Introduction:
Minor strokes, mini-strokes, small strokes and Transient ischemic attacks (TIAs) are one and the same. TIAs are common neurologic events characterized by stroke-like symptoms that completely resolve. They were previously thought to be benign but research over the past decade has revealed the high risk of further neurologic and cardiac events following TIA[1]
My submission in this article is that TIAs are ill-omened and call for immediate admission, comprehensive investigations, acute interventions, including carotid endarterectomy (CEA). Due to the high early risk of recurrent stroke in the acute period after TIA and minor stroke, more intensive antiplatelet regimes given over a short period may be beneficial.[2]
Definition:
About TIAs
TIA is a transient episode of neurologic dysfunction lasting a few minutes and no more than 24 hours. Many have queried and quarrelled with this definition, arguing that this might delay presentation to hospital and also delay treatment with proven efficacious medications. They would prefer that patients and doctors do not wait for resolution before urgent presentation to hospital
Signs and Symptoms:
TIAs and strokes cause the same symptoms, such as contra lateral paralysis (opposite side of body from affected brain hemisphere) or sudden weakness or numbness. A TIA may also cause sudden dimming or loss of vision (amaurosis fugax), aphasia, slurred speech (dysarthria) and mental confusion. But unlike a stroke, the symptoms of a TIA can resolve within a few minutes or 24 hours. Brain injury may still occur in a TIA lasting only a few minutes. Having a TIA is a risk factor for eventually having a stroke[3] [4]
Management:
Immediate admission and treatment
A substantial proportion of patients with TIA and minor stroke become disabled largely due to recurrent events.[5] [6] Urgent evaluation and immediate initiation of treatment reduces stroke after a TIA dramatically.[7] Rapid assessment and treatment in the emergency department or in specially designed 'TIA clinics' appear to reduce stroke rate.[8] [9] TIA patients should be evaluated with a history and physical examination, laboratory tests, electrocardiography, and head and neck imaging (Brain scan and carotid ultrasonography).[4] CT is faster and more accessible than MRI, and therefore is the better neuroimaging modality for the treatment of acute stroke.[10]
Risk factors such as hypertension, HIV, tobacco and other substance abuse, use of oral contraceptives, hyperlipidemia, and diabetes mellitus need to be defined. Neurological examination, blood pressure measurement in both arms and, when appropriate, a test for postural hypotension, measurement of pulse rate and rhythm, cardiac auscultation, and peripheral vascular examination are essential. Arterial pulses and bruits should be described.
Neurological consultation is important for patients with neurological symptoms or signs. Some patients with concurrent medical illnesses (eg, pulmonary, renal, hematologic, hepatic, and other diseases) will require an evaluation to assess surgical risk.
An electrocardiogram is mandatory. Additional cardiac evaluation and consultation should be considered to seek potential cardiac sources of embolism that might have caused the brain ischemia and to assess the presence and severity of coexistent coronary artery disease.
Hospitalization allows neurologic monitoring after a TIA so that tissue plasminogen activator (tPA) can be given promptly if a subsequent event occurs. Hospitalization also increases the likelihood that atrial fibrillation, carotid artery stenosis, and other conditions will be quickly evaluated and treated.
The ABCD (2) score11
The risk of stroke after a TIA is very high overall and can be quickly stratified with a simple score based on age, blood pressure, history of diabetes, and the duration and features of the TIA (ABCD2).[11] An ABCD2 score > 3 was significantly associated with the combined endpoint of cerebral or cardiovascular ischemic events, and death of vascular or unknown cause. An ABCD2 score > 3 is associated with an increased general risk for vascular events in the medium to long-term follow-up after TIA.[12] The ABCD2 score is calculated as shown in the table (Table 1).
Table 1
Prediction of risk of stroke after a TIA: ABCD2 Score11
Characteristic
Points
AGE 60 and above
1
BLOOD PRESSURE 140/90 mmHg and above
1
EVIDENCE OF TIA
Weakness
2
Speech Impairment
1
DURATION
More than an hour
2
DIABETES
1
TOTAL SCORE
1-7
Thrombolytic therapy
The majority of strokes are due to blockage of an artery in the brain by a blood clot. Most ischemic strokes in adults are caused by thrombotic or embolic occlusions of an artery. Prompt treatment with thrombolytic drugs can restore blood flow before major brain damage has occurred. Successful treatment could mean that the patient is more likely to make a good recovery from their stroke. Overall, thrombolytic therapy appears to result in a significant net reduction in the proportion of patients dead or dependent in activities of daily living. At present, intravenous tPA at 0.9mg/kg as licensed in many countries appears to represent best practice.[13] With tPA, inactive plasminogen is converted into the active form plasmin, which promotes thrombolysis by cleaving fibrin.
The data from trials using intravenous tPA, from which there are the most evidence on thrombolytic therapy so far, suggest that it may be associated with less hazard and more benefit.[14] Patients older than 80 years achieved similar benefit to those aged 80 years or younger, particularly when treated early.[13] The evidence indicates that intravenous rt-PA increased the proportion of patients who were alive with favourable outcome and alive and independent at final follow-up.[13] Thrombolytic drugs however, can also cause serious bleeding in the brain which can be fatal. Training and certification in the use of tPA is necessary for its safe administration and guidelines are widely available on the internet (Table 2).
Table 2
Use Intravenous tPA
Caveat/ Exclusion
0.9 mg per Kg body weight
No more than 90 mg to be given
Give immediate 10% as IV bolus
Give the rest as IV infusion over 60 minutes
Age less than 80 years
Within 4 hours of stroke
Brain CT scan show hemorrhage
Avoid in minor stroke or rapidly improving patients
Avoid in wake up stroke patients
Less than 6 hours in basilar artery thrombosis
Give intra arterial via angiographic techniques
Avoid in patients on Aspirin, oral anti coagulants
Blood Pressure must be controlled
Avoid if BP more than 180/105 mmHg
Avoid if recent head injury, operation, gastrointestinal bleed, previous stroke, seizures at onset of stroke, low platelet count and moderate hyperglycemia
Carotid Ultrasound scan and Carotid endarterectomy
Carotid artery disease and carotid artery stenosis can be evaluated using Carotid ultrasound scan and Carotid angiography (using CT, MRI or Digital Subtraction Angiography). Ultrasound using pulsed Doppler has been accepted by some investigators in qualified laboratories as a satisfactory means of determining the severity of carotid artery stenosis. Duplex examinations (combined B-mode ultrasound and pulsed Doppler), is also an accepted and accurate technique for determining the severity of carotid artery stenosis. The accuracy is dependent on the skill of the radiologist.
Patients with carotid stenosis 70%¬-99% should be offered carotid endarterectomy (CEA) as soon as possible before another stroke event.[15] Cerebral thromboembolism is one of the main risks of carotid artery occlusive disease and CEA is a preventive operation to reduce the incidence of embolic stroke.[16] Performing CEA within a 2 week period after the stroke episode, has been shown to be both possible and efficacious.[17] Carotid endarterectomy should be performed as soon as possible after a TIA, if indicated. Complete carotid occlusion (100%) does not need an operation.
Medical Management of Symptomatic Patients
One of the most important approaches to the medical management of patients with CAD with respect to stroke risk reduction has been the use of antiplatelet drugs, principally aspirin. Newer drugs, such as ticlopidine, have shown some improvement over the effect of aspirin. Combination therapies such as aspirin plus dipyridamole are however no better than aspirin alone. Clopidogrel is better than the combination of aspirin and dipyridamole.
Conclusion:
TIA and stroke share common causes, risk factors, pathophysiology, and treatment. This article proposes that prompt intervention or hospitalization is required and a patient who had a TIA the previous day should be told to go immediately to the emergency department for admission, investigation and treatment. Head and neck imaging should be done on all such patients. Those with acute neurological deficits (within a 3 hour window) who will benefit from Thrombolysis should be offered it. There is also data that some patients might benefit up to 6 h after stroke.
Those with carotid artery disease who will benefit from CEA should be referred urgently to the vascular surgeons or neurosurgeons skilled in the practice. Further, patients with other risk factors such as atrial fibrillation should be adequately managed. These may lead to significant reduction in stroke risk and improved life expectancy for such patients.
Finally, of course, continued therapy with anti platelet agents, risk factor modification and management, life style modification and exercise is to be recommended for all patients.
References:
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2.. Investigators CS. The effectiveness of dual antiplatelet treatment in acute ischemic stroke patients with intracranial arterial stenosis: a subgroup analysis of CLAIR study. Int J Stroke. 2013;8(8):663-668.
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14. Wardlaw JMZG, T. Y, E. B. Throbmolysis for acute ischaemic stroke. Vol 3: Cochrane Database Syst Rev.; 2003.
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