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There are limited data on the contribution of the African continent to neuroscience research and publications. This review aims to provide a clear view on the state of neuroscience research among African countries, and to compare neuroscience research within the 52 African countries. A literature review search was conducted for all published articles by African authors in both local and international journals using Medline and other primary databases. Neuroscience represents 9.1% of the total medical publications. The highest percentage of neuroscience publications comes from South Africa. There is a positive correlation between the Gross Domestic Product and the total number of neuroscience publications among African countries. There is therefore an urgent need to develop strategies to improve neuroscience research in African countries.

Tuesday May 26, 2015, will be remembered as an historic day in the fight against epilepsy. On that date, the World Health Assembly approved unanimously the Resolution on the "Global Burden of Epilepsy and the Need for Coordinated Action at the Country Level to Address its Health, Social and Public Knowledge Implications," which urges Member States to implement a coordinated action against epilepsy and its consequences. This event, which comes almost 20 years after the establishment of the Global Campaign against Epilepsy, is another landmark in the longstanding collaboration among the World Health Organization (WHO), the International League Against Epilepsy (ILAE), and the International Bureau for Epilepsy (IBE) in addressing the needs of people with epilepsy. It also acted as a catalyst for other professional societies, including the World Federation of Neurology (WFN), to join forces in promoting a common action against epilepsy. The Resolution did not happen by chance, but came at the end of a long journey that involved the hard and tireless work of many dedicated individuals around the globe., (Wiley Periodicals, Inc. © 2015 International League Against Epilepsy.)

When the WHO's Topic Advisory Group for Neurology (TAG) started work on revision of the ICD-10 diagnostic codes in June 2009, the issues were daunting. The existing classification was produced a generation ago and the need to move to the digital age was becoming imperative. Appreciating modern advances in genetics and immunology, and the consequent changes in understanding of the pathophysiology of disorders of the nervous system, WHO's charge to the TAG was to produce a comprehensive, up-to-date disease classification, while providing published or consensus evidence for each coding change. In addition, the task would be to focus on ways to reduce the treatment gap while considering the utility of ICD-11 when used in primary care and nonspecialist settings. The project mushroomed over the 3 years since our first meeting and continues to do so. The work was made even more difficult as the group needed to add "content models" for the major codes for the first time (i.e., providing a definition for each disorder, along with appropriate diagnostic tests and outcome). The ICD-11 is meant to be updated as new knowledge develops, rather than waiting some years for another whole-scale revision, but this process has yet to be defined.

We present a rare case of pustular vasculitis secondary to streptococcal infection. The majority of cases described in the literature predominantly involve the dorsal hands, and may subsequently spread to involve the lower limbs. However, our case demonstrates a rare case where primary involvement of the lower limbs was present with secondary involvement at the dorsum of the hands. The patient responded well to intravenous methylprednisolone reflected both clinically and by his acute phase response.

We have developed a series of aminoacetylenic isoindoline-1,3-dione compounds and showed their anti-inflammatory activities by reducing carrageenan-induced rat paw edema and modulating proinflammatory and anti-inflammatory cytokines. In the present study and due to efficacy reasons, we are exploring only two of these compounds, namely, ZM4 and ZM5, to reveal their analgesic activity and toxicity. Following oral administration, both compounds were effective in reducing significantly (P < 0.05-0.001) acetic acid-induced writhing behavior, hot plate latency test, and formalin-induced paw licking time as antinociceptive indicators in mice and rats, respectively. Regarding the toxicity, the acute (20, 50, and 150 mg/kg) and repeated oral administration (10, 20, and 50 mg/kg) of these compounds for ten days did not produce any mortality and the compounds were considered well tolerated. However, repeated oral administration of 50 mg/kg of both compounds induced erythropoiesis by means of increasing significantly red blood cells, hemoglobin, and packed cell volume. Moreover, these compounds did not induce gastric lesions in the stomach of experimental animals at the doses that exhibited analgesic and anti-inflammatory activity compared to indomethacin as a positive control. The results indicate that ZM4 and ZM5 possess potential analgesic activity while being preliminarily safe and have minimal ulcerogenic activity.

Hypothyroidism is a procoagulant state; hypothyroid females have greater risk of DVT than hypothyroid males. We present a case of primary hypothyroidism who presented with euvolemic hyponatremia and DVT that required thyroxine replacement and correction of hyponatremia. This highlights that hypothyroidism can present as euvolemic hyponatremia and deep vein thrombosis.

Background: Despite frequent use, little is known about the metabolic and endocrine side-effects of antipsychotics in individuals with intellectual disability., Aims: To compare indices of obesity, glucose, lipids and prolactin between antipsychotic-treated and antipsychotic-naive individuals with intellectual disability and also between participants with intellectual disability and controls from the general population., Method: Observational study comparing 138 antipsychotic-treated and 64 antipsychotic-naive participants with intellectual disability in one National Health Service trust with general population controls., Results: Antipsychotic treatment comprised: risperidone 48%,olanzapine 18%, thioxanthenes 10%, other 24%; monotherapy 95% of participants; mean treatment duration 8 years;median daily chlorpromazine equivalent dose 108 mg(range 16–667). Metabolic indices were the same or more favourable in the intellectual disability group than the general population control group but overweight/obesity and type 2 diabetes were more prevalent in the women in the intellectual disability group than the control group. Metabolic indices were similar, statistically or clinically, between the antipsychotic-treated and the antipsychotic-naive groups but there was a non-significant trend towards a higher rate of type 2 diabetes in the antipsychotic group. A total of 100%and 70% of participants on amisulpride/sulpiride and risperidone respectively had hyperprolactinaemia, with secondary hypogonadism in 77% and 4% of affected women and men., Conclusions: Antipsychotics, on average, did not increase metabolic risk,although the existence of a susceptible subgroup at risk of diabetes cannot be excluded. Some antipsychotics induced hyperprolactinaemic hypogonadism, requiring active management. However, our findings suggest that antipsychotics at the low doses routinely prescribed for people with intellectual disability are generally safe in relation to metabolic adverse effects, even if efficacy remains poorly defined.

Neurocysticercosis is a major cause of epilepsy and other neurological morbidity in endemic areas of the world but is exceptionally rare in the West. We have recently had experience of eight patients with this condition, seven presenting with epilepsy and single or multiple small, enhancing parenchymal lesions and one with hydrocephalus caused by a midbrain lesion. One lesion was stereotactically excised after it persisted, but in five other cases spontaneous cyst resolution was observed during expectant management with anticonvulsants. Two patients with multiple lesions were referred to us for further management but were free of active infection. Recent studies show that neurocysticercosis may often be diagnosed based upon the clinical, epidemiological and radiological features. Spontaneous cyst resolution is to be expected in this condition and suspected patients should be carefully observed and surgery avoided. We believe that this disease presents more commonly than has been appreciated in the UK and propose a protocol for management.

Higher auditory function in a patient was investigated following a right hemisphere infarction between the middle and posterior cerebral artery territories involving the insula. The patient complained of lack of musical appreciation and a battery of tests confirmed a dissociated receptive musical deficit in the presence of normal appreciation of environmental sounds and speech. The ability to detect continuous changes in sound frequency in the form of sinusoidal frequency modulation was preserved. There was, however, a deficit in the analysis of rapid temporal sequences of notes which could underlie his musical deficit. This case provides further evidence for the existence of amusia as a distinct form of auditory agnosia, but does not support the hypothesis that bilateral lesions are required to produce such a deficit. Unexpectedly, the patient was also found to have a deficit in the perception of apparent sound-source movement. We suggest that this deficit is analogous to the visual phenomenon of akinetopsia, and is in accord with PET work suggesting involvement of areas outside primary auditory cortex in sound movement perception. A possible common deficit in auditory temporal and spatial 'scene analysis' is discussed.

Human listeners can localize sounds by the difference in both arrival time (phase) and loudness between the two ears. Movement of the sound source modulates these cues, and responses to moving sounds have been detected in animals in primary auditory cortex and in humans in other cortical areas. Here we show that detection of changes in the interaural phase or amplitude difference occurs through a mechanism distinct from that used to detect changes in one ear alone. Moreover, a patient with a right hemisphere stroke is unable to detect sound movement, regardless of whether it is defined by phase or by loudness cues. We propose that this deficit reflects damage to a distinct cortical area, outside the classical auditory areas, that is specialized for the detection of sound motion. The deficit is analagous to cerebral akinotopsia (motion blindness) in the visual system, and so the auditory system may, like the visual system, show localization of specialized functions to different cortical regions.

Defects of the mitochondrial respiratory chain are increasingly being recognized as an important cause of neurological disease in humans. In many of these patients, the biochemical defect results from an abnormality of the mitochondrial genome. Respiratory chain defects involving complex II, which is entirely encoded by the nuclear genome, are comparatively rare. We report the clinical and biochemical findings in 2 elderly sisters who presented with late-onset neurodegenerative disease. In both patients, a partial deficiency of complex II (approximately 50% of control values) was shown to be present in mitochondria from muscle and platelets. The enzyme defect was not expressed in cultured skin fibroblasts or immortalized lymphocytes. There was an overexpression of the 70-kd flavoprotein subunit in muscle mitochondria from both patients, although we showed that this subunit is present in normal amounts in mitochondrial membranes. Our studies highlight the diversity of the clinical presentation of respiratory chain disease and that complex II deficiency should enter the differential diagnosis of certain patients with late-onset neurodegenerative disease.

Twelve patients with Wilson's disease, aged 11-25 years, underwent brainstem auditory evoked potential (BAEP) study. The results were correlated to clinical, neuroradiological and laboratory data. Ten had prominent to severe neurological manifestations, suggestive of involvement of one or several CNS structures, and 2 were neurologically free. All had evidence of abnormal copper metabolism, and 8 had CT scan evidence of brain atrophy, or hypodense areas in basal ganglia, or both. The 2 patients without neurological manifestations as well as one with neurological signs had normal BAEP. One patient with neurological signs had increased N1 latency due to cochlear hearing loss, but normal interpeak intervals, while 8 of 10 patients with prominent neurological symptoms and signs had abnormal BAEPs (prolongation of NIII-NV interpeak interval). The value of NIII-NV interpeak interval correlated with the number of different neurological signs (neurological score) attributable to involvement of different CNS structures (r = 0.64 at P = 0.001). Abnormal BAEPs do not seem to be an early finding in Wilson's disease.

In an attempt to categorize the diverse neurological manifestations of Behçet's syndrome, a group of 10 patients was prospectively studied; the diagnosis of Behçet's syndrome was not known in any of them prior to their neurological presentation. A reasonably clear distinction can be made to divide the manifestations into three general categories with some overlap. Category I includes patients with increased intracranial pressure with or without cerebral venous sinus thrombosis. Category II are those presenting with a stroke. Category III are those patients who present with spinal cord involvement and CSF pleocytosis. Brainstem involvement was noted independently of the group. In general, patients with Neuro-Behçet's syndrome showed little ocular involvement. The course of the illness both in morbidity and mortality tended to be better in category I, and mortality was only seen in category II patients. In populations susceptible to the disease, the clinical categorisation proposed may alert the clinician to the possibility of neuro-Behçet's syndrome whenever patients with pseudotumour cerebri, dural sinus thrombosis, stroke in the young, unexplained myelitis or possible multiple sclerosis are encountered.

Thirty-three epileptic patients were randomly divided into two treatment groups. One group of 18 patients was given sodium valproate; the other 15 patients were given phenytoin. Periods of treatment ranged from 9 t0 48 months (mean, 30 months). Any patient who developed a seizure while on the first drug was changed to the other drug, provided the serum level of the first drug was in the accepted therapeutic range. Six required the change from phenytoin to sodium valproate, and three from sodium valproate to phenytoin. Side effects were not a major problem with either drug during the trial period. Phenytoin has been widely prescribed alone; our results indicate that sodium valproate may also be used as a single drug in the treatment of several types of epilepsy.

Brucellosis rarely can present with involvement restricted to the nervous system. We describe a total of 19 cases of neurobrucellosis in whom the clinical presentation lay in three distinct categories. The first was an acute presentation with meningoencephalitis. The disease also presented in a chronic form where the brunt of the illness can either be in the peripheral or the central nervous system (CNS). The chronic peripheral form is that of a proximal polyradiculoneuropathy. The central form is that of diffuse CNS involvement, predominantly with myelitis or cerebellar involvement with or without cranial nerve palsies. Although the two chronic forms, 'peripheral' and 'central', are distinct, some overlap is possible. This was not observed for the acute form. The pathology of the three presentations may be different, being a direct effect of infection in the acute form, and an immune-related process, possibly demyelinating in nature, in the chronic forms. The response to treatment in the acute and chronic forms is also different, being much better in the acute form. Awareness of the condition and performance of the appropriate serological tests will differentiate neurobrucellosis from other chronic CNS infections, especially tuberculosis and neurosyphilis.

A 39-year-old previously healthy patient with combined pulmonary and neural cryptococcosis was successfully managed by pulmonary resection and antifungal chemotherapy. The pulmonary mass was removed under cover of miconazole and 5-fluorocytosine even though the patient had concomitant active meningitis. He recovered dramatically after the surgical procedure and remained well 2 years later. We suggest that, as in our patient, early removal of a pulmonary cryptococcal mass under antifungal cover may in other similar patients obviate the need for protracted antifungal therapy and lead to an excellent response of the neural cryptococcosis.

Total serum thyroxine (T4), triiodothyronine (T3), T3 resin uptake (T3U), thyrotrophin (TSH), and reverse T3 (rT3) were measured in 209 healthy adults 20--89 yr old. Mean T4 values for men were stable throughout life, but in females under age 60, T4 values were significantly higher than in older women. Values for T3U in males were significantly higher than in females throughout all decades, although females had a significant increase in T3U after age 60. TSH values increased significantly in females over age 60. Throughout all decades, males had stable TSH levels that were slightly higher than the female results before age 60 and lower thereafter. Mean serum T3 declined similarly for both sexes with increasing age, although not to the extent previously reported. Men had significantly higher mean rT3 values over all decades than females, although female rT3 levels decreased after age 50 whereas males maintained stable values. The physiologic reasons for these findings may be due to sex-related changes in binding proteins and alterations in metabolic clearance rates, production, and degradation of these hormones with increasing age.

The diagnosis of central nervous system (CNS) brucellosis was made by determining Brucella-specific IgG, IgM and IgA in cerebrospinal fluid (CSF) specimens, using an enzyme-linked immunosorbent assay (ELISA) method. A total of 68 CSF specimens including 10 from patients with brucellosis of the nervous system, 4 with Brucella infection but without CNS involvement, 38 with meningitis other than due to Brucella and 16 with no meningitis were studied. Of the 10 CSF specimens from patients with CNS brucellosis, Brucella-specific IgG was detected in all 10, IgM in 7 and IgA in 8. The 10 patients were also seropositive for anti-Brucella IgG and IgM, and 9 were seropositive for IgA. No Brucella-specific IgG, IgM or IgA was detected in the CSF of 4 patients with brucellosis but without CNS involvement, even though the blood of these patients had high titres of anti-Brucella IgG, IgM and IgA. In addition, none of the CSF specimens from the 38 patients with meningitis other than due to Brucella, or from the 16 patients without meningitis, had detectable anti-Brucella antibodies. This study indicates that the Brucella ELISA on CSF is a reliable, rapid, sensitive and specific assay in the diagnosis of CNS brucellosis.

Twenty-one patients with myasthenia gravis underwent a course of plasma exchange combined with immunosuppressive therapy. In fifteen there was dramatic clinical improvement which has been maintained for periods up to 19 months. Nine of these patients now take no anticholinesterase drugs. Six patients had a recurrence 3--9 months after the first course but in the three given a second course remissions were again obtained.

Mollaret's meningitis is a rare condition with a characteristic clinical and cerebrospinal fluid picture. In many ways it resembles recurrent hereditary polyserositis (familial Mediterranean fever) in its natural history, pattern of attacks, and response to colchicine. Association of the two conditions has been reported, so far, in two patients only. In our patient the symptoms of both conditions were induced by a metaraminol provocative infusion. We have previously introduced this as a specific diagnostic and confirmatory test for recurrent hereditary polyserositis. The possibility that the two conditions represent different manifestations of a single disease is therefore strengthened.

To investigate the role of folate deficiency in neuropathy caused by anticonvulsants, electrophysiological studies of peripheral nerve function were carried out on 29 epileptic patients on long-term anticonvulsant therapy. All but three patients showed abnormalities in one or more electrophysiological measurements, the main abnormality being in amplitude of sensory nerve action potential--this was reduced or absent in 76% of patients. All patients had low concentrations of folate in serum and CSF, these being below the normal ranges in 19 patients. These 19 patients were treated with folate, either 5-formyltetrahydrofolate (10 patients) or folic acid (9 patients), over a period of one month. After therapy all patients had normal levels of folate in serum and CSF, slightly higher levels in CSF being obtained in those receiving 5-formyltetrahydrofolate. Folate therapy significantly reversed abnormalities in motor and sensory nerve distal latencies; the effect was greater with 5-formyltetrahydrofolate, apparently because this produced higher CSF folate concentrations than folic acid. We conclude that folate deficiency may be involved in the development of peripheral neuropathy due to anticonvulsants.

Twelve patients with neurobrucellosis and 17 patients with systemic brucellosis without neurological involvement underwent a brainstem auditory evoked potentials (BAEP) study. All neurobrucellosis patients (100%) showed abnormalities in their BAEP recordings, suggestive of brainstem lesions at various levels. On the other hand, only 5 (29%) of the 17 patients with systemic brucellosis had mild unilateral BAEP abnormalities, while the remaining 12 had normal responses. Comparison of pooled data between the systemic brucellosis and neurobrucellosis groups showed highly significant differences in all BAEP parameters. The recording of BAEP is thus considered a sensitive supplementary method to reveal CNS lesions in patients with neurobrucellosis.

Twenty chronic epileptics receiving phenytoin and either phenobarbitone or primidone have been studied. All patients had frequent seizures and had serum concentrations of phenytoin below 410 mumol/1. Phenytoin dosage was increased to study the effect on the frequency of seizures and the serum concentrations of phenytoin and phenobarbitone. There was no effect on minor seizures but in ten out of sixteen patients major seizures were abolished or reduced. Serum concentrations of phenobarbitone rose as the phenytoin dose was increased. This may cause deviations from the expected relationship between dose and serum concentrations of phenytoin; this would explain deficiencies which were found in a nomogram for predicting the therapeutic dose of phenytoin.