Sunday, May 31, 2009

Are electrotherapy & cardiac rhythm devices (CRD) really incompatible or risky?

Review of the literature and of recommendations from CRD manufacturers suggests that TENS, Diathermy, and Interferential Electrical Current Therapy are best avoided in patients with CRDs.
But several case reports have demonstrated there are no interactions between various physiotherapy modalities and cardiac rhythm devices (CRD).

However, in my graduation days it was criminal not to ask the patient whether he was having a CRD or not. I have seen students fail in practical examinations if they omitted this query while interviewing the patients. Till date I have also maintained the same precautionary measure in my set up. Here is a recent paper I am discussing which investigated on the fact that “Is there really an interaction various physiotherapy modalities with CRD that contraindicates or cautions it’s application”.

This review will help many to

1. Reduce fear of potential interactions. This may lead to not implementing a treatment strategy that would be helpful to the patients’ ailments.
2. Reduce the chances of suboptimal utilization of physiotherapy treatments in CRD patients.

Digby & Colleagues reviewed existing guidelines regarding the use of physiotherapy modalities in patients with pacemakers and/or implantable cardioverter-defibrillators (ICDs).

In a local physiotherapy facility in Ontario, Canada 25 patients ware treated with CRD (22 pacemaker and 3 ICD patients) for a total of 230 visits (9.2 visits/patient).

5 patients received TENS and all 25 were administered additional treatment in the form of ultrasound (15), acupuncture (19), Laser (7), traction/manual therapy (12), exercise (8), education (18), taping (5), and/or moist heat (5).

The results are as follows:
1. No complications occurred. It may be possible to safely deliver these modalities in a proper setting with device and patient monitoring.

Further readers:
2. There are no specific international policies regarding the administration of physiotherapy modalities in CRD patients and, thus, there are no specific guidelines to be implemented at the local level.

Reference:
Digby GC et al; Europace. 2009 May 2. [Epub ahead of print]


Saturday, May 30, 2009

Prescribing exercises for the upper limb- Be aware of unequal BP in arms




A rare cause of upper limb exercise intolerance- Atherosclerosis !!!
Atherosclerotic occlusive disease of the subclavian artery is seen and occasionally will cause pain in the upper extremities. This pain is typically brought on by exercise and especially with repetitive movements of the upper extremity such as brushing one's hair. It is relatively rare for atherosclerosis to affect the upper extremities and cause symptoms. For reasons that again are unclear, it is more common for the atherosclerotic plaque to accumulate on the left side than it is on the right side.

Other associated features may be:
1. Difference in the quality of the pulse between the left wrist and the right wrist. The pulse on the left side may appear weaker.
2. Arm to arm blood pressure differences in upper extremities.

There have been reports of surprising variation in arm-to-arm blood pressure differences. But these variations were no more than 10- 15% and were in the elderly. The hypertension expert of MAYO clinic refers 10 mm Hg in diastolic & 20 mm Hg in systolic BP are within limits of variation of arm BPs. How ever the differential diagnosis in this arm-to-arm blood pressure differences in BP are as follows:

1. Congenital conditions: aortic coarctation and thinning of one of the subclavian, axillary, or brachial arteries.
2. Acquired arterial conditions include aortic dissection, atheroma, thrombus, embolus, and extrinsic compression (as might be seen in association with a mass in the upper chest).

The investigations of choice in this condition are:
1. Contrast-enhanced CT of the chest (to effectively define among the possibilities mentioned above).
2. Vascular ultrasound (transthoracic echocardiography or transesophageal echocardiography).
3. Angiography

The sub-clavian steal syndrome presenting as unequal arm-to-arm blood pressure.
"subclavian steal syndrome": In certain instances repetitive exercise of the left upper extremity can cause not only pain in the left arm but also dizziness and, in fact, patients have been known to actually faint. This condition is called "subclavian steal syndrome".

Cause of "subclavian steal syndrome": Usually there is an atherosclerotic plaque in the subclavian artery on the left side with decreased flow to the left arm. With exercise, the left upper extremity can actually "steal" blood from the brain through the vertebral artery by causing a reversal of blood flow from the brain and down into the left arm. This can result in "syncope" (fainting).

Confirmation of the diagnosis: The diagnosis is suspected by the history and confirmed by the finding of a markedly decreased blood pressure in the left upper extremity compared to the right side and further confirmed by noninvasive testing and ultimately by angiography.

References: 1. Vascularnet.com 2. Own contribution

Friday, May 29, 2009

Exercise is a hope for vascular claudication patients.


Peripheral arterial insufficiency is a product of progressive arterial degenerative disease. Further arterial insufficiency is associated with an increased morbidity and mortality in the suffering population. Usually this condition presents with decreases exercise tolerance and intermittent claudication.

Enhanced physical activity is one of the most effective means of improving the life of affected patients. Researchers tried to answer how enhanced physical activity helps in this regards?

They found following answer to that:

Exercise training-induce vascular adaptations to ischemic muscle. Vascular remodeling assumes an important means for improved oxygen exchange and blood flow delivery. Relevant exercise-induced signals stimulate angiogenesis, within the active muscle (e.g. hypoxia), and arteriogenesis (enlargement of pre-existing vessels via increased shear stress) to increase oxygen exchange and blood flow capacity, respectively.

This above statement is supported by following evidences from pre-clinical studies:

1. There is increase in collateral blood flow over time as the exercise progresses.
2. This is accompanied by significant enlargement of isolated collateral vessels.
3. Increased production of angiogenic growth factors (e.g. VEGF, FGF-2) is seen.

Thus, enhanced physical activity can be an effective means of enlarging the structure and function of the collateral circuit.

However findings illustrate clear distinctions between the processes influencing angiogenesis and arteriogenesis. Further, sympathetic modulation of the collateral circuit does not eliminate the increase in collateral circuit conductance induced by exercise training. These findings indicate that structural enlargement of the collateral vessels is essential to realize the increase in collateral-dependent blood flow capacity caused by exercise training. This raises the potential that meaningful vascular remodeling can occur in patients with intermittent claudication who actively participate in exercise training.

Reference:

Yang HT et al; J Physiol Pharmacol. 2008 Dec;59 Suppl 7:57-70.


Thursday, May 28, 2009

Which frozen shoulder patient respond to physical therapy & why many frozen shoulder patients are poor responders to normal physiotherapy protocol.





I treat about 8-10 frozen shoulder (FS) cases a day. My impression from what ever I know as a specialist physiotherapist is as follows:

1. We take frozen shoulder as an easy diagnosis because the movement restrictions & end feel are characteristics of diagnosis.
I take capsular pattern as the hall mark sign of diagnosing a frozen shoulder. Further the capsular (lethery) end feel confirms my diagnosis. As patients present to us at various duration after the onset & even after various treatments, they show different grades of pain, stiffness & psychological impacts on over all shoulder function. I find clearly defined clinical subgroups among the presenting population of frozen shoulders.

2. After the realization of the entity (FS) we remain so much pre-occupied with the technique administration among myriad of physiotherapeutic probabilities that we many time forget to notice the postural attitude of the patients. In majority cases I find UCS (upper crossed syndrome) & scapular fixation abnormalities & poor neuromuscular & dynamic stability. Whether this posture is antecedent or consequential occurrence in frozen shoulder is a debatable question. However one may find normal person with increased kyphosis (rounded upper thoracic spine) without shoulder pain but reduced external rotation, over head abduction & hand behind back. This description emulates a capsular tightness. How this posture contributes to the clinical subgroups in frozen shoulder is also unexplored. I would like to draw attention that I such cases where the posture of the patient is ignored active exercises especially the overhead abduction ensues an impingement of sub-acromion structures. The patient complains of relapse of pain in shoulder. The clinician in this case can mark that despite the ROM of the shoulder improving the pain has increased either in the rotator cuff tendons & exposed part of the subdeltoid bursa.

3. A research paper by Yang JL & colleagues throws some more light on this issue.
i. The purpose of Yang JL & colleague’s study was to identify the kinematic features of patients with frozen shoulder who are more likely to respond to physical therapy.
ii. 34 FS patients received same standardized treatment with passive mobilization/stretching techniques, physical modalities (i.e. ultrasound, shortwave diathermy and/or electrotherapy) and active exercises twice a week for 3 months.
iii. Initially, subjects were asked to perform full active motion in 3 tests: abduction in the scapular plane, hand-to-neck and hand-to-scapula. These motions ware studied by a 3-D electromagnetic motion-capturing system.

During a multivariate analysis 2 variables ware identified who have predictive value. They are:
1. Scapular tipping >8.4 degrees during arm elevation
2. External rotation >38.9 degrees during hand to neck

The presence of these two variables (positive likelihood ratio=15.71) increased the probability of improvement with treatment from 41% to 92%.

Reviewer’s comment: For predicting the success of frozen shoulder scapular tipping is one of the predictor. Further changed scapular tipping & external rotation are the features of poor posture associated with rounded shoulders (thoracic spine kyphosis)

Reference: Yang JL et al; Man Ther. 2008 Dec;13(6):544-51. Epub 2007 Oct 2.

Wednesday, May 27, 2009

Operative interventions in stiff elbow- A mini review



Introduction:

Two intermediate joints i.e. the elbow and the knee are the most affected by myositis ossificans. Stretching to regain ROM in the post immobilization period is not out of danger of acquiring myositis. Contracted elbow poses difficulty to both operative and non-operative treatment (7).
In my more than a decade of carrier as a graduate & specialist physiotherapist I have hardly seen case non-responding to physiotherapy for stiff elbow except cases associated with bony block. The part of world where I live in orthopedic surgery is not common for elbow stiffness. Recently I saw a case presenting with post operative stiff elbow. To my assessment stiffness was due to capsule as the stiffness was bi-directional and characteristic end-feel. Despite 15 days of oscillatory mobilization, stretching & other rehabilitation exercises, there was o remarkable change. I have no provision of serial casting in my set up. So I tried to get in to reviewing operative interventions in elbow stiffness cases. The following is the summary of that review.

Posttraumatic stiffness in elbow (2): Patients may present with extrinsic, intrinsic contractures or mixed contractures (combined extrinsic and intrinsic contractures) in a stiff elbow.
1. Initial traumas may be isolated fractures or dislocation and complex fracture-dislocations.
2. Initial treatments may be nonoperative, radial head resection, and ORIF.

Operative procedures
Posttraumatic elbow stiffness can impose severe functional limitations on the performance of activities of daily living. Patients who have failed a minimum of six months of nonsurgical management and who are motivated to comply with postoperative rehabilitation are candidates for surgical release. Unlike earlier studies the current studies suggest that posttraumatic stiffness of the elbow, particularly when the articular surface is left intact, may be treated reliably (7). There are several effective surgical approaches and techniques available. The choice of surgical approach and technique is dictated by the location of the pathology, condition of the skin, and degree of arthritic changes (5).

A. Capsulectomy: Capsulectomy is employed many times for posttraumatic stiffness. According to reports (1) patients are operated twice where the first operation dictates it. In a study by Ring & colleagues, average improvement in ulnohumeral motion after surgery for capsular release was 53 degrees (The average flexion was 98 degrees). The patients who subsequent repeat elbow contracture release had gained an additional 24 degrees, leading to a final average flexion arc 103 degrees. How ever in postoperative period Ulnar neuropathy was reported.

B. Column procedure: This surgical approach is a limited surgical approach. Because the procedure elevates muscles from the anterior and posterior aspects of the lateral supracondylar osseous ridge, we called it the column procedure. It allows anterior capsular exposure through an interval in the brachioradialis and extensor carpi radialis longus. A static adjustable splint rather than physical therapy is used in postoperative period. According to Morrey Column procedure can be successful in the majority of patients undergoing surgical release for capsular & extrinsic contracture of the elbow. Similarly, Mansat & colleagues reported the same column procedure which can both approach anterior and posterior aspects of the capsule is associated with a low rate of complications and is safe and effective for the treatment of a limitation in flexion or extension resulting from an extrinsic contracture of the elbow.

C. Arthrolysis (2,3): Arthrolysis refers to operative loosening of adhesions in an ankylosed joint. Adhesive structures can exist both anteriorly and posteriorly about the joint to prevent motion (3). Arthrolysis can be open or arthroscopic. Severely stiff elbow is one of the main indications of open arthrolysis in the patients without muscle atrophy (14). Open elbow release with excision of tethers and blocks is a valuable procedure for post-traumatic stiffness (3). According to Kayalar & Colleagues, sequential open arthrolysis is an effective way to simultaneously to obtain good range of motion especially in severe stiff elbows and to maintain the ligamantous stability of the elbow joint.
Cikes & colleagues (2) evaluated the results of open arthrolysis for posttraumatic elbow stiffness. The findings are as follows:

1. The mean total increase in range of motion was 40 degrees (13 to 112 degrees), with a mean gain in flexion of 14 degrees (0 to 45 degrees) and 26 degrees in extension (5 to 67 degrees).
2. There is no correlation between the type of stiffness, the surgical approach used, and the results.
According to the findings of these authors there is no complication of open arthrolysis such as elbow instability or post operative osteoarthritis. Interestingly, patients with the greatest preoperative stiffness had significantly better improvement of mobility. The best results were obtained in patients who had arthrolysis done within 1 year after the initial trauma. However, according to Tan & colleagues recurrence in postoperative period is common but is responsive to manipulation under anesthesia and repeat releases.

D. Arthroscopic surgery for stiff elbow: The appreciable aspect of arthroscopic method is minimal invasive nature of arthroscopic techniques & it is an effective procedure for limitation of motion of the elbow with minimal morbidity (4). According to Kim & colleagues report (4):
1. The elbow ROM shows a progressive increase until 1 year after surgery.
2. Even after 1 year post op. ROM shows little additional increase.
3. ROM show more improvement in patients whose duration of symptoms is less than 1 year as compared to patients of symptoms more than 1 year.
4. Post op. arthroscopic ROM results for posttraumatic stiffness & degenerative stiffness are similar even though in posttraumatic stiffness cases extension is more limited.
5. In more than 90% patient significant improvement in ROM can be achieved after arthroscopic procedures.

Do releases after heterotopic ossification (but not complete bony ankylosis) & capsular contracture alone restricting elbow motion have different outcomes. It is commonly believed that in cases with heterotopic ossification is associated with diminished motion after release. Lindenhovius & colleagues in their comparative study consisting of cohorts of heterotopic ossification & capsular contracture found, open release of post-traumatic elbow stiffness is more effective when heterotopic ossification hindering motion is removed than when there is capsular contracture alone.
Reviewer’s Comment: However, from the above said study, it is clear the capsular fibrotic tissues are less amenable to that of bony blocks associated with heterotopic ossification.

Different approaches for elbow surgeries in stiff-elbow

1. Anterior capsular release for extension losses in elbow: According to Aldridge & colleagues release of a pathologically thickened anterior elbow capsule through a predominantly anterior approach to correct diminished elbow extension is a safe and effective technique. Furthermore, compared with splinting in extension alone, the utilization of continuous passive motion during the postoperative period increases the total arc of motion.

2. Modified lateral release for extension losses in elbow: This approach is a modification of the procedure described by Nirschl for resection and repair of lateral elbow tendinosis (tennis elbow). This modified approach allows visualization of the entire anterior elbow joint without disturbing the common extensor origin or the collateral ligaments. If necessary, a second, posterior triceps-splitting incision is used to access the olecranon fossa. Medial approach or transhumeral perforation is not at all required in this procedure.
Kraushaar & colleagues used this technique for 12 patients. According to Kraushaar & colleagues (9), all patients were treated after operation with the elbow splinted in extension for 3 days, after which they were started on an aggressive physical therapy regimen. There were no wound complications, no neurovascular injuries, and no formations of heterotopic bone.

3. Medial release in elbow for post traumatic contractures: A medial approach is useful to reveal and excise the pathological changes in the medial collateral ligament. This technique employs a single medial approach. The posterior oblique bundle of the medial collateral ligament is resected, followed by posterior and anterior capsulectomies. An additional lateral release through a separate incision is employed if required.
Wada & colleagues employed this release method on 14 elbows. Contrary to the expectation of elbow instability ala medial collateral ligament resection all 14 elbows showed scarring of the posterior oblique bundle of the medial collateral ligament. In this study neither the interval from injury to operative release nor the age of the patient affected the results. Hence Wada & colleagues consider this approach as a useful tool to reveal and excise the pathological changes in the medial collateral ligament and effective route through which to correct post-traumatic contracture of the elbow.

4. Lateral release in elbow for post traumatic contractures: Cohen & colleagues described & performed a modified lateral approach allows release of post-traumatic contracture without disruption of the lateral collateral ligament or the origins of the extensor tendon at the lateral epicondyle of the humerus. The advantages include a simplified surgical procedure, less operative morbidity, and unrestricted rehabilitation. Both pain and function in the elbow (humeroulnar joint) improved significantly in post-traumatic stiffness of the elbow in 22 patients using this modified technique.

5. Isolated release of the medial collateral ligament over elbow stiffness: Contracture of the collateral ligaments is considered to be an important factor in post-traumatic stiffness of the elbow. Ruch & colleagues found isolated release of the medial collateral ligament called partial surgical release of the medial collateral ligament is associated with improved range of movement of the elbow in patients with post-traumatic stiffness, but was less effective in controlling pain.
Ruch & colleagues performed the operation through a longitudinal posteromedial incision centred over the ulnar nerve. After decompression of the ulnar nerve, release of the medial collateral ligament was done sequentially starting with the posterior bundle and the transverse component of the ligament, with measurement of the arc of movement after each step.

Post surgical complications in operations for stiff elbow include:

1. Wound dehiscence
2. Wound infection
3. Cubital tunnel syndrome
4. Reflex sympathetic dystrophy
5. Instability
6. Operative failure

Reference(s):
1. Ring D et al; J Hand Surg [Am]. 2006 Oct;31(8):1264-71.
2. Cikes A et al; J Orthop Trauma. 2006 Jul;20(6):405-9.
3. Tan V et al; J Trauma. 2006 Sep;61(3):673-8.

4. Kim SJ et al; Clin Orthop Relat Res. 2000 Jun;(375):140-8.

5. Issack PS et al; Bull Hosp Jt Dis. 2006;63(3-4):129-36.

6. Lindenhovius AL et al; J Shoulder Elbow Surg. 2007 Sep-Oct;16(5):621-5. Epub 2007 Jul 23.
7. Morrey BF; Clin Orthop Relat Res. 2000 Jan;(370):57-64.
8. Aldridge JM 3rd et al; J Bone Joint Surg Am. 2004 Sep;86-A(9):1955-60.

9. Kraushaar BS et al; J Shoulder Elbow Surg. 1999 Sep-Oct;8(5):476-80.

10. Wada T et al; J Bone Joint Surg Br. 2000 Jan;82(1):68-73.

11. Cohen MS et al ; J Bone Joint Surg Br. 1998 Sep;80(5):805-12.

12. Ruch DS et al; J Bone Joint Surg Br. 2008 May;90(5):614-8.

13. Mansat P et al; J Bone Joint Surg Am. 1998 Nov; 80(11):1603-15.

14. Kayalar M et al; Arch Orthop Trauma Surg. 2008 Oct;128(10):1055-63. Epub 2008 Apr16.

Sunday, May 24, 2009

Stiff elbow & static progressive splinting for it- A mini Review

Elbow is a highly constrained synovial hinge joint (3). A 50% reduction of elbow motion can reduce the upper extremity function by almost 80% (1). Elbow motion is essential for upper extremity function to position the hand in space (2). Stiffness of the elbow impairs hand function, because this is highly dependent on elbow extension and flexion and forearm rotation (1).

Elbow joint is prone to stiffness following a multitude of traumatic and atraumatic etiologies. Diagnosis depends on a complete history and physical exam, supplemented with appropriate imaging studies (2).

Søjbjerg JO defined stiff elbow as reduction in extension greater than 30 degrees, and/or a flexion less than 120 degrees. According to him supination and pronation are also often reduced as well but this author says contracture of the elbow is not related to forearm rotation. However, it seems this description matches the capsular restriction.

General guideline of treatment (1, 2 & 3):

1. Elbow contracture is challenging to treat, and therefore prevention is of paramount importance (2, 3).
2. When preventive approach fails, non-operative followed by operative treatment modalities should be pursued (2). The non-operative treatments are as follows:
3. Upon initial presentation in those who have minimal contractures of 6-month duration or less, static and dynamic splinting, serial casting, continuous passive motion, occupational/physical therapy, and manipulation are non-operative treatment modalities that may be attempted (2).
4. Surgery of the posttraumatic stiff elbow is a challenging and demanding procedure (1). A stiff elbow that is refractory to non-operative management can be treated surgically, either arthroscopically or open, to eliminate soft tissue or bony blocks to motion (2). Advanced postoperative rehabilitation can improve the final outcome (1).

Results of a retrospective study on static progressive splinting for posttraumatic elbow stiffness:

Doornberg JN et al evaluated a retrospective case series to examine the effect of static progressive splinting in helping patients with posttraumatic elbow stiffness regain functional motion and avoid operative treatment for stiffness. 29 patients with elbow stiffness after trauma (flexion contracture greater than 30 degrees or flexion less than 130 degrees) were treated with static progressive elbow splinting when a standard exercise program was no longer achieving gains in motion. In this study, Doornberg & colleagues found static progressive splinting can help gain additional motion when standard exercises seem stagnant or inadequate, particularly after the original injury. Operative treatment of stiffness was avoided in most these 29 patients (4).

References:

1. Søjbjerg JO; Acta Orthop Scand. 1996 Dec;67(6):626-31.
2. Nandi S et al; Hand (N Y). 2009 Apr 7. [Epub ahead of print]
3. Evans PJ et al; 2009 Apr;34(4):769-78.
4. Doornberg JN et al; 2006 Jul;20(6):400-4.



Tuesday, May 19, 2009

Truths from a clinical neurophysiology tool (Microneurography)

Microneurography is a method using metal microelectrodes to investigate directly identified neural traffic in myelinated as well as unmyelinated efferent and afferent nerves leading to and coming from muscle and skin in human peripheral nerves in situ.

1. Microneurography is particularly important to investigate efferent and afferent neural traffic in unmyelinated C fibers, in particular, recording of efferent discharges in postganglionic sympathetic C efferent fibers innervating muscle and skin (muscle sympathetic nerve activity; MSNA and skin sympathetic nerve activity; SSNA).
2. It provides direct information about neural control of autonomic effector organs including blood vessels and sweat glands.
3. Sympathetic microneurography has become a potent tool to reveal neural functions and dysfunctions concerning blood pressure control and thermoregulation.
4. This recording has been used not only in wake conditions but also in sleep to investigate changes in sympathetic neural traffic during sleep and sleep-related events such as sleep apnea.
5. The same recording was also successfully carried out by astronauts during spaceflight.
6. Recordings of afferent discharges from muscle mechanoreceptors have been used to understand the mechanisms of motor control. Muscle spindle afferent information is particularly important for the control of fine precise movements.
7. It may also play important roles to predict behavior outcomes during learning of a motor task.
8. Recordings of discharges in myelinated afferent fibers from skin mechanoreceptors have provided not only objective information about mechanoreceptive cutaneous sensation but also the roles of these signals in fine motor control.
9. Unmyelinated mechanoreceptive afferent discharges from hairy skin seem to be important to convey cutaneous sensation to the central structures related to emotion.
10. Recordings of afferent discharges in thin myelinated and unmyelinated fibers from nociceptors in muscle and skin have been used to provide information concerning pain.
11. Recordings of afferent discharges of different types of cutaneous C-nociceptors identified by marking method have become an important tool to reveal the neural mechanisms of cutaneous sensations such as an itch.

Reference:

Mano T et al; Clin Neurophysiol. 2006 Nov;117(11):2357-84. Epub 2006 Aug 10.


Sunday, May 17, 2009

Sympathetic nerve activity connects vestibulosympathetic reflex to cardiovascular reflexes

Form 1997 onwards various researchers have started investigating keenly on vestibule-sympathetic reflex’s interaction with cardiovascular reflexes. Ray CA has studied regulation of MSNA activity by vestibular system in humans by using head-down rotation (HDR) in the prone position. These studies have clearly demonstrated increases in muscle sympathetic nerve activity (MSNA) and calf vascular resistance during HDR. These responses are mediated by engagement of the otolith organs and not the semicircular canals.

Saturday, May 16, 2009

MSNA- muscle sympathetic nerve activity

this following is a part of my review i am going to send for a renowned journal.


Comparison of impacts of activation of SNA via metaboreflex & chemoreflex (21)
Bothdynamic and static exercise are associated with a metaboreflex activation of sympathetic activity. Both dynamic and static exercises are associated with a metaboreflex activation of sympathetic activity. Arterial hypoxemia is associated with a peripheral chemoreflex-mediated increase in sympathetic activity. Symathoexcitation manifests by increases in heart rate, blood pressure, and ventilation.
Characteristics of metaboreflex induced SNA: Increases in ventilation and heart rate being most prominent during dynamic exercise and blood pressure most prominent during static exercise.
Characteristics of chemoreflex induced SNA: Increases in ventilation and heart rate, but no change in blood pressure. Although an increase in systolic blood pressure has been reported in subjects who performed dynamic exercise in hypoxic conditions, the effects of static exercise on blood pressure in hypoxia are not well documented.

Interaction between metaboreflex & chemoreflex mechanisms in sympathoexcitation

At least 3 previous studies (Hanada A et al, Saito M et al, Seals DR et al), that these two mechanisms may interact in producing the autonomic responses. All three studies indicate that the sympathetic response to exercise during hypoxia is greater than to exercise or to hypoxia separately.

Arterial (high pressure) baroreceptors
Baroreceptors & Baroreflex:
Baroreceptors act in response to detected stretch on the blood vessel walls to elicit a negative feedback system called the baroreflex. This stretch on blood vessel wall signals to the nervous system. The output is by means of increase or decrease total peripheral resistance and cardiac output. Further because of these adjustments; as soon as there is a change from the usual blood pressure, return to the pressure to a normal level. However, they represent only a short term blood pressure regulation mechanism & over a period of 1-2 days they reset to a new BP value.
Typpes of baroreflex:
Baroreceptors can be divided into two categories
1. High pressure arterial baroreceptors and
2. Low pressure baroreceptors.
We are more concerned with the arterial baroceptors in the present context of discussion.
Arterial (high pressure) baroreceptors
Arterial baroreceptors are present in the aortic arch and the carotid sinuses of the left and right internal carotid arteries. They are vastly scattered sensory nerve endings lying in the tunica adventitia of the artery, not drug-binding molecules as the term 'receptor' may suggest. A depolarisation of these sensory endings which results in action potentials is a result of change in the mean arterial pressure. These action potentials are conducted to the central nervous system by axons and have a direct effect on the cardiovascular system through autonomic neurons. Baroreceptors are present in carotid arteries & aorta and are called carotid baroreceptors & aortic baroreceptors respectively. The efferent inputs from these baroreceptors travel through 9th & 10th cranial nerve respectively.
Baroreflex & MSNA (23, 25, 26):
Many researches have found that baroreflex is a major determinant of sympathetic discharge during exercise especially static exercise. But there is a lot of argument which baroreceptors are the major contributors i.e. the sinoaortic (receptors of aortic arch) or the caroid. Researchers Walgenbach & Donald (1983) has found during exercise, the carotid baroreflex acts to balance finely the opposing effects of sympathetic vasoconstriction and metabolic vasodilation25. However according to sherrer U & colleagues it is the sinoaortic baroreceptors which plays the dominant role. Further they also have shown in their study that in healthy humans sinoaortic baroreflex acts an effective buffer to the reflex sympathetic action caused by static muscle action23.
ABR function is impaired in hypertension and many other cardiovascular diseases. In clinical setting impaired baroreceptor function may lead to exaggerated increases in the sympathetic outflow & arterial pressure during exercises in patients with hypertension, heart failure & advancing age23. However, according to Giulliano G et al physical training improves ABR sensitivity in neurally mediated syncope patients and could be applied as a non-pharmacological therapeutic alternative for these patients26.
Thermal stress, ABR & MSNA:
At rest, whole-body heating enhances arterial baroreflex control of MSNA. This occurrence is likely to afford protection against potential decreases in arterial blood pressure in an effort to preserve orthostatic tolerance during heat stress 24.



Friday, May 8, 2009

ICU update- Sympathetic Storming

Brain injury is one of the most common types of traumatic injury. In critical care units, patients with moderate to severe brain injury are often intubated and sedated in an effort to diminish the workload of the brain. Agitation or restlessness is common in these patients and can be associated with fever, posturing, tachycardia, hypertension, and diaphoresis. This exaggerated stress response, known as sympathetic storming, occurs in 15% to 33% of patients with severe traumatic brain injury who are comatose (score on Glasgow coma scale [GCS] ≤ 8).

Signs and symptoms of sympathetic storming:
Posturing, dystonia, hypertension, tachycardia, pupillary dilatation, diaphoresis, hyperthermia, and tachypnea. The episodes appear unprovoked and can last for hours or end abruptly. Sympathetic storming often occurs after discontinuation of administration of sedatives and narcotics in the intensive care unit (ICU).

Sympathetic storming can occur within the first 24 hours after injury or up to weeks later. Precise mechanism for the increase in activity of the sympathetic nervous system is unknown, but the increased activity is thought to be a stage of recovery from severe traumatic brain injury.

Original Author:
Denise M. Lemke, MSN, APNP-BC, CNRN

Lumbar pathologies & muscle sympathetic activity in lower extremity

Both disc & vertebral abnormalities commonly presents with clinical symptoms affecting the lower extremities. Patients commonly present with pain, numbness and sensory disturbance in lower extremities. Some times these symptoms are suggested to be related to sympathetic nerve disturbance.

Akihiko N & colleagues examined whether these patients experience a difference in sympathetic nerve flow in terms of muscle sympathetic nerve activity (MSA) compared to healthy subjects. Salient points from the study are as follows:

1. Basic MSAs (muscle sympathetic activities) for IDH (inter-vertebral disc Hernia) and SCS (spinal canal stenosis) patients that were introduced from a common peroneal nerve.
2. MSA behavior and muscle blood flow introduced from the tibialis anterior muscle over 30 seconds while performing the Valsalva maneuver are examined.

NB:
1. Valsalva Maneuver is a well known technique that artificially facilitate MSA
2. Sympathetic activity in muscle has a vaso-constrictive response.

The findings are as follows:

1. Muscle sympathetic activities are statistically higher than those of the healthy subjects in basic MSAs via common peroneal nerve.
2. Muscle blood flow was inversely proportional to MSA for the normal subjects, and this relationship was observed for IDH patients as well as SCS patients.
3. But, MSA behavior and muscle blood flow introduced from the tibialis anterior muscle via Valsalva technique, showed slower changes than healthy subjects.

Hence maintained but delayed vaso-constrictive response is observed in cases affected by lumbar pathologies. According to the authors these findings suggest that the systemic physiological response to the maneuver is maintained, but that, some local modification mechanisms exist.

Reference:
Journal of Nippon Medical School; Vol. 72 (2005) , No. 2 pp.96-104

Thursday, May 7, 2009

Cervical spondylotic amyotrophy (CSA)

Shinomiya K reported dissociated motor loss due to cervical spondylosis and disc herniation presenting with deltoid paresis in the absence of sensory deficits or myelopathy (5). The clinical entity is recognized as CSA or Cervical spondylotic amyotrophy.

Cervical spondylotic amyotrophy is the clinical syndrome in cervical spondylosis characterized by severe muscular atrophy in the upper extremities, with an absent or insignificant sensory deficit. Pathophysiology of this particular syndrome has not been well understood. However, pathophysiology of this syndrome may be multisegmental damage to the anterior horns caused by dynamic cord compression, possibly through circulatory insufficiency (2). Abnormal venous circulation within the cord may cause the selective involvement of the gray matter (3).

Signs/symptoms:

1. Unilateral muscle weakness and atrophy in the deltoid and biceps muscles (1).
2. Very little/insignificant or no significant sensory deficit (2).
3. Age of onset 30-60 years (3)
4. Men were more frequently affected than women (3).

Why the sensory component is not affected in CSA?
According to Kaneko & colleagues; Pathophysiologic feature of CSA involves longitudinal gray matter lesion. Further, less damage to the lateral posterior column is the reason for the preservation of sensory function in the patients especially with distal-type cervical spondylotic amyotrophy.

The Deltoid in CSA:

Shinomiya K reported 4 types of neural injury associated with deltoid pareses associated with CSA patients. The first included isolated C5 nerve root lesions; the second, C6 nerve root lesions; the third, both C5 and C6 nerve root liaisons, and finally, intrinsic pathology.

2 types of CSA according to presentation:

Weakness and atrophy without prominent sensory changes were started from the proximal muscles are proximal type, and from the distal muscles distal type (3).
Distal type patients often presented cold paresis and/or postural finger tremor, which occasionally was the initial symptom. Distal type patients usually do not have extension of atrophy to the proximal muscles during a long course of their illness. But patients of proximal type may have muscular atrophy extended to the distal end. Most patients of proximal type had neurogenic changes on electromyography extended to the distal muscles (3).

2 types of CSA basing on Radiological pathology (5):

Basing on multiple radiological modalities CSA patients were divided into 2 pathologic types;
Type I: The first showed focal bony spur and disc herniation with axial cord rotation and nerve root compression
Type II: The second type demonstrated ventral cord flattening.

Neuroradiological examination:

As revealed on neuroradiological examinations by various authors the compressive paththology can involve anterolateral spinal cord compression or ventral root compression at the C4-5 and C5-6 spaces (1).
Proximal type CSA patients had a cord atrophy at C4/5 intervertebral level, and distal type had cord atrophy at C5/6,6/7. Hence the responsible lesion for the cervical spondylotic amyotrophy is in anterior horn at C5-T1 cord level for the proximal type, and at C7-T1 for the distal type (3).
CSA with intramedullary lesion Fujiwara has demonstrated a case study of a patient who showed severe wasting of the left triceps muscle without any sensory disturbance or long tract sign. A delayed (6 hours) CT scan after intrathecal injection of metrizamide revealed intramedullary left anterior horn cavitation or cystic necrosis. Thus Fujiwara was the first author to report a case of cervical spondylotic amyotrophy, in which intramedullary lesion was confirmed only at the affected side of the spinal cord (4).

Electrophysiologic studies in CSA:

These studies include evoked spinal potentials, motor evoked potentials, and evoked muscle action potentials. Usually Motor evoked potentials, recorded epidurally from the ventral aspect of the thecal sac and the nerve root are clinically significant in diagnosis of CSA.

EMG in distal type of CSA: Kaneko K reported attenuation of postsynaptic potentials with preserved presynaptic potentials at C4-C5, C5-C6, and C6-C7 was characteristic in the evoked spinal cord potentials after median nerve stimulation. The amplitude of the evoked spinal cord potentials after median nerve stimulation was preserved at C2-C3. Further these features implies that lateral posterior column in the spinal cord had less or no involvement in distal-type cervical spondylotic amyotrophy.

Differential diagnosis:

ALS (amyotrophic lateral scelerosis) poses a diagnostic challenge in Cervical spondylosis complicated by CSA.according to Sindo K et al muscle sympathetic nerve activity (MSNA) is the point of differentiation between cervical spondylotic amyotrophy (CSA) and amyotrophic lateral sclerosis (ALS) with cervical spondylosis (CS). During head-up tilting, changes in BP and MSNA were significantly less in patients with ALS than in patients with other subjects. MSNA at rest clearly differentiated CSA from ALS with CS.

Surgical Outcomes:

MORI Kentaro et al reported of 2 the patients surgically treated; one had good recovery of motor strength and the other had moderate recovery despite persistent motor atrophy. These authors have concluded that surgical intervention is effective in patients with CSA despite severe muscle atrophy unless MR imaging shows the presence of severe degenerative intramedullary lesion.
Kunihiko S et al retrospectively investigated the surgical outcomes and radiographically documented changes after microsurgical posterior foraminotomy with en bloc laminoplasty in patients with cervical spondylotic radiculo-myelopathy (CSRM), including cervical spondylotic amyotrophy (CSA), during a period greater than 2 years. This procedure yielded outstanding results both in CSRM & CSA.

References:
1. MORI Kentaro et al; Neurologia medico-chirurgica 46(7) pp.366-370 20060715 (The Japan Neurosurgical Society )
2. Kameyama, Takashi; Spine: 15 February 1998 - Volume 23 - Issue 4 - pp 448-452, Diagnostics
3. Tsuboi Y et al; Rinsho Shinkeigaku. 1995 Feb;35(2):147-52.
4. Fujiwara, Keiju; Spine; 15 May 2001 - Volume 26 - Issue 10 - pp E220-E222, Case Reports
5. Shinomiya K; Spine: January 1994 - Volume 19 - Issue 1
6. Kaneko K; Spine, 1 May 2004 - Volume 29 - Issue 9 - pp E185-E188, Case Report
7. Sindo K et al; Amyotroph Lateral Scler Other Motor Neuron Disord. 2002 Dec;3(4):233-8.
8. Kunihiko S; Journal of neurosurgery, August 2006 Volume 5, Number 2