ISCHEMIC STROKE

David Goldemund M.D.
Updated on 23/02/2024, published on 20/06/2023

Topical diagnosis in stroke refers to the localization of ischemia within the brain based on clinical signs and symptoms and neuroimaging. This approach helps to differentiate between different stroke subtypes, such as cortical versus subcortical strokes, or to identify specific vascular territories that may be affected (large vs. small vessel occlusion, anterior vs. posterior circulation). Accurate topical diagnosis is essential for timely and targeted intervention and can help determine the etiology of stroke and initiate appropriate secondary stroke prevention.

Both clinical examination and imaging should help answer the following questions:

→ Anatomy of cerebral arteries

→ Anatomical variants of cerebral arteries

The main regions to consider are:

• anterior circulation (carotid system) involving the internal carotid artery, middle cerebral artery, and anterior cerebral artery and their branches
• posterior circulation (vertebrobasilar system) involving the vertebral arteries, basilar artery, and posterior cerebral artery

• the common carotid artery (CCA) is most usually affected by atherosclerosis
  • extensive atherosclerosis may occur due to radiation-induced vasculopathy
• concentric wall thickening is a characteristic feature of Takayasu arteritis
• trauma/dissection (usually extending from the aortic arch) usually leads to sympathetic plexus disruption and the development of complete Horner’s syndrome
  • the extent of anhidrosis varies with the level of lesion
    • lesions affecting the plexus surrounding the CCA affect the entire half of the face
    • lesions affecting the plexus surrounding the ICA affect only the medial part of the forehead and the lateral aspect of the nose
  • in Horner syndrome, the upper eyelid never descends below the center of the pupil 
  • Pseudo-Horner syndrome is the coincidence of simple anisocoria (20% of the population) and measurable asymmetry in the width of the eye slits (15% of the population) with a narrower pupil and eye slit on the same side (3-4% of the population)
• CCA occlusion/stenosis may be asymptomatic or have a clinical presentation similar to ICA occlusion/stenosis (see below)
• ECA occlusion/stenosis is typically asymptomatic
  • ECA stenosis may become symptomatic if the ACE serves as the dominant collateral pathway in case of the ipsilateral ICA occlusion
  • inflammatory involvement has typical clinical presentation  → temporal arteritis

• variable clinical presentation, from asymptomatic occlusion to severe hemispheric infarct
  • massive MCA infarct (hemiparesis, hemisensory loss, aphasia/neglect syndrome, etc.)  
    
  • combined MCA+ACA infarct (MCA symptoms +frontal lobe syndrome) 
    
  • embolization into the ophthalmic artery with loss of vision (the transient form is called amaurosis fugax)
• presentation depends on:
  • the dynamics of the occlusion (progressive stenosis x acute thrombotic occlusion)
  • the location and extent of the occlusion (occlusion at the ICA origin  x terminal ICA occlusion +/-  proximal ACA and MCA involvement)
  • collateral circulation status
  • individual anatomical variations
• Border zone infarcts (BZIs) are also a specific finding in patients with ICA occlusion or severe stenosis 

• the ophthalmic artery supplies blood to the retina and other structures of the eye
• the symptoms of its occlusion are primarily visual; the severity can vary depending on the extent and speed of the occlusion
• usually sudden, painless monocular visual impairment (ranging from scotoma to complete amaurosis)→ see CRAO
• arteriolopathic changes lead to ischemic optic neuropathy (ION)
  • nonarteritic forms of ION usually do not result in total blindness
    
  • initially, there is edema of the optic nerve head, followed by its atrophy
    

• the Anterior Choroidal Artery (AChA) originates from the supraclinoid portion of the ICA (above the PComA) or MCA
• the AChA supplies several important brain structures:
  • choroid plexus in the lateral ventricles
  • optic chiasm, optic tract, and lateral geniculate body
  • internal capsule
  • medial part of the globus pallidus
  • amygdala and anterior segments of the hippocampus
  • hypothalamus, substantia nigra, and nucleus ruber
• a variety of symptoms may be seen depending on the specific area of the brain that is affected; confusion with other types of strokes or neurological disorders is frequent
  • contralateral homonymous visual field defects (lateral geniculate body)
  • contralateral hemiparesis (internal capsule)
  • contralateral hemihypesthesia (posterolateral thalamic nuclei)
  • bilateral lesions may cause akinetic mutism
  • memory deficit (if anterior segments of the hippocampus are involved)
  • dysfunction in the hypothalamus, substantia nigra, and nucleus ruber is less common
• AChA occlusion most commonly results from arteriolopathy or embolization

• clinical presentation can vary depending on several factors, such as the location and extent of the occlusion, the functionality of collateral circulation, such as the anterior communicating artery (AComA), and the individual’s unique anatomy.
• motor and sensory deficits:
  • hemiparesis – often more pronounced in the lower extremity than the upper extremity.
  • hemisensory loss – often parallel to the hemiparesis pattern
• cognitive and behavioral changes
  • frontal lobe syndrome
    • apathy, abulia, and reduced creativity
    • emotional incontinence and social disinhibition
    • dysexecutive syndrome
    • symptoms of frontal syndrome become more severe in cases of bilateral involvement (e.g. when both ACAs are supplied by a single carotid artery)
  • contralateral apraxia
• speech and language deficits
  • transcortical motor aphasia (dominant hemisphere) – characterized by good comprehension but poor speech production
    
• other symptoms:
  • Alien hand syndrome (nondominant hemisphere) – a person might experience involuntary hand movements
  • eyes and head may deviate toward the side of the infarct
• some perforating branches supplying the anterior portion of the internal capsule may originate from the A1 segment. Occlusion of the ACA may result in paresis of the CN VII and arm

• the vertebral artery (VA) most commonly originates from the subclavian artery, passes through the costotransverse foramina of vertebrae C6 to C2, and enters the skull through the foramen magnum
• segments (V0-4):
  • V0 – origin
  • V1 – segment before entering the transverse foramen (this happens most commonly at the level of vertebra C6)
  • V2 – intraforaminal segment
  • V3 – atlas loop (C2-dura)
  • V4 – intracranial segment
• major branches:
  • PICA (may arise uni- or bilaterally from the basilar artery) – supplies medulla oblongata (including the vestibular nuclei) and the inferior cerebellum
  • anterior and posterior spinal arteries
• atherosclerosis typically affects segments V1 and V4
• dissection mainly affects segment V3 (although concomitant thrombosis may occlude the entire vessel)
• steal syndrome may occur in the presence of significant subclavian artery stenosis
  • transient dizziness and other posterior circulation symptoms occur during physical activity involving the ipsilateral arm
    
• rarely, the VA may be compressed by head rotation (→ Bow Hunter’s syndrome)
• AV occlusion may remain asymptomatic; symptoms depend on the extent of the occlusion, the anatomic situation (is the dominant VA affected?), and whether distal embolization has occurred (to the BA or its branches)
  • ischemia typically occurs in the lateral medulla oblongata (symptoms are described in the PICA section)
    
  • extensive brainstem and cerebellar ischemia is also common

• etiopathogenesis:
  • thromboembolism from ostial vertebral stenosis (V0 segment)
  • thromboembolism from the V4 segment
  • embolization from the heart and the aortic arch
  • dissection (usually starting at the V3 segment; may lead to a complete VA occlusion)
• clinical presentation
  • cerebellar infarct 
    • involves part of the vermis and hemisphere
    • presenting with ataxia, vertigo, nystagmus (usually a simultaneous brainstem lesion occurs)
  • lateral medullary syndrome (Wallenberg syndrome) occurs when the PICA gives off branches to the oblongata (medulla oblongata is more commonly supplied by the VA and BA) 
    • ipsilateral: Horner’s syndrome, facial hypesthesia for all modalities, ataxia
    • contralateral: dissociated hypesthesia from the neck downward (impaired sensation of pain and temperature with preserved touch sensation)
      
    • vestibular syndrome – vertigo, nystagmus (inferior vestibular nuclei)
    • bulbar palsy (dysarthria, dysphonia, dysphagia), singultus
    • nausea and vomiting
    • singultus

• AICA arises from the lower part of the basilar artery and supplies:
  • the upper part of the medulla oblongata and cerebellum
  • the base of the pons
  • it may give off the labyrinthine artery (also known as the auditory artery or internal auditory artery), which may also arise from the BA
    
• clinical presentation of isolated AICA occlusion (AICA syndrome):
  • vestibular syndrome (nausea, vomiting, nystagmus, vertigo)
    
  • ipsilateral ataxia
  • sometimes contralateral hemiparesis
  • occlusion of the labyrinthine artery may cause hearing loss
    
  • ipsilateral facial weakness
  • sometimes contralateral hemiparesis ( if corticospinal tracts in the pons are involved )

• SCA arises from the rostral portion of the basilar artery, just below the PCA, and supplies:
  • the superior cerebellar peduncle
  • vermis
  • the upper part of the cerebellar hemisphere
  • the dorsolateral portion of the mesencephalon (midbrain)
    
  • dentate nucleus
• clinical presentation
  • neocerebellar syndrome with ataxia and tremor
  • dysarthria
  • Horner’s syndrome
  • central paresis of the CN VII
  • ipsilateral choreiform movements

• the basilar artery is a major blood vessel at the base of the brain that arises from the confluence of the two vertebral arteries, runs along the ventral surface of the brainstem, and gives off several branches before it branches into the two posterior cerebral arteries (PCAs)
• it supplies blood to the posterior part of the brain, including the cerebellum, brainstem, and occipital lobes
  • pons ((and sometimes medulla oblongata) are supplied via perforating and circumferential branches
• occlusion of the BA or its branches (embolic, atherothrombotic) results in a mix of symptoms caused by lesions in the brainstem, cerebellum, thalamus, temporal and occipital lobes (basilar artery syndrome)

• the posterior cerebral artery (PCA) is a terminal branch of the basilar artery
• the proximal segment gives off branches to the middle part of the mesencephalon, a substantial portion of the thalamus, and the lateral geniculate body
  • these branches may arise from a single PCA and supply both sides ⇒ extensive mesencephalic infarction may be thus present in unilateral PCA occlusion
• occlusion of the pre-communicating segment (P1) leads to infarction of the cerebral peduncles, thalamus, and mediobasal parts of the temporal and occipital lobes.
• peduncles and thalamus are spared when only the P2 segment (posterior to the PComA) is occluded