro-analgesics: Pain reliving modalities in electrotherapy
<br />2. Manual therapy:
<br />Maitland: transverse glide to C6-C7 on the painful side progressing to central PA of C6- may be up to T2 as per the condition.
<br />Mulligan: SNAGs to C6-C7 facets or spine as per the condition
<br />McKenzie: Chin retraction (Chin tucking) with or without extension
<br />Soft tissue therapy: I have found B/L rhomboids stretch to be very effective with digital ischemic pressures to tender points
<br />Neural mobilization: As symptoms abate add neural mobilization program
<br />
<br /><span style="font-weight: bold; font-style: italic; color: rgb(255, 0, 0);">N:B In my opinion C6-C7 syndrome is a mechanical derangement of minor grade due to repetitive positioning such as side lying. </span>
<br /><span style="font-weight: bold; color: rgb(0, 0, 153);">
<br />Reference:</span>
<br /><span style="color: rgb(0, 0, 153);">1. Smythe HA; J Rheumatol. 1994 Aug;21(8):1520-6. (The C6-7 syndrome--clinical features and treatment response).</span>
<br /><span style="color: rgb(0, 0, 153);">2. Walker JM, Helewa A (Physical therapy in arthritis): WB sounders & Company </span>
<br />
<br /></div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0tag:blogger.com,1999:blog-59305263331406079.post-36408323036776581852011-07-06T21:03:00.000+05:302011-07-07T11:37:44.772+05:30Stiff man syndrome: A neuromotor disorder- Know how for physios<div style="text-align: justify;"><br /><span style="font-weight: bold;">Synonyms:</span> stiff man syndrome (SMS), stiff person syndrome (SPS), stiff leg syndrome (a focal SMS) etc<br /><br /><span style="font-weight: bold;">Introduction & definition: </span><br /><br />Moerch and Woltman reported the first 14 cases with this syndrome for more than 50 years since 2010.<br /><br />Stiff man syndrome (SMS) is an uncommon (rare) neurological disease that manifests with disorder of motor function which is characterized by rigidity of axial musculature and fluctuating painful spasms, which are often induced by startle or emotional stimuli.<br /><br />Clinical and immunological findings indicate that SMS is a heterogeneous disease, suggesting the need to define its diagnostic criteria. But it has basic 2 forms either it can be generalized or focal. Criteria for the diagnosis of SPS were proposed but there are several variants of this syndrome described. These variants include focal variants of SMS.<br /><br />Variants include stiff limb syndrome (SLS), jerking SMS and progressive encephalomyelitis with rigidity and myoclonus (PERM). Recognition of the clinical spectrum of SMS is important, particularly the upper-limb, cervical, and cranial nerve involvement that occurs in paraneoplastic variants (Paraneoplastic SMS accounts for approximately 5% of all cases of SMS). However they all share the core clinical features of appendicular and axial rigidity caused by continuous involuntary motor unit activity, and superimposed stimulus-sensitive spasms.<br /><br />It is associated antineuronal autoimmunity and accompanying autoimmune diseases, most often noted in insulin-dependent diabetes mellitus with following C/F (see below). Several features suggest that SMS is an autoimmune-mediated chronic encephalomyelitis. Neurophysiological studies have demonstrated the presence of continuous motor unit activity in muscle at rest, with abnormally enhanced extereoceptive reflexes.<br /><br />The disease progresses over the span of months to years rendering many patients wheelchair-bound or bedridden.<br /><br /><span style="font-weight: bold;">Clinical features:</span><br /><br />1. Onset: Insidious & progressive<br />2. Fluctuating stiffness and paroxysmal spasms of the trunk and legs.<br />3. Symmetrical muscle stiffness and spasms that often lead to skeletal deformity.<br />4. The spasms characterized by hyperextension of the back (hyper-lordosis) and legs are both spontaneous as well as stimulus-sensitive. Spasms are excruciatingly painful.<br />5. SMS is frequently accompanied by symptoms of autonomic dysregulation.<br />6. Sometimes Hyperreflexia may be the only pathological finding on the neurological examination.<br />7. Mostly there is progressive gait impairment.<br />8. There may be a variety of additional neurological symptoms and signs such as eye movement disturbances, ataxia, or Babinski signs (progressive encephalomyelitis with rigidity and myoclonus), or be associated with malignant disease (paraneoplastic SMS).<br />9. Most patients show psychiatric disturbances suggestive of psychogenic movement disorder and this may cause delays in adequate pharmacotherapy.<span style="font-weight: bold;"> </span><br /><br /><span style="font-weight: bold;">EMG: </span><br /><br />The electromyographic examination shows continuous motor unit activity of the affected muscles at rest. Spasmodic reflex myoclonus is observed in nearly all SMS patients. It consists of well-reproduced reflex EMG-activity commencing 50-80 ms after medial or tibial nerve stimulation and lasting several seconds thereafter. The activity is first myoclonic then spasmodic in nature, and commonly begins in the muscles most severely affected before spreading bidirectionally along the neuraxis.<br /><br /><span style="font-weight: bold; font-style: italic;">Commonest clinical indicators to suspect SMS: </span><br /><br />The diagnosis is based on clinical, biochemical and electrophysiological findings.<br /><br />A characteristic group of symptoms and signs allows a tentative clinical diagnosis. Supportive ancillary findings include (1) the demonstration of continuous muscle activity in trunk and proximal limb muscles despite attempted relaxation, (2) enhanced exteroceptive reflexes, and (3) antibodies to glutamic acid decarboxylase (GAD) in both serum and spinal fluid.<br /><br /><span style="font-weight: bold;">Pathology:</span><br /><br />1. There is good evidence for a primary auto-immune aetiology. In addition to that there is clinical evidence of organ-specific autoimmunity predominantly encephalomyelopathic disorder resulting from B-cell-mediated clonal production of autoantibodies against presynaptic inhibitory epitopes on the enzyme glutamic acid decarboxylase (GAD) and the synaptic membrane protein amphiphysin.<br />However other antibodies such as anti-gephyrin, and anti-gamma-aminobutyric acid A receptor-associated protein (GABARAP) antibodies (14-kD protein localized at the postsynaptic regions of GABAergic synapses) are also detected along with GAD & anti-amphiphysin. In up to 65% of SMS patients, there are circulating anti-GABARAP antibodies that inhibit the GABA(A) receptor expression on GABAergic neurons. Paraneoplastic SMS is associated with anti-amphiphysin, anti-gephyrin, and anti-Ri antibodies. There is strong evidence that in SMS, GABAergic neurotransmission is impaired by these pathogenic autoantibodies; however, the exact antigenic target remains unknown.<br />Autoantibodies against glutamic acid decarboxylase- GAD in both serum and cerebrospinal fluid help to establish the correct diagnosis. Specifically GAD65 isoform, are present in serum or cerebrospinal fluid of 60-80% of patients with SPS and its variants. A paraneoplastic form of SPS is recognized in about 5%, associated with a different profile of auto-antibodies.<br />The correlation between antibody levels and severity of disease also offers evidence for a pathogenic role for the anti-GAD and anti-amphiphysin autoantibodies.<br /><br />2. The scarcity of neuropathological correlates stand in sharp contrast with the severity of the disability in affected individuals and suggests that functional impairment of inhibitory circuits without structural damage is sufficient to develop the full clinical spectrum of SPS.<br /><br /><span style="font-weight: bold;">Treatment options:</span><br /><br />There are 2 distinct options:<br />1. Immunomodulation<br />2. Symptomatic<br /><br />The rarity of this condition limits the feasibility of controlled clinical trials in the treatment of SPS, but the available evidence suggest that drugs that increase cortical and spinal inhibition such as benzodiazepines (clonazepam 4 mg/day) and drugs that provide immune modulation such as intravenous immunoglobulin, plasmapheresis, and prednisone are effective treatments.<br /><br />Rigidity and spasms may be treated symptomatically with benzodiazepines, baclofen, tiagabine and levetiracetam. An alternative of last resort is baclofen administered intrathecally via an implanted pump device.<br /><br />Treatments for cancer occasionally produce symptomatic improvement in patients with paraneoplastic SPS.<br /><br /><span style="font-weight: bold;">Prognosis:</span><br /><br />SPS remains a largely underdiagnosed condition.<br /><br />The syndrome varies from mild to severe, but if untreated it can be progressive and disabling. Generally after an initial progressive phase, patients with SPS generally stabilize over a period of months to years. However, 10% will require prolonged admission to intensive care at some stage during the disease. Sudden death has been reported in as many as 10% of patients because of unexplained metabolic acidosis or autonomic crises.<br /><br />The prognosis in paraneoplastic SPS, jerking SPS and PERM, in terms of mortality, is generally worse than in primary SPS. It has been reported that reported cases of patients with SPS who were positive for anti-GAD antibodies and subsequently developed cancer. Because SPS often develops before the diagnosis of cancer, patients diagnosed with SPS should be monitored for the development of cancer.<br /><br /><br /><span style="font-weight: bold; color: rgb(0, 0, 153);">References: </span><br /><span style="color: rgb(0, 0, 153);">1. Stayer C & Meinck HM; Neurologia. 1998 Feb;13(2):83-8. (Stiff-man syndrome: an overview).</span><br /><span style="color: rgb(0, 0, 153);">2. Meinck HM; CNS Drugs. 2001;15(7):515-26. (Stiff man syndrome).</span><br /><span style="color: rgb(0, 0, 153);">3. Fiol M et al; Neurologia. 2001 Feb;16(2):89-91. (Focal stiff-person syndrome).</span><br /><span style="color: rgb(0, 0, 153);">4. Duddy ME & Baker MR; Front Neurol Neurosci. 2009;26:147-65. Epub 2009 Apr 6. (Stiff person syndrome).</span><br /><span style="color: rgb(0, 0, 153);">5. Espay AJ & Chen R ; Muscle Nerve. 2006 Dec;34(6):677-90. (Rigidity and spasms from autoimmune encephalomyelopathies: stiff-person syndrome).</span><br /><span style="color: rgb(0, 0, 153);">6. Ishii A; Brain Nerve. 2010 Apr;62(4):377-85. (Stiff-person syndrome and other myelopathies constitute paraneoplastic neurological syndromes). [Article in Japanese]</span><br /><span style="color: rgb(0, 0, 153);">7. Dalakas MC; Curr Neurol Neurosci Rep. 2008 Jan;8(1):48-55. (Advances in the pathogenesis and treatment of patients with stiff person syndrome).</span><br /><span style="color: rgb(0, 0, 153);">8. Meinck HM & Thompson PD; Mov Disord. 2002 Sep;17(5):853-66. (Stiff man syndrome and related conditions).</span><br /><span style="color: rgb(0, 0, 153);">9. Saiz A et al; Ann Neurol. 1998 Mar;43(3):400-3. (Stiff-leg syndrome: a focal form of stiff-man syndrome).</span><br /><span style="color: rgb(0, 0, 153);">10. Gürol ME et al; Mov Disord. 2001 Nov;16(6):1189-93. (Stiff leg syndrome: case report).</span><br /><br /><br /><br /></div>satyajit mohantyhttp://www.blogger.com/profile/10478820484216397642noreply@blogger.com0