Parsonage-Turner Syndrome Revisited

Posted by Daniel Rubio, Drexel University College of Medicine Class of 2014

Parsonage-Turner Syndrome (PTS) is an inflammatory disorder that affects the brachial plexus an important network of nerves which lies deep in the armpit (axilla) giving off nerve brachnes including the axillary, radial, musculocutaneous, ulnar and median nerves which supply power to the shoulder and entire upper extremity.

What does PTS look like?

Unlike other brachial plexopathies, PTS begins spontaneously, without any prior injury to the arm, neck, or axilla.  The classical presentation is severe pain followed by patchy weakness in the shoulder, biceps, and the muscles controlling the thumb and first two fingers (index and middle).  It may also present with a finding known as winged scapula: the shoulder blade sticks out more from the back especially when pushing yourself off a wall.  Weakness may be so severe that the muscles may actually shrink (atrophy).  Pain may be found in the shoulder and along the outside of the upper arm and the thumb-side (lateral) of the forearm and hand.  Pain symptoms usually occur before the weakness and may last up to 4 weeks.  Patients may experience alteration in sensations in the upper extremity, specifically increased sensitivity to touch and temperature and/or tingling.  Symptoms may affect one or both sides, but they usually are asymmetric if they both sides.

 

What causes PTS?

Approximately 50% of patients describe some type of stressful event or illness prior to the onset of symptoms: infection, exercise, surgery, pregnancy, or vaccination.

Diagnosing PTS

Your neurologist can make the diagnosis based on signs and symptoms (especially if you do the above dance); however, sometimes further testing is required to ensure accurate diagnosis.  Suspicion of PTS should occur based upon pattern of initial sudden and severe pain followed by weakness in the upper extremity and slow recovery.  The neurologist may use nerve conduction studies and needle electromyography to document denervation to support clinical suspicion.  Blood tests and imaging rarely help make the diagnosis of PTS.

Help doctor! Fix me?

There is currently no specific treatment for PTS and management usually involves symptom relief.  Pain relief with short course of narcotics may be necessary.  A short course of steroids may be given, which may or may not help relieve symptoms or hasten recovery.  Physical therapy may be prescribed to maintain range of motion and decrease risk of atrophy.  Despite the above measures, there is no treatment to quicken recovery.

When will I be cured?

Recovery of symptoms begins 1-3 months following onset of symptoms; however, maximal recovery may take up to 1-3 years and some patients may be left with residual symptoms.

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Neuroscience Featured at MMC’s Chinese Medical Program Health Workshop

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Global warming, bad for MS patients!

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Wilhelm Uhthoff (1853-1927) a German neuro-ophthalmologist described an optic neuritis patient in 1890 who would develop episodes of temporary vision loss during physical exercise.

This condition, subsequently known as Uhthoff’s phenomenon, was later found to be caused by a rise in body temperature.

More than half of all multiple sclerosis (MS) patients spontaneously report being sensitive to environmental heat.

When specifically asked, as many as 70% MS patients report that high temperatures worsened their MS.

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Increased temperature blocks action potentials in compromised (demyelinated) neurons resulting in slower conduction velocities and/or temporary failure of conduction altogether (conduction block).

This explains the temporary exacerbations in neurologic dysfunction that underlie Uhthoff’s phenomenon.

So what can you do?

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Drugs like Ampyra (dalfampridine or 4-aminopyridine) improve conduction across demyelinated neurons, and can improve Uhthoff’s phenomenon, but these drugs are not currently FDA approved for this indication, and used off label can cost as much as $1200/month.  It might be cheaper to move to Alaska or buy a window box AC unit?

Post-operative peripheral neuropathy

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Post provided by Kevin Turezyn, Drexel University College of Medicine Class of 2013:

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While the overall risks of undergoing a procedure involving general anesthesia have decreased dramatically over the last 25 years, there is one phenomenon that still puzzles both anesthesiologists and surgeons: post-operative peripheral neuropathies.

Why a patient undergoing an appendectomy would wake up with weakness in their arm is still in large part a mystery. Luckily most patients recover fully, but a small subset suffer from permanent damage.

While relatively infrequent, peripheral nerve injury after anesthesia is one of the largest sources of professional liability for anesthesiologists. Estimates of its frequency range from .03% to .11% of patients who undergo anesthesia.

Interestingly, despite numerous attempts to decrease its incidence, anesthesiologists have had little success.

While the exact cause is unknown, many believe that it relates to patient positioning. There are several points in the body where nerves run very close to the surface leaving them vulnerable to injury. For example, the most commonly injured nerve is the Ulnar nerve of the arm. When this nerve goes through the elbow, it is very close to the surface where it has little body tissue for protection. People commonly hit this nerve in daily life, giving them a painful sensation called hitting your “funny bone”. Other commonly injured nerves include the radial nerve (compression in the spiral groove against the humerus), brachial plexus from traction on the arm, sciatic nerve in the buttock and peroneal nerve against the fibula head.

The American Society of Anesthesiologists has published guidelines for prevention of perioperative peripheral neuropathies. The guidelines focus on pre-operative assessment for patients who are at higher risk ( diabetics, alcoholics, patients with peripheral vascular disease) as well as proper positioning of the extremities and adequate padding.

Click here for the full guidelines.

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When peripheral nerve injury does occur, it frequently resolves on its own, although this can take take several months. During this time, there is little that can done to speed recovery. Physical therapy is often recommended to prevent muscle contractures and atrophy during this time period.

If a patient feels that they suffered a nerve injury during surgery, it is important that they be evaluated right away by a trained neurologist. Testing such as an electromyogram (EMG) can be done to determine the location of the injury and prognosis for recovery.

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CIDP Patient Impoves with Treatment

This 11-year-ol girl had a 4-month history or progressive proximal leg weakness leading to falls and difficulty with stairs. There was no back pain, numbness in the legs or difficulty with badder or bowel control.

Her exam showed leg weakness, absent reflexes and normal sensation.

Her serum CK was normal.  Her EMG showed features of acquired demyelinating neuropathy, most notably absent F-waves.  Her CSF showed a mildly elevated protein level without cells (“albuminocytologic dissociation”).  She was treated with a course of intravenous immune globulin and made a remarkable recovery within 4-weeks.

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Chronic inflammatory demyelinating polyneuropathy (CIDP)

CIDP is an acquired immune-mediated inflammatory disorder of the peripheral nervous system, causing demyelination, conduction slowing and conduction block:

Affected nerves fail to respond to stimuli causing progressive muscle weakness, loss of deep tendon reflexes (areflexia), fatigue, and abnormal sensations.

Most cases show evidence of demyelinating neuropathy on electrodiagnostic studies and albuminocytologic dissociation in the cerebrospinal fluid.

Early diagnosis and treatment is important in preventing irreversible axonal loss and improving functional recovery.

However, CIDP is probably under-recognized and under-treated due to its variable presentation and the limitations of clinical, serologic, and electrophysiologic diagnostic criteria.

Consultation with a sub-specialty trained neuromuscular physician is critical.

Monmouth Stroke Awareness Month Event, May 15 2013, 12pm

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Join us for a FREE education event

WHEN – Wednesday May 15, 2013 12-1pm

WHERE – Long Branch Senior Center

Dr Neil Holland, Medical Director of the Stroke Program and Neuroscience Institute, Monmouth Medical Center

Nanette DeLeon, Registered Dietician, Monmouth Medical Center

stroke

Learn about:

The warning signs and symptoms of a stroke,

How urgent care is crucial in saving lives and preventing disability,

The telltale symptoms of transient ischemic attack, sometimes referred to as “mini-stroke”,

Nutrition for stroke prevention.

CALL 732 571 6542 To Register!

Click here for directions.

Find out more about: the Monmouth Stroke Center, Monmouth TIA center, Strokes and TIAs.

Numb tingling hands, it’s probably carpal tunnel syndrome

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Numbness and tingling in the hands is most often from Carpal tunnel syndrome (CTS).

CTS is caused by compression of the median nerve as it travels across the wrist with the tendons between the carpal bones and the flexor retinaculum (also know as the transverse carpal ligament):

flexor retinaculum

CTS is caused by compression of the median nerve under the flexor retinaculum also known as transverse carpal ligament.

Compression an injury to the median nerve causes numbness and tingling mostly affecting the thumb, index finger, middle  finger, and half of the ring finger.

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CTS usually causes numbness and tingling mostly in the thumb, index and middle fingers

More severe cases also cause weakness and wasting of the muscle at the base of the thumb that abducts the thumb away from the fingers (abductor pollicis brevis or APB):

thumb abduction

Thumb abduction, the movement that is weak in more severe cases of CTS, where there is involvement of both motor and sensory median nerve fibers.

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Wasting of APB muscle belly (“thenar eminence”) in severe CTS

In severe cases, the numbness can seem to affect the whole hand, and can even radiate up the forearm and arm:

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Symptoms are often worse typing, driving, and frequently wake the affected patient up at night:

cts night

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CTS can usually be diagnosed on clinical grounds.  A helpful physical finding is a tingling in the wrist and fingers caused by a tap over the carpal tunnel (Tinel’s sign):
http://www.youtube.com/watch?v=VtrC9dnVrrQ&start=37&rel=0

In some cases, an electrodiagnostic study may be necessary to confirm the diagnosis:

cts emg

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CTS is usually “idiopathic” (we don’t know why it happened), but some cases are caused by diabetes, pregnancy, thyroid disease, joint swelling from rheumatoid arthritis, heavy manual work and work with vibrating tools.

Treatment usually begins with conservative measures, like avoiding exacerbating activities, and wearing a neutral position night splint:

cts splint

Patients who do not improve with these conservative measures can undergo a surgical procedure to release the compressed median nerve:

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Want to find out more?

Click here to take an on-line quiz to see if you have CTS.

Watch this on-line video tutorial explaining the causes and treatment of CTS:
http://www.youtube.com/watch?v=_p799CIpRL0&start=13&rel=0

If you think you might have CTS, you should make an appointment to see a neurologist.

Click here to use our physician finder service.