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Objective: Brain-derived neurotrophic factor (BDNF) and apolipoprotein E (ApoE) are thought to be implicated in a variety of neuronal processes, including cell growth, resilience to noxious stimuli and synaptic plasticity. A Val to Met substitution at codon 66 in the BDNF protein has been associated with a variety of neuropsychiatric conditions. The ApoE4 allele is considered a risk factor for late-onset Alzheimer's disease, but its effects on young adults are less clear. We sought to investigate the effects of those two polymorphisms on hemispheric and lateral ventricular volumes of young healthy adults.
Methods: Hemispheric and lateral ventricular volumes of 144 healthy individuals, aged 19–35 years, were measured using high resolution magnetic resonance imaging and data were correlated with BDNF and ApoE genotypes.
Results: There were no correlations between BDNF or ApoE genotype and hemispheric or lateral ventricular volumes.
Conclusion: These findings indicate that it is unlikely that either the BDNF Val66Met or ApoE polymorphisms exert any significant effect on hemispheric or lateral ventricular volume. However, confounding epistatic genetic effects as well as relative insensitivity of the volumetric methods used cannot be ruled out. Further imaging analyses are warranted to better define any genetic influence of the BDNF Val6Met and ApoE polymorphism on brain structure of young healthy adults.
This chapter investigates sarcoidosis-associated stroke syndromes. Sarcoidosis is often referred to as a "disease of exclusion". The definitive diagnosis of sarcoidosis requires histopathologic demonstration of noncaseating epithelioid granulomas that are not due to infection or malignancy. Patients can be classified as having possible, probable, or definite neurosarcoidosis based on the certainty of the diagnosis of multisystem sarcoidosis, the pattern of neurological disease, and the response to therapy. Corticosteroids are the mainstay of treatment for patients with symptomatic neurosarcoidosis; however, the severity and chronicity of this disease in some patients often leads to reluctance in subjecting patients to the long-term sequelae of corticosteroid treatment. Nonetheless, it is reasonable to decrease sarcoidosis-associated inflammation to decrease stroke risk. Anecdotal evidence suggests that concurrent use of corticosteroids and adjunctive agents is a reasonable approach. Antiplatelet agents has been used as a stroke-preventive strategy but have avoided thrombolytic interventions.
Sildenafil citrate has been shown to enhance neurogenesis, angiogenesis, synaptogenesis, and neurological outcome by augmentation of cyclic guanosine monophosphate (cGMP) levels in animal models of ischemic stroke. Whether sildenafil citrate may be helpful for recovery in human stroke is unknown at this time.
A 41-year-old woman with locked-in syndrome due to pontine infarction began receiving 150 mg of oral sildenafil citrate daily on a compassionate use basis in August 2003 and continues treatment at this time. Magnetoencephalography (MEG) was performed at 12 and 17 months after stroke.
No serious adverse events have occurred. Significant milestone recoveries including standing, use of both arms, talking, and full return of swallowing have occurred, particularly after nine months of treatment. The MEG showed a significantly increased amplitude in the somatosensory cortex.
Daily use of high dose sildenafil citrate appears to be safe in this patient with stroke resulting in locked-in syndrome. Further studies will be required to establish safety and efficacy.
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