Although there has been a limited description of signicant cerebral blood ow abnormalities in cases of encephalitis, signicant cerebrovascular abnormalities have been more notable in meningitis [60]. By varying mean arterial pressure (MAP) and measuring MCA MFV and jugular oxygen saturation, autoregulation was found to be impaired but temporarily recovered with hyperventilation in a series of patients with acute bacterial meningitis. Outcomes were good for those patients who recovered cerebral autoregulation; however, those who did not, either died or had a protracted hospital course [61, 62]. Three phases of tuberculous men­ingitis have been described with progressively worsening outcomes. The rst phase includes patients with focal reversible neurological decits and a GCS of 15 who have increased MCA ow velocities (MFV) and normal or slightly decreased PI.The second phase characterizes patients with focal neurological decits, a GCS 12–14, and decreased MCA MFV and PI.The third phase characterizes patients with GCS less than 12, severely reduced or absent MCA MFV, and severely reduced PI.Phase II and III patients have cerebral CT evidence of inammatory meningitis and infarction with clinical ndings of permanent neurological dysfunction or death [63]. Disturbed cerebral hemodynamics including MCA stenosis and an increased PI has been shown using TCCS in a small series of patients with non-HIV crypto­coccal meningitis. Good concordance between the TCCS ndings and those seen on MR angiography was not evident; however, the small number of study patients lim­its conclusions [64]. The same investigators have demonstrated in a small series of patients with tuberculous or cryptococcal meningitis that the presence of unilateral or bilateral MCA stenosis seen on TCCS was associated with 5.3 odds of a poor outcome (Barthel Index <12) at 6months [65].