This case is reported to raise awareness of herpes simplex encephalitis as a persisting brain disorder. A 66 year old immunocompetent man developed status epilepticus and died of pneumonia in the course of progressive hemiparesis, cognitive decline, and atrophy of the brain over a five year period after herpes simplex encephalitis. In addition to a completely destroyed left temporal lobe, necropsy revealed active encephalitis consisting of necrosis and lymphocyte infiltration with a large number of intranuclear inclusions in the neurones and glial cells in the markedly oedematous parenchyma of the right frontal and parietal lobes. Herpes simplex virus type 1 (HSV-1) antigen was detected by immunohistochemistry, HSV-1 DNA by in situ hybridisation, and herpes simplex virus nucleocapsids by electronmicroscopy. These clinical and pathological findings suggest that direct viral reactivation might result in a relapse of herpes simplex encephalitis, causing progressive clinical deterioration associated with the persistence of HSV-1 in the brain. This is the first case report demonstrating HSV-1 antigen, HSV-1 DNA, and herpes simplex virus nucleocapsids in a case of relapsing herpes simplex encephalitis.H erpes simplex encephalitis is the most common non-epidemic form of viral encephalitis. Its typical clinical presentation is of an acute febrile illness with behavioural abnormalities, decreased level of consciousness, and focal neurological signs. The common neurological sequelae of this disease include memory impairment, behavioural and cognitive abnormality, and secondary epilepsy.1 It has been reported recently, on the basis of the detection of viral DNA and persistent immunohistochemical activity in the brain, that herpes simplex virus type 1 (HSV-1) might persist within the human central nervous system following recovery from encephalitis.2 3 However, the role of persistence of the viral infection and its contribution to neurological sequelae after herpes simplex encephalitis remains obscure.We report the necropsy findings in a case of relapsing herpes simplex encephalitis presenting as progressive neurological deterioration over a five year period following the initial episode of herpes simplex encephalitis. The role of persistent herpes simplex virus infection and the pathogenesis of relapsing herpes simplex encephalitis are discussed in relation to the therapeutic problem. CASE REPORTA 61 year old man with a 10 year history of pneumoconiosis presented at our hospital with high fever and confusion. Three days later, he was admitted to our department because of a tonic-clonic seizure. On admission, he had global aphasia with no limb weakness or sensory disturbance. The initial diagnosis of herpes simplex encephalitis was made by the presence of intrathecal synthesis of antibodies specific to HSV-1 and the presence of HSV-1 DNA in the cerebrospinal fluid detected by polymerase chain reaction (PCR). Brain computed tomography (CT) and magnetic resonance imaging on the day of admission were normal, but single photon ...

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BackgroundAnkle exercise has been proven to be an effective intervention to increase venous velocity. However, the efficacy of ankle exercise for improving cerebral circulation has not been determined. We hypothesized that ankle exercise in the supine position would be able to increase oxyhemoglobin levels measured at the forehead.MethodsSeventeen community-dwelling elderly women participated in this study. We recorded blood pressure, heart rate (HR), and oxyhemoglobin (OxyHb) levels from the participants in the supine position. Participants repeated ankle plantar flexion and dorsiflexion movements for 1 min. Two types of exercise were used: active movement and passive movement. We used two-way analysis of variance to assess the differences in mean arterial blood pressure (MAP), HR, and OxyHb between different exercises (active and passive) and times (before and after exercise).ResultsThe HR and MAP increased during active exercise but not during passive exercise. On the other hand, the levels of OxyHb measured at the forehead were elevated during both active and passive exercises. This increase lasted at least 1 min after exercise. There was no significant difference between active and passive exercise with regard to OxyHb; however, a significant difference was observed between before and after exercise (p < 0.05, η2G = 0.153).ConclusionsThe physiological response of OxyHb to ankle exercise was different from that of the other cardiovascular functions. Both active and passive ankle exercises were able to increase cerebral blood oxygenation, whereas the other cardiovascular functions did not respond to passive exercise.