Neuropathic pain is a debilitating symptom reported by patients presenting with postherpetic neuralgia (PHN). Efforts to alleviate this pain have been projected to lie in individualization of pharmacological treatment through pain phenotyping and subsequent investigations into the genetic basis of PHN therapy. Understanding the various mechanisms related to these phenotypes can aid in improvement of available treatment options and discovery of new ones. Knowledge and application of genetic variations in PHN, structural proteins, and genes can aid in ascertaining risk, susceptibility to, severity of, and protection from PHN. This review summarizes the most recent information that has been published on phenotypes and genotypes with possible clinical applications and directions for future research.

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.

Introduction Knowledge of anatomical variations in the origin and in the course of the dorsal metatarsal arteries (DMTAs) is valuable for many procedures, including reconstructive surgeries and flap selection. However, there is a paucity of data on these arteries among black Africans. Materials and Methods The present study studied the origin and the location of DMTAs in 30 formalin-fixed cadaveric feet of adult black Kenyans at the Department of Human Anatomy of the University of Nairobi, Nairobi, Kenya. Results Dorsal metatarsal arteries were present in all of the cases. Of the right dorsalis pedis artery (DPA), in the majority of the cases, the 1st DMTA arose as the continuation of the DPA, while the 2nd to 4th DMTAs were given off as branches from the arcuate artery (AA). On the left feet, in the majority of the cases, the 1st DMTA arose as the continuation of the DPA, while the rest were given off as branches from the AA. In relation to the dorsal interossei muscles, all of the the arteries were either within the muscle fibers (53%) or beneath them (47%), on the right side. On the left side, the 1st DMTA was above the muscles in 40% of the cases; within the muscles in 53%; and beneath the muscles in 7%. The 2nd and 3rd DMTAs were above the muscles in 57% and in 53% of the cases, respectively. Conclusion These results reveal that the DMTAs show variation in their origin and position relative to the dorsal interossei muscles. These variations display bilateral asymmetry.

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Codeine is an opioid analgesic and antitussive that has been widely abused. Some adverse effects noted with its abuse include adrenocortical insufficiency and activation of the hypothalamic-pituitary-adrenal axis. The structural basis for these dysfunctions is not clearly understood. Twenty-five adult male rats were used for the study. They were divided into intervention and control groups that were administered 40 mg/kg of codeine phosphate and normal saline respectively by gavage daily for 50 days. Subsequently, both groups were given normal saline for a further fourteen days to note recovery changes. At day 0, 50 and 64, rats were randomly selected from both groups, euthanized and adrenal glands harvested for histological processing and analysis. At day 50 of codeine administration, the adrenal glands demonstrated an increase in zona fasciculata thickness but a decrease in zona reticularis thickness. Lower values were noted in the volume density of zona reticularis and cells count of the medulla in the experimental compared to the control groups (P-value<0.05). The experimental group also showed an increase in vascularization and connective tissue in the glands. After 14 days of recovery, most of the changes observed in experimental animals were reversed and the adrenal glands in both groups had similar features. A decrease in cell count of the adrenal medulla was however observed (P-value<0.05). In conclusion administration of codeine phosphate causes discernible changes in the microscopic structure of the adrenal gland, most of which appear to be reversed after two weeks recovery period.