[On 2 cases of cerebral mycosis caused by Torula hystolitica (Cryptococcus neoformans)].
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Biomedical subjects
Publications and source records attributed to R Zappoli.
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A case of mitochondrial encephalomyopathy followed by CT and magnetic resonance is reported. Magnetic resonance showed the cortical lesions of the disease better than CT but CT was superior in demonstrating basal calcium deposits, a nearly constant element of the disease.
The sensitivity of the CNV and somatosensory evoked potentials (SEP) was assessed in shoe industry workers suffering from neurotoxic effects of adhesive solvents. We have examined 21 patients with clear electroneuromiographic and clinical signs of polyneuropathy as well as EEG signs of diffuse brain damage. 10 normal volunteers served as a control group. The maximal motor conduction velocity (MMCV) was considerably reduced in all patients. The maximal sensory conduction velocity (MSCV) was in the lower normal range (or borderline) in 12 patients, whereas in 9 or more severe decrement was detected. In comparison with normal subjects, none of the patients showed clear differences in latency or amplitude of SEP components (p always greater than .2). It was very easy to elicit CNVs over all areas explored and all the 10 patients showed normal characteristics. These results, therefore, suggest that CNV and SEP are not helpful for an early diagnosis of toxic effects of the solvents on the function of the central and peripheral nervous system.
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Two cases have been studied by means of the usual method for eliciting CNV (S-1.5 OR 1 SEC-S-operant response) during and after the end of an episode of prolonged epileptic twilight state with almost continuous strictly unilateral temporal lobe discharge. From the clinical viewpoint in both cases the twilight state, lasting respectively about 12 and 48 hours, was characterized by a slightly clouded consciousness and moderate impairment of awareness and of psychic performances, at times associated with simple and complex psychomotor automatism and hallucinations. The EEG recorded an almost continous left temporal discharge of pseudorhythmic mixed slow waves and sharps. The third case had typical prolonged petit mal states with continuous spike-and-slow-wave activity, impaired intellectual and motor performances (very long reaction time etc.). In this patient for eliciting ERSPs, besides the standard method, we have used a paradigm in which S consisted of a colored slide, with various semantic contents, remaining visible for 5 seconds on a screen. At the trials of the standard paradigm during the epiliptic twilight state, all patients showed they had understood the signal to interrupt (S loud repetitive tone) in the shortest time possible and could clearly distinguish them from the S. The operant response was almost always made with sufficient precision and sometimes with fairly short reaction time, especially by the patients with temporal psychomotor status. During the episodes of prolonged clouded consciosness in all series of trials administered to the patients, no negative slow potential shifts were observed in the averaged EEG recordings obtained from F-T, F-T or F, FCZ and referred to to linked mastoids. On repetition of the examinations some time after the end of the epileptic twilight state, fairly normal ERSPs were obtained in all cases. Taking also into account the results of previous researches, these studies show that the temporal lobe and "centrencephalic" epileptic discharges, under certain conditions, may influence negatively the neurophysiological mechanisms which contribute to the information of complex contingent connections and which also underly the particular attentional, cognitive and sensorimotor functions involved in the inhibiting the appearance of ERSPs probably related to more specific perceptual and integrative functions. Some AA. maintain that negative slow potential shifts express the functional activity of the brain structures, particularly of determined cerebral cortex regions, involved not only in attentional, perceptual, cognitive and psychomotor functioning, but also in information processing (memory recording mechanism). Hence, the negative influence of prolonged temporal lobe or meso-diencephalic epileptic discharges on these structures may explain the almost complete amnesia that patients generally show at the termination of this kind of twilight state.
Six epileptic patients are described to whom the addition of Valproic Acid (VPA) to a previously unsatisfactory antiepileptic treatment caused a toxic encephalopathy. This was characterized by alterations of the state of consciousness in all patients a few days after the beninning of the treatment with VPA. These ranged from a marked drowsiness to coma and were often associated with gastrointestinal and neurological (ataxia, asterixis) symptoms. In all cases very high blood ammonia values were found and the EEGs showed a diffuse slowing down of the activity. After the discontinuation of the drug the toxic symptoms quickly ceased and ammonia values returned to the normal values. It is hypothesized that the interference of VPA on the metabolism of ammonia could play an important role in the pathogenesis of the VPA-induced toxic encephalopathy.
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Auditory and somatosensory evoked potentials were recorded from 10 patients suffering from Friedreich's ataxia. All patients were subjected to audiological tests and EMG-ENG study. Acoustic evoked potentials recordings included brainstem acoustic evoked potentials and long latency components. Peripheral and central components of somatosensory evoked potentials were obtained by stimulating the median nerve at the wrist and elbow. Various abnormalities of the cortical components were observed in all patients for both acoustic and somatosensory evoked potentials. Analysis of brainstem acoustic evoked potentials and of the early components of somatosensory evoked potentials showed a different incidence of abnormalities. The main feature of brainstem acoustic evoked potential changes was the frequent absence of one or more waves; the greatest abnormalities occurred in patients whose disease was of long duration. Long latency components (N85) were significantly prolonged in all but one patient. There was often an absence or reduction of early somatosensory evoked potentials with normal or near normal latencies, even though cortical responses were markedly prolonged. The sensory conduction velocity between stimulation sites at wrist and elbow was normal in all patients. Clinically brainstem acoustic evoked potentials may prove to be a reliable means of monitoring the progression of the disease, while long latency components and somatosensory evoked potentials could be used as complementary procedures in early diagnosis.