Transient ischemic attack

Transient ischemic attack
Classification and external resources
ICD-10 G45.9
ICD-9 435.9
DiseasesDB 13253
MedlinePlus 000730
eMedicine emerg/604
MeSH D002546

A transient ischemic attack (spelled ischaemic in British English)[1] (abbreviated as TIA, often colloquially referred to as “mini stroke”) is a change in the blood supply to a particular area of the brain, resulting in brief neurologic dysfunction that persists, by definition, for less than 24 hours. If symptoms persist longer, then it is categorized as a stroke.[2]

A cerebral infarct that lasts longer than 24 hours, but less than 72 hours is termed a reversible ischemic neurologic deficit or RIND.

Contents

Symptoms

Symptoms vary widely from person to person, depending on the area of the brain involved. The most frequent symptoms include temporary loss of vision (typically amaurosis fugax); difficulty speaking (aphasia); weakness on one side of the body (hemiparesis); and numbness or tingling (paresthesia), usually on one side of the body. Impairment of consciousness is very uncommon. There have been cases where there has been a temporary paralysis of a part of the face and the tongue. The symptoms of a TIA are short lived and usually lasts a few seconds to a few minutes and most symptoms disappear within 60 minutes. Some individuals may have a lingering feeling that something odd happened to the body. Dizziness, lack of coordination or poor balance are also symptoms related to TIA. The symptoms may vary in severity.

Diagnosis

The diagnosis of a TIA includes a history and a physical exam. There are several radiological tests that are done to evaluate patients who have had a TIA. This includes a CT scan or an MRI of the brain, Ultrasound of the neck, an echocardiogram of the heart. In most cases, the source of atherosclerosis is usually identified with an ultrasound.[3]

Effects of a TIA

Prognosis

Patients diagnosed with a TIA are sometimes said to have had a warning for an approaching stroke. If the time period of blood supply impairment lasts more than a few minutes, the nerve cells of that area of the brain die and cause permanent neurologic deficit. One third of the people with TIA later have recurrent TIAs and one third have a stroke due to permanent nerve cell loss.[4]

Causes

The most common cause of a TIA is an embolus that occludes an artery in the brain. This most frequently arises from a dislodged atherosclerotic plaque in one of the carotid arteries (i.e. a number of major arteries in the head and neck) or from a thrombus (i.e. a blood clot) in the heart due to atrial fibrillation. In a TIA, the blockage period is very short lived and hence there is no permanent damage.[5] The cholesterol build up is gradual and eventually narrows the lumen. With time, blood flow to that side of the brain is reduced and a stroke may result. In other cases, cholesterol particles from the atherosclerotic plaque may suddenly break off and fly into the brain. In some people, these fragments come off from the heart and go to the brain. This often happens during a heart attack or an infection of the valves.[6]

Other reasons include excessive narrowing of large vessels due to an atherosclerotic plaque and increased blood viscosity due to some blood diseases. TIA is related with other medical conditions like hypertension, heart disease (especially atrial fibrillation), migraine, cigarette smoking, hypercholesterolemia, and diabetes mellitus.

Differential

1. Atypical migraine if visual symptoms occur such as perception of wavy or jagged lines or tiny specks of light and if a headache occurs. Typically a history of prior migraines is present.
2. partial seizure in the parietal area of the brain can mimic TIA symptoms.
3. Glucose abnormalities can mimic TIAs. Ask about history of Diabetes Mellitus and Loss of Consciousness
4. Electrolyte abnormalities
5. Hypertensive Encephalopathy (Headache, delirium, hypertension, cerebral edema)
6. Subdural Hematoma (H/O trauma, headache, LoC)
7. Brain Tumor (Mode of onset, progressive headaches, increased ICP)
8. Demylenating Disease
9. Conversion disorder

Prevention

A TIA may be prevented by changes in lifestyle, although most of these recommendations have no solid empirical data, most medical professionals believe them to be so. These include:

Treatment

The mainstay of treatment following acute recovery from a TIA should be to diagnose and treat the underlying cause. It is not always immediately possible to tell the difference between a CVA (stroke) and a TIA. Most patients who are diagnosed at a hospital's emergency department as having suffered from a TIA will be discharged home and advised to contact their primary physician to organize further investigations. TIA can be considered as the last warning. The reason for the condition should be immediately examined by imaging of the brain.

The initial treatment is aspirin, second line is clopidogrel, third line is ticlopidine. If TIA is recurrent after aspirin treatment, the combination of aspirin and dipyridamole is needed (Aggrenox).

An electrocardiogram (ECG) may show atrial fibrillation, a common cause of TIAs, or other arrhythmias that may cause embolisation to the brain. An echocardiogram is useful in detecting thrombus within the heart chambers. Such patients benefit from anticoagulation.

If the TIA affects an area supplied by the carotid arteries, an ultrasound (TCD) scan may demonstrate carotid stenosis. For people with a greater than 70% stenosis within the carotid artery, removal of atherosclerotic plaque by surgery, specifically a carotid endarterectomy, may be recommended. Surgery is the gold standard and includes anesthesia. The blood vessel is opened up and the plaque is removed. The procedure is not difficult but one of its complications is inducing a stroke. The stroke can happen during surgery or after the procedure. With both procedures, the chances of a stroke are about 1–4 percent.[7]

Some patients may also be given modified release dipyridamole or clopidogrel.

To reduce recurrence of an attack ACE Inhibitors are used. The aim is not to lower blood pressure in a hurry as too low too fast may increase ischemic injury due to low perfusion pressure.

Medication

The use of anti-coagulant medications, heparin and warfarin; or anti-platelet medications such as aspirin. Antiplatelet drugs prevent platelets from sticking to each other and thin the blood. These drugs thin the blood to ensure that small particles do not form and fly off to the brain. These drugs require frequent monitoring. These drugs also have more side effects like easy bruising and bleeding from mild trauma.[8]

Risk factors

References

  1. http://www.nhs.uk/Pathways/stroke/Pages/Landing.aspx
  2. Transient Ischemic Attacks: Stroke (CVA): Merck Manual Home Edition
  3. Transient Ischemic Attack eMedicine. Retrieved on 2010-03-07
  4. Transient ischemic attack Mount Sinai Hospital, New York
  5. What is a TIA or transient ischemic attack? American Heart Association. Retrieved on 2010-03-07
  6. Transient Ischemic Attack MedLine Plus. Retrieved on 2010-03-07
  7. Transient Ischemic Attacks(TIA) Merck, Sharpe & Dohme. Retrieved on 2010-03-07
  8. Brain Stroke Overview Retrieved on 2010-03-07
  9. African Americans and Stroke National Stroke Association. Retrieved on 2010-03-07

External links