A Clinical Guide to Stroke Syndromes
Definition
A stroke is a clinical syndrome defined by the World Health Organization (WHO) as rapidly developing clinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting 24 hours or longer or leading to death, with no apparent cause other than of vascular origin (1). This definition is critically important as it encompasses both ischemic events (blockage of a vessel) and hemorrhagic events (rupture of a vessel), both of which represent a time-critical medical emergency requiring immediate and distinct management pathways.
Epidemiology
Globally, stroke remains a major public health crisis and a leading cause of death and long-term disability. Ischemic strokes are the most prevalent type, accounting for approximately 87% of all cases, while hemorrhagic strokes, though less common at 13%, often carry a more severe prognosis (6). In Malaysia, stroke is consistently ranked among the top five principal causes of death and is a primary driver of adult disability, placing a substantial and growing burden on patients, their families, and the national healthcare system. The long-term care, rehabilitation needs, and loss of economic productivity associated with stroke are significant challenges. [While global data points to varying risks among different populations, specific prevalence and incidence data for ethnic distribution in Malaysia are not readily available in national health surveys and should be interpreted with caution].
Etiology
The etiological classification of ischemic stroke is a cornerstone of effective management, as it is crucial for guiding targeted secondary prevention strategies. The most widely used framework is the Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification, which categorizes strokes based on their underlying cause after a thorough diagnostic workup (2, 5).
Large-Artery Atherosclerosis (LAA): This refers to strokes caused by significant (>50%) stenosis or occlusion of a major extracranial (e.g., internal carotid artery at the bifurcation) or intracranial artery (e.g., middle cerebral artery) due to atherosclerosis. The stroke mechanism can be an in-situ thrombosis, where a plaque ruptures and a clot forms locally, or an artery-to-artery embolism, where debris from a proximal plaque travels distally to block a smaller vessel (9).
Cardioembolism (CE): This involves the formation of a thrombus within the heart that subsequently embolizes to a cerebral artery. The most common underlying cause is atrial fibrillation, where blood stasis in the non-contracting left atrial appendage promotes clot formation. Other high-risk sources include recent myocardial infarction with a mural thrombus, mechanical prosthetic valves, infective endocarditis, and dilated cardiomyopathy (10). The presence of infarcts in multiple vascular territories is highly suggestive of a cardioembolic source.
Small-Vessel Occlusion (SVO) / Lacunar: These strokes result from the occlusion of a single, small penetrating artery deep within the brain (e.g., lenticulostriate arteries). The primary pathology is intrinsic disease of these small vessels, most commonly lipohyalinosis (a degenerative process from chronic hypertension) or microatheroma (a tiny plaque at the vessel origin). These pathologies are strongly associated with long-standing, poorly controlled hypertension and diabetes mellitus (26).
Stroke of Other Determined Etiology: This category is a repository for uncommon but important causes that are specifically identified through further testing. Examples include non-atherosclerotic vasculopathies (e.g., arterial dissection, vasculitis), inherited or acquired hypercoagulable states (e.g., antiphospholipid syndrome, sickle cell disease), and genetic conditions like CADASIL (2).
Stroke of Undetermined Etiology: This is assigned when the cause remains unclear after a comprehensive evaluation. This includes patients with a truly cryptogenic stroke (no cause found), those with an incomplete workup, or those with two or more competing potential causes (e.g., a patient with both atrial fibrillation and significant ipsilateral carotid stenosis). A key subgroup is the Embolic Stroke of Undetermined Source (ESUS), which describes a non-lacunar infarct without an identified source, suggesting a covert embolic mechanism that warrants careful investigation (2).
Pathophysiology
The pathophysiology of stroke is fundamentally divided into two distinct pathways, ischemia and hemorrhage, each with a unique cascade of cellular injury.
Ischemic Stroke: This occurs when a cerebral blood vessel is occluded, leading to a rapid cessation of blood flow, oxygen, and glucose delivery. The brain tissue in the core of the affected vascular territory, which has severely reduced blood flow (<20%), undergoes irreversible cell death (infarction) within minutes due to energy failure. Surrounding this core is the ischemic penumbra—tissue that is functionally impaired but still structurally intact and viable, maintained by limited collateral blood flow. This penumbral tissue is the primary target of acute therapy. If perfusion is not restored, the penumbra will succumb to a cascade of neurotoxic events, including excitotoxicity (excessive glutamate release), oxidative stress, and inflammation, eventually leading to its infarction and a larger final stroke volume (9).
Hemorrhagic Stroke: This is caused by the rupture of a blood vessel, leading to bleeding directly into the brain parenchyma (intracerebral hemorrhage) or into the subarachnoid space. The initial damage is mechanical, caused by the direct compression and disruption of brain tissue by the expanding hematoma. This is followed by secondary injury mechanisms, including increased intracranial pressure, perihematomal edema (swelling around the clot), and the potent neurotoxic and inflammatory effects of blood products like iron and thrombin breaking down in the brain parenchyma (5).
Clinical Presentation
The clinical presentation of a stroke is a direct map of the vascular territory affected. The Oxfordshire Community Stroke Project (OCSP) or Bamford classification is a simple, powerful bedside tool for categorizing strokes based on initial signs and symptoms, which helps in prognostication and localization (6).
Total Anterior Circulation Syndrome (TACS): This implies a large cortical stroke (e.g., MCA stem occlusion) and requires all three of the following, indicating massive hemispheric damage:
Unilateral weakness and/or sensory deficit affecting the face, arm, AND leg.
Homonymous hemianopia (loss of the same half of the visual field in both eyes).
Higher cerebral dysfunction (e.g., global aphasia if in the dominant hemisphere, or profound visuospatial neglect if in the non-dominant hemisphere).
Partial Anterior Circulation Syndrome (PACS): This suggests a less extensive cortical infarct, such as an occlusion of a branch of the MCA. It is diagnosed when only two of the three TACS components are present, or the patient has isolated higher cerebral dysfunction (e.g., Wernicke's aphasia with no motor deficit), or a motor/sensory deficit more restricted than a lacunar syndrome (e.g., weakness of only the face and hand) (6).
Lacunar Syndrome (LACS): Characterized by one of the classic subcortical syndromes (pure motor, pure sensory, sensorimotor, or ataxic hemiparesis). The defining feature is the complete absence of any cortical signs like aphasia, neglect, or visual field defects. This clinical purity points to a small, deep, subcortical infarct affecting structures like the internal capsule or thalamus (6).
Posterior Circulation Syndrome (POCS): This diagnosis localizes the stroke to the brainstem, cerebellum, or occipital lobe. Features are diverse and include one or more of the following:
Ipsilateral cranial nerve palsy with contralateral motor/sensory deficit ("crossed signs").
Bilateral motor or sensory deficit.
Disorder of conjugate eye movement (e.g., gaze palsy).
Profound cerebellar dysfunction (the "5 D's": Dizziness, Diplopia, Dysarthria, Dysphagia, Dystaxia/Ataxia).
Isolated homonymous hemianopia (often from a PCA infarct) (6).
⚠️ Red Flag Signs & Symptoms
Sudden, severe "thunderclap" headache: This is the classic presentation of a subarachnoid hemorrhage. It is a neurological emergency requiring immediate investigation to rule out a ruptured aneurysm (5).
Rapidly deteriorating level of consciousness (GCS): This is an ominous sign that may indicate a large stroke with significant cerebral edema causing raised intracranial pressure, hemorrhagic transformation of an ischemic infarct, or direct brainstem compression from a swelling cerebellar stroke (63).
Signs of brainstem compression: In a patient presenting with dizziness and ataxia (cerebellar signs), the subsequent development of a depressed GCS, new pupillary abnormalities (e.g., pinpoint pupils), or irregular breathing patterns suggests life-threatening compression of the adjacent brainstem and requires an urgent neurosurgical consultation (64).
Severe uncontrolled hypertension (e.g., >220/120 mmHg): While hypertension is common in acute stroke, extreme elevations may indicate hypertensive encephalopathy or significantly increase the risk of hemorrhagic transformation of an ischemic stroke, requiring careful and controlled reduction (10).
Complications
Complications after stroke are common and can be divided into neurological and systemic categories.
Neurological:
Acute: Cerebral edema can cause a dangerous rise in intracranial pressure, leading to herniation. Hemorrhagic transformation of an ischemic stroke is a feared complication, especially after thrombolysis. Seizures occur in a minority of patients. Obstructive hydrocephalus is a life-threatening complication specific to cerebellar strokes (63).
Chronic: Central post-stroke pain (Dejerine-Roussy syndrome) is a debilitating neuropathic pain condition. Spasticity, post-stroke depression and anxiety, and vascular cognitive impairment are common long-term sequelae.
Systemic:
Aspiration pneumonia is common due to dysphagia (impaired swallowing) and is a leading cause of post-stroke mortality.
Venous thromboembolism (DVT and pulmonary embolism) is a major risk due to immobility.
Urinary tract infections (often related to catheter use), pressure sores, and cardiac complications like arrhythmias or heart failure are also frequent.
Prognosis
The OCSP classification is a powerful and validated clinical tool for predicting outcome. For ischemic stroke, the prognosis varies dramatically by the initial clinical syndrome:
TACS: Carries the worst prognosis by a significant margin. The massive area of infarction leads to a one-year mortality rate of approximately 60%, with only 4% of survivors regaining functional independence (1).
PACS: Has an intermediate prognosis. The smaller infarct volume results in a much lower one-year mortality of ~4% and a 56% rate of functional independence, although significant disability can still occur (1).
LACS & POCS: Generally have the best prognosis for survival and functional recovery. One-year mortality rates are low (2% and 7% respectively), and over 60% of patients achieve functional independence, defined as being able to care for themselves without assistance (1, 14). Factors such as age, baseline NIHSS score, and pre-stroke comorbidities also heavily influence the final outcome.
Differential Diagnosis
Several conditions can mimic the symptoms of an acute stroke, and it is vital to consider them in the initial assessment.
Hypoglycemia/Hyperglycemia: Metabolic derangements are the most common stroke mimics and can produce focal neurological deficits. They must be ruled out immediately with a bedside blood glucose test, as hypoglycemia is easily reversible.
Seizure (Todd's Paresis): A post-ictal state following a focal seizure can cause transient hemiparesis that perfectly mimics a stroke. The history of tonic-clonic movements or other seizure phenomena is key, and the deficit typically resolves within hours.
Migraine with Aura: Complicated or hemiplegic migraines can present with transient focal neurological symptoms, including weakness or sensory changes. A prior history of similar episodes and the characteristic gradual "march" of symptoms can help differentiate it from the abrupt onset of a stroke.
Brain Tumour or Abscess: These space-occupying lesions typically have a more subacute onset of symptoms. However, they can present acutely if there is hemorrhage into the tumour or if they trigger a seizure.
Peripheral Vertigo: Benign conditions like vestibular neuritis or labyrinthitis can cause severe vertigo, mimicking a cerebellar or brainstem stroke. The key to differentiation is a meticulous search for the "plus" signs of a central cause: gait ataxia, dysarthria, limb incoordination, or other neurological deficits. The HINTS exam (Head-Impulse, Nystagmus, Test-of-Skew) is a highly sensitive bedside tool for this purpose (7).
Investigations
Immediate & Bedside Tests
Capillary Blood Glucose: This is the most critical bedside test to perform immediately on every patient with suspected stroke to rule out hypoglycemia, a common and easily reversible stroke mimic (90).
Electrocardiogram (ECG): An ECG is mandatory in the initial workup to screen for atrial fibrillation, which is a major and treatable cause of cardioembolic stroke, and to detect any signs of concomitant acute myocardial infarction (10).
Diagnostic Workup
First-Line Investigation: An urgent non-contrast computed tomography (NCCT) scan of the head is the single most important initial imaging investigation. Its primary, non-negotiable purpose is to definitively exclude intracranial hemorrhage (the rationale), as this is an absolute contraindication to thrombolysis and fundamentally alters the entire management pathway (the action). Early signs of ischemia, such as the hyperdense MCA sign or loss of the insular ribbon, may be visible but are often absent in the first few hours (9).
Gold Standard (for Ischemia): Magnetic Resonance Imaging (MRI) with Diffusion-Weighted Imaging (DWI) is the gold standard for diagnosing acute ischemic stroke. It is far more sensitive than CT in the hyperacute phase and can detect an infarct within minutes of onset (the rationale), making it invaluable for confirming the diagnosis, especially in cases of small lacunar or posterior circulation strokes where the CT may be normal (the action). The concept of a DWI-FLAIR mismatch can identify patients in the thrombolysis window even if their onset time is unknown ("wake-up stroke") (9).
Vascular Imaging: CT Angiography (CTA) of the head and neck should be performed concurrently with the NCCT in potential candidates for mechanical thrombectomy. It provides rapid and detailed visualization of the major cervical and intracranial arteries (the rationale) to identify a large vessel occlusion (LVO) that is amenable to endovascular treatment (the action) (9).
Monitoring & Staging
National Institutes of Health Stroke Scale (NIHSS): This validated 15-item scale is performed serially to objectively quantify the neurological deficit (the rationale). It is essential for tracking the patient's clinical progress or deterioration and is a key component in determining eligibility for reperfusion therapy (the action) (94).
CT Perfusion (CTP): In selected patients, particularly those presenting in the extended time window (6-24 hours), CTP provides physiological maps of the brain. It can identify the ischemic penumbra (salvageable tissue) versus the infarct core (irreversibly damaged tissue) (the rationale). A favorable "mismatch" (small core, large penumbra) helps to select patients who may still benefit from thrombectomy long after the conventional window has closed (the action) (85).
Management
Management Principles
The management of acute stroke is governed by the hyperacute principle that "time is brain." The overarching goals are to ensure medical stability, rapidly restore blood flow via reperfusion therapies for eligible ischemic stroke patients, prevent complications, and initiate strategies for secondary prevention based on the determined etiology.
Acute Stabilisation (The First Hour)
Airway/Breathing: Ensure a patent airway. Patients with a reduced GCS are at high risk of aspiration. Administer supplemental oxygen only if the patient is hypoxic (SpO2 <94%) (the action), as routine use of oxygen in non-hypoxic patients may be harmful (the rationale) (92).
Circulation: Secure two large-bore IV cannulas for access. For the rare hypotensive patient, administer a stat fluid bolus of IV Normal Saline (the action) to restore cerebral perfusion (the rationale). However, most stroke patients are hypertensive.
Disability: Check blood glucose immediately. Obtain an urgent NCCT head scan to differentiate between ischemic and hemorrhagic stroke (the action), as this is the most critical decision point that dictates all subsequent therapy (the rationale) (9).
Blood Pressure Control: This is a critical, nuanced aspect of acute care.
If the patient is a candidate for thrombolysis, blood pressure must be carefully and promptly lowered to <185/110 mmHg before and during treatment (the action) to reduce the risk of hemorrhagic transformation, the most feared complication of thrombolysis (the rationale). IV Labetalol or Nicardipine are common first-line agents (16).
If the patient is not eligible for reperfusion, a state of "permissive hypertension" is often allowed (do not treat unless BP >220/120 mmHg) (the action). This is done to maintain cerebral perfusion pressure to the ischemic penumbra, which relies on this higher pressure for its collateral blood supply (the rationale) (10).
Definitive Therapy
First-Line (for eligible ischemic stroke): Intravenous Thrombolysis (IVT): Administer Alteplase (rt-PA), a fibrinolytic agent, at a dose of 0.9 mg/kg (maximum 90 mg), with 10% given as a bolus over 1 minute and the remainder infused over 1 hour. This "clot-busting" drug must be given within a strict time window, typically 4.5 hours from the time the patient was last known well, after meticulously checking all inclusion and exclusion criteria (16, 101).
First-Line (for Large Vessel Occlusion): Endovascular Thrombectomy (EVT): For patients with an ischemic stroke due to an LVO in the anterior circulation (e.g., ICA or MCA), mechanical thrombectomy is the standard of care. This neuro-interventional procedure involves navigating a catheter to the clot and physically removing it with a stent retriever or aspiration device (the rationale). It has been shown to dramatically improve functional outcomes (the action) and can be performed up to 6 hours from onset. In selected patients with a favorable perfusion imaging profile, this window can be extended up to 24 hours (18).
Supportive & Symptomatic Care
Aspiration Prevention: Keep the patient Nil By Mouth (NBM) until a formal swallow screen has been performed by a trained nurse or speech and language therapist (the action). This is a critical step to prevent aspiration pneumonia, a common and potentially fatal complication (the rationale) (10).
Glycemic Control: Maintain blood glucose in a target range (e.g., 7.8-10.0 mmol/L), avoiding both significant hyperglycemia and any hypoglycemia, as both are associated with worse neurological outcomes.
Fever Management: Treat fever (e.g., temperature >38.0°C) aggressively with paracetamol, as fever increases the metabolic demand of the brain and can worsen outcomes in the setting of ischemia.
DVT Prophylaxis: Use intermittent pneumatic compression devices early. Pharmacological prophylaxis (e.g., subcutaneous heparin) is typically deferred for the first 24 hours, especially after thrombolysis, to minimize bleeding risk.
Key Nursing & Monitoring Instructions
Strict hourly neurological observations (GCS, pupil size and reactivity, limb power) for at least the first 24 hours, especially post-thrombolysis.
Continuous cardiac monitoring and frequent vital signs monitoring, with close attention to blood pressure.
Strict input/output chart monitoring to ensure adequate hydration.
Maintain the head of the bed elevated at 30 degrees to optimize cerebral venous drainage and reduce intracranial pressure.
Inform medical staff immediately if there is any neurological deterioration, a severe headache develops, nausea/vomiting occurs, or blood pressure exceeds target limits.
Long-Term Plan & Patient Education
The long-term plan is dictated by the stroke etiology (TOAST classification) and focuses on aggressive, multifactorial secondary prevention to reduce the high risk of recurrence.
Antithrombotic Therapy: This is tailored to the stroke cause.
For non-cardioembolic stroke (LAA, SVO), antiplatelet therapy (e.g., lifelong Aspirin or Clopidogrel) is the mainstay. For minor strokes or high-risk TIAs, a short course of dual antiplatelet therapy (Aspirin plus Clopidogrel) for 21 days is often used first (20).
For cardioembolic stroke (e.g., atrial fibrillation), long-term oral anticoagulation (e.g., a DOAC like Apixaban or Rivaroxaban, or Warfarin) is indicated and is significantly superior to antiplatelets in preventing recurrent embolic events (20).
Risk Factor Management: Aggressive, evidence-based control of vascular risk factors is critical.
Hypertension: Target <130/80 mmHg.
Hyperlipidemia: High-intensity statin therapy (e.g., Atorvastatin 80mg) with a target LDL <1.8 mmol/L.
Diabetes: Target HbA1c ≤7.0%.
Lifestyle: Smoking cessation, a heart-healthy diet (e.g., Mediterranean style), regular physical activity, and moderation of alcohol intake are foundational (21).
Patient Education: Educate the patient and family on the importance of medication adherence, lifestyle modifications, and how to recognize the signs of a recurrent stroke (F.A.S.T.) to ensure they seek immediate help.
Rehabilitation: A comprehensive, multidisciplinary rehabilitation plan involving physiotherapy, occupational therapy, and speech and language therapy should be initiated as early as possible to capitalize on the period of greatest neuroplasticity and maximize functional recovery (110).
When to Escalate
Call Your Senior (MO/Specialist) if:
The patient shows any signs of neurological deterioration (e.g., a drop in GCS, worsening weakness, new cranial nerve signs), as this may signal stroke progression or a complication.
The patient develops a severe headache, nausea, or vomiting after receiving thrombolysis, as this is a classic sign of potential hemorrhagic transformation.
Blood pressure cannot be controlled within the target range despite initial treatment.
The patient has a seizure.
You are considering a patient for thrombolysis; it is good practice to discuss all potential candidates with a senior to confirm eligibility.
Referral Criteria:
Neurosurgery: Refer immediately for any patient with a cerebellar stroke showing signs of hydrocephalus or brainstem compression on imaging or examination, any patient with a large hemispheric stroke causing significant mass effect and midline shift, or any patient with a diagnosed subarachnoid hemorrhage.
Cardiology: Refer for further evaluation and management if the stroke is suspected to be cardioembolic (e.g., for management of newly diagnosed atrial fibrillation, or for a transesophageal echocardiogram to look for a clot).
Vascular Surgery: Refer patients with a recent non-disabling stroke or TIA who are found to have significant (e.g., >70%) symptomatic carotid stenosis for consideration of carotid endarterectomy, ideally within two weeks of the event (21).
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