Stroke and TIA: Risk Factors and Symptoms

• Stroke is a sudden focal neurological deficit.
• Strokes can be ischemic or hemorrhagic.
• Ischemic strokes account for 85% of all strokes, while hemorrhagic strokes make up the remaining 15%.
• Ischemic stroke results from the occlusion of a cerebral blood vessel, leading to cerebral infarction.
• Transient ischemic attack (TIA) is a temporary neurological deficit, lasting less than 1 hour.
• TIA is caused by a cerebrovascular disease, without clinical or imaging traces.

Risk Factors

• Age, gender, ethnicity, and genetic factors are non-modifiable risk factors.
• Cardiac disease, hypertension, dyslipidaemia, cigarette smoking, diabetes mellitus, physical inactivity, and drug abuse are potentially modifiable risk factors.

Non-Modifiable Risks

• The risk of stroke doubles for each year after age 55.
• Strokes occur approximately twice as often in blacks and Hispanics compared to whites.
• Men have a 50% higher chance of stroke than women.
• A family history of stroke or TIA increases the risk.

Pathology of Underlying Etiology

• Ischemic infarction accounts for 85% of strokes and can be thrombotic, embolic, or hemodynamic.
• Hemorrhage accounts for 15% of strokes and can be intracerebral, subarachnoid, or subdural/extradural.

Thrombosis

• Vascular wall issues may include atherosclerosis and vasculitis like SLE.
• Blood element issues may include hyperviscosity or hypercoagulable states such as polycythemia and thrombocytosis, as well as tumors, pregnancy, and puerperium.
• Hemodynamic circulatory issues may include heart failure and systemic hypotension.

Embolism

• Emboli can occlude any vessel, whether diseased or healthy.
• Heart conditions are the most common source of emboli.
• Arteries, such as the aortic arch and carotids, can be sources of emboli.
• In rare cases, the emboli source can be remote.

Pathophysiology of Ischemic Stroke

• Inadequate blood flow in a single brain artery is often compensated for by an efficient collateral system.
• Normal variations in the Circle of Willis, atherosclerosis, and other arterial lesions can interfere with collateral flow, increasing the chance of brain ischemia.
• Mild ischemia means damage proceeds slowly; 3-6 hours may pass before brain tissue is completely lost with perfusion at 40% of normal.
• Severe ischemia persisting for more than 15-30 minutes leads to infarction of the affected tissue.
• Promptly restoring blood flow to ischemic but not irreversibly damaged tissues may reduce or reverse injury.
• Intervention might salvage moderately ischemic areas (penumbras) around severe ischemia, which exist because of collateral flow.
• Penumbra is an area of reversible ischemia surrounding the core of an infarct.
• The infarcted (necrotic) zone is the region of dead cells in the core of the lesion.
• Mechanisms of ischemic injury are edema, microvascular thrombosis, programmed cell death (apoptosis), and infarction with cell necrosis.

Determinants of Damage

• The duration and degree of cerebral hypoperfusion is a factor.
• Which artery is affected is a factor.
• The site of vascular occlusion (or hemorrhage) is a factor.
• Previous brain damage is a factor.
• Collateral circulation is a factor.
• General body health is a factor.

Clinical Presentation of Ischemic Stroke

• Symptoms and signs of ischemic stroke depend on the affected brain part.
• Deficits typically become maximal within minutes of onset in embolic stroke.
• Deficits evolve slowly, over 24-48 hours (evolving stroke/stroke in evolution), usually in atherothrombotic stroke.
• Evolution of stroke typically involves unilateral neurologic dysfunction, often beginning in one arm and spreading ipsilaterally, without headache, pain, or fever.
• Progression is usually stepwise, with periods of stability.
• A stroke with residual function in the affected area is considered submaximal, meaning viable tissue is at risk.
• Embolic strokes often occur during the day and may be preceded by headache.
• Thrombi tend to occur during the night and are discovered on awakening.
• Seizures may occur at stroke onset, more often with embolic than thrombotic stroke, or months to years later because of scarring or hemosiderin deposition at the site of ischemia.
• Occasionally, fever develops.
• Impaired consciousness from cerebral edema, not extension of the infarct, leads to Deterioration within 48-72 hours of symptoms.
• Unless the infarct is large/extensive, function improves in the first few days; further improvement occurs gradually for up to 1 year.

Arteries

• Anterior cerebral artery occlusion can cause contralateral hemiparesis (maximal in the leg), urinary incontinence, apathy, confusion, poor judgment and gait apraxia.
• Middle cerebral artery occlusion can cause contralateral hemiparesis (worse in the arm and face than in the leg), dysarthria, hemianesthesia, contralateral homonymous hemianopia, aphasia (if the dominant hemisphere is affected) or apraxia, and sensory neglect (if the nondominant hemisphere is affected).
• Posterior cerebral artery occlusion can cause contralateral homonymous hemianopia, unilateral cortical blindness, memory loss, unilateral 3rd cranial nerve palsy or hemiballismus.
• Ophthalmic artery occlusion causes monocular loss of vision (amaurosis).
• Vertebrobasilar system occlusion can cause unilateral or bilateral cranial nerve deficits, truncal or limb ataxia, crossed sensory and motor deficits, impaired consciousness, coma, and death (if basilar artery occlusion is complete), as well as tachycardia and labile blood pressure.
• Lacunar infarcts may produce pure motor hemiparesis, pure sensory hemianesthesia, combined hemiparesis and hemianesthesia, ataxic hemiparesis, or dysarthria–clumsy hand syndrome, but signs of cortical dysfunction are absent and multiple infarcts may result in multi-infarct dementia.
• Lacunar infarcts have an absence of cortical deficits
• Ipsilateral facial sensory loss or motor weakness with contralateral body hemianesthesia or hemiparesis indicates a lesion at the pons or medulla.

Diagnosis of Ischemic Stroke

• Primarily a clinical evaluation.
• Also Neuroimaging
• Evaluation to identify the cause
• CT is done first to exclude intracerebral hemorrhage, subdural or epidural hematoma, and rapidly growing tumors.
• Evidence of even a large anterior circulation ischemic stroke on CT may be subtle during the first few hours, including effacement of sulci, loss of the gray-white junction between cortex and white matter, and a dense middle cerebral artery sign.
• Within 6-12 hours of ischemia, medium-sized to large infarcts become visible as hypodensities in CT scans.
• Small infarcts (lacunar infarcts) may be visible only with MRI.
• Diffusion-weighted MRI is highly sensitive for early ischemia and can be done after CT neuroimaging.

Other Investigations

• Testing for cardiac causes typically includes ECG, telemetry or Holter monitoring, serum troponin, transthoracic or transesophageal echocardiography.
• Testing for vascular causes may include MRA, CTA, carotid and transcranial duplex ultrasonography and conventional angiography.
• Routine blood-related testing includes CBC, metabolic panel, prothrombin time/partial thromboplastin time (PT/PTT), fasting blood glucose, hemoglobin A1C and lipid profile.
• Additional tests may include testing for thrombotic disorders (antiphospholipid antibodies, protein S, protein C, antithrombin III, factor V Leiden).
• Testing for rheumatic disorders, syphilis serologic testing, and urine drug screen for cocaine and amphetamines may also be done.

Treatment of Ischemic Stroke

• General stroke treatments are necessary.
• Acute antihypertensive therapy is used only in certain circumstances.
• Reperfusion with recombinant tissue plasminogen activator and/or mechanical thrombectomy is sometimes used for acute treatment.
• Carotid endarterectomy or stenting is sometimes used.
• Antiplatelet therapy is used.
• Anticoagulation is sometimes necessary.
• Long-term control of risk factors.
• Long-term treatment, and rehabilitation is important.