amyloid-beta-peptides and Subarachnoid-Hemorrhage

Atraumatic convexal subarachnoid hemorrhage (cSAH) in elderly patients is a rare entity that has been associated with cerebral amyloid angiopathy (CAA) and intracerebral hematomas (ICH). To characterize this entity and to study these associations, 22 patients over 60 with cSAH were included in a multicenter ambispective cohort study. Clinical data, magnetic resonance imaging (MRI) studies, APOE genotyping, and cerebrospinal fluid (CSF) biomarkers were evaluated. Results were compared with data from healthy controls (HC), non-cSAH CAA patients (CAAo), and Alzheimer disease patients. Convexal subarachnoid hemorrhage presented with transient sensory or motor symptoms. At follow-up (median 30.7 months), 5 patients had died, 6 survivors showed functional disability (modified Rankins Scale (mRS)>2), and 12 cognitive impairment. Four patients had prior ICH and six had an ICH during follow-up. CSF-Aß40 and Aß42 levels were lower in cSAH and CAAo compared with HC. Convexal subarachnoid hemorrhage presented an APOE-ɛ2 overrepresentation and CAAo had an APOE-ɛ4 overrepresentation. On MRI, all patients fulfilled CAA-modified Boston criteria and 9 showed cortical ischemia in the surrounding cortex or the vicinity of superficial siderosis. The neuropathologic study, available in one patient, showed severe CAA and advanced Alzheimer-type pathology. Convexal subarachnoid hemorrhage in the elderly is associated with cognitive impairment and lobar ICH occurrence. Our findings support the existence of an underlying CAA pathology.

Topics: Aged; Aged, 80 and over; Amyloid beta-Peptides; Apolipoproteins E; Cerebral Amyloid Angiopathy; Disease-Free Survival; Female; Follow-Up Studies; Genotype; Humans; Magnetic Resonance Angiography; Male; Middle Aged; Peptide Fragments; Radiography; Subarachnoid Hemorrhage

Convexal subarachnoid hemorrhage (cSAH) is sometimes experienced in cerebral amyloid angiopathy (CAA), but ones that are repeated within a brief time period are not common. Also, it is often difficult to diagnose CAA when you experience a case of cSAH.. We examined the clinical course of 2 cases that showed cSAH repeatedly. We examined cerebrospinal fluid (CSF) concentrations of amyloid β protein (Aβ) 40 and 42 and tau protein as additional evidence for a diagnosis of CAA.. Case 1 presented with transient motor paresis of the left hand and case 2 with transient sensory disturbance of the left hand. CT scans showed cSAH on the right central sulcus in both patients. Case 1 showed development of intracerebral hemorrhage on the frontal lobe near the right central sulcus. Case 2 showed relapse of cSAH with recurrence of the same symptoms. These cases could not be diagnosed by image analysis, but were considered CAA by Aβ40, Aβ42 and tau protein in CSF.. Aβ in CSF can be presented here as support for the diagnosis of CAA that is difficult to diagnose by Boston criteria.

Topics: Aged; Amyloid beta-Peptides; Brain; Cerebral Amyloid Angiopathy; Diagnosis, Differential; Female; Humans; Middle Aged; Peptide Fragments; Subarachnoid Hemorrhage; tau Proteins; Tomography, X-Ray Computed

The mechanism underlying the association between possession of the APOEepsilon4 allele and less favorable outcome after subarachnoid hemorrhage (SAH) remains to be determined. After SAH the level of apolipoprotein E (apoE) in the cerebrospinal fluid (CSF) is decreased, and lower levels are associated with more severe injury and less favorable outcome. This study examined serial CSF samples to determine the time course for the decrease in CSF apoE and the relationship between CSF apoE and amyloid beta-protein (Abeta), testing the hypothesis that apoE-Abeta interactions occur in vivo after SAH.. Enzyme-linked immunosorbent assay was used to assay apoE, Abeta1-40, and Abeta1-42 in serial ventricular CSF samples from 19 patients with SAH and 13 controls. CSF S100B and tau were assayed as surrogate markers of brain injury.. There was a sustained decrease in CSF apoE (P<0.001) and Abeta (P<0.001) after SAH in contrast to the observed elevation in CSF S100B (P<0.001) and tau (P<0.001) concentration. There was significant correlation between CSF Abeta concentration and clinical outcome (r=0.65, P<0.01), and the decrease in CSF Abeta concentration correlated significantly with that of apoE (r=0.85, P<0.0001).. After SAH both apoE and Abeta levels decrease in the CSF, supporting the concept that interactions between these proteins occur in vivo. The possibility that apoE and Abeta influence outcome after SAH warrants further investigation.

Topics: Adolescent; Adult; Amyloid beta-Peptides; Apolipoproteins E; Biomarkers; Disease Progression; Humans; Middle Aged; Nerve Growth Factors; Peptide Fragments; S100 Calcium Binding Protein beta Subunit; S100 Proteins; Subarachnoid Hemorrhage; tau Proteins; Time Factors