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Xavier De Tiège

Publications and source records attributed to Xavier De Tiège.

6 recordsLinked to original sources

Herpes simplex encephalitis: diagnostic problems and late relapse.

A 5-year-old female presented with prolonged afebrile right-sided focal seizures, right brachio-facial paralysis, and dysarthria; consciousness was not altered. Fever appeared 20 hours after onset of neurological symptoms. At admission (day 1) cerebral computerized tomography and cerebrospinal fluid (CSF) analyses were normal including undetectable alpha-interferon (alpha-IFN) and negative herpes simplex virus (HSV) polymerase chain reaction (PCR). Acyclovir was started at a dosage of 60mg/kg/day for 21 days and neurological symptoms improved. Cerebral magnetic resonance imaging (MRI) showed lesions in the left thalamus and left parietal lobe. On day 8, CSF contained an elevated leukocyte count with a predominance of lymphocytes, but alpha-IFN and HSV DNA were still undetectable. Delayed intrathecal synthesis of specific anti-HSV antibodies was found on day 26 and confirmed herpes simplex encephalitis (HSE) diagnosis. Twenty months after this episode, the patient presented with a febrile meningeal syndrome. PCR detected HSV DNA in CSF and cerebral imaging showed a new left temporal lesion. At relapse onset, intrathecal synthesis of specific anti-HSV antibodies had disappeared. Acyclovir was started at a dosage of 60mg/kg/day for 21 days and neurological status improved. At discharge, neurological examination showed right hemiparesis and bucco-facial dyspraxia. Diagnostic problems of HSE diagnosis in children are highlighted. It is suggested that the premature disappearance of intrathecal synthesis of a specific anti-HSV antibody might play a permissive role in the resurgence of cerebral viral replication.

Acyclovir↗

Coexistence of idiopathic rolandic epilepsy and CSWS in two families.

PURPOSE: To report two families combining benign childhood epilepsy with centrotemporal spikes (BCECS) and cryptogenic epilepsy with continuous spike-waves during sleep (CSWS) in first-degree relatives. METHODS: Clinical, EEG, and cerebral imaging data are described. RESULTS: FAMILY 1: The proband was 3 years old at epilepsy onset. First seizures were convulsive, with centrotemporal spikes on EEG. At age 5 years, he had complex partial seizures, psychomotor regression, and centrotemporal CSWS. [(18)F]fluorodeoxyglucose (FDG) positron emission tomography (PET) showed left parietal hypermetabolism. After several antiepileptic drug (AED) trials, valproate (VPA) and ethosuximide (ESM) induced seizure remission, CSWS disappearance, and psychomotor improvement. Learning disabilities, however, persisted. Family history was remarkable for BCECS in his father. FAMILY 2: The proband was 2 years old at epilepsy onset. First seizures were convulsive, with centrotemporal CSWS on EEG. Despite several AED trials including corticosteroids, focal negative myoclonia, atypical absences, and psychomotor regression occurred, leading to severe mental retardation. FDG-PET showed bilateral parietal hypermetabolism. Vagus nerve stimulator was implanted. Her family history was remarkable for BCECS in her father and febrile convulsions in infancy in her mother. CONCLUSIONS: These data suggest the existence of a common genetic basis between BCECS and cryptogenic epilepsies with CSWS. The higher expression in patients with CSWS could be related to other genetic or acquired factors. These data suggest that these epileptic syndromes constitute edges of a continuum.

Cerebral Cortex↗

Postinfectious immune-mediated encephalitis after pediatric herpes simplex encephalitis.

We report a 3-year-old patient who presented a secondary acute neurological deterioration clinically characterized by a partial Kluver-Bucy syndrome, 1 month after the onset of herpes simplex encephalitis. This episode is unlikely due to continuation or resumption of cerebral viral replication but might be related to an immune-inflammatory process. In children, postinfectious immune-mediated encephalitis occurring after HSE are usually clinically characterized by choreoathetoid movements. This type of movement disorder was, however, not observed in this patient. On the basis of this case and a review of the literature, we hypothesize the existence of a spectrum of secondary immune-mediated process triggered by herpes simplex virus cerebral infection ranging from asymptomatic cases with diffuse white matter involvement to secondary acute neurological deteriorations with or without extrapyramidal features.

Brain↗

Limits of early diagnosis of herpes simplex encephalitis in children: a retrospective study of 38 cases.

The prognosis of herpes simplex encephalitis (HSE) depends on the early and appropriate administration of specific antiviral therapy. We retrospectively reviewed 38 cases of children with proven HSE, to evaluate the reliability of polymerase chain reaction results, according to the time of cerebrospinal fluid (CSF) sampling. Initial negative results were observed in 8 of 33 CSF samples drawn before day 3 of the disease and were significantly associated with a low level of protein and <10 leukocytes/mm3 in the CSF.

Adolescent↗

Brain function in the vegetative state.

Positron emission tomography (PET) techniques represent a useful tool to better understand the residual brain function in vegetative state patients. It has been shown that overall cerebral metabolic rates for glucose are massively reduced in this condition. However, the recovery of consciousness from vegetative state is not always associated with substantial changes in global metabolism. This finding led us to hypothesize that some vegetative patients are unconscious not just because of a global loss of neuronal function, but rather due to an altered activity in some critical brain regions and to the abolished functional connections between them. We used voxel-based Statistical Parametric Mapping (SPM) approaches to characterize the functional neuroanatomy of the vegetative state. The most dysfunctional brain regions were bilateral frontal and parieto-temporal associative cortices. Despite the metabolic impairment, external stimulation still induced a significant neuronal activation (i.e., change in blood flow) in vegetative patients as shown by both auditory click stimuli and noxious somatosensory stimuli. However, this activation was limited to primary cortices and dissociated from higher-order associative cortices, thought to be necessary for conscious perception. Finally, we demonstrated that vegetative patients have impaired functional connections between distant cortical areas and between the thalami and the cortex and, more importantly, that recovery of consciousness is paralleled by a restoration of this cortico-thalamo-cortical interaction.

Cerebral Cortex↗