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Biomedical subjects

M Trillet

Publications and source records attributed to M Trillet.

At least 73 records · Page 4Linked to original sources
PubMed1983

[Cataplectic falls disclosing hypercalcemia].

Clinical manifestations of hypercalcaemic encephalopathy were heralded in three patients by isolated cataplexy-like falls without loss of consciousness. In one patient the falls with global hypotonia occurred every 5 to 10 seconds and were unaccompanied by changes in E.E.G. The falls disappeared after hypercalcaemia was corrected by excision of a parathyroid adenoma in two patients and by calcitonin injections in one. For this reason, there is little doubt that they were due to the hypercalcaemia, but their mechanism is poorly understood; it probably involves metabolic disturbances in the reticular systems of the brain stem. The connections between calcium metabolism and neuromediators in the brain stem are discussed.

Adenoma↗
PubMed1983

[Familial paroxysmal ataxia responsive to acetazolamide].

From their early twenties, a 56 year-old french woman and her 33 year-old son suffered from paroxysmal attacks of gait ataxia, incoordination of both hands, dysarthria and nystagmus. These attacks lasted from one to three hours and occurred at the rate of one to seven per week. On examination between attacks, there was only a bilateral horizontal and upward-beating gaze nystagmus. This was documented by E.O.G. Biological investigations were normal with the exception of a mild elevation of glucose blood level. Treatment with acetazolamide 250 mg daily, completely abolished the attacks in both patients. These cases meet the criteria of familial paroxysmal ataxia, a disorder only described in the United States up to the present. Although rare, this disease should be recognized because of its dramatic response to acetazolamide.

Acetazolamide↗
PubMed1982

[Peripheral neuropathy due to N-hexane in a drug addict (author's transl)].

After voluntary inhalation of a domestic solvent containing N-Hexane and N-Heptane for three months, a 23-year-old woman developed motor deficit of the lower limbs, sensory symptoms and areflexia. Clinical disorders continued to progress after discontinuation of the intoxication, with a parallel aggravation of the E.M.G. disturbances. A nerve biopsy with ultrastructural study showed axon dilatation with accumulation of neurofilaments. The clinical, electrophysiological and pathological features of neuropathies induced by hexacarbon solvents are reviewed and their pathogenesis is discussed.

Adult↗
PubMed1982

[Primary non-Hodgkin's lymphoma of the brain, sarcoidosis, thyroid cancer and immunity cell deficiency (author's transl)].

A 66-year-old man presented with a primary malignant lymphoma of the cerebellum and brain stem. The lymphoma was of type V (Bryon's classification) with predominant B cells, and was associated, as in previously reported cases, with a peripheral blood T lymphocyte deficiency. This case was unusual, in that autopsy revealed an active multivisceral sarcoidosis (considered as being cured more than 10 years previously), a clear-cell renal adenoma demonstrating nearly all the characteristics of a Grawitz's tumor, and a papillary epithelioma of the thyroid gland. These findings lead to discuss the significance of immuno-surveillance lack in this particular case: was it dependent on the sarcoidosis (during which a reduction in T lymphocytes is known to occur), or was it primary and perhaps genetic, a son of the patient having Hodgkin's disease? Whatever the case may be, the encephalic proliferation of the B lymphocyte clone, the peripheral epitheliomas, the sarcoidosis, and the deficit in T lymphocytes in the peripheral blood constitute a group of factors singularly rich in questions, this being, apparently, the first case of this type reported in the published literature.

Aged↗
PubMed1980

[Amnesic syndrome of posterior cerebral ischemia].

30 patients with acute onset of memory disturbances and visual impairment (cortical blindness or hemianopsia) are reported. For all of them, there was evidence of posterior cerebral artery ischemia. This clinical syndrome is compared with Dide and Botcazo's case report. The amnesia never recovered in 17 patients and was transient in 13 patients: in 4 of them it occurred during vertebral angiography and in 4 during general anaesthesia with anoxia. The main clinical features of the syndrome and the related bibliography are reviewed.

Adult↗
PubMed1980

[Chronic polyradiculitis with cutaneous and endocrine signs suggesting a plasmocytic dyscrasia to IgA (author's transl)].

A case of chronic disabling sensory-motor polyradiculitis occurring in a female patient and followed up for 18 months is reported. Clinical findings were papilledema, hypertrichosis, abnormal pigmentation of the skin, generalized edema, and spontaneous cutaneous necrosis. The diagnosis of a plasmocytic dyscrasia to IgA Lambda was made at a late stage of the disease. There were no signs of a solitary plasmocytoma or of diffuse myeloma. At autopsy, there were mild lesions in the peripheral nervous system, but no plasmocytic infiltration or amylosis was seen on optical or electron microscopy. This case is similar to other clinical cases reported mainly by Japanese authors.

Chronic Disease↗
PubMed1979

[Adrenomyeloneuropathy: an adult form of adrenoleukodystrophy spastic paraparesis, and chronic adrenal insufficiency (concerning 3 cases) (author's transl)].

Three cases of adult males with spastic paraparesis and adrenal insufficiency are reported. The adrenal insufficiency is primary and in one case associated with Leydig cell insufficiency. Ultrastructural examination of peripheral nerve revealed abnormal cytoplasmic inclusions in Schwann cells. A decrease in the percentage of linoleate to total fatty acids was found in the sera. A child with adrenoleucodystrophy and an adult with adreno myeloneuropathy were observed in the same family. It allows adrenomyeloneuropathy to be considered as an adult form of adrenoleucodystrophy.

Addison Disease↗
PubMed1977

[Multiple and familial meningiomatosis. A syndrome bordering on Recklinghausen's neurofibromatosis].

The authors present three cases of multiple, intra-cranial meningiomatosis with contact hyperostosis affecting the grandmother, mother and daughter, in a very stereotypic manner. No other sign of von Recklinghausen's disease was noted, except for two tiny neurofibromas on the left hand in the mother. Only the latter suffered from bilateral deafness, but it was not possible to give definite proof of the presence of an acoustic neuroma in this patient. Anatomical verification in the first case, and surgical intervention in the last, confirmed that it was in fact a meningioma. Thus, a new clinical form of expression of neuro-fibromatosis has been found.

Adult↗
PubMed1976

[Striato-nigral degeneration. A propos of 2 anatomo-clinical cases].

Two sporadic cases of striato-nigral degeneration were characterized by the onset at the age of 61 of an akinetic-hypertonic syndrome and of a minimal or absent rest tremor, with a pyramidal syndrome, sphincter disorders, dysphonia, difficulty in swallowing and an unfavorable development in the space of two or three years not affected by L-Dopa. In one case, total insomnia was demonstrated by means of 3 polygraphic recordings during the night, two of them consecutive, and aprobenecide test showed a definite fall in H.V.A. and 5 H.I.A.A. in the lumbar cerebrospinal fluid. Anatomical verification showed, in one case, isolated putamino-nigral degeneration, and in the other associated with lesions of the olivo-cerebellopontine system. Much of the excess pigmentation found only in the putamen was melanotic in character and resulted perhaps from the striato-nigral degeneration, making it possible to classify this more accurately among the other multisystem degenerations, especially olivo-ponto-cerebellar atrophy and Shy-Drager syndrome

Brain Diseases↗