Document Type : Original Article
- Fode Abass Cisse 1
- Foksouna Sakadi 1
- Nana Rahamatou Aminou Tassiou 1
- Amadou Talibe Balde 1
- Arcel Steven Nitche Woga 1
- Aissatou Kenda Bah 1
- Souleymane Djigue Barry 2
- Ibrahima Sory Souare 2
- Mohamed Lamine Toure 2
- Amara Cissé 1
1 Department of Neurology, University Hospital of Conakry, Guinea
2 Department of Neurosurgery, University Hospital of Conakry, Guinea
Background: The diagnostic certainty of medullar tuberculosis (TB) without Pott disease is difficult to establish in a tropical environment with the large group of infectious, parasitic, and systemic myelopathies, despite the increasing availability of magnetic resonance imaging (MRI) data and improvement of biological exploration platforms.
Methods: We retrospectively analyzed the files of 186 patients hospitalized in the Department of Neurology and Neurosurgery of the University Hospital Center of Conakry, Guinea, between 2008 and 2016 for the management of non-compressive and compressive myelopathy. Biological evidence of TB infection was demonstrated for 13 (6.9%) patients.
Results: Infectious clinical picture prior to the development of neurological signs was reported in 11 patients (84.6%). The neurological signs were summed up by the existence of a sensitivo-motor semiology of progressive evolution (100% of cases) with sphincter disorders in 11 patients (84.6%) and a medullary compression symptomatology with a lesion and under lesion syndrome from the outset in 4 patients (30.8%). Medullary MRI revealed an extensive intramedullary hypersignal in 9 patients with non-compressive myelopathy and in 4 cases, the lesions appeared in T1 hypersignal and T2 isosignal were localized. Lumbar puncture (LP) revealed lymphocytic pleocytosis, hypoglucorrhage (0.3 to 0.5 g/l), and leukocytosis.
Conclusion: This study reveals a classic clinical, biological, neuroradiological, and evolutionary profile of compressive and non-compressive myelopathies. These results are important for the therapeutic and evolutionary discussion of TB myelopathies for good management.