[Parkinsonism secondary to the use of sertraline].
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Biomedical subjects
Publications and source records attributed to J Roquer.
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Isolated angiitis of the central nervous system (IAC) is an idiopatic, recurrent vasculitis confined to the CNS involving small blood vessels. We describe the clinical, angiographic, and neuropathological data in two patients with IAC and delineate the main clinical and neuropathological features in both cases as well as the importance of a complete autopsy for discovering subclinical vasculitic lesions outside the CNS. Patient 1 concerned a 40 year-old-man that evolved for the last three years, initially with focal seizures, headache, and neurological focal deficits, later on the left sided hemihyposthesia and preferentially left parieto-occipital dysfunctions. He presented an oligoclonal band in CSF with slight hyperproteinorraquia and 25 lymphocytes. A cerebral angiography was compatible with angiitis and a leptomeningeal/cerebral biopsy showed lymphocytic vasculitis in the leptomeningeal and intraparenchymatous cerebral small vessels. These results lead to start a treatment with Cyclophosphamide associated to high dose of steroids. The patient clearly improved and now is almost asymptomatic. Patient 2 concerned a 67 year-old-man that evolved for 4 years with encephalic ischemic lesions distributed and confined throughout the brain stem and cerebellum, temporary remissions occurred and the patient required high-dose steroids and Cyclophosphamide to improve. Conventional and MRI angiographies only suggested the diagnosis that was confirmed at autopsy. The patient died after a massive pulmonary thromboembolism and a complete necropsic study showed abundant lymphocytic infiltrates, without granulomatous lesions, in the intraparenchymatous and leptomeningeal cerebral small vessels specially at the brain stem and cerebellar level where many demyelinated greyish areas and few infarctions were to be seen. The inflammatory cells were, in both cases, predominantly CD4+ T lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
We report 3 cases of dorsal ischemic myelopathy indicative of aneurysm of the abdominal aorta. In 2 cases the aneurysm was dissecting and in all patients medullary symptoms were preceded by sudden lumbar or abdominal pain. Neurological symptoms were slightly different in each case. One patient experienced 3 episodes of acute paraparesis and rapid regression evoking transitory medullary ischemic accidents (intermittent medullary claudication). Another patient suffered progressive asymmetric paraparesis which first stabilized and later improved partially after surgical treatment of the aneurysm. The third suffered acute paraplegia related to irreversible ischemia of the anterior 2/3 of the medulla. The great variety of clinical manifestations of spinal cord ischemia related to aneurysms of the descending aorta can be explained by the topography of the aneurysm, pecularities of medullary vascularization and, especially, by the diversity of etiopathogenetic mechanisms that give rise to ischemia. We conclude that in the face of symptoms suggesting dorsal ischemic myelopathy, the possibility that an aneurysm of the abdominal aorta may be the cause must be considered, whether or not pain has been experienced prior to signs of medullary involvement.
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We carried out a prospective study to determine the frequency and evolution of carpal tunnel syndrome (CTS) in patients with hyperthyroidism. An initial survey revealed CTS in 5% of these patients when hyperthyroidism was diagnosed. During the clinical and neurophysiologic follow-up for a two-year period, four more patients developed CTS; of these, two had uncontrolled hyperthyroidism, and the other two had iatrogenic hypothyroidism. The clinical and neurophysiologic evolution suggests a relationship between both diseases. The symptoms of CTS remitted if endocrinopathy is controlled. Surgery is, in general, not necessary. CTS can be considered another peripheral neurological manifestation associated with hyperthyroidism.
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BACKGROUND: Twenty-four patients with neurologic involvement and anti-Hu antibodies were studied with the aim of defining the type of tumor associated, evaluating whether the clinico-pathologic picture agreed with the concept of paraneoplastic encephalomyelitis (PEM) and evaluating the treatments used. METHODS: The study was retrospective with the clinical histories being reviewed to define the neurologic syndromes, their evolution and response to the different treatments, time of appearance and type of tumor as well as the neuropathologic changes in the patients undergoing autopsy. RESULTS: In 18 patients a neoplasm was diagnosed as small cell pulmonary carcinoma (SCPC) in 89% of the cases. The neurologic picture preceded the tumor by an average of five months. The clinical pictures included: sensitive neuropathy (20 patients), cerebellous and truncus encephalicus involvement (8 patients), motor neuropathy (6 patients), cortical involvement (5 patients) and neurovegetative dysfunction (4 patients). In 55% of the patients more than one area was altered. Post mortem studies carried out on 5 patients demonstrated inflammatory infiltrates and neuronal loss in multiple areas of the nervous system. None of the patients improved with treatment. The 9 patients who only received immunodepressants evolved in a way similar to those who were not treated. In 7 of the 11 patients who received antitumoral therapy, the neurologic syndrome stabilized for at least 6 months. CONCLUSIONS: The clinicopathological picture and the associated tumor seen in patients with anti-Hu antibodies are identical to those seen in PEM. Antitumoral treatment seems to be more effective than immunodepressant treatment.
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BACKGROUND AND PURPOSE: The role of lipoprotein abnormalities in the development of ischemic cerebrovascular disease has not been sufficiently clarified. The aim of this study was to identify the lipoprotein profile in ischemic cerebrovascular disease and the possible role of apolipoprotein E polymorphism. METHODS: The relation between the concentrations of lipoprotein(a), intermediate density lipoproteins, apolipoprotein A-I, apolipoprotein B, apolipoprotein E, and other lipoproteins was studied in 100 men with ischemic cerebrovascular disease (48 atherothrombotic, 28 lacunar, and 24 of unknown type) and in 100 healthy age-matched men as a control group. RESULTS: Patients with ischemic cerebrovascular disease had significantly higher levels of lipoprotein(a), lipids carried by intermediate density lipoproteins, and low density lipoprotein cholesterol and lower levels of high density lipoproteins than control subjects. Patients with atherothrombotic infarction had higher total serum cholesterol and low density lipoprotein cholesterol concentrations than patients with lacunar infarction. To assess lipoprotein abnormalities in normolipidemic subjects, a subgroup of 38 patients with ischemic cerebrovascular disease and 53 control subjects, both with serum cholesterol levels < 5.2 mmol/l (200 mg/dl) and triglycerides < 2.3 mmol/l (200 mg/dl), was analyzed. Serum lipoprotein(a), lipids carried by very low density lipoproteins and intermediate density lipoproteins, and low density lipoprotein triglycerides were significantly higher in normolipidemic patients compared with normolipidemic control subjects, whereas high density lipoprotein cholesterol levels were lower. Apolipoprotein E polymorphism in our ischemic cerebrovascular patients differed from that of the control group, with the epsilon 4 allele being more prevalent. CONCLUSIONS: Increased serum lipoprotein(a) levels and intermediate density lipoprotein abnormalities together with decreased high density lipoprotein levels are major risk factors for ischemic cerebrovascular disease, even in normocholesterolemic and normotriglyceridemic subjects. Finally, the epsilon 4 allele could probably be a predisposing genetic marker for ischemic cerebrovascular disease.
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