Background Area postrema syndrome (APS) is considered to be one of the most specific clinical presentations of neuromyelitis optica spectrum disorders (NMOSDs). In sub-Saharan Africa, NMOSDs and even more so those revealed by an APS, are rarely reported. However, studies among mixed populations have shown that NMOSDs disproportionately affect black people with relatively more frequent encephalic involvement. We report a case of APS revealing an NMOSD associated with central nervous system (CNS) tuberculosis in a young Togolese woman residing in Togo (West Africa). Case presentation A 28-year-old Togolese woman was admitted for left hemibody sensory problems with ataxia. These problems were observed while the patient was hospitalized for a few days in the hepato-gastroenterology department for persistent vomiting, abdominal pain and hiccups lasting for about a month. The examination confirmed left hemibody ataxia with nystagmus when looking to the left, pronounced left osteotendinous reflexes, and left hemibody hypoesthesia up to the base of the neck. Encephalic magnetic resonance imaging (MRI) showed a hypersignal lesion in the bulbar more lateralized on the left in the fluid-attenuated inversion recovery sequence, not enhanced after a gadolinium injection. Biological assessment showed the presence of Mycobacterium tuberculosis deoxyribonucleic acid in the cerebrospinal fluid and a sedimentation rate of 120 mm in the 1st hour. The result of the anti-AQP4 antibody test was positive. Two months from the onset of digestive problems with Lhermitte’s sign and hand and foot contracture access without vesico-sphincter problems were established. Cervical medullary MRI showed an additional intramedullary hypersignal lesion in the T2 sequence at the C2 level, not enhanced after a gadolinium injection. A second course of intravenous corticosteroids was administered, and anti-tuberculosis treatment was continued. The outcome was favorable. After 8 months of anti-tuberculosis treatment, the patient started immunosuppressive therapy (azathioprine 50 mg twice daily) to limit the risk of recurrence of NMOSD. Conclusion The recognition of an APS is an additional challenge for the diagnosis of NMOSDs, especially in countries with limited resources. CNS tuberculosis must be tested when faced with an NMOSD because it seems to be a major cause.

Spinocerebellar ataxias (SCAs) are rare neurodegenerative disorders of adults characterized by autosomal dominant inheritance. Machado-Joseph disease (MJD) or ASC type 3 is the most common worldwide. We report the first cases of MJD in a Togolese family. We performed a cross-sectional study based on a case of MMJ disease confirmed by genetic testing. We then conducted a family survey to identify suspected familial cases of the disease. The confirmed case was a 46 year old Togolese woman of Ewe ethnicity (south of Togo), hypertensive, who was seen in consultation for speech and walking disorders that had been progressively worsening for 9 years and had been confined to a wheelchair for 3 years. In the family history, we noted similar cases without a precise diagnosis. On examination, we noted cerebellar dysarthria, difficulties in performing calculations, spastic tetraparesis at 4/5, kinetic and static ataxia. Brain magnetic resonance imaging showed cerebral atrophy more marked in the posterior fossa. Genetic analysis revealed the presence of an expanded allele located in the pathological zone at the ASC3 locus, which confirmed the diagnosis. The family investigation allowed us to identify six suspected cases on clinical grounds. This observation confirms the ubiquitous nature of MJD. The existence of a family history of gait disorders in a patient with cerebellar ataxia should raise the possibility of ASC.

Introduction Neuromyelitis optica spectrum disorders (NMOSD) would disproportionately affect blacks within mixed populations. However, they are rarely reported in black African. The objective of this work was to report the experience of Togo, a West African country in terms of NMOSD. Methods This is a series of six cases diagnosed between 2015 and 2020 in the only three neurology departments in Togo. The diagnosis of NMOSD was made according to the criteria of the International Panel for NMO Diagnosis (2015) and the patients had a minimum clinical follow-up of 6 months after the diagnosis. The search for anti-aquaporin 4 (AQP4) antibodies was performed by immunofluorescence on transfected cells. Results The mean age was 25.33 years and the sex ratio female/male was 5/1. The average time between the first attack and the diagnosis was 122.83 days. Clinically, there was isolated medullary involvement (2/6), simultaneous opticomedullary involvement (3/6), and area postrema syndrome (1/6). Five patients were anti-AQP4 positive. All six patients had extensive longitudinal myelitis. At 6 months of follow-up, there was one case of death and one case of blindness. Conclusion The rarity of NMOSD cases in Togo could be linked to an underestimation. To better characterize the NMOSDs of the black African population, multicenter and multidisciplinary studies are necessary.

Background:Encephalitis of Rasmussen is an inflammatory hemiencephalopathy of unknown etiology. It is a cause of drug-resistant epilepsy.Aim:To report two cases of Rasmussen’s encephalitis (RE) in a low-income setting.Clinical Observation:The cases concerned were that of an 8-year-old boy and a 4-year-old girl. The illness began with daily several seizures at the age of 28 months in the boy and 23 months for the girl. Epileptic seizures were generalized in the elder one and focal in the younger. The elder presented right hemiplegia with severe cognitive impairment. In the younger child, the expression of the language was disturbed, associated with right hemiparesis at 4/5. The electroencephalography recording showed background theta asymmetric rhythm associated with discharges of periodic lateralized epileptiform discharges (PLEDs) into the left hemisphere in the two cases. Brain imaging showed left hemisphere atrophy. The seizures had decreased in intensity after association of several anticonvulsant molecules over a period of 3–6 months. The diagnosis of RE was based on clinical, paraclinical, therapeutic, and evolution arguments.Conclusion:There was a delay to establish the diagnosis. Further studies are needed to evaluate rehabilitation capacities in children with RE before brain maturation.

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