07-17-2006, 10:25 AM
Still not confident for answer.
Intracranial hemorrhage accounts for 8-13% of all strokes.
ICH is more likely to result in death or major disability than ischemic stroke or subarachnoid hemorrhage.
ICH and accompanying edema may disrupt or compress adjacent brain tissue, leading to neurological dysfunction. Substantial displacement of brain parenchyma may cause elevation of intracranial pressure (ICP) and potentially fatal herniation syndromes.
Chronic hypertension produces a small vessel vasculopathy characterized by lipohyalinosis, fibrinoid necrosis, and development of Charcot-Bouchard aneurysms, affecting penetrating arteries throughout the brain including lenticulostriates, thalamoperforators, paramedian branches of the basilar artery, superior cerebellar arteries, and anterior inferior cerebellar arteries.
Predilection sites for ICH include the basal ganglia (40-50%)
lobar regions (20-50%),
thalamus (10-15%),
pons (5-12%), cerebellum (5-10%), and other brainstem sites (1-5%).
Annually, more than 20,000 individuals in the United States die of ICH.
ICH has a 30-day mortality rate of 44%.
Pontine or other brainstem ICH has a mortality rate of 75% at 24 hour
ICH has a slight male predominance, though study results have been conflicting.
Cerebral amyloid angiopathy may be more common among women.
Phenylpropanolamine use has been associated with ICH in young women
Incidence of ICH increases in individuals older than 55 years and doubles with each decade until age 80 years
Onset of symptoms of ICH is usually during daytime activity, with progressive (ie, minutes to hours) development of the following:
Alteration in level of consciousness (approximately 50%)
Nausea and vomiting (approximately 40-50%)
Headache (approximately 40%)
Seizures (approximately 6-7%)
Focal neurological deficits
Physical: Clinical manifestations of ICH are determined by the size and location of hemorrhage, but may include the following:
Hypertension, fever, or cardiac arrhythmias
Nuchal rigidity
Subhyaloid retinal hemorrhages
Altered level of consciousness
Anisocoria
Focal neurological deficits
Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, aphasia, neglect, or apraxia
Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion
Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia
Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion
Brain stem - Quadriparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability
Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousness
SAH
About 6-8% of all strokes are caused by SAH from ruptured berry aneurysms.
Hypertension (previously documented acute severe hypertension with diastolic value over 110 mm Hg), smoking, alcohol, multiple aneurysms, increasing aneurysm size, fatty metamorphosis of the liver, long-term analgesic use, and oral contraceptives have been linked to aneurysmal SAH.
Race: North American blacks have been found to have a 2.1 times greater risk of SAH than whites.
Sex: The incidence of SAH is slightly higher in women than in men.
Age: The mean age for SAH is 50 years.
Aneurysmal SAH presents with severe headache of sudden onset ("thunderclap headache") that can be accompanied by loss of consciousness at onset. The headache is frequently described as "worst headache of my life."
Neck stiffness, photophobia, and low back pain are symptoms of meningeal irritation. Nausea and vomiting are due to increased intracranial pressure (ICP) and meningeal irritation.
Focal neurological deficits may also occur.
Approximately 10-25% of patients with SAH have a seizure, usually in the first few minutes after onset. This is due to the sudden rise in ICP or direct cortical irritation by blood.
An estimated 10-15% of patients with ruptured aneurysms have symptoms related to their aneurysm prior to the rupture. The most common symptoms are headache (48%), dizziness (10%), orbital pain (7%), diplopia (4%), and visual loss (4%).
Signs present before SAH include sensory or motor disturbance (6%), seizures (4%), ptosis (3%), bruits (3%), and dysphasia (2%). Some studies estimate an even higher incidence of premonitory symptoms”as many as 40-50%, with signs appearing 10-20 days prior to rupture.
The premonitory symptoms may represent small leaks ("sentinel bleed") or expansion of the aneurysm.
Approximately 30-40% of patients are at rest at the time of SAH. Physical or emotional strain, defecation, coitus, and head trauma contribute to varying degrees in the remaining 60-70% of cases.
Physical:
The physical examination findings may be normal.
Global depression of neurological function may be noted, including altered level of consciousness and confusional state.
Focal neurological findings may include the following:
Cranial nerve deficits: Oculomotor palsy (posterior communicating artery aneurysm) is most frequent. Abducens palsy is usually due to increased ICP rather than a true localizing sign. Monocular loss of vision can occur with ophthalmic artery aneurysms.
Hemiparesis: With or without aphasia, hemiparesis is due to middle cerebral artery (MCA) aneurysm, ischemia or hypoperfusion in the vascular territory, or intracerebral clot.
Leg monoparesis or paraparesis with or without akinetic mutism/abulia points to anterior communicating aneurysm rupture.
Funduscopic findings include papilledema and subhyaloid retinal hemorrhages
Intracranial hemorrhage accounts for 8-13% of all strokes.
ICH is more likely to result in death or major disability than ischemic stroke or subarachnoid hemorrhage.
ICH and accompanying edema may disrupt or compress adjacent brain tissue, leading to neurological dysfunction. Substantial displacement of brain parenchyma may cause elevation of intracranial pressure (ICP) and potentially fatal herniation syndromes.
Chronic hypertension produces a small vessel vasculopathy characterized by lipohyalinosis, fibrinoid necrosis, and development of Charcot-Bouchard aneurysms, affecting penetrating arteries throughout the brain including lenticulostriates, thalamoperforators, paramedian branches of the basilar artery, superior cerebellar arteries, and anterior inferior cerebellar arteries.
Predilection sites for ICH include the basal ganglia (40-50%)
lobar regions (20-50%),
thalamus (10-15%),
pons (5-12%), cerebellum (5-10%), and other brainstem sites (1-5%).
Annually, more than 20,000 individuals in the United States die of ICH.
ICH has a 30-day mortality rate of 44%.
Pontine or other brainstem ICH has a mortality rate of 75% at 24 hour
ICH has a slight male predominance, though study results have been conflicting.
Cerebral amyloid angiopathy may be more common among women.
Phenylpropanolamine use has been associated with ICH in young women
Incidence of ICH increases in individuals older than 55 years and doubles with each decade until age 80 years
Onset of symptoms of ICH is usually during daytime activity, with progressive (ie, minutes to hours) development of the following:
Alteration in level of consciousness (approximately 50%)
Nausea and vomiting (approximately 40-50%)
Headache (approximately 40%)
Seizures (approximately 6-7%)
Focal neurological deficits
Physical: Clinical manifestations of ICH are determined by the size and location of hemorrhage, but may include the following:
Hypertension, fever, or cardiac arrhythmias
Nuchal rigidity
Subhyaloid retinal hemorrhages
Altered level of consciousness
Anisocoria
Focal neurological deficits
Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, aphasia, neglect, or apraxia
Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion
Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia
Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion
Brain stem - Quadriparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability
Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousness
SAH
About 6-8% of all strokes are caused by SAH from ruptured berry aneurysms.
Hypertension (previously documented acute severe hypertension with diastolic value over 110 mm Hg), smoking, alcohol, multiple aneurysms, increasing aneurysm size, fatty metamorphosis of the liver, long-term analgesic use, and oral contraceptives have been linked to aneurysmal SAH.
Race: North American blacks have been found to have a 2.1 times greater risk of SAH than whites.
Sex: The incidence of SAH is slightly higher in women than in men.
Age: The mean age for SAH is 50 years.
Aneurysmal SAH presents with severe headache of sudden onset ("thunderclap headache") that can be accompanied by loss of consciousness at onset. The headache is frequently described as "worst headache of my life."
Neck stiffness, photophobia, and low back pain are symptoms of meningeal irritation. Nausea and vomiting are due to increased intracranial pressure (ICP) and meningeal irritation.
Focal neurological deficits may also occur.
Approximately 10-25% of patients with SAH have a seizure, usually in the first few minutes after onset. This is due to the sudden rise in ICP or direct cortical irritation by blood.
An estimated 10-15% of patients with ruptured aneurysms have symptoms related to their aneurysm prior to the rupture. The most common symptoms are headache (48%), dizziness (10%), orbital pain (7%), diplopia (4%), and visual loss (4%).
Signs present before SAH include sensory or motor disturbance (6%), seizures (4%), ptosis (3%), bruits (3%), and dysphasia (2%). Some studies estimate an even higher incidence of premonitory symptoms”as many as 40-50%, with signs appearing 10-20 days prior to rupture.
The premonitory symptoms may represent small leaks ("sentinel bleed") or expansion of the aneurysm.
Approximately 30-40% of patients are at rest at the time of SAH. Physical or emotional strain, defecation, coitus, and head trauma contribute to varying degrees in the remaining 60-70% of cases.
Physical:
The physical examination findings may be normal.
Global depression of neurological function may be noted, including altered level of consciousness and confusional state.
Focal neurological findings may include the following:
Cranial nerve deficits: Oculomotor palsy (posterior communicating artery aneurysm) is most frequent. Abducens palsy is usually due to increased ICP rather than a true localizing sign. Monocular loss of vision can occur with ophthalmic artery aneurysms.
Hemiparesis: With or without aphasia, hemiparesis is due to middle cerebral artery (MCA) aneurysm, ischemia or hypoperfusion in the vascular territory, or intracerebral clot.
Leg monoparesis or paraparesis with or without akinetic mutism/abulia points to anterior communicating aneurysm rupture.
Funduscopic findings include papilledema and subhyaloid retinal hemorrhages