Hemorrhagic stroke physical examination

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Physical examination

Physical examination should include:^[1]^[2]^[3]^[4]

Vital signs
Level of consciousness (Glasgow Coma Scale (GCS))
Level of severity of neurological deficit (National Institutes of Health Stroke Scale (NIHSS))

Physical examination of patients with Intracerebral hemorrhage is usually varies based on the location of the bleeding.^[4]


Locations	Physical examination
Putamenal hemorrhage	Hemiplegia Hemisensory loss Homonymous hemianopsia Gaze palsy Stupor Coma
Thalamic hemorrhage	General signs: Downward gaze (paralysis of upward gaze) Small pupils (lack of light pupillary response) Depressed consciousness Apathy Hypersomnolence Disorientation Visual hallucinations Aphasia Impairment of verbal memory Visuospatial dysfunction
Thalamic hemorrhage	Behavioural patterns based on the four main arterial thalamic territories: Anterior: perservations, apathy, and amnesia Paramedian infarction: disinhibition, personality change and amnesia (severe retrograde and anterograde amnesia) Extensive lesions: “thalamic dementia” Inferolateral: Executive dysfunction and occasionally severe long term disability Posterior: No specific behavioural pattern however can include cognitive dysfunction, neglect, aphasia
Pontine hemorrhage	Decreased level of consciousness (most common) Long tract signs including tetraparesis Cranial nerve palsies Seizures Cheyne-Stokes respiration
Cerebellar hemorrhage	Small bleeds Ataxia Nystagmus Larger bleeds Impair consciousness Obstructive hydrocephalus (obstruct the fourth ventricle)
Lobar hemorrhage	The signs vary depending on the location of the hemorrhage: Acute neurological deterioration Decreased GCS Seizure Contralateral homonymous hemianopsia (occipital hemorrhage) Contralateral plegia/paresis of the leg with relative sparing of the arm (frontal hemorrhage)

References

↑ Bos MJ, Koudstaal PJ, Hofman A, Breteler MM (2007). “Decreased glomerular filtration rate is a risk factor for hemorrhagic but not for ischemic stroke: the Rotterdam Study”. Stroke. 38 (12): 3127–32. doi:10.1161/STROKEAHA.107.489807. PMID 17962600.
↑ Hackam DG, Mrkobrada M (2012). “Selective serotonin reuptake inhibitors and brain hemorrhage: a meta-analysis”. Neurology. 79 (18): 1862–5. doi:10.1212/WNL.0b013e318271f848. PMID 23077009. Review in: Evid Based Ment Health. 2013 May;16(2):54
↑ Qureshi AI, Tuhrim S, Broderick JP, Batjer HH, Hondo H, Hanley DF (2001). “Spontaneous intracerebral hemorrhage”. N Engl J Med. 344 (19): 1450–60. doi:10.1056/NEJM200105103441907. PMID 11346811.
↑ ^4.0 ^4.1 Fisher CM (1971). “Pathological observations in hypertensive cerebral hemorrhage”. J Neuropathol Exp Neurol. 30 (3): 536–50. PMID 4105427.

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[pmid17962600-1] Bos MJ, Koudstaal PJ, Hofman A, Breteler MM (2007). “Decreased glomerular filtration rate is a risk factor for hemorrhagic but not for ischemic stroke: the Rotterdam Study”. Stroke. 38 (12): 3127–32. doi:10.1161/STROKEAHA.107.489807. PMID 17962600.

[pmid23077009-2] Hackam DG, Mrkobrada M (2012). “Selective serotonin reuptake inhibitors and brain hemorrhage: a meta-analysis”. Neurology. 79 (18): 1862–5. doi:10.1212/WNL.0b013e318271f848. PMID 23077009. Review in: Evid Based Ment Health. 2013 May;16(2):54

[pmid11346811-3] Qureshi AI, Tuhrim S, Broderick JP, Batjer HH, Hondo H, Hanley DF (2001). “Spontaneous intracerebral hemorrhage”. N Engl J Med. 344 (19): 1450–60. doi:10.1056/NEJM200105103441907. PMID 11346811.

[pmid4105427-4] 4.0 ^4.1 Fisher CM (1971). “Pathological observations in hypertensive cerebral hemorrhage”. J Neuropathol Exp Neurol. 30 (3): 536–50. PMID 4105427.

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