[Conference at Salpêtrière. 7 October 1981. Lasting stupor, tetraparesis, decerebration and decortication in a 32 year-old woman].
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Biomedical subjects
Publications and source records attributed to P Brunet.
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Four cases of angioimmunoblastic lymphadenopathy associated to peripheral neuropathy are described. The neuropathy was mixed, sensory and motor, more or less extensive, always asymetrical. In two cases, the clinical symptomatology and the clinical course were very peculiar, characterized by sensory disorders of a precise topography, circumscribed and sometimes suspended and by a relapsing and remitting course. In the third case, the neurological signs were acute and rapidly extensive with mandatory respiratory assistance. In this case, death occurred after a few weeks and the exact diagnosis was only attained at post-mortem examination. In the fourth case the neuropathy was very painful but the course was slow. In all four cases marked and extensive pain was present prior to the neurological disorders. Electrophysiological abnormalities were a constant feature with a marked slowing down of nerve conduction velocity. CSF was normal at the beginning in one case but was otherwise markedly pathological with an increased number of cells due to a large number of lymphocytes ranging from 6 to 40 cells while protein ranged from 60 to 160 mg per 100 ml. Nerve and muscle biopsies were non specific, i.e. neurogenous muscular atrophy and demyelination, except in case n. 4 where specific angioimmunoblastic lymphadenopathy infiltrates were present both in nerve and muscle. In cases 1 and 3 a non specific lymphohistiocytic infiltrate was present in spinal roots and meninges. Corticotherapy was used and efficient in two cases. These data are compared with a review of the literature. Since 1976, 7 cases of angioimmunoblastic lymphadenopathy associated to peripheral neuropathy have been reported. Clinical, electrophysiological and biological features are similar. Only one case underwent a post mortem examination of the central nervous system: a non specific lymphocytic infiltration in the spinal roots and meninges was mentioned. The role of the dysproteinemia associated with the AIL in the occurrence of the neuropathies is discussed. It remains a possible factor only. The role of a massive specific localization of the pathological process is well established in only one case (case 4). Such localization in lymphomas are not unusual. In 2 of our cases as well as in 2 from the literature the pathological findings are non specific: mild lymphoplasmocytic infiltrates of spinal roots and meninges. Those lesions are similar to neuropathies associated to non metastasizing neoplasms or malignant hemopathies.
Relative to an industrial application, the authors relate results obtained from a peculiar study on the thermic degradation of bis (tri-n-butyltin) oxide (TBTO) at various temperatures and they account for the toxic effects observed after inhaling the combustion products in the mouse and guinea pig. Thermolysis of TBTO between 200 and 600 degrees C gives saturated hydrocarbon and olefin gas, a condensate of tetrabutyltin and dibutyltin oxide and a residue composed of stannous or stannic oxides according to the temperature. Pulmonary toxicity is very important at low temperatures but after heating, toxic effects decrease. The results are confirmed by localisation and histopathologic studies. At 600 degrees C no death appears but some behavioral troubles occur. It's possible that repeated exposures can induce delayed toxicity.
Two clinical cases are reported of similar oculomotor disorders presenting as a paralysis of the oculomotor nerve (III) on one side and isolated paralysis of the superior rectus on the other side. Previous reports of this clinical picture have not been found. Recent experimental studies have established that all the superior rectus motoneurons decussate and pass through the opposite II nucleus before entering the radicular portion. Therefore it is suggested that the reported syndrome results from an unilateral lesion in the III nucleus.
A case of rigid spine syndrome associated with a pleuropulmonary disease is reported. This case is the ninth known rigid spine syndrome but it is the first associated with a diffuse pleural and pulmonary involvement. Clinical examination showed limitation of flexion of the spine since early infancy and limitation of extension of the elbows. Fibrosis probably involved both the lung and the pleura, although microscopic examination showed limitation of flexion of the spine since early infancy and limitation of extension of the elbows. Fibrosis probably involved both the lung and the pleura, although microscopic examination are not available. Severity of respiratory failure is explained by involvement of lungs, pleura and chest wall. Future is explained by involvement of lungs, pleura and chest wall. Future studies of similar case are needed to answer the questions whether or not this association is casual and if lung and muscular involvement are linked.
Metabolic and hormonal tests to assess plasma renin, aldosterone, and catecholamine activity were conducted in three patients with idiopathic orthostatic hypotension. Blood pressure readings were then taken in decubitus and orthostatism during treatment with 10 to 15 mg of tyramine and 30 mg of tranylcypromine. Marked functional improvement was observed, with an increase in mean blood pressure in decubitus and a less marked reduction in orthostatism avoiding the onset of severe discomfort. Therapeutic indications are limited, however, because of a possible hypertensive response.
A case of facial quadriplegia of sudden onset in a 73 year old man is reported. Proprioceptive sensory disorders involved only the upper limbs. This suggested a medial infarction of the medulla the precise situation of which is discussed.
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In a 43 year old man we reported a spinal cord compression by extradural lipomatosis associated with long term corticosteroid therapy for periarteritis nodosa. Decompressive surgery at the 16th month of corticosteroid treatment resulted in regression of symptoms and signs. Corticosteroid therapy was felt to be responsible for this neurological complication, which is unknown in periarteritis nodosa, but has been seen in association with intraspinal lipomas.
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The authors describe three patients presenting several episodes of paralysis of the motor and sensory cranial nerves and discuss possible aetiological factors. The paralytic attacks were regressive and were repeated at irregular intervals over a period of several years. It was confirmed that no local or general cause for the symptoms existed and the conclusion was reached that they were part of an autonomous clinical syndrome of unknown aetiology. Other cases have been reported in the published literature in which a non-specific inflammatory mechanism is suggested but no biological or pathological basis exists to support this physiopathological hypothesis. The clinical syndrome follows a benign course, the paralysis being regressive and the affection remaining confined to the peripheral nervous system of mesencephalic origin.
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The authors report 5 personal cases (3 in the same family) of patients suffering from recurrent peripheral nerve palsies usually induced by pressure and review the relevant literature. There is evidence in such cases of a mild, chronic, diffuse, subclinical neuropathy which can be recognized by electrophysiological examination. Examination of peripheral nerve biopsy material in such cases shows evidence of both axonal and Schwann cell abnormalities with evidence of neurogenic atrophy of skeletal muscles. This chronic subclinical neuropathy which is often familial can be distinguished from other chronic primary neuropathies with or without myelin sheath proliferation and hypertrophy.
Pure dural arteriovenous fistulas are still not properly understood, and pose problems wich are far from being resolved. Among these, dural fistulas with cortical venous drainage represent a very special entity since they alone are expressed clinically by a neurological brain syndrome. Diagnosis is difficult and mistakes can be made as it is only by means of hyperselective arteriography of the branches of the external carotid that an accurate diagnosis can be made. However, their diagnosis assumes considerable importance since surgical or radiological treatment of hese fistulas brings about complete disappearance of clinical symptoms.
The authors studied 13 new cases of fistulae of the dura mater. With reference to these 13 cases, and to the literature, they propose a classification according to the type of drainage of the fistula: direct, into a dura mater lake, into a cortical vein. This clasification enables a better clinical and radiological approach to these anomalies.
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