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Biomedical subjects

M Giroud

Publications and source records attributed to M Giroud.

At least 181 records · Page 10Linked to original sources
PubMed1987

[Neuroendocrine disorders observed in the post-critical phase in epileptic patients].

In 10 epileptic patients with generalized seizures, plasma levels of ACTH, prolactin, FSH, LH, TSH, were measured first within 60 minutes after the crisis, then 3 to 5 days later without changes in antiepileptic drugs. Within 1 hour after the seizure, a significant rise of ACTH and prolactin 3 - 4 folds the levels observed in the 2nd measure was present. This was compared to measures made within 1 hour after a syncope in which case it was not present. The post-critic rise of ACTH and prolactin would appear to be a characteristic of generalized epileptic seizures.

Adolescent↗
PubMed1987

[Complications observed in the surgery of aneurysms of the circle of Willis in a perspective of early operation].

This report concern a series of 100 consecutive patients operated by direct attack for intracranial ruptured aneurysms (mortality: 14%, complete removal: 70%). 35% of this patients have been early operated before the 96e hour. In this series, only one case of spasm was observed. But we have observed other neurosurgical complications, analysed and compared to the postoperative course of the patients who had delayed operations.

Circle of Willis↗
PubMed1987

[Somnambulism and migraine in children. A non-fortuitous association].

Looking for frequency of somnambulism in 3 homogeneous groups of children, a first group of migrainous children, a second group of epileptic children and a third group of normal children, the authors have observed that an antecedent of somnambulism existed in 28% of migrainous children, when it was found in only 6% of epileptic children, and in 5% of normal children. This significant difference demonstrates that the association of migraine and somnambulism is real. The possibility that migraine and somnambulism appearing in the same patient at different ages might be the expression of a same neurochemical disorder is discussed. The practical interest to know this association is that somnambulism may be a real clinical marker of migrainous background that should be searched for in every patient presenting with chronic cephalalgia.

Adolescent↗
PubMed1986

[Etiological diagnosis errors corrected by x-ray computed tomography in acute hemiplegia].

Correlations between the clinical diagnosis on admission and the aetiological diagnosis revealed by computerized tomography (CT) were studied in 248 cases of acute hemiplegia. In 15% of the cases, hemiplegia was not due to a cerebral vascular accident. This mechanism was overestimated in 9% of the cases and missed in 14%. Ischaemia was overestimated in 15% of the cases and haemorrhage in 45%. With regard to transient deficit, CT scans showed that ischaemia was responsible for only 72% of acute hemiplegias, 28% of them being due to haematoma, tumour or subdural haematoma. In many cases where subdural haematoma or tumour was suspected on clinical grounds, CT confirmed that the suspicion was founded.

Acute Disease↗
PubMed1986

[Post-crisis elevation of adrenocorticotropic hormone and prolactin in epileptic children].

In six children, aged from 8 to 12 years, presenting with primary generalized epilepsy a significant rise in plasma ACTH and prolactin levels (as compared with levels measured 5 days later) was observed either during a generalized seizure demonstrated by EEG (3 cases) or within 1 hour of a generalized seizure (3 cases). The neurophysiological basis for these post-epileptic endocrine disturbances is a sudden depression of dopaminergic and GABA-ergic pathways. As a result, these endocrine changes, already well documented in adults, may be regarded as a good biological marker of the epileptic origin of a paroxysmal attack.

Adrenocorticotropic Hormone↗
PubMed1986

[Elevation of gamma-glutamyltransferase levels in treated epileptic patients].

Plasma levels of gamma-glutamyl transpeptidase were measured prospectively in 75 epileptic patients treated with one of the following drugs: phenobarbitone (n = 20), phenytoin (n = 23), carbamazepine (n = 18) or sodium valproate (n = 14). A significant increase in gamma-glutamyl transpeptidase levels was observed from the 7th day of treatment onward. The increase was particularly pronounced in the phenytoin group, with mean and maximum values of 104.10 and 215 mU/ml respectively, followed by the phenobarbitone group (mean 68.15, max. 124 mU/ml), the carbamazepine group (mean 49.83, max. 100 mU/ml) and the sodium valproate group (mean 35.42, max. 70 mU/ml). This was due to enzyme induction being highest with phenytoin and phenobarbitone which are strongly liposoluble and have prolonged half-life. Any epileptic patient with plasma gamma-glutamyl transpeptidase levels higher than those found in this study may be suspected of having viral or alcoholic hepatitis.

Adult↗
PubMed1986

A case of progressive familial encephalopathy in infancy with calcification of the basal ganglia and chronic cerebrospinal fluid lymphocytosis.

The authors report the ninth case of progressive familial encephalopathy in infancy, with calcification of the basal ganglia and chronic cerebrospinal fluid (CSF) lymphocytosis, as recently described by Aicardi and Goutieres. The encephalopathy appears during the first year of life with bilateral spasticity, continuing microcephaly, abnormal eye movements, and a rapid course toward a behavioral vegetative state. In every case, there is a mild lymphocytosis in the CSF and brain atrophy with calcification of the lenticular nuclei. No evidence of an infectious disease has been discovered. This syndrome constitutes a distinct type of leukodystrophy, transmitted as an autosomal recessive trait. Our case is a reminder that the presence of CSF lymphocytosis in infants, with encephalopathy and calcification of the lenticular nuclei, may be due to genetic degenerative encephalopathy.

Atrophy↗