ABSTRACT
We describe the follow-up of a cohort of 255 Alzheimer's disease (AD) patients (81 males, 174 females) treated by tacrine during 4 years. We performed the survey of hepatic, cholinergic and general tolérance. Drug efficacy was measured by MMS examination on weeks 0, 18, 30, 52, 104, 156 and 208. A total of 190 patients (74.5 percent) were dropped out of this study, 75 (29 percent) for adverse events. We found 85 hepatic (33 percent), 79 cholinergic (31 percent), 31 (12 percent) neuropsychiatric and 72 general (28 percent) side effects. In term of drug efficacy we observed a global decline of 2.5 MMS points during the first year and 2 MMS points between W52 and W156. Tacrine's symptomatic efficacy, defined as the number of patients improved or stabilized at W30, was present in 50 patients (46 percent) among the 109 patients reaching W30. The intensity of symptomatic efficacy was expressed by a 2.7 MMS points increase in 37 patients improved on W30. The long term effects of Tacrine, measured by the MMS score at one year, showed a positive impact as the MMS was 2.5 points above the expected score in non treated AD patients. This study raises the practical problem of optimal cholinesterase inhibitors use in AD and the theoretical question of long term action of cholinesterase inhibitors on cerebral lesions of AD.
Subject(s)
Alzheimer Disease/drug therapy , Cholinesterase Inhibitors/therapeutic use , Tacrine/therapeutic use , Aged , Cholinesterase Inhibitors/adverse effects , Cohort Studies , Female , Follow-Up Studies , Humans , Male , Patient Dropouts/statistics & numerical data , Tacrine/adverse effects , Time FactorsABSTRACT
We report two cases of unilateral upper cervical spinal cord infarction in the territory supplied by the anterior spinal artery. Early nonspecific MRI abnormalities consisted of hypointense T1 signal and hyperintense T2 signal. A late MRI study showed partial decrease in lesion size due to perifocal edema resorption with negative Gd-DTPA enhancement. The presumed cause of infarction was occlusion of a sulcocommissural artery or of the ipsilateral nutrient branch of the spinal artery.
Subject(s)
Infarction/diagnosis , Magnetic Resonance Imaging , Spinal Cord Diseases/diagnosis , Adult , Arteries , Functional Laterality , Hemiplegia/etiology , Humans , Infarction/complications , Male , Middle Aged , Spinal Cord/blood supply , Spinal Cord Diseases/complicationsABSTRACT
A report is given on a 25-year-old man who was admitted to the hospital because of severe headache (CSF: 280 cells per mm3, 90% lymphocytes, later normal). Headache persisted for one year when acute deterioration occurred. The CSF showed 140 cells per mm3 (100% lymphocytes), 1 g% protein. Improvement of the patient's state after corticosteroid therapy. 9 months later he interrupted the intake of prednisolon and provoked exacerbation of the disease with motor and sensor disturbances. 21/2 years after the beginning of the symptomatology he suddenly developed cerebral coma and died. The autopsy revealed ischemic necrosis of both the left and the right thalamus, hemorrhage with destruction of the left-sided thalamus, nucleus caudatus, internal capsula and rupture into the lateral ventricle. Histologically, preparations from all parts of the brain revealed granulomatous angiitis of arteries, capillaries and veins with fibrinoid necrosis, infiltration of lymphocytes, histiocytes, epitheloid and plasma cells as well as numerous giant cells. Microaneurysms were found frequently. The inflammatory process showed various stages of the development indicating that more and more vessels had been involved at different times. Contrasting to giant cell arteritis of A. temporalis, in giant cell angiitis of the brain the blood sedimentation rate is frequently normal. In all reported cases, vessels of the leptomeninges were involved. Therefore, leptomeningeal biopsy is regarded as diagnostic procedure. The own observation as well as data of the literature demonstrate that giant cell angiitis of the brain is distinct from temporal arteritis (Horton's disease), not only because of differences in location, but also because of differences in age incidence and prognosis. It is supposed that giant cell angiitis is not a nosological entity, but the expression of different etiologic and pathogenetic mechanisms.