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Stroke – Types, Causes, Symptoms, Diagnosis, Treatment

Stroke is a neurological deficit of cerebrovascular causes the sudden death of brain cells due to lack of oxygen, caused by blockage of blood flow or rupture of an artery to the brain. Sudden loss of speech, weakness, or paralysis of one side of the body can be symptoms. A suspected stroke may be confirmed by scanning the brain.

 is defined by the World Health Organization as a clinical syndrome consisting of rapidly developing clinical signs of focal (or global in case of coma) disturbance of cerebral function lasting more than 24 hours or leading to death with no apparent cause other than a vascular origin.’ A transient ischaemic attack () is defined as stroke symptoms and signs that resolve within 24 hours. There are limitations to these definitions. The symptoms of a TIA usually resolve within minutes or a few hours at most, and anyone with continuing neurological signs, when first assessed, should be assumed to have had a stroke. ‘Brain Attack’ is sometimes used to describe any neurovascular event and maybe a more transparent and less ambiguous term.

A cerebellar infarct (or cerebellar stroke) is a cerebrovascular event involving the posterior cranial fossa, specifically the cerebellum. Impaired perfusion reduces oxygen delivery and causes deficits in motor and balance control. In the case of hemorrhagic events, bleeding can directly damage tissue and worsen these deficits. While comprising a small fraction of strokes, cerebellar strokes are responsible for a disproportionate share of morbidity and mortality due to their sometimes subtle initial presentation and the adverse effects of reactive swelling in the posterior fossa. Cerebellar strokes account for 1% – 4% of all brain strokes.

Types of Stroke

Ischemic Stroke

  • Most strokes (87%) are ischemic strokes.1 An ischemic stroke happens when blood flow through the artery that supplies oxygen-rich blood to the brain becomes blocked. Blood clots often cause blockages that lead to ischemic strokes.

Hemorrhagic Stroke

  • A hemorrhagic stroke happens when an artery in the brain leaks blood or ruptures (breaks open). The leaked blood puts too much pressure on brain cells, which damages them.
  • High blood pressure and aneurysms—balloon-like bulges in an artery that can stretch and burst—are examples of conditions that can cause a hemorrhagic stroke.

There are two types of hemorrhagic strokes.

  • Intracerebral hemorrhage – is the most common type of hemorrhagic stroke. It occurs when an artery in the brain bursts, flooding the surrounding tissue with blood.
  • Subarachnoid hemorrhage – is a less common type of hemorrhagic stroke. It refers to bleeding in the area between the brain and the thin tissues that cover it.

Transient Ischemic Attack (TIA)

  • For Blanche Teal-Cruise, a smoker for 40 years who also had high blood pressure, the transient ischemic attack (sometimes called a mini-stroke) she had on the way to work was a wake-up call.
  • A transient ischemic attack (TIA) is sometimes called a “mini-stroke.” It differs from the significant types of stroke because blood flow to the brain is blocked for only a short time—usually no more than 5 minutes.

Features of middle cerebral artery stroke

  • Contralateral hemiparesis and hypesthesia (Weakness of arm& face is worse than in the lower limb)
  • Gaze towards to side of the lesion
  • Ipsilateral hemianopsia
  • Receptive or expressive aphasia is the dominant hemisphere is affected
  • Agnosia
  • Inattention, neglect

Features of anterior cerebral artery stroke

  • Speech is preserved, but there is a disinhibition
  • Mental status is altered
  • Judgment is impaired
  • Contralateral cortical sensory deficits
  • Contralateral weakness greater in legs than arms
  • Urinary incontinence
  • Gait apraxia

Posterior cerebral artery stroke

  • Cortical blindness
  • Contralateral homonymous hemianopsia
  • Altered mental status
  • Visual agnosia
  • Memory impairment

Vertebral/basilar artery stroke

  • Nystagmus
  • Vertigo
  • Diploma and visual field deficits
  • Dysarthria
  • Dysphagia
  • Syncope
  • Facial hyperesthesia
  • Ataxia

Subtypes

  • Pure motor hemiparesis – The patient presents with weakness on one side of the body (face, arm, and leg) without cortical signs and sensory symptoms.
  • Pure sensory stroke – The patient presents with unilateral numbness of the face, arm, and leg without cortical signs or motor deficits. All sensory modalities will be impaired.
  • Ataxic hemiparesis – These patients present unilateral limb ataxia and weakness that exceeds the strength/motor deficit. Patients may also exhibit other ipsilateral cerebellar signs such as dysarthria, dysmetria, and nystagmus without showing cortical signs.
  • Sensorimotor stroke – Patients present with weakness and numbness of the face, arm, and leg without cortical signs. Cortical function testing must be done meticulously to distinguish between a frontoparietal lobe (MCA) stroke and a subcortical stroke (posterior thalamus and internal capsule).
  • Dysarthria-clumsy hand syndrome – This is the least common of all lacunar syndromes. Patients present with facial weakness, dysarthria, dysphagia, and dysmetria/clumsiness of one upper extremity.

If the area of the brain affected includes one of the three prominent central nervous system pathways—the spinothalamic tract, corticospinal tract, and the dorsal column–medial lemniscus pathway, symptoms may include:

  • hemiplegia and muscle weakness of the face
  • numbness
  • reduction in sensory or vibratory sensation
  • initial flaccidity (reduced muscle tone), replaced by spasticity (increased muscle tone), exaggerated reflexes, and obligatory synergies.[rx]

In addition to the above CNS pathways, the brainstem gives rise to most of the twelve cranial nerves. A brainstem stroke affecting the brainstem and brain, therefore, can produce symptoms relating to deficits in these cranial nerves

  • altered smell, taste, hearing, or vision (total or partial)
  • drooping of the eyelid (ptosis) and weakness of ocular muscles
  • decreased reflexes: gag, swallow, pupil reactivity to light
  • decreased sensation and muscle weakness of the face
  • balance problems and nystagmus
  • altered breathing and heart rate
  • weakness in sternocleidomastoid muscle with the inability to turn head to one side
  • weakness in the tongue (inability to stick out the tongue or move it from side to side)

If the cerebral cortex is involved, the CNS pathways can again be affected but also can produce the following symptoms

  • aphasia (difficulty with verbal expression, auditory comprehension, reading, and writing; Broca’s or Wernicke’s area typically involved)
  • dysarthria (motor speech disorder resulting from neurological injury)
  • apraxia (altered voluntary movements)
  • visual field defect
  • memory deficits (involvement of temporal lobe)
  • hemineglect (involvement of parietal lobe)
  • disorganized thinking, confusion, hypersexual gestures (with the involvement of the frontal lobe)
  • lack of insight into their, usually stroke-related, disability

If the cerebellum is involved, ataxia might be present, and this includes

  • altered walking gait
  • altered movement coordination
  • vertigo and or disequilibrium

Symptoms associated with PCA strokes like diplopia, visual field defects, dysphagia, vertigo, alteration in consciousness, memory impairment, or difficulty reading may help us understand the stroke’s localization.

Visual Field Defects

  • PCA and deep branches of MCA supply the optic radiations. The lower part of the optic radiations receives blood supply from the PCA. The upper part gets blood supply from the MCA.
  • Unilateral infarctions of the occipital lobe may cause contralateral homonymous hemianopia with macular sparing.
  • Quadrantanopia may be seen if the defect is limited. If there is an infarction in the temporal lobe involving the Meyer loop or infracalcarine, it may present with superior quadrantanopia. Infarctions cause inferior quadrantanopia in the optic radiation of the inferior parietal lobe or supracalcarine. In a study with pure superficial PCA strokes in 117 patients, 26 (22%) presented with quadrantanopia. Twenty (17%) is superior.
  • Visual field defects (hemianopia, quadrantanopia, deuteranopia), hemisensory deficit, and neuropsychological dysfunction (transcortical aphasia, memory disturbances) may be seen after occlusion of the posterior choroidal artery.
  • Bilateral infarction of the occipital lobes may cause cortical blindness. The patient may have visual anosognosia. The patient is not aware of their deficit. The patient may confabulate and deny blindness.

Visual Dysfunction 

  • Visual Agnosia: Patients may not understand or describe uses for the objects seen. Patients can name things when they touch them or when the items are related to them. The two forms of visual agnosia are apperceptive and associative. Apperceptive involves poor perception and understanding, while associative involves a poor ability to match and use. It is caused by a large left PCA stroke, which likely causes a disconnect between language and visual systems.
  • Prosopagnosia is difficulty recognizing familiar faces due to lesions in the inferior occipital areas, fusiform gyrus, and the anterior temporal cortex. In literature, deficits are only shown in the right PCA territory.
  • Alexia refers to difficulty in reading. Alexia without agraphia (pure alexia) is caused by a lesion to the dominant occipital lobe and splenium of the corpus callosum and is often accompanied by right homonymous hemianopia.
  • Achromatopsia refers to difficulty perceiving colors. It is due to infarctions in the ventral occipital cortex and/or infracalcarine. The patient may present with hemiachromatopsia if the infarction is unilateral. Tests to check for achromatopsia are Ishihara color plates or the Farnsworth-Munsell 100-hue test.

Cognitive and Behavioral Dysfunction

  • Aphasia can be due to an infarction large enough to cover the left parietal or temporal lobe. Infarctions cause transcortical sensory aphasia to the parietal-occipital region on the left side. The patient may have amnestic aphasia (inability to name but repetition and comprehension intact) due to infarction to the left temporal lobe of PCA territory.
  • Memory impairment is caused by infarction of the hippocampus and parahippocampus.
  • Aggressive behavior can be caused by PCA strokes as well. In a study of 41 PCA stroke patients, 3 (7.3%) patients showed aggressive behavior such as shouting obscenities and hitting and biting others. These patients may become anxious, bold, and frustrated when stimulated by the environment.
  • Hallucinations are uncommon but may develop from PCA strokes on any side of the brain.
  • Palinopsia refers to seeing images persist even after an image has been removed. Infarctions can be in the lingual and fusiform gyri.

Other Dysfunctions

  • Midbrain infarction may present differently, depending on the location of infarction. Patients may present ataxic hemiparesis due to an anterolateral midbrain infarction or oculomotor or pupillary problems due to a paramedian rostral midbrain infarction.
  • Pure sensory stroke may result from a lesion in the ventral posterolateral nucleus, which receives the blood supply from thalamogeniculate (inferolateral) arteries.
  • Infractions to the artery of Percheron infarction can result in bilateral paramedian thalamus infarction with or without midbrain involvement. Patients may present with confusion, hypersomnolence, dysarthria, amnesia, and ocular movement disorders.
  • Infarctions cause Balint syndrome to the bilateral occipitoparietal border. This presents with optic ataxia (inability to reach targets one is looking at), oculomotor apraxia (inability to move eyes towards an object intentionally), and simultagnosia (inability to synthesize objects within a visual field).
  • Anton syndrome is due to a sudden onset of bilateral occipital strokes leading to cortical blindness. The patient will deny the blindness.

Symptoms of Stroke

The words FAST can help you recognize stroke signs:

  • (B)Balance: Sudden loss of balance.
  • (E)Eyes: Sudden loss of vision in one or both eyes
  • (F) ACE. Ask the person to smile. Check to see if one side of the face droops.
  • (A) RMS. Ask the person to raise both arms. See if one arm drifts downward.
  • (S)PEECH. Ask the person to repeat a simple sentence. Check to see if words are slurred and if the sentence is replicated correctly.
  • (T)IME. If a person shows any of these symptoms, time is essential. It is vital to get to the hospital as quickly as possible.

Common Signs of Stroke

Common signs of a stroke include sudden weakness, numbness and signs of paralysis, speech problems, trouble seeing, dizziness, difficulty walking, and a severe headache. Usually, only one side of the body is affected, making it impossible to move the right arm and right leg, for example. Nausea and vomiting are also possible symptoms. The type and severity of stroke symptoms depend on the affected area of the brain.

Signs and symptoms of stroke in both men and women may include:

  • Sudden numbness, weakness, or inability to move the face, arm, or leg (especially on one side of the body)
  • Confusion
  • Trouble speaking or understanding speech
  • Trouble seeing in one or both eyes
  • Dizziness, trouble walking, or loss of balance or coordination
  • Sudden, severe headache (often described as “the worst headache of my life”)
  • Trouble breathing
  • Loss of consciousness

If the area of the brain affected contains one of the three prominent central nervous system pathways—the spinothalamic tract, corticospinal tract, and dorsal column (medial lemniscus), symptoms may include:

  • hemiplegia and muscle weakness of the face
  • numbness
  • reduction in sensory or vibratory sensation
  • initial flaccidity (reduced muscle tone), replaced by spasticity (increased muscle tone), exaggerated reflexes, and obligatory synergies.
  • altered smell, taste, hearing, or vision (total or partial)
  • drooping of the eyelid (ptosis) and weakness of ocular muscles
  • decreased reflexes: gag, swallow, pupil reactivity to light
  • decreased sensation and muscle weakness of the face
  • balance problems and nystagmus
  • altered breathing and heart rate
  • weakness in sternocleidomastoid muscle with the inability to turn head to one side
  • weakness in the tongue (inability to stick out the tongue or move it from side to side)

If the cerebral cortex is involved, the CNS pathways can again be affected but also can produce the following symptoms:

  • aphasia (difficulty with verbal expression, auditory comprehension, reading, and writing; Broca’s or Wernicke’s area typically involved)
  • dysarthria (motor speech disorder resulting from neurological injury)
  • apraxia (altered voluntary movements)
  • visual field defect
  • memory deficits (involvement of temporal lobe)
  • hemineglect (involvement of parietal lobe)
  • disorganized thinking, confusion, hypersexual gestures (with the involvement of the frontal lobe)
  • lack of insight into his or her, usually stroke-related, disability

If the cerebellum is involved, ataxia might be present, and this includes:

  • altered walking gait
  • altered movement coordination
  • vertigo and or disequilibrium

Stroke Symptoms in Women

Stroke is the third leading cause of death in women (and the fifth leading cause of death in men).

Each year stroke kills twice as many women as breast cancer, according to the National Stroke Association.

The stroke symptoms women may experience can be different from those experienced by men. These include:

  • Fainting
  • Difficulty or shortness of breath
  • Sudden behavioral changes
  • Agitation
  • Hallucination
  • Nausea or vomiting
  • Seizures
  • Hiccups

Diagnosis of Stroke

A. Bedside history & examination

  1. Precise time-of-onset interview – Asking the patient, family, or witnesses exactly when symptoms began determines eligibility for time-sensitive treatments such as clot-busting drugs or thrombectomy and distinguishes stroke from migrainous aura or seizure post-ictal states.

  2. Past medical history screen – Rapid review of hypertension, atrial fibrillation, diabetes, prior stroke, smoking, and medication use (e.g., anticoagulants) pinpoints risk factors and bleeding likelihood, shaping acute therapy and secondary prevention choices.

  3. Vital-signs survey – Blood pressure, pulse, oxygen saturation, and temperature signal raised intracranial pressure, infection, or cardio-embolic sources and guide safe permissive hypertension or fever control strategies during the hyper-acute window.

  4. Focused cranial-nerve exam – Testing pupils, gaze, facial symmetry, swallow, and tongue movement localises the lesion and spots brain-stem or posterior-circulation strokes that can masquerade as benign dizziness.

  5. Motor strength grading – Simple arm-drop and leg-lift tests quantify hemiparesis severity, monitor progression, and feed into formal scales such as the NIH Stroke Scale.

  6. Sensory pattern mapping – Pinprick or light-touch asymmetry across dermatomes confirms a vascular rather than peripheral neuropathic pattern and may indicate thalamic or cortical involvement.

  7. Deep-tendon reflex and Babinski response – Hyper-reflexia or an up-going plantar reflex supports an upper-motor-neuron lesion and helps rule out functional (psychogenic) weakness.

  8. Cerebellar coordination checks – Finger-to-nose, heel-to-shin, and rapid alternating movements reveal ataxia from cerebellar or posterior circulation ischemia and warn of impending herniation if swelling evolves.

  9. Gait observation (if safe) – Early bedside walking or, if non-ambulatory, passive sitting balance uncovers truncal ataxia or neglect, useful for rehabilitation planning.

  10. Level-of-consciousness assessment (Glasgow Coma Scale) – Serial GCS scoring tracks declining arousal due to hemorrhage, hydrocephalus, or malignant cerebral edema and triggers airway protection.


B. Standardised neurological rating scales

  1. National Institutes of Health Stroke Scale (NIHSS) – The 11-item score (0–42) objectifies neurological deficit size, predicts outcome, and guides reperfusion thresholds; regular updates ensure contemporary stimuli and scoring consistency. ninds.nih.gov

  2. Modified Rankin Scale (mRS) – Though mainly an outcome scale, an early mRS baseline (0–5) helps document pre-stroke independence, influencing thrombectomy candidacy and discharge planning.

  3. Barthel Index of Activities of Daily Living – Ten everyday tasks (feeding, transfers, toileting) rate practical disability; a low score at admission steers early occupational-therapy priorities.

  4. ABCD² Score – In transient ischemic attack, this five-factor score (Age, BP, Clinical features, Duration, Diabetes) predicts stroke within 48 hours and supports urgent imaging triage.

  5. FOUR Score – A coma scale incorporating eye, motor, brain-stem reflex, and respiration items, useful when an endotracheal tube prevents full GCS verbal testing in severe hemorrhagic stroke.


C. Laboratory & molecular biomarkers

  1. Complete blood count (CBC) – Detects polycythemia, thrombocytopenia, or infection that might mimic stroke or alter thrombolysis safety.

  2. Serum electrolytes & renal panel – Sodium, potassium, creatinine abnormalities can provoke seizure or confusion mimicking stroke and flag contrast-induced nephropathy risk before CT angiography.

  3. Finger-stick and venous glucose – Hypo- or hyper-glycemia confounds neurological findings; urgent correction prevents secondary neuronal injury.

  4. Coagulation profile (PT/INR, aPTT) – Identifies warfarin effect or factor deficiencies that increase hemorrhagic conversion risk after alteplase.

  5. Cardiac troponin I/T – Elevated enzymes hint at concurrent myocardial infarction or cardio-embolic origin and necessitate dual cardiac–neurological management.

  6. Lipid profile – Baseline LDL supports statin initiation and secondary prevention counselling.

  7. Plasma D-dimer – High levels suggest large-vessel occlusion or underlying venous sinus thrombosis; when combined with GFAP improves stroke subtype detection.

  8. Blood urea nitrogen & creatinine – Beyond contrast safety, deranged values may indicate uremic encephalopathy rather than true stroke.

  9. Serum glial fibrillary acidic protein (GFAP) – An astrocytic injury marker that rises swiftly in intracerebral hemorrhage and extensive infarction; point-of-care assays aid early subtype triage. pubmed.ncbi.nlm.nih.govfrontiersin.org

  10. Multiplex GFAP + D-dimer panel for large-vessel occlusion (LVO) – A 2024 prospective tool pairs biomarkers with stroke-severity scales, boosting pre-hospital detection of thrombectomy-eligible occlusions. ahajournals.org


D. Structural & vascular imaging

  1. Non-contrast head CT (NCCT) – The first-line scan rules out hemorrhage, visualises early ischemic changes, and underpins Alteplase decision-making; speed trumps sensitivity.

  2. CT Angiography (CTA) – From aortic arch to vertex, CTA maps occlusion location, collateral status, and tandem lesions, informing thrombectomy strategy.

  3. CT Perfusion (CTP) – Automated colour maps distinguish irreversibly infarcted core from salvageable penumbra, extending reperfusion windows up to 24 hours in select patients.

  4. Conventional brain MRI – Superior for posterior fossa and small lacunar infarcts; sequences include T1, T2, FLAIR, DWI, and SWI.

  5. Diffusion-weighted imaging (DWI) – Within minutes of arterial blockage, restricted diffusion lights up, confirming brain ischemia even when CT is normal.

  6. Magnetic resonance angiography (MRA) – Time-of-flight or contrast-enhanced MRA non-invasively visualises intracranial vessels without radiation, albeit slower than CTA.

  7. MR perfusion (PWI) – Complements DWI; mismatch patterns mirror CT perfusion and guide late mechanical thrombectomy.

  8. Portable low-field MRI (e.g., Hyperfine Swoop®) – Bedside ultra-low-field (0.064 T) scanners provide rapid images in emergency or rural settings, with 2025 data showing good agreement with standard MRI for ischemic stroke triage. hyperfine.iobusinesswire.com

  9. Dual-energy CT (DECT) – Differentiates iodine contrast staining from true parenchymal hemorrhage after thrombectomy, preventing unnecessary anticoagulation delays.

  10. Susceptibility-weighted imaging (SWI) – Highly sensitive to micro-bleeds, thrombus (“susceptibility vessel sign”), and hemorrhagic transformation risk.

  11. Transcranial Doppler ultrasound (TCD) – Bedside insonation detects MCA flow arrest, micro-embolic signals, or vasospasm; also monitors reperfusion during thrombolysis.

  12. Carotid duplex ultrasound – Combines B-mode plaque imaging with Doppler velocity to grade carotid stenoses, screening for endarterectomy candidates.

  13. Intracranial vessel-wall MRI (VWI) – High-resolution black-blood sequences visualise vasculitis, intracranial dissection, or unstable atherosclerotic plaque missed by lumen-based angiography.

  14. Digital subtraction angiography (DSA) – The gold standard for vascular detail and endovascular therapy; supplies live road-mapping for clot retrieval.

  15. Contrast-enhanced carotid ultrasound (CEUS) – Micro-bubble agents highlight neovascularisation in vulnerable plaques, predicting embolic risk.


E. Cardiac rhythm & source evaluation

  1. 12-lead electrocardiogram (ECG) – Arrhythmias such as atrial fibrillation or flutter direct anticoagulation; acute ST-elevation alerts to concurrent myocardial infarction.

  2. 24-hour Holter monitor – Catches paroxysmal atrial fibrillation episodes that a single ECG may miss; detection rates climb with longer monitoring.

  3. Transthoracic echocardiography (TTE) – Screens for mural thrombus, cardiomyopathy, or patent foramen ovale that could shower emboli to the brain.

  4. Trans-esophageal echocardiography (TEE) – High-frequency probe via oesophagus gives superior views of left atrial appendage thrombus and aortic arch plaque.

  5. Implantable loop recorder – Three-year continuous monitoring uncovers elusive atrial fibrillation in cryptogenic stroke, transforming secondary prevention.


F. Physiological & adjunct tests

  1. Near-infrared spectroscopy (NIRS) cerebral oximetry – Real-time bedside monitoring of regional oxygen saturation during ambulance transport, reperfusion therapy, or hemicraniectomy.

  2. Electroencephalography (EEG) – Differentiates post-stroke seizures, periodic discharges, or non-convulsive status epilepticus that mimic deterioration.

  3. Ambulatory blood-pressure variability analysis – Excess peaks suggest sympathetic dysregulation post-stroke and correlate with poor functional outcome, guiding tighter pressure targets.

  4. Microwave or electromagnetic portable brain scanner (EMVision “backpack” device) – A compact unit detects hemorrhage or ischemia within minutes in pre-hospital settings, improving golden-hour decisions in rural regions. theaustralian.com.au

  5. Cerebrospinal-fluid (CSF) analysis via lumbar puncture – In suspected stroke mimics (e.g., meningitis, subarachnoid hemorrhage with negative CT), CSF xanthochromia or pleocytosis settles the diagnosis.

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