B Vitrani

University of Trieste

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Giovanni Masè

Azienda Ospedaliera Santa Maria Degli Angeli

Emanuele Biasutti

University of Udine

Marino Zorzon

University of Trieste

Giuseppe Cazzato

Istituto Nazionale di Fisica Nucleare, Sezione di Firenze

Giulia Tasca

Istituto Oncologico Veneto

F Urbán

Ca' Foncello Hospital

Renata Longo

Ospedale dei Bambini Vittore Buzzi

L Capus

Vall d'Hebron Hospital Universitari

Lucia Antonutti

Ospedale di Cattinara

M Frezza

Ospedale di Cattinara

Cooperative Institutions

University of Trieste

Ospedale di Cattinara

Istituti di Ricovero e Cura a Carattere Scientifico

Vall d'Hebron Hospital Universitari

University of Padua

Azienda Ospedaliera Santa Maria Degli Angeli

Cleveland Clinic

Istituto Oncologico Veneto

Agostino Gemelli University Polyclinic

Azienda Ospedaliera di Padova

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ACUTE ENCEPHALOPATHY AND POLYNEUROPATHY AFTER DISULFIRAM INTOXICATION

Alcohol and Alcoholism (1995)

Marino Zorzon Giovanni Masè Emanuele Biasutti B Vitrani Giuseppe Cazzato

A chronic alcoholic who had ingested a very high dose of disulfiram (29 g over a 1-week period) without simultaneous alcohol intake developed an acute encephalopathy and a severe flaccid tetraparesis that worsened over the course of several days, even after the intake of the drug had stopped. Recovery was both slow and incomplete. One year after intoxication, the patient still had distal weakness in the arms and legs, and hypesthesia in the hands and feet.

Tetraparesis

Hypesthesia

Disulfiram

Drug withdrawal

Toxic encephalopathy

Drug intoxication

10.1093/oxfordjournals.alcalc.a045773

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Citations (10)

Immediate prognosis of primary intracerebral hemorrhage using an easy model for the prediction of survival

Acta Neurologica Scandinavica (1995)

Giovanni Masè Marino Zorzon Emanuele Biasutti Giulia Tasca B Vitrani

We reviewed the medical records and CT scans of 138 patients hospitalized for spontaneous supratentorial hemorrhage and conservatively treated. Seventeen clinico-anamnestic variables and five CT desumed findings were collected. Using univariate analysis we found eight significant predictors of 30-day mortality: intraventricular spread (IVS) of blood, volume of the hemorrhage, Glasgow Coma Scale (GCS) score, midline shift, hyperglycemia, pupillary abnormalities, limb paresis and gaze deviation. With multivariate logistic regression analysis we found three independent predictors of 30-day mortality: IVS of blood, volume of the hemorrhage and GCS score. Using these three independent variables we developed an easy model which allows an immediate estimate of the probability of survival with a high degree of sensitivity and specificity.

Paresis

Univariate analysis

Midline shift

Univariate

10.1111/j.1600-0404.1995.tb07011.x

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Trigeminal neuralgia due to contralateral meningioma of the posterior cranial fossa.

Journal of Neurology Neurosurgery & Psychiatry (1994)

Giovanni Masè Marino Zorzon L Capus Emanuele Biasutti B Vitrani

Letters to the Editor sheaths, and anterior horn cells but no abnormalities in dorsal and ventral roots or in dorsal root ganglia.3A sural nerve biopsy study indicated axonal neuropathy.1 A necropsy study showed destruction of ante- rior horn cells but no abnormalities of dor- sal root ganglia and peripheral nerve.4Therefore the damage in this neuropathy could be located in the axon or in the nerve cell body.The studies carried out on our patient are characteristic of a pure axonal degeneration, but a coexisting lesion in the anterior horn cell cannot be ruled out.

Posterior cranial fossa

Posterior fossa

10.1136/jnnp.57.8.1010

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Citations (8)

Development of myasthenia gravis during interferon-alpha treatment for anti-HCV positive chronic hepatitis.

Journal of Neurology Neurosurgery & Psychiatry (1996)

Giovanni Masè Marino Zorzon Emanuele Biasutti B Vitrani Gerardo Cazzato

Myasthenia gravis in a patient with chronic active hepatitis C during inter- feron-a treatment Batocchi et all recently reported the occur- rence of autoimmune myasthenia gravis dur- ing interferon-a (INF-a) treatment in two patients with malignancies.We report a patient who developed myasthenia gravis after INF-a treatment for chronic hepatitis C. A previously healthy 54 year old man developed malaise and dyspepsia three years ago.Increased serum concentrations of ala- nine aminotransferase and aspartate aminotransferase led to a serological diagnosis of hepatitis C infection.Liver biopsy showed a histological picture of chronic active hepatitis.Two years later, in March 1993, the patient received INF-a-nl (Wellferon, Wellcome, UK) subcutaneously at a dose of 9 x 106 U on alternate days.After nine

Hepatitis C

10.1136/jnnp.60.3.348-a

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Citations (33)

Proton magnetic resonance spectroscopy during transient global amnesia

Journal of the Neurological Sciences (1998)

Marino Zorzon Renata Longo Giovanni Masè Emanuele Biasutti B Vitrani

Transient global amnesia

Cortical Spreading Depression

Proton magnetic resonance

Creatine

Depression

10.1016/s0022-510x(98)00029-x

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Transient Global Amnesia and Transient Ischemic Attack

Stroke (1995)

Marino Zorzon Lucia Antonutti Giovanni Masè Emanuele Biasutti B Vitrani

Background and Purpose The purpose of the present study was to make an attempt to ascertain the etiology of transient global amnesia (TGA), which is still disputed more than 30 years after the first description of this clinical entity. Methods In a case-control study, we compared the prevalence of vascular risk factors in 64 TGA patients with 64 first-ever transient ischemic attack (TIA) control subjects and 108 normal community-based control subjects matched for age and sex. We prospectively studied the vascular events and mortality rates of the TGA cases and of the TIA control subjects. Then we compared the outcome of the two groups using actuarial analysis based on survival curves. Results We did not find evidence of an increased risk of TGA associated with any vascular risk factor. In contrast to TIA control subjects, no TGA patient suffered stroke, myocardial infarction, or TIA during the follow-up period. Migraine was more common in TGA patients than in both normal and TIA control subjects. In three patients (4.5%), the TGA was eventually considered to be of epileptic origin. Conclusions The results of our case-control and longitudinal studies point to the conclusion that TGA and TIA do not share the same etiology. Since half of our patients had a precipitating event in their history, it is reasonable to hypothesize that spreading depression may play a role in TGA. The significant positive association between migraine and TGA may support this hypothesis. Epilepsy may mimic TGA in a minority of cases.

Transient global amnesia

Etiology

Stroke

Depression

10.1161/01.str.26.9.1536

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Citations (152)