Central nervous system disorders

V./4.4.: Physical examination

Physical findings in stroke depend on the location of ischemic area affected. Distribution follows arterial territories in most cases. Blood supply of the brain and arterial/vascular territories reviewed in details in the chapter on anatomy. Two paired arteries of internal carotid artery (ICA) and vertebral artery (VA) supply the brain with blood. The paired vertebral arteries join in front of the pons to form basilar artery (BA), the latter give rise to the paired posterior cerebral arteries (PCA).

Middle cerebral artery (MCA) and anterior cerebral artery (ACA) are the main branches of ICA. First segment of ACA (A1), bilateral MCA and both PCA form the Willis circle in addition with the anterior communicating artery (ACoA) which connects both ACA. ICA also gives rise to the posterior communicating artery (PCoA), originating proximally then ACA and MCA. PCoA connects ICA and PCA.

Ophthalmic artery (branch of ICA) stenosis or emboli result in ischemia of the retina that cause ipsilateral blindness, transient monocular blindness (TMB) or anterior ischemic optic neuropathy (AION). Infarction of the anterior choroidal artery (other direct branch of ICA) would cause contralateral hemiparesis and hemihypesthesia or additionally hemianopsy if lateral geniculate body were also involved.

Infarction in the ACA vascular territory results in contralateral lower extremity dominant hemiparesis or lower extremity monoparesis most often. Lesion of the medial surface in this region could also result the following: sensory disturbance in the contralateral lower extremity (postcentral gyrus), urinary incontinence (upper part of the frontal medial gyrus), abulia (mediobasal area of the frontal lobe), and primitive reflexes.

Symptoms highly depend on the exact location of the occlusion and the collateral circulation. Occlusion of the A1 segment of ACA with open ACoA would only cause infarction in case medial perforating branches such as recurrent artery of Heubner  is also affected. In that case ischemia in the internal capsule will result in upper extremity dominant hemiparesis and dysarthria; agitation and hyperactivity or on the contrary abulia, apathy and lack of initiative also could develop. Anatomic variation with missing unilateral A1 segment means that both ACA originate from the other side; in which case both ACA vascular territories are damage simultaneously by infarction.

Symptoms of the infarction in the MCA territory are contralateral faciobrachial dominant hemiparesis and hemihypesthesia, lesion of the dominant hemisphere could also cause aphasia; while lesion of the non-dominant hemisphere cause anosognosia or neglect syndrome. Lesion in the territory of anterior branches of the MCA result in contralateral motor and sensory disturbance with predominance of the face, hand and upper extremity, aphasia and gnostic symptoms could develop regarding side of the lesion. Isolated motor symptoms are possible. Contralateral gaze palsy or conjugated deviation toward the lesion in most severe cases could develop. In case of posterior branches of the MCA territory damage, motor symptoms will not, but contralateral hemisensory syndrome and hemi- or quadrantanopsy will develop.

Lenticulostriate arteries are the perforating branches of MCA. Ischemic lesion of that area may damage the caudate nucleus, putamen and internal capsule. Left sided lesion would not only cause hemiparesis but also cognitive disturbance, amnestic syndrome, confusion or subcortical aphasia. In case of right sided lesion, faciobrachial dominant hemiparesis will develop with occasional behavioural disturbance. Perforating branches supplying this region could also arise from the ACA (anterior lenticulostriate arteries and anterior choroidal artery).

Symptoms of the cortical PCA infarction are contralateral homonym hemianopsy and hemisensory syndrome occasionally. (Question 2). Bilateral lesion may result in cortical blindness, in which case cardioembolic origin or severe BA occlusive disease suspected.

The PCoA give rise to the tuberothalamic artery supplying the anterolateral part of the thalamus. Contralateral hemiparesis, emotional facial nerve palsy, neuropsychiatric symptoms; additionally aphasia (dominant hemisphere) or neglect syndrome (non-dominant hemisphere) could develop.

Posterolateral part of the thalamus is supplied by thalamogeniculate artery from PCA. Typically, Dejerine-Roussy syndrome will develop: contralateral paresthesia and pain (occasionally anaesthesia), astereognosis, thalamus hand, chorea (sometimes athetosis), hemiparesis and hemiataxia. Posteromedial and posterolateral branches of the choroidal artery from PCA supply the lateral geniculate body: contralateral hemianopsy will be found if damaged. Median or paramedian infarct of the thalamus is caused by occlusion of the thalamoperforating artery arising from the proximal PCA. In that case, transient hypnoid disturbance of consciousness followed by neuropsychiatric syndrome, vertical gaze palsy or internuclear ophtalmoplegia is typical.

Watershed zone infarctions are visible by neuroimaging methods. Anterior watershed area damage could cause contralateral lower extremity dominant hemiparesis, transortical motor aphasia, apathy or dysexecutive syndrome. In case of bilateral lesion gait apraxia and dementia could develop. Posterior watershed infarct will cause visual neglect, prosopagonsia, colour agnosia, contralateral hemisensory loss or visual defect. Bálint syndrome with simultaneous agnosia, optic ataxia and ocular apraxia is a result of bilateral damage. Deep subcortical watershed zone infarcts cause contralateral motor and sensory symptoms and possibly cognitive changes.

Lacunar infarction caused by microangiopathy will lead to typical clinical findings like isolated hemiparesis or pure motor stroke, pure sensory syndrome, motor and sensory symptoms (without visual defect or cortical damage), ataxic hemiparesis, dysarthria-clumsy hand syndrome and crossed brainstem syndromes.

In case of brain stem strokes, crossed and bilateral symptoms have to be briefly mentioned. Dysarthria, double vision, ataxia with dizziness and vomiting could develop. In case of crossed symptoms, the physical finding will be the so-called alternating hemiparesis (ipsilateral cranial nerve damage and contralateral projection pathway damage); the location of the lesion is suspected by the cranial nerve involvement. Basilar artery stenosis can cause cortical blindness and tetraparesis. Small perforating arteries of the brainstem lead to typical clinical syndromes.

Based on the Oxfordshire Community Stroke Project stroke patients could be divided in four groups on the physical findings from which size and location of the lesion can be judged. Prognosis in all four groups is markedly different. Total anterior circulation infarct (TACI) is characterized by contralateral hemiparesis, hemianopsy and cortical symptoms (aphasia, apraxia). Symptoms are not so extensive in partial anterior circulation infarct (PACI) then in TACI. In posterior circulation infarct (POCI) brain stem and/or cerebellar symptoms and hemianopsy are typical. In lacunar infarct (LACI) pure motor or sensory symptoms, ataxic hemiparesis, motor and sensory symptoms without visual or cortical involvement could be found.