[Ageusia caused by terbinafine].
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Biomedical subjects
Publications and source records attributed to J Peres Serra.
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Peduncular hallucinations are generally associated with lesions of the midbrain. We describe a 68-year-old man who developed left hemiparesis, paraesthesias on the left side and vivid visual hallucinations, suggesting peduncular hallucinosis. MRI demonstrated a right posterior thalamic infarct as the sole lesion.
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The association of trigeminal neuralgia and Arnold-Chiari malformation (ACM) is uncommon. We report two cases of trigeminal neuralgia as the first and single clinical feature of an ACM. The pathophysiological relationship between ACM and trigeminal malformation is discussed. Also, the need for magnetic resonance imaging in trigeminal neuralgia is emphasized, as this is a noninvasive study which may provide valuable etiological information and prevent the progression of the disease.
Diffuse leptomeningeal melanoma is an uncommon condition; its diagnosis is difficult, and requires the detection of atypical melanic cells in the CSF or the performance of meningeal biopsy. We report a 34-year-old patient with progressive symptoms of intracranial hypertension of 2 months duration, in whom meningeal biopsy was required for a definitive diagnosis. The patient's age, the neuropathological abnormalities and the images of computed tomography scan (CT), and also a through clinical and paraclinical investigation, led us to the conclusion that the patient had diffuse primary leptomeningeal melanoma.
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A case of insulinoma is reported with disease of the peripheral nervous system and pathological demonstration of a primary nerve lesion. On admission the female patient gave a history of hypoglycemic episodes and paresthesias and loss of strength in both hands. Physical examination disclosed loss of strength and atrophy of the distal musculature of the extremities, predominating in the upper ones and without fasciculations. Muscle biopsy demonstrated changes suggestive of neurogenous atrophy, and biopsy of the sural nerve showed reduction of the myelin fibers with axonal degeneration, important signs of demyelinization, and remyelinization figures. The neuropathy was unchanged two months after removal of the insulinoma. The exact location of the nerve lesion in insulinoma is controversial, some authors placing it in the peripheral nerve while others believe the motor neurons of the anterior horns to be diseased. The pathological findings in the present case suggest primary nerve disease, but an associated lesion of the anterior horns could also be present.
The authors report three cases of multiple sclerosis which presented, during its course, paroxysmal attacks, also denominated brain-stem seizures. They review the literature with special reference to the incidence and the clinical forms of these paroxysmal phenomena, and they discuss the proposed pathogenic mechanisms. According to the authors, the literature review and the clinical picture of their cases, have shown a direct relation between these paroxysmal symptoms and a neighboring bout of the disease. They may also appear as an isolate "abortive bout". A partially demielinated lesion at brain-stem level, possibly by a transversely spreading ephatic activation, is suggested to explain the clinical phenomena.
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BACKGROUND: Fasciculation, double discharge, myokymia and neuromyotonia are different kinds of involuntary muscular activity that originate in ectopic discharges of the motor axons. Electrophysiological studies are needed in all cases for the diagnosis. Non rigorous electrophysiological studies in some cases is the cause of the historically unclear nosological delimitation of the neuromyotonic syndromes. OBJECTIVE: To report the clinical picture and electrophysiological findings in patients with congenital neuromyotonia. PATIENTS AND METHODS: Four patients with congenital neuromyotonia were studied. Electrophysiological exam included nerve conduction measurements, study of the after-discharges and conventional EMG. Spontaneous discharges were displayed after applying a low pass filter, signal trigger and delay line. RESULTS: In one case positive motor features predominate (continuous muscle fiber activity). On the contrary, two cases, showed neuropathic deficitary signs with a Charcot-Marie-Tooth type II disease phenotype; neuromyotonia was, in both cases, an electrophysiological feature. In the last patient, motor signs were limited to the facial muscles but electrophysiological study discovered generalized neuromyotonia. Treatment with carbamazepine or oxcarbazepine was useful in the four cases. CONCLUSION: Congenital neuromyotonia is a clinically heterogeneous syndrome with uniform electrophysiological features that permit its qualification.
In the necropsy exam of the brains of 13 patients with acquired immune deficiency syndrome (AIDS) cerebrovascular lesions were seen in 5 cases, three of them having AIDS encephalopathy. Hyalinosis was noted in 3 cases, and endarteritis obliterans and fibrinoid necrosis in one case each; both of them had associated perivascular lymphocytic infiltrates. Cerebral infarction was observed in one case, but no hemorrhages were seen. The neuropathological anomalies in four children affected with the AIDS are reported too, being an extensive calcified vasculopathy and changes suggesting active AIDS encephalopathy the main findings.
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Spatial and temporal dissemination of demyelinating lesions continue to provide the basis for diagnosing multiple sclerosis (MS). We describe 20 patients (from a series of 234 with MS) who experienced flare-ups consistent with sensory suspension syndrome (SSS). The presence of syringomyelic cavities (non communicating syringomyelia) was ruled out by nuclear magnetic resonance imaging (NMR). We discuss the possible locations of lesions responsible for this syndrome: the trigeminus, dorsal root entry zones, anterior medullary white matter, and the mid-lateral portion of the spinothalamic tract. MS should be included as a differential diagnosis in young patients presenting with SSS.