Neurology >

“Acute neurologic condition due to a disruption in cerebral perfusion”

  • There are two types:
    • Ischaemic
      • May be caused by a thrombotic (blood clot forms in a blood vessel that supplies brain tissue commonly caused by atherosclerosis) or embolic (fragment of a clot that formed in another part of the body) event
    • Haemorhagic
      • Divided into Intracerebral and Subarachnoid
Frequent Presentation
  • Focal loss of function
  • No warning, sudden/rapid onset
  • Maximal loss in all parts, no gradual spread
  • Facial drooping, Arm weakness, Speech difficulties, Time
  • Transient Ischaemic Attack (TIA):
    • Temporary, focal cerebral ischemia resulting in neurologic deficits without acute infarction or permanent loss of function (< 24 hours)
  • Ischaemic Stroke:
    • Most common, in 85% of cases
    • Cerebral infarction due to insufficient cerebral blood flow (hypoperfusion), resulting in ischemia and neuronal injury
    • Causes:
      • Embolism
      • Thrombus (atherosclerosis)
      • Vessel occlusion (lacunar stroke)
      • Systemic hypoperfusion (watershed stroke)
    • Risk factors:
      • Age > 65 years
      • Hypertension
      • Diabetes mellitus
      • AF
      • Carotid artery stenosis
    • Clinical features:
      • Neurological deficits have a sudden onset
  • Intracerebral Haemorrhagic Stroke:
    • Presents in 10% of cases
    • Bleeding within the brain parenchyma
    • Causes:
      • Ruptured cerebral artery or microaneurysm
      • Trauma
      • Arteriovenous malformation
      • Reperfusion injury after ischaemic stroke
    • Risk factors:
      • Age > 65 years
      • Hypertension
      • Vasculitis
      • Malignancy
      • Ischemic stroke
    • Clinical features:
      • Headache
      • Confusion
      • Nausea
      • Sudden onset of focal neurologic deficits
  • Subarachnoid Haemorrhagic Stroke:
    • Presents in 5% of cases
    • Bleeding into the subarachnoid space
    • Causes:
      • Ruptured berry aneurysm
      • Arteriovenous malformation
      • Trauma
    • Risk factors:
      • Hypertension
      • Tobacco use
      • Family history
    • Clinical features:
      • Rapid onset of severe headache
      • Meningeal signs
      • Sudden onset of focal neurologic deficits

The ischaemic cascade causing neurons to break down

  • Vessel obstruction →↑↓ reduced blood flow → ↓O2 → ↓ATP → anaerobic metabolism → x15 less ATP + lactic acid
    • ↓ATP → ↓ neuron Na+/K+ pump function → ↑­ intracellular Na+ → ­↑ H2O diffusing into cell → cytotoxic oedema
    • ↓ATP  →↓ neuron Na+/Ca2+ pump function → ­↑ intracellular Ca2+ → excitotoxicity → ­↑ glutamate release → ↑ ­ excitation of local neurons → toxicity (over-excitement of neurons is toxic)
    • ↓ATP  → ↓ neuron Na+/Ca2+ pump function → ­↑ intracellular Ca2+ → ­↑ degradative enzymes (proteases & lipases) + ­↑ free radicals and reactive oxygen species → breakdown of the neuron cell membrane
  • ↑ Harmful chemicals → ↑ ­ mitochondrial death → ↑­ apoptotic factor  → cellular apoptosis
  • ↑ Blood vessel degradation/ rupture → blood breaches blood-brain barrier → extracellular space in brain parenchyma → vasogenic oedema ­↑ swelling → ↓ brain function + mass effect → cingulate, uncal and cerebellar tonsil brain herniation
  • ↑ Ischemia → brain cell death → ­↑ release of DAMP* → ­↑ inflammatory response  ­ macrophage release → ↑­ anti-inflammatory cells → ­ liquefactive necrosis begins → cystic cavity formation + loss of functional brain tissue
Clinical Presentation

Stroke presentation can be varied depending on where the occlusion or haemorrhage occurred, how long it has lasted, how quickly treatment was obtained and how large the area affected is. Recovery is also dependant on these factors.

  • Middle Cerebral Artery – deep and lateral hemispheres (~65-75%)
    • The MCA arises from the Circle of Willis and supplies most of the cerebral cortex on the lateral surfaces of the frontal lobe, the anterolateral surface of the parietal lobe, and the superolateral surface of the temporal lobe, as well as part of the basal ganglia and internal capsule. The MCA is the most commonly occluded artery in ischemic strokes.
    • Contralateral sensory loss (numbness) and weakness in the arm, lower limb and lower half of face, gaze deviation to the side of infarction
    • Contralateral homonymous hemianopia without macular sparing
    • Aphasia – Wernicke’s (unable to comprehend speech) and/or Broca’s (comprehends but cannot respond) if a stroke occurs in dominant hemisphere
  • Anterior Cerebral Artery – medial anterior hemispheres (~5-10%)
    • The ACA arises from the Circle of Willis and supplies the medial portions of the frontal and parietal lobes, much of the corpus callosum, the caudate nucleus, and the anterior portion of the internal capsule.
    • Contralateral weakness in the lower limbs > upper limbs
    • Contralateral sensory loss in the lower limbs > upper limbs
    • Abulia (disinterest and a slowed mental state)
    • Urinary incontinence
    • Dysarthria (impaired articulation due to dysfunction of the tongue, lips, or vocal cords)
    • Transcortical motor aphasia (difficulty initiating speech and expressing a thought process)
    • Apraxia (inability to perform coordinated, purposeful, and/or learned voluntary movements e.g. brushing hair, putting on socks/shoes)
  • Posterior Cerebral Artery – occipital & medial temporal lobe ~ 20-30% of strokes
    • The PCA arises from the Circle of Willis and supplies most parts of the occipital cortex, inferior and medial temporal cortices, thalamus, and midbrain.
    • Contralateral homonymous hemianopia with macular sparing
    • Contralateral sensory loss (due to lateral thalamic involvement – light touch, pinprick, and positional sense may be reduced)
    • Memory deficits, vertigo, nausea
    • In left PCA territory: Alexia without agraphia (can write but are unable to read), anomic aphasia (can understand speech and repeat words and sentences but may struggle to supply words for things they want to talk about), visual agnosia (inability to recognise or interpret visual information)
    • Right PCA territory: prosopagnosia (inability to recognize familiar faces
    • Midbrain Syndrome:
      • Medial midbrain syndrome (Weber syndrome)
      • Lateral midbrain syndrome (Claude syndrome)
      • Paramedian midbrain syndrome (Benedikt syndrome)
      • Dorsal midbrain syndrome (Parinaud syndrome)
    • Thalamic Syndrome:
      • Decreased arousal
      • Variable sensory loss
      • Aphasia
      • Visual field losses
      • Apathy, agitation, personality changes
  • Basilar Artery
    • Consciousness is usually preserved
    • Vertebrobasilar insufficiency
      • Vertigo, drop attacks, tinnitus, hiccups, dysarthria, dysphagia (swallowing issues)
      • Ipsilateral cranial nerve deficits
      • Diplopia (double vision)
      • Gait ataxia (staggering gait with irregular, uncoordinated movements)
      • Paresthesias (abnormal sensation, such as tingling or “pins and needles”
    • Pontine syndromes
      • Ventral pontine syndrome
      • Lateral pontine syndrome
      • Inferior medial pontine syndrome
      • Locked-in syndrome (bilateral basilar artery occlusion)
    • Cerebellar syndromes
  • Identify risk factors for ischemic or haemorrhagic stroke
  • Determine the time of onset of symptoms (the time of stroke onset determines whether thrombolytic therapy/tPA is an option)
    • Ischaemic stroke patients with onset <6 hours aren’t eligible for thrombolytic
  • Visualise haemorrhagic in CT scan, FLAIR MRI (distinguish old from new) and cerebral angiography
  • Carotid ultrasound + echocardiography → identify thrombus/ source of emboli
  • Fasting lipid profiles  + haemoglobin A1C levels → identify atherosclerosis + diabetes
  • Ischaemic stroke: “prevent and bust clots
    • Time dependant thrombolytic enzymes (tPA – alteplase, tenecteplase)
    • Reperfusion therapy (reestablish blood flow and prevent further tissue ischemia),
    • Aspirin (prevent more clots)
    • Thrombectomy surgery to mechanically remove clot (suction and wire), stenting, carotid endarterectomy (plaque removal) if necessary
  • Haemorrhagic stroke: “manage symptoms and complications”
    • Antihypertensive (beta-blockers, calcium channel blockers),
    • Prevent vasospasm (oral nimodipine)
    • Reverse anticoagulation
    • Anticonvulsant
    • In patients with ­ ICP: intubation with hyperventilation, head elevation (30°), IV mannitol
  • Surgical intervention to prevent further injury and bleeding: clipping or coil embolisation

Prevention of future stroke and symptom management

  • Clinical:
    • Monitoring of patient following a stroke
    • Rehabilitation (physiotherapy, speech therapist, mental health support.)
    • Control other comorbidities (diabetes, HTN, CVD, etc.)
  • Lifestyle:
    • Stop smoking
    • Improve diet, ↓ salt, exercise
    • Minimise alcohol consumption
  • Pharmacological:
    • Anti-hypertensives/ACE inhibitors (ramipril)
    • Antiplatelet therapy (aspirin, clopidogrel in non-cardioembolic)
    • Anticoagulation therapy (e.g. warfarin in cardioembolic)
    • Cholesterol management (e.g. simvastatin, atorvastatin)
  • Coma and potentially brain death
  • Cardiac dysfunction: arrhythmia, MI
  • Deep vein thrombosis and pulmonary embolism
  • Delirium and Depression
  • Bleeding (e.g., gastrointestinal bleeding)
  • Aspiration pneumonia
  • Neurologic C/X: ­↑ ICP, brain herniation, seizures, hemiparesis, aphasia, disability, central post-stroke pain, neuropathic pain, SIADH
  • Ischemic stroke: haemorrhagic transformation, vascular dementia
  • Haemorrhagic stroke: recurrent haemorrhage, Intraventricular haemorrhage, hydrocephalus, vasospasm
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