Symptomatic idiopathic intracranial hypertension triggered by Ramadan intermittent fasting: a case report.

BACKGROUND: Idiopathic intracranial hypertension (IIH) is a disorder that primarily affects obese women of reproductive age. The exact pathogenesis of IIH is unknown though multiple etiologies have been proposed. CASE PRESENTATION: We report a case of IIH triggered by first-time Ramadan intermittent fasting (RIF) in an 18-year-old woman. Our patient developed new onset headaches, diplopia, and pulsatile tinnitus with examination notable for bilateral papilledema and lumbar puncture revealing an elevated opening pressure. Her symptoms resolved after cessation of RIF, apart from persistent left sided tinnitus which later resolved with acetazolamide administration. CONCLUSION: This case report uniquely illustrates that RIF may provoke symptomatic IIH. We hypothesize that a decreased concentration of glucagon-like peptide-1 (GLP-1) induced by fasting results in decreased GLP-1 receptor activation in the choroid plexus, allowing for increased CSF secretion into the ventricles invoking increased intracranial pressure (ICP). This theoretical mechanism provides further insight as to the possible underlying pathophysiology of IIH.

Genetic variation at CR1 increases risk of cerebral amyloid angiopathy.

OBJECTIVE: Accumulated evidence suggests that a variant within the CR1 gene (single nucleotide polymorphism rs6656401), known to increase risk for Alzheimer disease (AD), influences ß-amyloid (Aß) deposition in brain tissue. Given the biologic overlap between AD and cerebral amyloid angiopathy (CAA), a leading cause of intracerebral hemorrhage (ICH) in elderly individuals, we investigated whether rs6656401 increases the risk of CAA-related ICH and influences vascular Aß deposition. METHODS: We performed a case-control genetic association study of 89 individuals with CAA-related ICH and 280 individuals with ICH unrelated to CAA and compared them with 324 ICH-free control subjects. We also investigated the effect of rs6656401 on risk of recurrent CAA-ICH in a prospective longitudinal cohort of ICH survivors. Finally, association with severity of histopathologic CAA was investigated in 544 autopsy specimens from 2 longitudinal studies of aging. RESULTS: rs6656401 was associated with CAA-ICH (odds ratio [OR] = 1.61, 95% confidence interval [CI] 1.19-2.17, p = 8.0 × 10(-4)) as well as with risk of recurrent CAA-ICH (hazard ratio = 1.35, 95% CI 1.04-1.76, p = 0.024). Genotype at rs6656401 was also associated with severity of CAA pathology at autopsy (OR = 1.34, 95% CI 1.05-1.71, p = 0.009). Adjustment for parenchymal amyloid burden did not cancel this effect, suggesting that, despite the correlation between parenchymal and vascular amyloid pathology, CR1 acts independently on both processes, thus increasing risk of both AD and CAA. CONCLUSION: The CR1 variant rs6656401 influences risk and recurrence of CAA-ICH, as well as the severity of vascular amyloid deposition.

Vascular risk factors in cocaine users with stroke.

OBJECTIVES: To determine if the classic stroke risk factors, chronic hypertension, diabetes, cigarette smoking, chronic alcohol abuse, older age, and male sex, are also risk factors in cocaine-related ischemic and hemorrhagic stroke. METHODS: A computer search of ICD-9 codes identified 100 patients admitted to two inner city hospitals between 1986 and 1995 with acute ischemic or hemorrhagic stroke who also tested positive for cocaine in the urine. The case records of these patients were reviewed retrospectively. The ischemic and hemorrhagic stroke groups were compared with a control group of 109 cocaine users without a history of stroke. Multiple logistic regression was performed to see if the classic stroke risk factors independently increased the risk of cocaine-induced ischemic and/or hemorrhagic stroke. RESULTS: A total of 66 stroke patients in the study group had ischemic stroke, whereas 34 had hemorrhagic stroke. The stroke and control groups were similar in racial and gender composition. The mean ages of patients with ischemic and hemorrhagic stroke (both 41 years) were greater than the control group (34 years) (P<.01). Only chronic hypertension (odds ratio [OR] 5.2, P<.0001) and older age (OR 1.08/year increase of age, P<.0006) were independent risk factors for ischemic stroke. Female sex (OR 3.2, P<.015) and older age (OR 1.1/year increase of age, P<.0002) were independent risk factors for hemorrhagic stroke. CONCLUSIONS: Chronic hypertension and older age may magnify the risk of cocaine-related ischemic stroke, whereas female sex and older age may increase the risk of cocaine-related hemorrhagic stroke.