Brucella spp. should be considered in the differential diagnosis of acute meningitis of children living in areas where brucellosis is endemic.
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Virology Department, Institut Pasteur de Dakar, 36 Avenue Pasteur, Dakar 200, Senegal.
Neurological manifestations associated with human parvovirus B19 (B19V) infections are rare and varied. Acute encephalitis and encephalopathy are the most common, accounting for 38.8% of all neurological manifestations associated with human B19V.
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Breathing Research and Therapeutics Center, Department of Physical Therapy, University of Florida, Gainesville, Florida, United States.
We present a case report of a 42-year-old female with post-West Nile virus meningoencephalitis who exhibited unique, long-latency diaphragm potentials evoked by transcranial and cervical magnetic stimulation after exposure to acute intermittent hypoxia (AIH). The subject was recruited for a study investigating AIH effects on respiratory motor function in healthy individuals. She had contracted West Nile virus infection 5 years before assessment that resulted in hospitalization and persistent allodynia but was not reported to the research team.
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GloNeuro, Sector 107, Vishwakarma Road, Noida 201301, Uttar Pradesh, India.
Meningitis is the acute or chronic inflammation of the protective membranes, surrounding the brain and spinal cord, and this inflammatory process spreads throughout the subarachnoid space. The traditional drug delivery methods pose a disadvantage in limiting the capacity of crossing the blood-brain barrier (BBB) to reach the central nervous system (CNS). Hence, it is imperative to develop novel approaches that can overcome these constraints and offer efficient therapy for meningitis.
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View Article and Find Full Text PDFTraumatic brain injury causes early aggregation of beta-amyloid peptides and NOTCH3 reduction in vascular smooth muscle cells of leptomeningeal arteries.
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Department of Clinical Sciences, Lund Brain Injury Laboratory for Neurosurgical Research, Lund University, 222 20, Lund, Sweden.
Traumatic brain injury (TBI) often leads to impaired regulation of cerebral blood flow, which may be caused by pathological changes of the vascular smooth muscle cells (VSMCs) in the arterial wall. Moreover, these cerebrovascular changes may contribute to the development of various neurodegenerative disorders such as Alzheimer's-like pathologies that include amyloid beta aggregation. Despite its importance, the pathophysiological mechanisms responsible for VSMC dysfunction after TBI have rarely been evaluated.
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