MSC Neuro 25 p2

MSC–NeurologyandNeurosurgery2025

PART – 2

1.Classification of cerebral circulation disorders. Sharp and chronic shapes. Syndromology.

1.Definition

Transient disturbances of cerebral circulation with complete reversibility of neurological symptoms within 24 hours.

If symptoms last longer than 24 hours → classified as stroke.

2.Forms

Typical TIA: Brief focal neurologic deficits due to transient ischemia.

Hypertensive cerebral crises: Sudden high blood pressure causing cerebral dysfunction.

General cerebral dysfunction (WHO classification): Short-term syncope-like episodes due to vertebral artery compression (e.g., neck rotation).

3.Syndromology

Carotid Pool TIAs (anterior circulation)

Transient hemiparesis or monoparesis.

Hypoesthesia (sensory loss) on one side.

Speech disturbances (usually motor aphasia).

Transient vision loss (amaurosis fugax), dysarthria.

Optic-pyramidal syndromes.

Vertebrobasilar TIAs (posterior circulation)

Systemic dizziness with autonomic symptoms.

Headache, occipital pain, nystagmus, diplopia.

Hemianopsia, visual symptoms.

Alternating syndromes, Wallenberg syndrome variants.

Drop attacks and syncope-like episodes.

Transient global amnesia and disorientation.

4.Diagnosis

Comprehensive blood tests (clinical and biochemical).

EEG for brain function.

Brain imaging: CT or MRI.

Doppler ultrasound of head and neck vessels.

Sometimes angiography and ECG.

5.Treatment

Hospitalization mandatory if:

Age >45 years, repeated TIAs, cardiovascular disease, or symptoms ongoing <2 days.

Outpatient treatment only if immediate hospitalization available upon recurrence.

Prevent recurrence with:

Antiplatelet drugs (aspirin, clopidogrel)

Anticoagulants (in selected cases)

Vascular tone regulation

Control of hypertension, diabetes, and other risk factors

Lifestyle modification (diet, smoking cessation, exercise)

6.Prevention

Aggressive management of vascular risk factors.

Early detection and treatment ofTIAs reduce risk of stroke.

Patient education on recognizing symptoms and seeking urgent care.

2. Pathogenetic variants of ischemic stroke. Atherothrombotic ischemic stroke. Middle cerebral artery occlusion syndrome.

1.Definition

Ischemic stroke is caused by sudden reduction or blockage of blood flow in a brain artery, leading to focal brain tissue necrosis (infarction).

2.Pathogenetic Variants

Atherothrombotic stroke:

Due to atherosclerotic lesions and thrombosis in extracranial/intracranial arteries (e.g., carotid artery bifurcation).

Cardioembolic stroke:

Emboli from heart (atrial fibrillation, myocardial infarction, valve issues) or large arteries occlude cerebral vessels.

Hemodynamic stroke:

Occurs with severe stenosis and sudden blood pressure drops, affecting watershed brain regions.

Lacunar stroke:

Small infarcts in deep brain areas due to small vessel disease, often linked to hypertension.

Rare causes: Vasculitis, antiphospholipid syndrome, venous thrombosis, dissection, hematologic diseases, contraceptives, infections (e.g.,AIDS).

3.Clinical Features

Atherothrombotic: Symptoms may develop gradually or in steps (stuttering progression); onset often at night.

Cardioembolic: Sudden onset; often involves large vessel territories; associated with seizures, loss of consciousness.

Hemodynamic: Signs of border zone ischemia with bilateral or watershed deficits.

Lacunar: Pure motor or sensory deficits with no cortical signs; often gradual onset.

Symptoms vary based on artery involved (carotid vs vertebrobasilar).

4.Diagnosis

Imaging: CT and MRI to localize ischemia and identify type.

Vascular studies: Doppler ultrasound, MR/CT angiography to assess vessels.

Cardiac evaluation: Echocardiography (transthoracic and transesophageal) for embolic source.

EEG for seizure activity.

Lab: Coagulation profile, blood glucose, lipids.

5.Treatment

Hospitalization within 4-6 hours preferred.

Supportive care: maintain airway, respiration, hemodynamics.

Control blood pressure, blood sugar, temperature.

Pharmacotherapy:

Antiplatelets, anticoagulants (when indicated).

Neuroprotective agents (e.g., citicoline, cerebrolysin).

Osmotic agents and corticosteroids for cerebral edema.

Manage complications: seizures, deep vein thrombosis, aspiration.

Rehabilitation: early mobilization, physical therapy.

6.Prevention

Control hypertension, diabetes, dyslipidemia, smoking cessation.

Antithrombotic therapy post-TIAor stroke.

Lifestyle modification.

3. Pathogenetic variants of ischemic stroke. Cardioembolic ischemic stroke. Risk factors, clinic features. The syndrome occlusion of the posterior inferior cerebellar artery.

Cardioembolic Ischemic Stroke

Risk Factors

Atrial fibrillation (most common)

Recent myocardial infarction with left ventricular thrombus

Valvular heart disease (rheumatic or prosthetic valves)

Dilated cardiomyopathy

Patent foramen ovale and paradoxical embolism

Infective endocarditis with vegetations

Heart failure

Other cardiac arrhythmias (e.g., sick sinus syndrome)

Clinical Features

Sudden onset to maximal neurological deficit (often within minutes)

Fluctuating symptoms possible due to embolus fragmentation or recanalization

Loss of consciousness and epileptic seizures more common than other stroke types

Symptoms depend on artery involved:

Middle cerebral artery embolism: unilateral facial weakness, aphasia (especially Wernicke’s), hemiplegia, sensory aphasia, neglect of opposite space

Anterior cerebral artery embolism: sudden weakness mainly in contralateral leg

Posterior cerebral artery: homonymous hemianopia, cortical blindness

Basilar artery embolism: drowsiness, bilateral cortical blindness

Posterior Inferior Cerebellar Artery (PICA) Occlusion Syndrome (Wallenberg-

Zakharchenko Syndrome)

Clinical Features

Ipsilateral Horner’s syndrome (ptosis, miosis, enophthalmos)

Ipsilateral hypoesthesia of the face

Paresis of soft palate and larynx leading to dysphagia and dysphonia

Vertigo, nausea, vomiting, nystagmus

Ipsilateral limb ataxia

Contralateral hemihypesthesia below the neck

Dysfunction of cranial nerves and cerebellar signs may coexist

Diagnosis

Brain imaging (CT, MRI) to identify infarct location and subtype

Doppler ultrasound and magnetic resonance angiography for vessel assessment

Echocardiography (transthoracic and transesophageal) to identify cardiac embolic sources

Electroencephalography may show focal slowing or epileptic activity

Blood tests: coagulation, lipids, glucose, etc.

Treatment and Prevention

Early hospitalization (within 4-6 hours if possible)

Management of vital functions (airway, breathing, circulation)

Blood pressure control (prefer smooth reductions)

Antiplatelet or anticoagulant therapy depending on stroke subtype and etiology

Neuroprotective agents and cerebral edema management (osmotic diuretics, corticosteroids)

Seizure control

Prevention of complications - prevent deep vein thrombosis, infections

Address cardiac causes to prevent recurrence (anticoagulation for atrial fibrillation)

Rehabilitation and physical therapy post-acute phase

4.Stroke risk factors. Prevention of strokes.

Stroke Risk Factors

Non-modifiable risk factors:

Age (risk increases with age)

Family history of stroke or cardiovascular disease

Male sex (generally higher risk than females)

Race/ethnicity (some groups likeAfricanAmericans have higher risk)

Modifiable risk factors:

Hypertension: strongest and most common risk factor

Diabetes mellitus: raises stroke risk by endothelial damage and atherosclerosis promotion

Atherosclerosis: carotid and intracranial vessel disease

Cardiac disease: atrial fibrillation, valvular heart disease, myocardial infarction, cardiomyopathy

Hyperlipidemia: high cholesterol and triglycerides

Obesity and physical inactivity

Smoking: causes vascular damage and thrombosis risk

Excessive alcohol consumption

Poor diet: high salt, saturated fats, low fruits and vegetables

Psychosocial stress and depression

Stroke Prevention

Primordial prevention (population-level healthy living)

Promote non-smoking, healthy diets, physical activity, weight control

Primary prevention (individual risk factor control)

Blood pressure control (target <130/80 mmHg for many)

Diabetes management and glucose control

Lipid lowering therapy (statins)

Antiplatelet therapy in at-risk patients (aspirin, clopidogrel)

Control cardiac arrhythmias (e.g., anticoagulation in atrial fibrillation)

Manage psychosocial factors and stress

Secondary prevention (after stroke or transient ischemic attack)

Continued and intensified management of above risk factors

Rehabilitation and lifestyle modifications

Medication adherence and monitoring for recurrent disease

5.Non-traumatic parenchymal haemorrhage. Etiologic, clinical, diagnosis and treatment. Indications for surgical treatment.

Etiology

Most common cause: Hypertension - chronic high blood pressure weakens small intraparenchymal arteries leading to rupture.

Other causes:

Cerebral amyloid angiopathy (especially in elderly; lobar hemorrhages)

Ruptured cerebral aneurysm or arteriovenous malformation (AVM)

Brain tumors with hemorrhagic necrosis

Coagulopathies (anticoagulant therapy, thrombocytopenia)

Hemorrhagic transformation of ischemic stroke

Vasculitis, infections, or systemic diseases

Clinical Features

Sudden onset with severe headache, nausea, vomiting.

Rapid development of focal neurological deficits (hemiparesis, hemianesthesia, aphasia, homonymous hemianopia) depending on hemorrhage location.

Consciousness impaired early; coma possible.

Hemorrhage in basal ganglia/internal capsule → contralateral hemiparesis, sensory loss, homonymous hemianopia.

Brainstem/cerebellar hemorrhage → ataxia, ophthalmoplegia, pinpoint pupils, respiratory failure.

Face may be red and edematous from increased ICP; pulse often slow and strong, blood pressure elevated.

Signs of raised intracranial pressure and brain herniation may develop.

Diagnosis

CT scan: modality of choice to identify hemorrhage and its size, location.

MRI useful for further characterization but less practical in emergency.

Cerebral angiography for suspected vascular malformations or aneurysms.

Blood tests: coagulation profile, platelets, metabolic screen.

Lumbar puncture contraindicated due to risk of herniation.

Treatment

Conservative:

Manage airway, breathing, circulation.

Blood pressure control (avoid hypotension, prevent hematoma expansion).

Osmotic agents (mannitol) for cerebral edema.

Antiepileptics for seizures.

Supportive care with monitoring ICP.

CT scan head: first-line for detection of blood in subarachnoid space (within 6 hours very sensitive).

Lumbar puncture: if CT negative but SAH still suspected; shows xanthochromia or blood.

Cerebral angiography or MR angiography: to localize aneurysm or vascular malformation.

Additional tests: MRI, digital subtraction angiography if needed.

Treatment

Early surgical clipping or endovascular coiling of ruptured aneurysm (ideally mild to moderate cases).

Intensive bed rest for 3 weeks post-bleed to prevent rebleeding.

Avoid straining, coughing, and other maneuvers increasing ICP.

Blood pressure control: maintain systolic 130-150 mmHg, avoid hypotension and hypovolemia.

Nimodipine (calcium channel blocker) to prevent/treat cerebral vasospasm (days 4-21 post-hemorrhage).

Avoid antifibrinolytics routinely (risk of vasospasm, hydrocephalus).

Symptomatic treatment for pain, agitation, seizures as needed.

Indications for Surgery

Accessible ruptured aneurysms for clipping or coiling.

Large hematomas causing mass effect.

Hydrocephalus needing CSF diversion.

Persistent or recurrent bleeding despite medical management.

Prevention

Control hypertension, avoid smoking and drug abuse.

Screening in high-risk patients (family history, known aneurysms).

7.Emergency therapy of strokes: basic and differentiated treatment.