Atrial fibrillation (AF) is a major risk factor for TIA and Stroke.
It is estimated that AF accounts for >20% of all strokes.
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.
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.
We have urged you to call 911, and get to the hospital by Ambulance.
Certified stroke centers, like Monmouth Medical Center, have established protocols to get brain scans and blood work done as quickly as possible.
But what about if the Neurologist can’t get to the hospital quickly enough?
Suppose it’s late in the evening on July 4th, and the Neurologist gets stuck in traffic driving to the hospital.
You’re sitting in the emergency room with a stroke losing precious minutes.
Teleneurology allows the Neurologist to use a secure video conferencing system to examine and counsel an emergency room patient from wherever he or she may be:
Monmouth Medical Center is currently investing in telemedicine and teleneurology to improve patient care.
Watch this space for more information!
Post written by Dr. Farida A. Malik , PGY3 Medical Resident, Monmouth Medical Center
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.
The family was reassured about the benign nature of the condition and she was discharged home the next day still with memory lag.
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.
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.
This 46-year-old woman was healthy except for a history of occasional migraine headaches and cigarette smoking. On the day of admission she had fallen down a short flight of steps carrying a heavy box. About 2 hrs later she complained of some neck pain. Then later that evening developed abrupt onset left sided weakness. She arrived at the emergency room within 1.5 hrs of the onset of weakness. On examination, she was alert, but she had a right gaze deviation (she wouldn’t look to the left side) and the left side was completely paralyzed. She had a normal brain CT scan.
The stroke team was notified, and she was given intravenous thrombolytic (“clot busting”) drug therapy within 1/2 hr of her arrival at the hospital and 2 hrs since the onset of her symptoms.
Carotid ultrasound subsequently showed no flow in the right internal carotid artery, and carotid arteriography subsequently showed near occlusion of the artery from an arterial dissection (see image below, red arrow):
What is cervical artery dissection?
Cervical artery dissection is caused by bleeding inside the wall one of the major arteries in the neck.
This process is thought to be triggered by local injury to the inside layer of the vessel wall.
Cervical artery dissections occur from blunt trauma:
Cervical artery dissection can also occur after minor trauma, particularly in someone with a genetic predisposition:
What diseases predispose to arterial dissection?
There are some specific syndromes such as Marfan syndrome, Pseudoxanthoma elasticum and Ehlers- Danlos syndrome type IV that are associated with a weakness in the arterial wall making an arterial dissection more likely:
In other cases, the specific cause of arterial weakness is unknown, but there is ongoing research to try to identify genetic links.
What happens after a cervical artery dissection?
Symptoms can be caused from the damaged arterial wall itself (local symptoms) and some affected patients will later develop strokes.
Local symptoms include neck pain, unusual headache and/or Horner’s syndrome.
What about stroke?
Stroke symptoms only occur in 25-30% dissections and can occur several days after the neck trauma and/or onset of local symptoms.
The arterial dissection narrows the space inside the blood vessel (the lumen), so less blood flow gets to the brain:
Cervical arterial dissections can also cause stroke when pieces of blood clot break off and move with the blood flow only to block small arteries further inside the brain (cerebral thromboembolism), or if the dissection tracks across (and blocks off) an arterial branch (see below):
How is arterial dissection diagnosed?
Magnetic resonance imaging is probably the easiest way to make the diagnosis:
How is it treated?
In most cases the arterial dissection ultimately heals on its own without any surgical intervention. There has been some controversy surrounding the use of anticoagulant vs anti-platelet drugs for stroke prevention after cervical artery dissection, but most current data favors the use of the anti-platelet drug aspirin:
Of course, for patients presenting with symptoms of acute stroke, throbolytic therapy is also an option, and can improve outcome without increased risk in stroke from dissection:
Click here to find out more about cervical artery and dissection and stroke.
Click here to find out what to do if you think your having a stroke.
Click here to find out more the certified stroke center at Monmouth Medical Center.