Sporadic choreas: analysis of a general hospital series.

The incidence of sporadic chorea among general hospital admissions is unknown, and the relation of clinical manifestations and etiological factors to neuroimaging findings has been little investigated in this condition. We reviewed the 7,829 cases admitted to the neurology departments of two general hospitals over 3.25 years and identified 23 (8 male and 15 female) cases of apparently sporadic chorea. Analysis of the records of these patients permitted etiological classification as follows: drug-induced chorea (5 patients), vascular chorea (6 patients), chorea-vasculitis (1 patient), Sydenham's chorea (1 patient), AIDS-related chorea (5 patients) and in 4 patients neither etiological factors nor neuroradiological alterations were found. Finally in 1 patient, the genetic test for Huntington's disease was positive. Thirteen patients had pathological neuroimaging findings; however, in only 3 were basal ganglia lesions considered to be the cause of the chorea. We conclude that sporadic chorea is not rare among neurological department admissions (we found 2.94 cases per 1,000 admissions) and only in a minority of cases is the symptomatology attributable to gross basal ganglia lesions; HIV infection is an emerging cause of chorea.

Chorea as a symptom of neuroborreliosis: a case study.

Borrelia burgdorferi (Bb) can cause a large number of neurological symptoms. Although extrapyramidal disturbances are rare (representing less than 2% of all neurological complications), diffuse choreic dyskinesias have been described during the course of mild encephalitis. The data published in the literature suggest that there are clinical and neurological analogies between neuroborreliosis and multiple sclerosis (MS). The presence of specific anti-Bb antibodies in cerebrospinal fluid is a discriminating factor that allows a diagnosis of neuroborreliosis to be made. We describe the case of a patient with Lyme disease, characterised by widespread chorea and behavioural disturbances. Emphasis is placed on the atypical onset and evolution, the difficulties encountered in formulating a diagnosis, and the uncertainties concerning the pathophysiology and clinical/neuroradiological correlations of the disease.

Hyperosmolar hyperglycemic nonketotic coma in Waldenström's macroglobulinemia associated with type II diabetes and complicated by pulmonary tuberculosis.

In this paper we describe a successfully treated case of hyperosmolar hyperglycemic non ketotic coma (HHNC). The HHNC was observed in a patient affected by Waldenström's macroglobulinemia, associated with type II diabetes and complicated by pulmonary tuberculosis. Hyperosmolar hyperglycemic nonketotic coma is a clinical condition with a high mortality rate associated with a severe increase in blood viscosity. This increase in blood viscosity justifies several clinical manifestations of the HHNC. We believe that an increase in the blood viscosity produced by the simultaneous presence of the single diseases mentioned above may have encouraged the development of hyperosmolar coma in the case reported.