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A García Pastor

Publications and source records attributed to A García Pastor.

2 recordsLinked to original sources

[Acute encephalopathy and myoclonic status induced by vigabatrin monotherapy] .

Vigabatrin (VGB) is a new antiepileptic drug useful in refractOry partial seizures. Psychosis as a secondary effect of VGB is well known. This drug may even induce new epileptic seizures. We report a 69-year-old hypertensive patient with multiple cerebral infarcts. She was diagnosed as having late onset symptomatic partial epilepsy (complex partial seizures and generalized secondary motor partial seizures). She had been receiving VGB 3 g/day in monotherapy. She came to the emergency room in a psychotic state with new epileptic seizures. We performed an EEG and video during the ictal phase. The patient was awake, conscious and partially oriented. The video showed generalized myoclonic jerks involving facial and limb muscles, separated by non-convulsive intervals lasting three minutes. The EEG showed spike and wave discharges over a diffuse slow-wave background activity. The patient was conscious throughout the recording. The electroclinical picture was considered as an encephalopathy-associated generalized myoclonic status. VGB was replaced by phenytoin. Two weeks later, and after a clinical improvement, a new recording showed the disappearance of signs of encephalopathy and the myoclonic status. Epileptic seizures induced by VGB are well reported. Several pathogenic mechanisms have been suggested. In our case the myoclonic status was related to a non-dose dependent encephalopathy induced by VGB. The electroclinical improvement after withdrawal of the drug supports this possibility.

Acute Disease↗

[Intracranial tumors simulating transient ischemic attacks].

INTRODUCTION: Occasionally intracranial tumors present a clinical picture similar to that seen with transient ischemic attacks (TIA). The mechanism for this is not clear. The differential diagnosis of these two disorders is important since their treatment is quite different. CLINICAL CASES: Two men and two women aged between 53 and 72 years of age, with no known cardiovascular risk factors, complained of one or several episodes of neurological deficit (hemisensitive deficits, transient blindness and isolated aphasia), lasting between 3 minutes and 6 hours. Neuroimaging investigations (CT and MR) showed images compatible with space occupying lesions localized to the convexity (parietal, frontotemporal and frontoparietal) and in one case at the edge of the sphenoid bone. Three patients were operated on. The lesions were confirmed as tumors (two cases of meningiomas and one of glioblastoma). Symptoms did not recur after a mean follow up period of nine months. Various mechanisms have been suggested to explain this phenomenon: vascular compression due to pressure from the mass, changes in intracranial pressure, vascular steal phenomenon, negative focal seizures, Leao s cortical depression and others. The absence of risk factors which would justify a vascular cause, the correlation between localization of the tumour and the clinical signs, and the disappearance of symptoms following surgery would seem to support the hypothesis that in our cases the symptoms observed were due to intracranial space occupying lesions. CONCLUSION: The presence of an intracranial tumour should be ruled out by using neuroradiological investigations in patients complaining of transient episodes of neurological deficits.

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