Click here to see the abstract.
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.
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.
PGY III resident Dr Mohamed Sheta won overall best prize, as well as the medicine and cardiology prizes, for his research project analyzing the 6-month outcome data from Monmouth’s innovative new TIA Rapid Evaluation Center.
Unfortunately, Dr Sheta was not able present his outstanding data in person, but here are pictures of him presenting some of the same data at the 2013 International Stroke Meeting in Hawaii earlier this year (left) and also at the 2013 Drexel University Research Day (right):
PGY I-III residents Drs Martin Miguel Amor, Paavani Atluri, Alan Hamza (left and right), Michael Chan (right only) and Mohamed Sheta (above) won the best poster award.
One of their findings was that most acute stroke patients not given thrombolytic therapy because of too “mild” a neurologic deficit still needed in-patient rehabilitation, so we should probably lower our threshold for administering the drug.
We also had a neuroscience poster by PGY II residents Drs Nagakrishnal Nachimuthu and Michael Chan on an acute stroke case we have already featured on this blog:
Case presentation prepared by Drs N. Nachimuthu and M Chan, Residents, Dept of Internal Medicine, Monmouth Medical Center
When feasible, administration of tissue plasminogen activator (tPA) is the standard of care for treatment of acute ischemic stroke to improve outcomes. Treated patents may be found on subsequent work up to have significant stenosis of one or both carotid arteries. Carotid endarterectomy (CEA) has been shown to be more effective than medical therapy for preventing subsequent strokes in patients with symptomatic stenosis. However, the timing of CEA after ischemic stroke with or without administration of tPA remains controversial, particularly in patients with critical stenosis or unstable symptoms.
To better illustrate this dilemma, we present the case of a 43 year old male who presented with symptoms of acute stroke, was given tPA within the recommended time frame, but was subsequently found to have high grade carotid stenosis and fluctuating symptoms. We follow with a review and discussion of recent literature showing that in select cases, CEA can be done early with no increase in perioperative complications or adverse events.
A 43 year old man presented to our Emergency Room after he was found to be restless in bed by his wife at 12:30am on the day of admission. He was also unable to express himself and was noted to have had a right sided facial droop. He was last observed to be asymptomatic 1 hour and 45 mins earlier when he was getting ready for bed at 10:45pm.
The patient arrived at the ER at 1:15am and a code stroke was immediately called. Initial examination revealed aphasia, disorientation, and right-sided facial droop, with a NIH stroke score of 5. There was no motor weakness and the rest of the neurologic exam was unremarkable. Vital signs were stable and within normal limits. A stat CT scan was done which did not show any hemorrhage or findings of ischemia:
After the CT scan, the patient initially showed some improvement in speech and orientation with the NIH stroke score dropping to 2. It seemed that treatment with tPA might not be necessary.
However, at 2am the patient’s symptoms again worsened acutely. Repeat NIH stroke score was 6 at 1:50am. tPA was given at 2:10am, 3 hours and 25 mins from last known normal.
Following tPA administration, the patient seemed to be improving again and was admitted to the ICU for close observation. However, a few hours later, at 6am, the patient again worsened. He had new right sided weakness and worsening of his aphasia and right facial droop. Given the fluctuating course of the patient’s symptoms he underwent a repeat stat CT of the head to rule out a bleed. This was negative. A CT angiogram of the head and neck was done at the same time, and this showed severe stenosis (almost total occlusion) of the left internal carotid artery:
At this point, our multidisciplinary stroke team suggested that he undergo emergent carotid endarterectomy to prevent further deterioration of his neurologic status. This was a controversial decision, but after discussing the risks and benefits of the procedure, the patient consented and a carotid endarterectomy was done urgently and completed at 12:05am on the second hospital day, or 21 hours and 55 mins from administration of tPA.
Intraoperatively, the patient was found to have left internal carotid artery narrowing secondary to hemorrhagic plaque and dissection:
The patient experienced no intraoperative complications. Post-operatively, he was started on Lovenox at 1mg/kg every 12 hours. He did develop a hematoma on the site of the CEA, and Lovenox and antiplatelets were immediately stopped. Aspirin at 325mg daily was resumed after a day and Plavix 75mg daily was resumed the next day, after the hematoma had shown signs of resolution. The patient experienced no further complications.
He underwent a repeat CT scan after surgery, more than a day from symptom onset, which did show an evolving left hemispheric stroke:
However, clinically, in the hours following CEA, his right sided weakness improved.
By the time the patient was discharged to a rehabilitation facility, he had only mild aphasia, a residual right facial droop, but no motor deficits.
Many vascular surgeons suggest waiting 6-8 weeks after acute stroke before considering CEA, because of fear or bleeding or extension of cerebral infarction during the surgery. However, this delay can lead to recurrent stroke or complete occlusion of the carotid artery. Moreover, more recent studies have shown that urgent early CEA can be performed on patients with evolving symptoms without additional risks.
We feel that our patient’s near complete recovery was the direct result of early CEA, done despite the recent stroke and potential hemorrhagic complications associated with the use of tPA.
These types of complicated medical decisions can only be made after discussion between neurologists, intensivists and vascular surgeons in a multidisciplinary stroke center.
Click here to find out more about Monmouth’s Certified Stroke Center.
Most strokes are caused by a blocked artery that starves an area of the brain of it’s blood supply, leading to an abrupt loss of brain function.
This can lead to the sudden onset of:
Paralysis on one side (including a drooping face):
Loss of vision in one eye or to one side:
Or a change in speech:
There’s a FDA approved treatment for acute stroke which can open up that blocked artery, and increase your chances of getting better, but only if administered within a few hours of the onset of your symptoms, and even then sooner the better.
However, studies show that less than 5% of acute stroke patients get this clot busting therapy, mostly because they do not get the hospital in time.
A recent study found that only 2/3 of stroke patients came to the hospital by ambulance. Furthermore, if they did come by ambulance, they were 50% more likely get the clot busting therapy.
So, if you think you are having a stroke, ACT FAST, call 911 and get to the hospital right away!
On May 11, 1989, President George Bush signed Presidential Proclamation 5975 designating May as National Stroke Awareness Month at the urging of National Stroke Association.
Since then, the National Stroke Association has been honoring this special time of the year to increase public awareness of stroke in an effort to conquer it.
Check our “events” tab for special stroke awareness month educational events emphasizing this message.
If you are found to have a carotid artery blockage (stenosis), the chances are you can find a doctor who will want to operate or put a stent in to open it up for you, no matter whether you have had symptoms or not.
And, it it true that if you have had a recent TIA or a stroke and have a carotid stenosis, you should consider having surgery as soon as possible to prevent another cerebrovascular event.
However, we have already blogged about how the benefits of having surgery over medical therapy are much lower for patients who are found to have a carotid stenosis on a routine screening study, without ever having had any symptoms, i.e. asymptomatic carotid artery stenosis.
The scientific evidence for avoiding surgery on asymptomatic carotid disease just got a little stronger.
A recent study followed 4319 patients with a history of known arterial disease (coronary heart disease, abdominal aortic aneurysm, or peripheral arterial disease) or risk factors for atherosclerosis (diabetes mellitus, hypertension, and hyperlipidemia), but no previous TIA or stroke. All patients underwent carotid artery doppler, and 293 (about 7%) had a carotid stenosis (>50%). All patients underwent intensive medical management, and were followed for 5-6 years. The risk of stroke was 0.35%/yr overall and 0.4%/yr for patients with carotid stenosis (50-99%), not a statistically significantly difference.
The bottom line here is that if you have carotid stenosis, the first step is to determine if that stenosis is symptomatic or asymptomatic. If there is any doubt about this, you should consult with a stroke expert to be sure. If your carotid stenosis is asymptomatic, it is probably more important to quit smoking, treat blood pressure, treat high blood sugar and treat high cholesterol, and take an anti platelet agent like aspirin, than rush in to getting surgery.