[Visual impairment due to optic neuropathy in 2 patients on amiodarone, and ethambutol and isoniazide therapy, respectively].
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Biomedical subjects
Publications and source records attributed to W Verslegers.
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The syndrome of acquired aphasia and convulsive disorders in childhood has received ample discussion since the initial description by Landau and Kleffner in 1957. Despite numerous investigations considering the linguistic and epileptic phenomena of the syndrome, the symptomatology still remains of a puzzling nature. Two aspects of the syndrome, the acquired nature of the aphasia and the type of linguistic symptomatology, have not been discussed thoroughly. In our case not only a history of developmental language pathology was present but language symptomatology also revealed a predominantly motor aphasia during a language deterioration phase. A careful review of the literature as presented here yields data in agreement with our findings. First we found further evidence in the literature that Landau-Kleffner's syndrome is not exclusively a primarily receptive language disturbance. Secondly, evidence in favour of a developmental type of Landau-Kleffner's syndrome was found in 25 additional cases. In this group of children with developmental language disturbances at least two distinct types seem to emerge. A group in which the already existing developmental language disturbances did not fluctuate during the course of the illness and a group in which a considerable deterioration of the developmentally disturbed language functions took place. The different patterns of language evolution not only seem to suggest the possibility of an acquired language pathology within a context of developmental language disturbances but also a congenital onset of the syndrome of Landau-Kleffner as the probable cause of developmental language pathology.
The single- and repeated-dose pharmacokinetics of sabeluzole have been determined in six elderly patients with [senile] dementia of the Alzheimer type. After a single oral dose of 10 mg sabeluzole, the peak plasma concentration was attained at 1 to 4 h; it averaged 42 ng.ml-1. On repeated dosing (10 mg b.d.), steady-state was virtually attained after 3 days of treatment. Steady-state mean trough and peak plasma concentrations fluctuated between 53 and 94 ng.ml-1. The mean terminal half-life after a single dose and at steady-state was of the order of 33 h. Sabeluzole was well tolerated and at the end of treatment, no systematic changes in blood haematology, biochemistry or urinalysis were seen.
Three patients presented with an acute agitated delirium as the earliest sign of bilateral posterior cerebral artery infarction. All patients showed a unique slow progressive deterioration with a remarkably long interval between the first neuropsychological and subsequent visual and neurological symptoms, ranging from 3 to 30 days. Repeated CT scans demonstrated hypodensities in the posterior artery territory only after a long interval of 9-12 days, in case 3, and between 33 and 48 days in case 2. In the latter case MRI was still negative 33 days after onset. In 2 patients the cortical blindness was complicated with anosognosia for blindness. Clinical condition worsened progressively in all patients, leading to death, probably due to brainstem infarction. In all 3, the combination of clinical and radiological findings indicated a 'top of the basilar' distribution, which could be confirmed in two by autopsy.
A 78-yr-old woman presented with transient echolalia and palilalia. She had suffered from Parkinson's disease for 2 yr. Routine laboratory examination showed hypotonic hyponatremia, but was otherwise unremarkable. Brain mapping revealed a bifrontal delta focus, more pronounced on the right. Single photon emission computed tomography (SPECT) of the brain with technetium-99m labeled d,l hexamethylpropylene-amine oxime (99mTc-HMPAO), performed during the acute episode showed relative frontoparietal hypoactivity. Brain mapping performed after disappearance of the echolalia and palilalia, which persisted only for 1 day, was normal. By contrast, SPECT findings persisted for more than 3 wk. Features of particular interest in the presented patient are the extensive defects seen on brain SPECT despite the absence of morphologic lesions, the congruent electrophysiologic changes and their temporal relationship with the clinical evolution.
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Following a cardiac arrest, a 21-year-old man developed a Parkinson syndrome. This was due to, as shown by brain computerized tomography (CT) and magnetic resonance imaging (MRI), symmetrical infarctions of the basal ganglia, especially the globi pallidi. The levels of homovanillic acid (HVA) in the CSF were lower than normal, pointing to a possible alteration of the central dopaminergic activity. An alteration of the opioid system may also be supposed because of the extremely high levels of methionine-enkephalin (Met-Enk).
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Due to methanol intoxication, a 38-year-old male developed permanent parkinsonism with visual impairment. Brain computerized tomography (CT) and magnetic resonance imaging (MRI) revealed cystic resorption of the putamen. An alteration of the central noradrenergic activity and the opioid system can be assumed because of increased dopamine beta-hydroxylase (D beta H) activity and decreased methionine-enkephalin (Met-Enk) levels in the cerebrospinal fluid (CSF).