Following infection the disease progresses through two stages. During stage-1 the parasites proliferate in the blood, lymphatic system and peripheral organs. However, the most serious form of HAT, stage-2, occurs when the trypanosomes circumvent the blood-brain barrier (BBB) to enter and establish within the CNS. Gambiense infections are associated with a chronic progressive course and can take months to years before stage-2 disease is reached, while rhodesiense infections are more acute with parasites entering the CNS within a matter of weeks . The progression of the infection to the CNS-stage is associated with the development of a neuroinflammatory reaction described in only a limited number of human cases , . This neuroinflammatory response to trypanosome infection has been mirrored in both rodent and primate models of the human disease and is characterised by inflammatory cells, including lymphocytes, macrophages and plasma cells, infiltrating the meninges and choroid, followed by inflammation of the parenchymal vessels and lastly the development of encephalitis. Astrocyte and microglial cell activation accompany this response although little neuronal damage or demyelination occur until the terminal stages of the disease are reached , , , .