speech (Garcia- Grimshaw et al., 2018). For instance, a Japanese patient with TBM that had been veried by bacteriology complained of memory loss, low motivation, and speech problems. ere were no other meningitis- related symptoms. Brain im­aging showed substantial ventricular enlargement (Dev et al., 2019; Kobayashi et al.,

Indirect consequences of TBM include uid retention (hydrocephalus), cerebral oe­dema, or an inammatory reaction in the brain tissue that results in diuse cor­tical or subcortical processes that can result in neurocognitive problems (Chen et al., 2015; Kirmi et al., 2009). Additionally, the infectious agent of TBM, Mycobacterium tuberculosis, can attack and infect neurons directly. Neurons can phagocytose bac­teria but to a lesser extent than do microglia and astrocytes (Randall et al., 2014). e neuronal infection aects function and the intercellular interactions during host im­mune responses (Davis et al., 2019b). As reported in studies of Alzheimer’s disease, TBM inammation- induced disruption of the blood– brain barrier causes and fur­ther induces a variety of tissue damage leading to synaptic and neuronal dysfunction and cognitive decits (Barisano et al., 2022). Other possible pathologies underlining the cognitive impairment in TBM are focal and discrete structural abnormalities in the brain, including vasculopathy leading to brain ischemia or tuberculomas (Chen et al., 2015; Davis et al., 2023; Wasay et al., 2018). Numerous studies have shown that the immune and neurological systems interact and that maintaining a healthy im­mune system is essential for sustaining cognitive function (Marin & Kipnis, 2013; Yirmiya & Goshen, 2011). Microglia and astrocytes in particular communicate with peripheral immune cell, such as T cells and macrophages, which play an important role in infectious illness (Yirmiya & Goshen, 2011). Glia and other brain immune cells alter their morphology and function when the immune system is severely en­gaged by infection, damage, and extremely stressful situations and secrete high levels of proinammatory cytokines, prostaglandins, and excitatory neurotrans­mitters, including glutamate (Rohlwink et al., 2019). ese inammatory mediators disrupt the delicate balance needed for the neurophysiological actions of immune processes, causing neuro- excitotoxicity and producing direct detrimental eects on memory, neural plasticity, and neurogenesis (Yirmiya & Goshen, 2011). Numerous

infectious pathogens have been identied as potential initiators of neurodegenera­tive illnesses, particularly Alzheimer’s disease. In addition to an indirect impact by infectious pathogens, this appears to be caused at least in part by microglia activa­tion, long- acting inammation, neuronal change, oxidative stress, and amyloid- beta accumulation (Marin & Kipnis, 2013; Stroolini et al., 2021; Williamson et al., 2011). Compared to Alzheimer’s disease or syphilis patients, cerebrospinal uid (CSF) from non- HIV TBM patients had relatively little amyloid deposition (amyloid- beta 1- 42) (Stroolini et al., 2021), which is one of the early pathological indicators of de­mentia, such as Alzheimer’s disease (Hampel et al., 2021; Murphy & Levine, 2010).

e characteristic feature of TBM in postmortem studies is the presence of a thick, gelatinous inammatory exudate in the basal cisterns and subarachnoid spaces of the brain, which may extend into the spinal canal. ese locations in the brain, primarily basal, have important ramications, such as the major cerebral vessels becoming encased in exudate, as seen in their small perforators. e middle cere­bral artery and its perforators around the ventricle oor are commonly involved. Vascular pathology from TBM includes an inammatory inltrate from the adven­titia of arteries and veins inward, resulting in a peri- arteritis— or pan- arteritis— that involves a segment or the entire thickness of the vascular wall tissue. e evolution of vascular inammation may involve thickening of the vessel intima resulting in vessel stenosis or occlusion. Furthermore, vasospasm is also an important contrib­utor to brain ischemia (Davis et al., 2019b; Rock et al., 2008).

e expansion of exudate material into the basal cisterns causes an accumulation of exudate around the midbrain and a blockage in CSF ow around the upper brain­stem, which prevents the circulation of CSF. A build- up of exudate may also obstruct CSF ow through the ventricular system around the cerebral aqueduct of the third and fourth ventricles (Davis et al., 2019b). Fiy- six to 80 percent of TBM patients ex­perience hydrocephalus (Dian et al., 2020; Misra et al., 2010). Gray and white matter may be adversely aected by the pressure of brain oedema brought on by pathologic processes, which can result in pallor and diuse myelin loss. Increased intracranial pressure has the potential to seriously impair cerebral blood ow.

physical treatments should be provided in the acute period of TBM since early re­habilitation aects functional outcomes in critically ill patients (Schweickert et al.,

2009). As previously indicated, a thorough assessment of neurocognitive impair­ment is essential for more specialized rehabilitation techniques to hasten the re­covery from deciencies in memory, executive function, and mental processing speed. For TBM, there is currently no specic strategy to treat cognitive impair­ment. Given the high prevalence of motor impairments, depression, and cognitive decits in TBM, the commonly used stroke rehabilitation methods may be bene­cial (Ganaraja et al., 2021; Quinn et al., 2021; Wasay et al., 2018). Tele- rehabilitation, including home- based exercises such as resistance, endurance, and balance training, has yielded gains in cognition and motor ability in post- Covid- 19 infection patients (Rolin et al., 2022) and could be tried for TBM patients, mainly for those who have no motor decits. Rehabilitation may be cost- eective since the population of those aected with TBM (mean age 35 years) is in the most economically active period of life (Quinn et al., 2021).