From 108 cases of new daily persistent headaches, clinical or laboratory evidence was found suggesting extracranial or systemic infections in: 28 cases (25.9%) of gastrointestinal mainly Salmonella, 28 (25.9%) urinary Coli, 16 (14.8%) Streptococcal, 4 (3.7%) each of Epstein Barr virus or Toxoplasma, and 1 (0.9%) each of Herpes Zoster or pneumonia. A group of 26 (24.1%) showed high Proteus OX titer or clinical adenoviral involvement. All had normal neurological examinations plus selective negative neuroimaging or spinal taps. The mean headache duration was 13.8 days, and mean age 28.8 years. Prominent symptoms were fever in 37 (34.2%) cases, nausea/vomiting in 30 (27%) and vertigo in 17 (15.7%). Diarrhea, dysuria, and abdominal discomfort were rare. Headache was a solitary symptom in 36 (33.3%). The predominant sign was painful cervical lymphadenopathy in 61 (56.5%). These cases represent 1.2% of our 9060 neurology patients.
Four patients with congenital toxoplasmosis serologically diagnosed by the Sabin-Feldman test (SFT) and the IgM-indirect fluorescent antibody test (IgM-IFAT) in the first year of life presented with eye disease between the age of 21 months and ten years. Repeated serological testing revealed increasing levels of specific antibodies as measured by the SFT. IgM antibodies to Toxoplasma gondii were detected in all four patients by the immunosorbent agglutination assay, in two by the IgM-IFAT and in three by the IgM-indirect haemagglutination test. Findings suggest that specific IgM antibodies reappear at the time of reactivation of congenital toxoplasmosis later in life, or possibly persist for an extraordinary long period (up to ten years)
The association of unusual types of aphasia and epilepsy (Landau-Kleffner syndrome) has been described in three children. The children were 5 to 11 years of age and all have EEG abnormalities. Speech disorders appeared after epileptic seizures. No organic causes of the disease have been found in axial computed tomography. In all described cases the increased titer of IgG antibodies against Toxoplasma gondii has been observed. The authors suggest that the Toxoplasma gondii infection should be taken into account as a possible cause of Landau-Kleffner syndrome.
The authors report 4 cases of toxoplasmosis in patients with acute disseminated lupus erythematosus (ADLE). In one case, a pregnant patient with serology indicative of chronic infection, infected the neonate who died of subacute toxoplasmosis. Although ADLE is a classical cause of immunodepression, toxoplasmosis is a rare complication; only 5 cases were found in a review of the literature. Toxoplasmosis infection may resemble an exacerbation of lupus; an accurate diagnosis is essential as the treatment of the two conditions is radically different. The problems of diagnosis of toxoplasmosis in immunodepressed patients are reviewed and the therapeutic approach, especially in pregnant patients, is discussed. In ADLE, the authors recommend checking toxoplasmosis serology before starting and during treatment with corticosteroids. Special attention should be paid to pregnant women with apparently chronic serological changes as neonatal infection may occur.
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.
We report here a case of polymyositis and toxoplasmosis, and review the previous examples of this association. We suggest that in most cases this relationship is due to reactivation of latent infection in an immunocompromised host. Gross immunological aberrations underline the pathogenesis of polymyositis and these predispose the patient to the development of toxoplasmosis. Anti-protozoal therapy is necessary and produces some clinical benefit, but it does not cure the polymyositis.
The presence of positive antibody titres to Toxoplasma and Toxocara in an adult epileptic population has been examined in relation to other observations of aetiological importance. With Toxoplasma, and more particularly with Toxocara, a higher incidence of positive antibody titres was recorded than in nonepileptic populations. Comparison with previous studies in childhood epilepsy indicate that the incidence of positive titres increased with age throughout adult life. Despite attention to the age of onset of epilepsy, presumed aetiological factors, and electroencephalographic and clinical observations, no causal relationship between parasitic infection and the aetiology of epilepsy was established.
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.