Friday, September 2, 2016

Localization of stroke based on clinical findings


This post focuses on the localization of the lesion in stroke, re-written from Harrison.
I divide this post into "Important to know" and "Extra notes" which are optional to learn about.

What's a stroke?
A stroke, or cerebrovascular accident, is defined by this abrupt onset of a neurologic deficit that is attributable to a focal vascular cause. Causes of ischemic stroke here.

Stroke syndromes are divided into:
(1) large-vessel stroke within the anterior circulation,
(2) large vessel stroke within the posterior circulation
(3) small-vessel disease of either vascular bed.

During vivas, you'll mostly be asked to localize the lesion into anterior circulation (ACA vs MCA). They don't expect much, but you should at least know the divisions (anterior circulation vs posterior circulation), occlusion of which artery involves speech, monoparesis of a leg is seen in stroke involving which artery, etc. Just the basics.

Stroke within the Anterior Circulation:
The internal carotid artery and its branches (MCA + ACA) comprise the anterior circulation.

Middle cerebral artery:
Important to know:
- If the entire MCA is occluded at its origin, the clinical findings are contralateral hemiplegia, hemianesthesia and homonymous hemianopia. Dysarthria is common because of facial weakness.

- When the dominant hemisphere is involved, global aphasia is present.

- When the nondominant hemisphere is affected, anosognosia, constructional apraxia, and neglect are found. (Mnemonic: pH - Parietal lobe - Hemineglect, NN - Neglect, Non dominant hemisphere)

- Occlusion of a lenticulostriate vessel produces small-vessel (lacunar) stroke within the internal capsule. This produces pure motor stroke or sensory-motor stroke contralateral to the lesion.

Extra notes:
- A combination of sensory disturbance, motor weakness, and nonfluent aphasia suggests that an embolus has occluded the proximal superior division.

- If a fluent (Wernicke’s) aphasia occurs without weakness, the inferior division of the MCA supplying the posterior part (temporal cortex of the dominant hemisphere is probably involved. Jargon speech and an inability to comprehend written and spoken language are prominent features, often accompanied by a contralateral, homonymous superior quadrantanopia.

- Hemineglect or spatial agnosia without weakness indicates that the inferior division of the MCA in the nondominant hemisphere is involved.

- Ischemia within the genu of the internal capsule causes primarily facial weakness followed by arm then leg weakness as the ischemia moves posterior within the capsule.

Anterior cerebral artery:
Important to know:
Occlusion of a single A2 segment of the ACA results in the contralateral symptoms such as:
- Paralysis of opposite foot and leg due to involvement of the motor leg area
- Cortical sensory loss over toes, foot, and leg due to involvement of sensory area for foot and leg
- Paresis of opposite arm because of arm area of cortex or fibers descending to corona radiate
- Urinary incontinence due to involvement of sensorimotor area in paracentral lobule

Extra notes:
- The ACA is divided into two segments: the precommunal (A1) circle of Willis, or stem, which connects the internal carotid artery to the anterior communicating artery, and the postcommunal (A2) segment distal to the anterior communicating artery

- The A1 segment gives rise to several deep penetrating branches that supply the anterior limb of the internal capsule, the anterior perforate substance, amygdala, anterior hypothalamus, and the inferior part of the head of the caudate nucleus.

- Occlusion of the proximal ACA is usually well tolerated because of collateral flow through the anterior communicating artery and collaterals through the MCA and PCA.

Stroke within the Posterior Circulation: 
Important to know:
- The posterior circulation is composed of the vertebral arteries, the basilar artery, and the posterior cerebral arteries.

Two clinical syndromes are commonly observed with occlusion of the PCA:

P1 syndrome:
Midbrain, subthalamic, and thalamic signs, which are due to disease of the proximal P1 segment of the PCA or its penetrating branches (thalamogeniculate, Percheron, and posterior
choroidal arteries)
- Infarction usually occurs in the ipsilateral subthalamus and medial thalamus and in the ipsilateral cerebral peduncle and midbrain. A third nerve palsy with contralateral ataxia (Claude’s syndrome) or with contralateral hemiplegia (Weber’s syndrome) may result.

P2 syndrome:
Cortical temporal and occipital lobe signs, due to occlusion of the P2 segment distal to the junction of the PCA with the posterior communicating artery.
- Occlusion of the distal PCA causes infarction of the medial temporal and occipital lobes. Contralateral homonymous hemianopia with macula sparing is the usual manifestation.

Extra notes: 
- Occlusion of the posterior cerebral artery can produce peduncular hallucinosis (visual hallucinations of brightly colored scenes and objects).

- Bilateral infarction in the distal PCAs produces cortical blindness (blindness with preserved pupillary light reaction). The patient is often unaware of the blindness or may even deny it (Anton’s syndrome).

Vertebral and posterior inferior cerebellar arteries:
Important to know:
Only the fourth segment of the vertebral artery gives rise to branches that supply the brainstem and cerebellum. The posterior inferior cerebellar artery (PICA) in its proximal segment supplies the lateral medulla and, in its distal branches, the inferior surface of the cerebellum.

- Embolic occlusion or thrombosis of a V4 segment causes ischemia of the lateral medulla.

- The constellation of vertigo, numbness of the ipsilateral face and contralateral limbs, diplopia, hoarseness, dysarthria, dysphagia, and ipsilateral Horner’s syndrome is called the lateral medullary (or Wallenberg’s) syndrome. Most cases result from ipsilateral vertebral artery occlusion; in the remainder, PICA occlusion is responsible. Hemiparesis is NOT a feature of vertebral artery occlusion.

Extra notes:
- Complete basilar occlusion causes bilateral long tract signs (sensory and motor) with signs of cranial nerve and cerebellar dysfunction. A “locked-in” state of preserved consciousness with quadriplegia and cranial nerve signs suggests complete pontine and lower midbrain infarction. 

- Occlusion of the superior cerebellar artery results in severe ipsilateral cerebellar ataxia, nausea and vomiting, dysarthria, and contralateral loss of pain and temperature sensation over the extremities, body, and face (spino- and trigeminothalamic tract).

- Occlusion of the anterior inferior cerebellar artery (AICA) produces variable degrees of infarction because the size of this artery and the territory it supplies vary inversely with those of the PICA. The principal symptoms include: ipsilateral deafness, facial weakness, vertigo, nausea and vomiting, nystagmus, tinnitus, cerebellar ataxia, Horner’s syndrome, and paresis of conjugate lateral gaze; and contralateral loss of pain and temperature sensation.

That's all!
Lemme know if that helped! 
Here's a quote by Van Gogh: I would rather die of passion than of boredom (:


  1. These posts are excellent. Bridging basic science (in this case neuro-anatomy) with clinical medicine in perfectly pertinent ways.


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