The apparent inception of neurological involvement during early-stage infections has been identified previously in animal models of trypanosomiasis. The presence of trypanosomes within the CNS, only hours following infection, was demonstrated in a murine model of sleeping sickness . Here the authors used intravital microscopy to show fluorescently tagged T.b.rhodesiense IL1852 and T.b.brucei GVR35 in the cortical microvasculature and brain parenchyma 5 h following intravenous infection. A recent study by Laperchia et al.  demonstrated the presence of parasites and T-cells in the brain parenchyma at day 9 post-infection in a T.b.brucei rat model of HAT. The authors present confocal images illustrating parasite traversal of the blood vessel endothelia to enter the neuropil on day 9 post-infection and show high parasite burdens by day 21 post-infection. In addition, this study detected the occurrence of sleep-onset rapid eye movement (SOREM) episodes in the rats during the first week following infection and demonstrated that the number and duration of these episodes did not correlate with the trypanosome load found in the brain parenchyma. SOREM periods represent a disruption of the normal sleep architecture and are typically thought to be associated with CNS-stage infections . However, in the Laperchia study they became apparent early after infection demonstrating the presence of neurological features associated with early-stage disease. In human cases of sleeping sickness, caused by T.b.rhodesiense, a similar disconnect between the incidence of neurological signs, and development of stage-2 infection occurs . Patients presenting with either early and late-stage infections exhibited symptoms such as altered gait, tremors, incontinence, cranial nerve palsy, somnolence and reduced Glasgow coma score. Indicating that these neurological signs can occur prior to progression to stage-2 disease.