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Background Hypoplasia of cerebral arteries predisposes to stroke and cerebral aneurysms which have an increased incidence in sub-Saharan Africa. The frequency and pattern of cerebral artery hypoplasia, however, shows population variations, and data from the African population remain scanty. Objectives This study aimed to determine the percentage of hypoplasia in the anterior, middle, and posterior cerebral, anterior and posterior communicating, basilar, and vertebral arteries. Materials and Methods Sections of the basilar, vertebral, posterior, and anterior communicating arteries and anterior, middle, and posterior cerebral arteries were taken, processed for histology, and examined with a light microscope at ×40. The images of the vessels were taken by a photomicroscope and circumference analyzed with the aid of Scion image analyzer. The average diameter of 10 sections was taken to be the diameter of the artery in analysis. Hypoplasia was then defined as internal diameter ≤1 mm. Photographs of representative samples of asymmetry were taken, data were analyzed using SPSS, and gender differences were analyzed using the Student's test. Results were presented in tables. Results Two hundred and eighteen formalin-fixed brains of adult Kenyans at the Department of Human Anatomy, University of Nairobi, were studied. Of the 218, 48 brains (22%) did not have vessels with any form of hypoplasia while 170 (78%) did have vessels. Of these, anterior circulation hypoplasia (anterior cerebral artery and posterior communicating artery) was seen in 100 brains (46%) and posterior circulation hypoplasia (middle and posterior cerebral, basilar, and vertebral arteries) in 69 brains (32%). Conclusion Cerebral arterial hypoplasia is frequent in the select adult Kenyan population.

Background: Secondary brain insults after traumatic brain injury such as electrolyte dysfunctions are associated with poor outcomes. This study aimed at determining the incidence of serum sodium ion abnormalities and their association with clinicoradiological parameters. Methods: A prospective crosssectional study of one hundred and seventeen patients with severe head injury. Data collected included patient demographics, prehospital interventions, clinical examination findings, computed tomography (CT) scan head findings, serum sodium ion levels (at admission and 48 h later), and outcome (30 days). Results: At admission, 93(79.5%) patients had normal serum sodium ion levels. However, 48 h post-admission, hypernatremia was  prevalent in 56(63.6%) patients (p < 0.001). Hypernatremia was significantly associated with the use of mannitol (p = 0.036), lower Glasgow  Coma Score (p = 0.047), higher Injury Severity Score (p = 0.015), presence of subdural hematoma (p = 0.044), midline shift >5 mm (p = 0.048), compressed/absent basal cistern (p = 0.010), and higher Rotterdam CT Score (p = 0.003). Hypernatremia reported 48 h  postadmission was associated with a high 30-day mortality rate [odds ratio (OR) 3.55, p = 0.0095]. Risk of mortality associated with hyponatremia and hypernatremia at admission was not statistically significant. Conclusion: While both hyponatremia and hypernatremia can occur in serious TBI patients, hypernatremia predominates 48 hours post- admission and is associated with statistically significant increased risk of death.

Introduction: Neurofibromatosis type 1 (NF-1) is an autosomal dominant disorder characterized by pigmented lesions (café-au-lait macules, skinfold freckling, and Lisch nodules), and dermal neurofibromas. In some subjects, NF-1 presents with complications such as brain tumors, skeletal abnormalities, peripheral nerve tumors, and behavioral abnormalities. Patient concerns: We report the case of a 30-year-old man who presented with sudden bilateral lower limb paralysis and acute-onset lower back pain following a fall while rising from a seated position. He denied a history of back pain or muscle weakness before the index event. On examination, the patella and Achilles tendon reflexes were absent bilaterally. The patient presented with a power grade of 0 in all lower limb muscle groups and normal muscle bulk. Diagnosis: Bilateral lower limb paralysis was associated with sensory loss in the T11 dermatome. X-ray, computed tomography, and magnetic resonance imaging (MRI) showed vertebral canal enlargement (dural ectasia) at multiple levels suggestive of a lateral meningocele associated with neurofibromatosis. After repeated MRI studies, herniation of nerve root sleeves was noted, with marked compression of the traversing nerve roots. Notably, there was no evidence of cord compression on either the computed tomography or MRI. The cerebrospinal fluid studies were unremarkable. Interventions: No particular intervention was performed to address specific NF symptoms. In the hospital, the patient received analgesics and antibiotics (gentamicin and cefuroxime) for a urinary tract infection, lactulose for constipation and enoxaparin as anticoagulant prophylaxis. Outcomes: The patient experienced a clinical decline unrelated to his initial symptoms and succumbed to sepsis 6 weeks after admission. The cause of death was not directly linked with NF-1. Conclusion: We report a case of NF-1 with dural ectasia presenting with sudden bilateral lower limb paralysis and lower back pain following mild trauma. Although 70% of dural ectasia cases are associated with NF-1, there are few reports of NF-1 patients with dural ectasia and associated orthopedic complications. Here, we note that dystrophic changes in NF-1 may lead to rapidly aggravating neurological symptoms even after trivial trauma.