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עמוד בית
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November 2009
November 2006
D. Soffer
 Cerebral amyloid angiopathy is characterized by deposition of amyloid in the walls of leptomeninged and cerebral blood vessels. Its most common form, sporadic CAA[1] that results from deposition of β-amyloid peptide, which is the subject of this short review, is present in virtually all cases of Alzheimer diseases and is also common among non-demented subjects where its prevalence increases with age. Stroke due to massive cerebral lobar hemorrhage is the main clinical presentation of CAA, but transient neurologic symptoms due to microhemorrhages may also occur. CAA is also a risk factor for cerebral infarction and there is increasing evidence that CAA contributes to cognitive impairment in the elderly, usually in association with white matter abnormalities on imaging. Although the definitive diagnosis of CAA is neuropathologic, reliable diagnosis can be reached clinically, based on the occurrence of strictly lobar hemorrhages, particularly in the cortico-subcortical area when using gradient-echo or T2*-weighted magnetic resonance imaging. Experimental studies have shown that the origin of the vascular amyloid is neuronal, and age-related degenerative changes in the vessel walls prevent its clearance from the brain along perivascular spaces and promote Aβ[2] aggregation and CAA formation. The entrapped Aβ aggregetes are toxic to various vascular wall components, including smooth muscle cells, pericytes and endothelial cells, leading to their eventual destruction and predisposition of the vessel wall to rupture and hemorrhage. However, more research is necessary to decipher the mechanism of CAA formation and its relation to cognitive decline in the elderly.







[1] CAA = cerebral amyloid angiopathy

[2] Aβ = β-amyloid peptide


R. Segal, A. Furmanov and F. Umansky
 Background: The recent occurrence of a spontaneous intracerebral hemorrhage in Israel’s Prime Minister placed the scrutiny of local and international media on neurosurgeons as they made therapeutic decisions. In the ensuing public debate, it was suggested that extraordinary measures (surgical treatment) were undertaken only because of the celebrity of the patient.

Objectives: To evaluate the criteria used to select surgical versus medical management for SICH.

Methods: We retrospectively reviewed the files of 149 consecutive patients admitted with SICH[1] from January 2004 through January 2006 to our medical center. Their mean age was 66 (range 3–92 years), and 62% were male. SICH localization was lobar in 50% of patients, thalamus in 23%, basal ganglia in 15%, cerebellum in 13%, intraventricular in 6%, and pontine in 1%. Mean admission Glasgow Coma Score was 9 (range 3–15). Risk factors included hypertension in (74%), diabetes mellitus (34%), smoking (14%) and amyloid angiopathy (4%). Fifty percent of patients were on anticoagulant/antiplatelet therapy, including enoxaparin (3%), warfarin (7%), warfarin and aspirin (9%), or aspirin alone (34%).      

Results: Craniotomy was performed in 30% of patients, and ventriculostomy alone in 3%. Rebleed occurred in 9% of patients. Six months after the treatment 36% of operated patients were independent, 42% dependent, and 13% had died. At 6 months, 37% of non-operated patients were independent, 15% dependent, and 47% had died.

Conclusions: One-third of the SICH patients, notably those who were experiencing ongoing neurologic deterioration and had accessible hemorrhage, underwent craniotomy. The results are good, considering the inherent mortality and morbidity of SICH.


 





[1] SICH = spontaneous intracerebral hemorrhage


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