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H Vespignani

Publications and source records attributed to H Vespignani.

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

Lafora disease is not linked to the Unverricht-Lundborg locus.

Lafora disease and Unverricht-Lundborg disease are two forms of progressive myoclonus epilepsies (PME). Recently the gene for Unverricht-Lundborg disease (EPM1) was mapped to chromosome 21q22.3. Using three highly polymorphic DNA markers (D21S212, PFKL, and D21S171) which flank the EPM1 locus, we performed linkage analysis to investigate whether or not the EPM1 gene is also implicated in Lafora disease. Linkage was excluded in three North-African pedigrees each comprising at least two affected individuals. This result suggests that differential diagnosis of Lafora disease and Unverricht-Lundborg disease may be facilitated by molecular genetic analysis.

Adolescent↗
PubMed1994

[Herpetic meningoencephalitis in the elderly. Apropos of 13 cases].

In a retrospective analysis of 13 cases of Herpes simplex encephalitis (mean age: 67.2 +/- 6.4 years; ten women, three men), the authors conclude that this infection is more often due to Herpes simplex virus 1 in the elderly. Diagnosis is difficult at an early stage, and must be suspected in case of confusion (9/13), especially feverish (11/13), associated with neurological signs (10/13), and particularly epilepsy (5/13). It requires a lumbar puncture which collect a clear and lymphocytic fluid. Prognosis of this encephalitis depends on early diagnosis and an presumptive therapy with acyclovir. EEG is helpful showing periodic activity (10/13). CT scan and MRI can show unspecific abnormalities, but often too late. Laboratory findings will secondarily confirm the diagnosis quite frequently, using new Elisa methods. Polymerase chain reaction allows earlier diagnosis. Geriatric cases seem more often due to reinfection or to endogen virus reactivation rather than to primary infection.

Aged↗
PubMed1994

[Subacute leukoencephalopathy of the rhombencephalon after pituitary radiotherapy].

Two patients had early delayed leucoencephalopathy mainly confined to the brainstem after radiotherapy for pituitary tumours. To our knowledge, we report the first MRI description. The patients had somatotroph cell adenomas (associated with prolactin secretion, patient 2). Surgical removal of the adenomas were complete (patient 1) and partial (patient 2). Both underwent pituitary irradiation: patient 1, 55.8 Gy (31 x 1.8 Gy); patient 2, 54 Gy (27 x 2 Gy). Six weeks after completion of radiation, the patients had low vigilance, sleepiness, cerebellar symptoms, optic neuropathy (patient 1), CSF inflammatory reaction. T2-weighted MRI scans showed hypersignal in brainstem, cerebellar peduncles (both patients), temporal lobe white matter (patient 2). T1-weighted images showed hyposignals, pseudonecrotic and contrast-enhanced images in brainstem (patient 1). Both patients responded to intravenous then oral steroid treatment with a progressive and complete clinical recovery. Radiological abnormalities improved with clinical statement. Present characteristics support a demyelinating mechanism of early delayed cerebral radiation injuries.

Adenoma↗
PubMed1992

[Value of transcranial Doppler ultrasonography in patients with suspected brain death].

Transcranial Doppler ultrasonography (TCD) is a non invasive technique which assesses blood flow velocitics in basal cerebral arteries. Specific patterns have been observed in brain death. In a continuous series of 72 patients, the TCD recordings from the intracranial internal carotid and middle cerebral arteries were compared with the results from the usual investigations for brain death, such as electroencephalogramme (EEG), and arteriography. All the patients were clinically brain dead: Glasgow score of 3, apnoea, bilateral mydriasis, loss of cortical function and cerebral reflexes. This clinical diagnosis was confirmed by and isoelectric EEG with or without angiographic circulatory arrest. Two characteristic patterns were identified: an oscillating to and fro signal, with a positive sharp systolic peak and a negative diastolic reflux; and a systolic peak without any diastolic component. The absence of signal on both sides did not allow any conclusion, except when this pattern occurred during follow-up. The oscillating pattern was seen on both sides in 60 patients (83%), and, in 3 other patients, only on one side, always combined with a contralateral systolic peak pattern, in 3 other patients. A bilateral systolic peak pattern was identified in 7 patients (10%). The TCD results were compared with angiography in 37 cases. TCD circulatory arrest preceded angiographic arrest by six hours in three cases. Hypotension was the main limitation to this technique. n the other hand, TCD may be used in patients treated with sedative drugs. The non invasive character of TCD, its low cost, the possibility of repeating it at the patient's bedside make TCD a very interesting diagnostic tool.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

[Papilledema and dural fistula].

A retrospective analysis of three cases of papilledema was made, initially attributed to idiopathic raised intracranial pressure on the basis of the following data: symptoms and signs of raised intracranial pressure, no other neurological signs, normal electroencephalogram, normal computerised tomography, and normal cerebrospinal fluid. The discovery of a dural arteriovenous malformation was made only after a period over six months, by cerebral angiography. After a survey of medical data concerning the incidence of papilledema in dural fistulae, a description of the supposed pathogenic mechanisms of papilledema formation in this disease is proposed. Venous hypertension was found to be the main factor leading to papilledema. It could be in relation with obstruction of the involved venous sinus, and with the high level of blood flow of the dural arteriovenous malformation. It appeared that drainage with involvement of subarachnoid veins was the main characteristic for arteriovenous malformations to be directly responsible for papilledema. The possible lack or delay of suggestive signs such as intracranial bruit and the potential seriousness of the vital and visual prognosis led us to routinely carry out angiologic investigations comprising first doppler ultra-sound of the cervical vessels and secondly cerebral angiography, before diagnosing benign raised intracranial pressure.

Adult↗
PubMed1989

[Intracerebral cavernous angioma].

Thirty four cases (18 operated, 16 non-operated), of cavernous angioma are reported. The presenting symptoms and signs were epilepsy in 22 cases, neurologic deficit in 9 and cerebromeningeal hemorrhage without vigilance disorders in 3. In the operated group 15 angiomas were supratentorial, 3 were subtentorial. In the non-operated group symptoms and signs were epilepsy in 11 cases and a neurologic deficit related to a brain stem lesion in 4/5 cases. Follow-up of 2 to 39 years after the first fit episode and of 1 to 7 years after initial diagnosis suggested that the risk of hemorrhage is low. Indications for neurosurgery are discussed as a function of the site of the angiomas and of the operative hemorrhagic risk.

Adolescent↗
PubMed1988

[Neurological manifestations of alveolar echinococcosis].

Among 78 cases of alveolar echinococcosis reported in Lorraine, France, 5 had neurologic complications which in 3 cases revealed the disease. Results of parasitic tests are discussed and emphasis is placed on differences between this disease and hydatidosis. Encephalic localizations (3 cases) were multiple making neurosurgery impossible. The outcome was fatal in 2 cases: 1 month after the initial neurologic signs in the absence of treatment (case 1) and 4 months after treatment with flubendazole (case 2). This drug was however effective in the 3rd case (hepatic, pulmonary and cerebral form) with follow-up now at 4 years. Epidemiologic, histopathologic, clinical, diagnostic characteristics and course of these encephalic localizations are reviewed. Spinal localizations (2 cases) presented with a picture of spinal cord compression. After laminectomy and flubendazole, the course was marked by relapse with death in one case and a satisfactory neurologic course with a 4 year follow-up in the other one.

Aged↗
PubMed1987

[Electroencephalographic impact of propofol anesthesia].

Two groups of patients were studied. In group A, propofol was used alone, given by repeat injections of 2.5 mg X kg-1 in 30 s, in 5 patients undergoing percutaneous thermocoagulation of the Vth cranial nerve. In group B, a series of 12 patients undergoing lumbar disc hernia surgery, propofol was given as a bolus of 2.5 mg X kg-1 in 60 s followed by an infusion of 7 to 12 mg X kg-1 X h-1 together with vecuronium and fentanyl. The EEG recording was carried out during the whole length of anaesthesia and for 1 h after its end. The recordings were all stereotyped, within five successive phases: the awake physiological pattern (phase 0) was desynchronized a mean 52 s after the start of the propofol injection; it was followed by an increase in amplitude of the alpha rhythm (phase I); within a mean of 132 s were seen phases II to V. Phase V corresponded to surgical anaesthesia and could be kept up by a rate of infusion of 9 mg X kg-1 X h-1 propofol. An increase in this rate gave rise to burst suppressions which lasted as much as 15 s or more, and disappeared very quickly when the infusion rate was slowed. After stopping the anaesthesia, the EEG phases were quickly reversed, V to 0: in a mean of 11.1 min, the EEG pattern had returned to the awake state (extremes 4.3 to 19 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1987

[Five years after a first epileptic seizure appearing late in life].

A first epileptic seizure in adulthood leads to fear a brain tumor and other important features of late epilepsies have received little attention. We have analyzed the etiologies in a group of 392 patients consecutively seen from 1977 to 1980. Our data are in keeping with previously reported data. One hundred and eighty patients were followed for five years or more. Fifty eight had only a single seizure (only 23 were treated, and 20 stopped therapy). Seizures recurred in 122 patients (97 untreated). The characteristics of recurrence have been analyzed. Some predictive factors appear significant. Socio-professional results have been considered. By and large, the prognosis was good for 75 p. 100 of patients.

Adult↗
PubMed1986

[Value of mazindol in Gélineau's disease. Apropos of 10 cases].

Ten narcoleptic patients were treated daily with Mazindol 2-6 mg for 42.2 months (31-63 months). The response was excellent on narcoleptic attacks in 6 and on cataplexy in 7 cases. However, the nocturnal sleep disturbance persisted unchanged. The improvement was poor in 1 case and inexistant in 1 subject. Minor side effects (dry mouth) occurred in 3 cases, and urinary retention obliged to stop the medication in 2 cases.

Adolescent↗