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J F Hurtevent

Publications and source records attributed to J F Hurtevent.

At least 37 records · Page 2Linked to original sources
PubMed1995

[Acute and reversible myoclonic encephalopathy, extrapyramidal syndrome, polyneuropathy caused by chronic disulfiram poisoning].

This 44-year woman was admitted for weight loss and global intellectual slowing. She had mild chronic alcoholic neuropathy. She was discontinued alcoholic consumption for 6 months and was given disulfiram (1.5 g/day) since then. She developed over a 5-day period acute neuropathy, confusion and extrapyramidal symptoms with oculo-cephalogyric and dystonic movements and myoclonus. Electromyography revealed a severe polyneuropathy. After disulfiram withdrawal, confusion and extrapyramidal symptoms disappeared within a few days, but sensitivo-motor deficit improved more slowly. Nerve biopsy was suggestive of a pure axonal neuropathy.

Acute Disease↗
PubMed1994

[Unilateral paralysis of the glossopharyngeal, vagus and hypoglossal nerves].

A 32-year-old woman complained of swallowing difficulty after a general seizure. Neurological examination revealed unilateral palsies of the 9th, 10th, and 12th cranial nerves. CT, MRI and internal carotid artery angiogram were normal. Selective catheterization of the external carotid artery and ascending pharyngeal system suggested a cranial nerve ischaemic arterial syndrome. The apparent sparing of the eleventh nerve may be explained by the double vascularization of this nerve. This may also be related to the double innervation of the trapezius and sterno-cleido-mastoid muscles by the 11th nerve and cervical spinal nerves.

Adult↗
PubMed1993

Unilateral loss of facial flushing and sweating with contralateral anhidrosis: harlequin syndrome or Adie's syndrome?

A 45-year-old woman presented with a 10 year history of asymmetrical facial flushing and sweating after exertion or in hot weather. During these episodes the right side of her face remained dry and white, while the left side normally flushed. Sweating was impaired on the left side in the limbs and trunk. She also had areflexia in the lower limbs and slow pupillary reactions to light and darkness, as seen in Adie's syndrome. The topography of the sweating disorder suggested that the lesion involved the sympathetic pathways at the level of spinal cord. The relationship with the harlequin syndrome and related disorders is discussed.

Adie Syndrome↗
PubMed1993

[Bulbar hematoma of the olivary area. An analysis of the autonomic syndrome].

The consequences of an anterolateral medullary hematoma in a 50 year old patient are reported. The lesions principally involved the inferior olive nuclei, the lateral reticular nucleus, and, partially, the nucleus ambiguus. Long-lasting postural control deficit and hypotonia were observed, associated with alpha motoneurons hyperexcitability. Analysis of the heart rate regulation showed a severe reduction of the normal accelerating reactions and a relative preservation of slowing down reactions that suggested a deficit of the ortho-sympathetic control. Unilateral palsy of the tongue and pharynx was also observed without sensory or sensorial deficit. The long term course was favourable.

Autonomic Nervous System Diseases↗
PubMed1992

Myasthenia gravis and steroid-induced myopathy of the respiratory muscles.

OBJECTIVE: We report a case of corticosteroid-induced myopathy with involvement of respiratory muscles observed in a myasthenic patient. PATIENT: A 37-years-old woman, under corticosteroid treatment for two years for typical myasthenia gravis was admitted to ICU for acute myasthenic respiratory failure. Weaning from mechanical ventilation remained impossible despite 4 plasma exchanges and azathioprine. The patient exhibited a progressive 12 kg weight loss with muscular weakness and atrophy. MEASUREMENTS AND RESULTS: Peripheral and diaphragmatic electromyography as well as histological study were consistent with a steroid-induced myopathy. Discontinuation of corticosteroid treatment was followed by a rapid weight gain with general improvement and allowed weaning from mechanical ventilation with a complete recovery. CONCLUSION: This case provides evidence that corticosteroid-induced myopathy may be observed in myasthenia gravis and may involve the respiratory muscles as well as the peripheral musculature.

Adrenal Cortex Hormones↗
PubMed1992

[Stiff-Man syndrome with late onset].

We report a case of Stiff-Man syndrome according to Gordon, Januszko and Kaufman's criteria. Onset at age 76, association with insomnia and a rapid course leading to death within 2 years were the characteristic features. CSF data, electromyographic and immunological findings suggest abnormalities of catecholaminergic and GABA ergic systems, with release of segmental or suprasegmental inhibitory influence. The presence of antibodies against glutamic acid decarboxylase, considered a useful marker of this syndrome, raises the possibility of an autoimmune pathogenesis.

Aged↗
PubMed1992

[Mixed pre- and postsynaptic neuromuscular block].

We report a new case of neuromuscular block overlap between Myasthenia Gravis and Eaton-Lambert syndrome. A 64-year-old man with a 4-months history of gait disturbance was admitted for ophthalmoplegia worsening during exercise and decreasing at rest. Clinical examination after exercise, revealed limbs weakness and areflexia, palsy of the left eye abduction and a left ptosis. The level of anti-acetylcholin-receptor antibodies was high. Electrophysiological explorations revealed a decrement at 3 Hz and a increment at 30 Hz, with a reduction in amplitude of the initial motor potential. This patient improved under a combination of guanidine and anticholinesterase drugs. From this case and 9 previously reported cases, we propose 4 criteria for the diagnosis of such neuromuscular blocks: 1) exercising symptoms and signs, including areflexia, 2) presence of anti-acetylcholin-receptor antibodies, 3) reduction of the amplitude of the initial motor potential, with a decrement at 3 Hz, and an increment at 30 Hz, and 4) clinical and electrophysiological improvement under guanidine and anticholinesterasic drugs therapy.

Cholinesterase Inhibitors↗
PubMed1991

[Contribution of early electromyography in the prognostic assessment of facial paralysis].

26 patients suffering from total facial palsy of different etiologies underwent an electromyography of the facial muscles between the 5th and 15th day, and were followed up for one year. The muscular activity in forced mimetics, the blink reflex, and the electric response latency were studied after stimulation of the stylomastoid foramen. Early EMG with detection of one or several motor units is a decisive factor in the final prognosis. The methodology and advantages of EMG are compared to those of electroneuronography.

Adolescent↗
PubMed1990

[Benign, monomelic juvenile amyotrophy of a hand (Hirayama type): a new case report].

Benign, monomelic juvenile amyotrophy of the hand (Hirayama type): new data.--Within the space of a few months a 21-year-old man developed isolated amyotrophy and paresis of the right hand; thirteen years later the clinical picture was unchanged. Medullo-cervical MRI was normal. The EMG confirmed the involvement of the anterior horn. Unilateral chronic distal juvenile amyotrophy located in an upper limb (Hirayama type) was diagnosed on clinical findings. But the spread of electrical abnormalities to the lower limbs suggested a transitional form between this syndrome and other disorders of the anterior horn.

Adult↗
PubMed1990

[Rhythmical myoclonus and tremor at rest disclosing mesencephalic metastasis].

We report a case in which rhythmical myoclonus and tremor at rest revealed a thalamo-subthalamic metastasis from a bronchial carcinoma. Tremor of the upper limbs and face (4 Hz) disappeared with sustained posture and action. A cogwheel phenomenon, hypotonia and disorders of automatic and voluntary movements were also present. Surface electromyographic recordings showed a rhythmical, synchronous activity of the biceps brachialis and triceps muscles at rest. Pathology disclosed lesions of the red nucleus and neighbouring area and severe compression of the substantia nigra which were likely to be the cause of the signs and symptoms.

Adenocarcinoma↗
PubMed1987

[Study of congenital hemiplegia: value of x-ray computed tomography of the brain and of somatosensory evoked potentials].

21 cases of children with congenital hemiparesis have been studied by computerized tomography (CT) of the head and somatosensory evoked potentials (SEP). Computerized tomography is correlated with clinical features and may disclose cerebral lesions and their physiopathological mechanisms. Somatosensory evoked potentials allow a more functional approach of the handicap but are not perfectly correlated with the motor deficit. SEP are correlated with the topography of cerebral lesions showed by CT. These two investigations seem to be interesting and complementary for the exploration of congenital hemiparesis.

Adolescent↗
PubMed1987

[Neuropathies and almitrine. 14 cases].

Previously reported cases of peripheral neuropathies occurring during almitrine therapy had only a few weeks follow-up after having stopped the drug. We have studied clinical and electrophysiological data 6 to 12 months after almitrine had been given up in 9 patients from a group of 14 whose epidemiologic, clinical, electrophysiological and pathological data had been registered. In 7 of them, without any chronic respiratory deficiency, almitrine was administered as almitrine bismésilate and raubasine, and in 7 others (6 with chronic respiratory deficiency) as almitrine bismesilate alone. In patients who had another possible cause of neuropathy, clinical disorders appeared after a lesser total quantity of almitrine (p less than 0.05). Clinical data were suggestive of sensory peripheral neuropathies of feet and lower third of legs. Electrophysiological data suggested distal axonopathy in spite of the absence of denervation: amplitudes of sensory potentials were reduced and nerve conduction velocities were moderately decreased. Biopsies revealed mild neurogenic atrophy of muscles and distal axonopathy. Clinical improvement was very slow and 6 to 12 months later, most of the patients still presented decreased vibration sense and ankle reflexes loss, but all of them were still improving. Amplitudes of sensory potentials and sensory nerve conduction velocities were significantly improved (p less than 0.05) but motor nerve conduction velocities were not (p greater than 0.05). Our study shows: 1) clinical, electrophysiological and pathological data similar to those previously reported; 2) subclinical disturbances of motor functions in lower limbs and sensory functions in upper limbs; 3) some patients presented with unusual signs: posture tremor (3 cases), painful legs and moving toes (1 case); 4) peripheral neuropathies may occur during almitrine therapy even in patients without any chronic respiratory insufficiency; 5) peripheral neuropathies occurred with lower doses in patients with other factors predisposing to neuropathies; 6) patients' improvement was very slow; 7) in 9 cases the imputability of these peripheral neuropathies to almitrine is plausible. We suggest not to prescribe almitrine without caution, especially in patients with other factors of neuropathy. Treatment should be regularly interrupted.

Aged↗