Monmouth Neuroscience at the 2014 NJ Stroke Conference

We are happy to report that Monmouth’s stoke program was well represented at the 2014 New Jersey Stroke Conference earlier this month.

Two department of medicine residents, Drs Amor and Chan, presented our TIA center data in the poster session:

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Dr Holland gave a talk on the role of telemedicine in stroke rehabilitation.

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Data from our TIA Rapid Evaluation Center (TREC) at the 2014 International Stroke Convention

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Click here to see the abstract.

Click here and here to find out more about this innovative program.

Atrial Fibrillation? Better ask your doctor about anticoagulation.

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Atrial fibrillation (AF) is a major risk factor for TIA and Stroke.

It is estimated that AF accounts for >20% of all strokes.

This risk can be lowered by as much as 60% by taking an anticoagulant such as warfarin (Coumadin).

Current guidelines recommend anticoagulation for all patients with AF, even paroxysmal (intermittent) AF:

1. If they have had a prior TIA or stroke, or

2. If they have two or more of the following risk factors: (1) age > 75 years, (2) history of hypertension, (3) diabetes mellitus, and (4) moderately or severely impaired left ventricular systolic function and/or heart failure.

If you have AF, click here to calculate your CHADS2 score and stroke risk, and click here to calculate your risk of bleeding from anticoagulation.

Your risk of stroke is much higher than your bleeding risk, right?

Many AF patients don’t get anticoagulants because they are considered a fall risk. If you had AF and need anticoagulation, you would have to fall more than 300 times a year for the harm from the falls to outweigh the benefits of anticoagulation.

Despite these guidelines, recent studies have shown that:

1. Less than half of AF patients with a high stroke risk receive anticoagulants.

2. Even less patients with paroxysmal (intermittent) AF than those with permanent AF receive anticoagulants (31 vs 49%), even though the stroke risk is the same in both groups.

3. Too few patients with new onset AF are started on anticoagulants (only 52%).

We need to do better.


Click here to download a booklet about AF and stroke.

Click here to download a worksheet that you and your doctor can use to decide if anticoagulation is right for you.

Memory misplaced

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Post written by Dr. Farida A. Malik , PGY3 Medical Resident, Monmouth Medical Center

Case Summary

This 69 year old lady had a remote history of breast cancer, hypertension and hypothyroidism.  She was brought to the Emergency Room by her husband because of abrupt onset confusion after waking up that morning. She was disoriented and was noted to ask the same questions over and over again. She had no difficulty walking, talking or dressing herself. She denied having headache or visual problems. There was no history of head trauma, seizures or any prior similar episodes.

When she was seen in the in the ER she knew her name and recognized her husband.  She was able to follow simple commands.  She had no recollection of events since morning or the day before. She repeatedly asked how she got to the hospital, despite being told several times that her husband brought her. Neurological examination otherwise was unremarkable.

CT scan of head, MRI of the brain and EEG were all normal.

She was diagnosed with TRANSIENT GLOBAL AMNESIA.

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The family was reassured about the benign nature of the condition and she was discharged home the next day still with memory lag.

Discussion

Transient global amnesia (TGA) is a clinical syndrome of reversible anterograde amnesia accompanied by repetitive questioning that occurs in middle-aged and elderly individuals.

The incidence of TGA is 5.2 to 10 per 100,000 per year overall, but 23.5 to 32 per 100,000 per year in adults aged 50 and over.

During a TGA episode recall of recent events simply vanishes. One may also draw a blank when asked to remember things that happened a day, a month or even a year ago.  Unlike “soap opera amnesia” (Jason Bourne) affected patients do remember who they are and recognize the people they know well.  But that doesn’t make their memory loss less any less disturbing.

Fortunately, episodes are usually short-lived, recover spontaneously, and are unlikely to recur.

The precise cause of TGA is unknown.  Atherosclerotic risk factors (eg. hypertension, diabetes, hypercholesterolemia) are not associated with TGA.
However there may be a link between TGA and history of migraines.

The primary site of neurologic functional disturbance is the medial temporal lobe and hippocampus.
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The pathogenesis of this transient disruption is unknown. Current theories include arterial ischemia, venous congestion, and migraine, but no theory explains all of the clinical features.

The diagnosis is made by the following signs and symptoms:

  • Sudden onset of memory loss, verified by a witness
  • Retention of personal identity despite memory loss
  • Normal cognition, such as the ability to recognize and name familiar objects and follow simple directions
  • Absence of signs indicating damage to a particular area of the brain, such as limb paralysis, involuntary movement or impaired word recognition
  • Duration of no more than 24 hours
  • Gradual return of memory
  • No evidence of seizures during the period of amnesia
  • No history of active epilepsy or recent head injury

Some common triggers identified are:

  • Sudden immersion in cold or hot water
  • Strenuous physical activity
  • Sexual intercourse
  • Medical procedures, such as angiography or endoscopy
  • Mild head trauma
  • Acute emotional distress, as might be provoked by bad news, conflict or overwork

There are no confirmatory diagnostic tests. The initial evaluation and management of patients with TGA focuses on excluding other diagnoses and should include the following:

  • If the patient is symptomatic on presentation, the patient should be observed in the hospital until the amnesia resolves.
  • Diagnostic testing includes oxygenation status, serum electrolytes, glucose, and a toxicology screen.

The need for further testing varies depending on the circumstances, such as how typical the event is for TGA, the presence of vascular risk factors, and whether the ictus was observed. Patients with recurrent or brief episodes, or activity suggesting motor automatism should be evaluated with EEG for possible epilepsy. A neuroimaging study may be performed in all patients, preferably a brain MRI with DWI, to exclude acute ischemia, head trauma, and other causes.

Treatment is not required for TGA. The condition usually does not recur, and the patient does not need to be restricted from driving unless events are recurrent.

There is no increased risk of mortality, epilepsy, or stroke following TGA as compared with age-matched controls.

What’s best for stroke prevention, aspirin, clopidogrel or both?

We have already blogged about the benefits of anti-platelet agents in stroke prevention.

We haven’t talked about how they work, or which one(s) are best.

Platelets are an important component of blood clotting (or hemostasis) – the normal process that stops us bleeding and facilitates healing after a cut or other injury:

This same platelet led coagulation cascade can lead to blood clot formation inside intact but diseased arteries laden with atheroma – the result of years of hypertension, high cholesterol and smoking:

These small blood clots then break off and travel down the artery causing (in the case of a cerebral blood vessel) a TIA or stroke.

There are three currently available  anti-platelet medications  – aspirin, modified release dipyridamole with aspirin (Aggrenox) and clopidogrel (Plavix) which inhibit platelet activation and aggregation.

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Comparative studies have shown that all three drugs reduce the risk of ischemic stroke in high risk patients who have had a previous stroke or TIA.  Aspirin is the cheapest of the three.  Aggrenox is more effective than aspirin alone, but can cause troubling headache in some patients.  Clopidogrel can be used in patients who are allergic or immune to aspirin.

Because these drugs work in different ways, investigators have asked whether combining them might be even more beneficial.

The initial studies said No.  The MATCH (2004), CHARISMA (2006) and SPS3 (2012) trials all showed that long term use of the combination of aspirin and clopidogrel failed to reduce the risk of major vascular events and also led to significant increased life-threatening bleeding complications (mainly intracranial and gastrointestinal) compared with either drug alone.

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However, new data from the CHANCE study presented at this year’s international stroke meeting shows that a short course of combined treatment might be helpful:

The study enrolled 5170 patients who had suffered a TIA or minor stroke within the previous 24hrs, randomly assigned to one of two treatment groups:  The first group received aspirin (75-300 mg one-day loading dose followed by 75 mg/day).  The second group received the same aspirin regimen plus clopidogrel (loading dose of 300 mg followed by 75 mg/day) for 21 days, then just the clopidogrel alone after that.

The study showed that the 90d stroke incidence was lower in those who received both aspirin and clopidogrel.

The risk of hemorrhagic stroke and other severe bleeding was the same in the two groups.

In other words, short term combination anti-platelet therapy might be more effective in preventing stroke in this high risk TIA and minor stroke group, and this is something we will be offering patients seen in Monmouth’s innovative TIA Rapid Evaluation Center.

Dr Holland and Monmouth Neuroscience Institute’s TIA Rapid Evaluation Center Honored at the 2013 Heart Ball

The American Heart Association and American Stroke Association gathered to recognize Dr. Neil Holland and Dr. June Duck as this year’s medical honorees at the annual Heart Ball on June 21 at the Ocean Place Resort and Spa in Long Branch.

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Drs Holland and Duck with their awards.

Dr. Holland was recognized for excellence in stroke care. Commended for his role in developing a TIA and Minor Stroke Rapid Evaluation Center, Dr. Holland has focused care to optimize stroke prevention without the need for hospitalization in high-risk patients.

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The Monmouth TIA Center Team – L to R – Neuroscience ARNP Florence Armour, Hospital VP Shirley Hwang, Program Director Dr Holland, Neuroscience Coordinator Felesia Swanson & Dept of Medicine Chairman Dr Allan Tunkel

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Dr Holland with his partners – L to R – Drs Gennaro, Anayiotos, Gilson, Holland, Herman, Davis, Mendelson & Ponce.
The success of the TIA Center is the result of close cooperation between hospital administration, all of the doctors in the practice, the Emergency Room, and many many other members of the hospitals medical and technical staff.

Find out about Monmouth’s Stroke Service and TIA Center.