Neurocognitive outcomes of tuberculous meningitis in a primarily HIV-positive Ugandan cohort

Abstract

Background: The toll of tuberculous meningitis (TBM) in both mortality and disability is considerable, but advancements in rehabilitation have the potential to improve the functional abilities and the quality of survivors’ lives. However, the typical phenotype of neurocognitive impairment in TBM survivors remains unstudied in HIV-predominant populations in sub-Saharan Africa. Methods: We tested 36 survivors of TBM in Uganda with a comprehensive battery of neurocognitive assessments at 8 and 24 weeks after diagnosis, and compared results to a representative cohort of HIV-uninfected Ugandans. Results: While participants had a broad range of impairments at eight weeks, there was marked improvement by 24 weeks, when a phenotype of impairment including deficits in motor functioning, verbal learning and memory, processing speed, and executive function emerged. These deficits were present despite good clinician-rated functional status. The majority (23/27, 85%) had evidence of moderate to severe depression at week 8, and at week 24 (18/24, 75%). Conclusion: These findings highlight the need for more comprehensive neurocognitive assessment in the survivors of TBM, and further investment in and study of rehabilitation, including management of depression, to improve long-term outcomes in this population.

Glutamate Neurotoxicity and Destruction of the Blood–Brain Barrier: Key Pathways for the Development of Neuropsychiatric Consequences of TBI and Their Potential Treatment Strategies

“…If inflammation was closely associated with those symptoms, then conditions with significant neuroinflammation and stress, such as encephalitis, meningitis, and sepsis, would also present with associated neuropsychiatric diseases such as depression, anxiety, aggression, and dementia to a similar degree as after TBI. However, studies show little if any association between those conditions of neuroinflammation and neuropsychiatric disease or show the presence of neuropsychiatric diseases that are secondary to the neuroinflammation itself [ 61 , 62 ].…”