We studied a Japanese patient who developed parkinsonian symptoms over 3 months before the diagnosis of acquired immunodeficiency syndrome. Brain MRI showed multiple lesions with mass effect and ring enhancement in the basal ganglia and subcortical white matter suggesting Toxoplasma infection. Anti-Toxoplasma therapy and highly active antiretroviral therapy for 6 months allowed improvement of parkinsonism, brain MRI findings, and immune system.
A 34 year old woman with AIDS presented with adynamia and obsessive-compulsive behaviour. CT scan revealed bilateral toxoplasmic lesions involving basal ganglia. The neuropsychological picture resolved under specific antitoxoplasmic treatment. However, relapse of toxoplasmosis occurred in associating with the same behavioral changes. This is the first case of such a syndrome due to infectious lesions, and in which improvement through transient, was observed.
A case-control study evaluating the association between mental retardation and toxoplasmosis was conducted among 845 school children in Belo Horizonte, MG, Brazil. Cases (450) were mentally retarded children attending a Public school for special education. Controls (395) were children from the regular public school system. Clinical and anthropometric examinations and interviews were carried out to determine risk factors for toxoplasmosis and mental retardation. Diagnosis of Toxoplasma gondii infection was based upon an indirect immunofluorescent test (IFA); 55% of cases and 29% of controls were positive. The Relative Odds of mental retardation in children with positive serology was 3.0 (95% CI 2.2-4.0). Maternal exposure to cats and contact with soil were associated with an increased risk of mental retardation. Retinochoroiditis was fourfold more prevalent among cases than controls and was only diagnosed in T. gondii IFA positive participants. Congenital toxoplasmosis, in its subclinical form, appears to be an important component in the etiology of mental retardation, especially in high risk (lower socioeconomic) groups. The population attributable risk was estimated as 6.0-9.0%, suggesting the amount of mental retardation associated with this infection.
Explicit consolidation of memory, or fixation of declarative belief, appears to be physically represented in changes of synaptic conductances of neurons in the parietal-temporal-occipital association cortex (PTO) of the mammalian forebrain. This fixation of belief in PTO is postulated to be critically dependent on a diffuse reinforcement signal via the inferior temporal cortex (ITC) ultimately caused by an increased output of the CA1 pyramidal cells of hippocampus. Analogous to the reinforcing mechanisms of other forebrain systems, this updating of the connection weights of the neural nets in PTO by the output of the critical neurons in CA1 is directly related to concentrations of dopamine (DA). We propose that the delusions (i.e., unreasonable beliefs) of paranoid schizophrenia are caused by a hyperactivity of the same DA-sensitive CA1 neurons that are responsible for the fixation of normal beliefs. The dramatic reduction in delusions with administration of neuroleptics, as DA D2 blockers, in schizophrenics may thus be explained by their acting to ameliorate the hyperactivity of these CA1 DA D2 receptors.
Childhood autism may be caused by damage to three phylogenetically distinct regions of the brain, or their major pathways and connections. Injury to the neocortex results in loss of language and cognitive function, while injury to the limbic cortex results in autistic withdrawal and abolition of play behaviour. Injury to the more primitive striatal complex, mammalian counterpart of the brain of reptiles, results in a bizarre and truncated form of stereotyped and ritualistic behaviour. The causes of brain injury in childhood autism could be those common in the perinatal period including cerebral anoxia, haemorrhage, phenylketonuria, neurolipidoses , meningitis, toxoplasmosis, and congenital rubella. All these conditions have previously been shown to be associated with childhood autism.
Intradermal tests using toxoplasmin were performed among three hundred mentally handicapped patients admitted to the "10 de Octubre" Clinical-Surgical Teaching Hospital in Havana between 1976--1977 and 100 healthy subjects. A statistically significant difference between reactors among patients (54,7%) and reactors among healthy subjects (30,0%) was found. Results are compared to those from a similar paper performed in the Psychiatric Hospital of Havana in 1967. It is concluded that the higher the severity of affections the higher the percentage of reactors in the surveyed series.