Case report: an area postrema syndrome revealing a neuromyelitis optica spectrum disorder associated with central nervous system tuberculosis in a young Togolese (black African) woman

Abstract

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.

Anti‐aquaporin‐4 antibody‐positive neuromyelitis optica spectrum disorder associated with central nervous system tuberculosis

“…3,6 Although this phenomenon of mycobacterial antigens presence has been documented in multiple sclerosis, 9,10 the evidence of confluence of these events in NMOsd is scarce and appears to be limited to previous cases reports of exclusively active M. tuberculosis, or even atypical mycobacteria pulmonary, abdominal or renal infection with variable AQP4 antibodies serostatus. 13 In the present report, we describe two cases of tuberculosis (Tb) CNS infection associated with seropositive NMOsd, although it is not the first attempt to document this association. 13 In the present report, we describe two cases of tuberculosis (Tb) CNS infection associated with seropositive NMOsd, although it is not the first attempt to document this association.…”

Neuromyelitis optica spectrum disorder and active tuberculosis

“…An association between NMOSD and TB has been reported over the past 50 years 6 14–22. Silber et al 15 described eight patients with pulmonary TB and myelitis or optic neuropathy without evidence of central nervous system TB: six developed NMOSD, one an acute necrotising myelopathy and one an optic neuropathy.…”

Intractable Vomiting and Hiccups: An Atypical Presentation of Neuromyelitis Optica

“…This region is particularly rich in aquaporin-4, which is the primary site of attack by anti-AQP4 antibodies responsible for NMOSDs. Therefore, APS is considered to be one of the most specific clinical manifestations of NMOSDs [13]. Since most APS attacks precede the inflammatory attack on the optic nerves or spinal cord, this makes it an important warning sign.…”