Intracerebral Hemorrhage Flashcards
Which are the two types of hemorrhagic stroke
1) Intracerebral hemorrhage
2) Subarachnoid hemorrhage
What is the percentage of intracerebral hemorrhage among strokes
10-15%
Intracerebral Hemorrhage: Risk Factors
- Hypertension
- Smoking
- Heavy alcohol use
- Low cholesterol levels
- Genetics (apolipoprotein E ε2 ε4 alleles)
Intracerebral Hemorrhage: Causes
A) Most common causes Hypertension Cerebral amyloid angiopathy Vascular malformations (arteriovenous fistula or malformations, cavernous angiomas) Ruptured aneurysm Hemorrhagic transformation of an ischemic stroke Neoplasm
B) Less common causes Endocarditis with septic embolism Coagulopathy Severe thrombocytopenia Sympathomimetic drug abuse Anticoagulant or antiplatelet therapy
C) Rare causes Herpes simplex encephalitis Cerebral vasculitis Reversible cerebral vasoconstriction syndrome Cerebrovenous occlusion Moyamoya disease
Putamen Hemorrhage symptoms
The hallmark of putamen hemorrhage is contralateral hemiparesis, hemisensory loss, or both, due to involvement of the adjacent internal capsule.
Smaller putamen hemorrhages may mimic the deficits seen with lacunar infarction, including pure motor
hemiparesis, pure hemisensory sensory stroke, and ataxic hemiparesis.
Rarely, a movement disorder (eg, hemiballism) follows hemorrhage limited to the putamen itself.
Larger putaminal hemorrhage often causes cortical signs in addition to contralateral hemiplegia, including aphasia (language dominant hemisphere), contralateral hemineglect (either hemisphere), visual field disturbances, and ipsilateral gaze preference.
Massive putamen hematoma can cause coma.
Caudate Hemorrhage symptoms
Bleeding into the caudate often extends into the ventricular system, causing severe headache, nuchal rigidity, nausea, and vomiting.
There may be decreased verbal fluency or aphasia, but persistent language disturbance is uncommon.
Many patients are apathetic or abulic.
Hemiparesis, when present (about 30%), is usually mild.
Ventricular extension of blood may cause acute hydrocephalus, with coma and oculomotor palsies.
Thalamic hemorrhage symptoms
Most patients with thalamic hemorrhage have a rapid onset of contralateral weakness and hemisensory loss to all modalities.
A minority experience initial hemisensory symptoms with subsequent appearance of hemiparesis.
Receptive aphasia or hemineglect may be present.
Small anterior or medial thalamic hemorrhages
can cause amnesia or abulia with preserved motor
and sensory function.
Small lateral thalamic hemorrhages rarely mimic the thalamic lacunar syndrome of so-called pure sensory stroke.
Massive thalamic hemorrhages cause a rapid descent into coma, either due to acute hydrocephalus from intraventricular extension or due to hematoma dissection into the midbrain reticular activating system.
Occular signs in thalamic hemorrhage
These include:
- tonic downward gaze deviation with upgaze palsy
- horizontal gaze deviations to either the ipsilateral or contralateral side
- mid-position, unreactive pupils
- retractory nystagmus upon attempted upgaze
*These ocular signs are probably the result of damage to the oculomotor complex in the mid-brain or acute obstructive hydrocephalus.
Pontine hemorrhage symptoms
Eighty percent of patients have rapid descent into coma, accompanied by quadriplegia, stiffening of the limbs, extensor posturing, pinpoint reactive pupils, facial diplegia, absence of gag and swallowing reflexes, loss of spontaneous and reflexic horizontal eye movements, and loss of corneal reflexes.
Other eye movement abnormalities include ocular bobbing (rapid conjugate downward saccade with slow return to neutral position).
Rare patients have predicate symptoms of headache, deafness, numbness, or nausea, usually lasting a few minutes and followed by coma.
Autonomic symptoms include high fevers and respiratory abnormalities.
Mortality from large pontine hemorrhage is nearly 100%.
Occasionally, patients have small unilateral pontine hemorrhages, most often due to AVM rupture or bleeding from cavernous malformations. Such patients have syndromes that mimic lacunar infarction in the pons, such as pure motor stroke, ataxic hemiparesis, or isolated cranial neuropathies.
Cerebellar hemorrhage symptoms
The most common symptom is the inability to stand or walk independently, with a “drunk” or unstable feeling.
Vomiting, headache, and neck pain and stiffness are also common.
Neurologic examination usually discloses nystagmus, dysarthria, occasional ipsilateral peripheral facial and gaze palsy (from compression of the ipsilateral pons), and ipsilateral appendicular incoordination.
Frank weakness of the extremities is uncommon and, if present, suggests brainstem compression.
The level of consciousness may range from normal to
coma and is a crucial clinical variable.
Common locations of intraparenchymal
hemorrhage
A: Lobar hemorrhage often due to cerebral
amyloid angiopathy
B: Hemorrhage of basal ganglia and internal capsule
C: Thalamic hemorrhage
D: Pontine hemorrhage
E: Cerebellar hemorrhage
*B–E are often
due to hypertension
