We conducted a case-control study of 116 patients with the clinical diagnosis of Alzheimer's disease (AD) in seven Italian centers. One hundred sixteen hospital controls and 97 population controls were matched by age, sex, and region of residence to the cases. A structured questionnaire was administered to the next-of-kin of cases and controls by trained interviewers to identify possible risk factors. Genetic, viral, toxic, immunologic, medical, surgical, and personality factors were investigated. Dementia among first- or second-degree relatives and advanced age of the mother at subject's birth (age over 40) were associated with AD. Head trauma was more frequent in cases than in either hospital or population controls, but the differences were not significant. Our data did not confirm the previously reported association with antecedent thyroid disease or family history of Down's syndrome.
Diphenylhydantoin (DPH) is known to induce reversible paroxysmal dyskinesias and paranoid psychosis in humans, but its interactions with dopamine (DA) metabolism are not clear. Single doses of DPH (60-100 mg kg-1), with serum levels over 10 micrograms ml-1, reduced homovanillic acid (HVA) levels in rat striatum. The DPH-induced HVA decrease was enhanced by supersensitivity of postsynaptic DA receptors following chronic haloperidol (Hal) administration. DPH 60 mg kg-1 given acutely enhanced the HVA decrease induced by apomorphine (Apo) and partially counteracted the HVA increase following acute Hal (0.1-0.5-2 mg kg-1). After chronic DPH treatment, Apo was ineffective in reducing striatal HVA levels. Concomitant chronic treatment with DPH and Hal counteracted the development of supersensitivity of postsynaptic DA receptors to Apo. Single doses of DPH (30-60-100 mg kg-1) increased cyclic AMP striatal content; this effect was blocked by Hal. A dopaminomimetic DPH action and a subsensitivity of postsynaptic DA receptors after chronic DPH seem to be suggested. These effects could be related to the dyskinetic and psychotic syndromes produced by the drug.
Herpes zoster of the ophthalmic division of the left fifth cranial nerve with contralateral hemiparesis was observed in a 30-year-old man. Left carotid angiography showed segmental constrictions consistent with cerebral arteritis, possibly provoked by direct viral infection along the intracranial part of the ophthalmic nerve. An ischaemic lesion revealed by computed tomographic scan was considered secondary to arteritis and responsible for the hemiparesis. The presence of an immune response within the blood-CSF barrier was suggested by an increase of oligoclonal CSF IgG and IgA.
Isoelectric focusing and quantitative estimation of serum and CSF IgG were performed in 85 patients with idiopathic polyneuropathy (IP), subdivided according to the clinical course (acute, subacute, recurrent, chronic). Acute IP very frequently had an increase of oligoclonal and/or polyclonal serum IgG during the progressive phase and blood-CSF barrier damage accompanied by polyclonal IgG intrathecal synthesis during the stationary phase. Polyclonal IgG intrathecal synthesis was also present in several not acute IP and seemed to forecast unfavorable course. Oligoclonal IgG synthesis occurs very rarely within CSF but is a frequent finding in serum of patients with IP. Abnormalities of the IgG serum pattern are neither specific for any clinical course of IP nor of prognostic value. The possible significance of such findings is discussed.
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