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Biomedical subjects

T De Broucker

Publications and source records attributed to T De Broucker.

At least 19 recordsLinked to original sources

[Treatment of tuberculous meningitis].

INTRODUCTION: Tuberculous meningitis and brain tuberculomas are currently rare in the western world but remain serious. Improved outcome requires early recognition and treatment of these conditions. STATE OF ART: Treatment is usually begun before diagnostic confirmation. Therapeutic principles are now better defined thanks to recent recommendations and studies. Antituberculous therapy begins with two months of a combination of four drugs: isoniazid, rifampicin, ethambutol and pyrazinamid. Then follows a longer phase of bitherapy with isoniazid and rifampicin, lasting at least four months but usually extended to seven or ten months as a precaution. Patients at risk of toxic neuropathy should receive pyridoxine supplementation. Corticosteroids must be systematically added during the first eight weeks of treatment, beginning with high dose before progressive tapering. Hyponatremia is common, often induced by emesis and cerebral salt wasting syndrome. Therefore saline supply rather than water restriction is required. Non-obstructive hydrocephaly can usually be managed with diuretic therapy including acetazolamid, sometimes complemented by serial lumbar punctures. Neurosurgical interventions are rarely needed. Monitoring of treatment tolerance and efficacy is mainly clinical. Central nervous system imaging and cerebro-spinal fluid analysis are only required to explain clinical deterioration. CONCLUSION: With adequate and prompt anti-tuberculous, anti-inflammatory and supportive treatment, the prognosis of central nervous system tuberculosis can be greatly improved.

Adrenal Cortex Hormones↗

[Isoniazid induced neuropathy: consider prevention].

INTRODUCTION: Antituberculous treatment is effective but has numerous side effects. Among these isoniazid induced neuropathy is easily preventable. CASE REPORT: A female patient of 42 years, infected with HIV, presented with general deterioration associated with an interstitial pulmonary infiltrate and mediastinal lymphadenopathy. Tuberculosis was not confirmed bacteriologically but she responded to antituberculous treatment. Three months later she developed distal leg pains extending proximally. There was superficial sensory impairment up to the groins and loss of the ankle reflexes. The dose of isoniazid was reduced from 5 to 2.5 mg/kg/day on account of slow acetylator status and treatment with pyridoxine 250 mg/day commenced. The clinical signs resolved in a few weeks. CONCLUSIONS: Isoniazid neuropathy develops in the presence of risk factors (HIV, alcoholism, diabetes, renal failure, malnutrition, pregnancy and lactation, neurotoxic medication) and manifests itself initially by burning feet. Pyridoxine is preventative in low dosage and curative in high dosage. The development of symptoms should lead to measurement of acetylator status, and a reduction of the isoniazid dose to 3 mg/kg/day or even less in slow acetylators.

Acetylation↗

[Hereditary Creutzfeldt-Jakob disease caused by a mutation at codon 200].

INTRODUCTION: A typical case of genetic Creutzfeldt-Jakob disease in a 39-year-old woman without remarkable familial history is described. CASE REPORT: Initial symptoms were disequilibrium, cerebellar syndrome and complex neurovisual complaints. EEG was pseudoperiodic. NSE and 14-3-3 protein levels were elevated in the CSF. MRI showed anomalies of the anterior parts of the putamen and the caudate nuclei on the MRI T2 FLAIR sequence, mainly on diffusion sequences. A quinacrine test did not yield any effect. Death eventually occurred 8 months after the first symptoms. CONCLUSION: Current data on genetic Creutzfeldt-Jakob disease are briefly reviewed.

14-3-3 Proteins↗

[Acute neurological disclosure of B12 avitaminosis induced by folic acid administration].

A paradigmatic case of acute combined spinal cord degeneration and delirium due to inappropriate administration of folic acid in the context of chronic cobalamin deficiency is described. Rapid improvement was obtained with immediate cessation of folate administration and parenteral cobalamin supplementation. Folic acid and cobalamin prescription rules are recalled. Pathophysiological hypotheses tentatively explaining the neurotoxicity of folic acid in case of vitamin B12 deficiency are summarized.

Acute Disease↗

[Cadasil].

Explore the source record for details and available documents.

CADASIL↗

[Management of stroke in France. Results of 3 national surveys].

Three surveys were performed in France, in March 1999, to analyze the management of acute stroke patients. Three hundred forty five Emergency departments, 93 departments of Neurology and 258 Rehabilitation units participated. Fifty per cent of patients with stroke arrive at the emergency department within 3 hours of symptom onset. Only 40 p. cent of the patients are admitted in a neurological department and 5 p. cent in an acute stroke unit. The mean length of acute hospital stay is often very long (more than three weeks) because of the delay to transfer to a rehabilitation unit. This study shows that acute stroke management is herogeneous and not structured in France.

Acute Disease↗

[Cerebral amyloid angiopathy presenting as a pseudotumor: 2 cases with spontaneously favorable outcomes].

A rare clinical and radiographical presentation of cerebral amyloid angiopathy mimicking a brain neoplasm was observed in 2 patients. The signs and symptoms included seizures and focal parieto-occipital dysfunction in 1 case, massive left hemisphere dysfunction and akinetic mutism in the other. Brain CT and MRI showed nonspecific focal white matter abnormalities suggestive of the diagnosis of low-grade glioma. Gradient echo T1 and T2-weighted images showing multiple areas of signal void suggesting multiple disseminated petechial hemorrhages led to the diagnosis of cerebral amyloid angiopathy. An eventless brain biopsy confirmed the diagnosis. The neuropathology examination disclosed amyloid angiopathy of the pial and cortical vessels selectively stained by anti A-beta protein antibodies. The clinical course was remarkable in the two cases with almost complete clinical recovery without any particular treatment.

Aged↗

[Cerebral infarction disclosing neurocysticercosis].

An ischaemic stroke related to neurocysticercosis observed in the Paris neighbourhood is reported. A 32-year-old man originating from Cape Verde presented a left lacunar stroke. CT scan showed multiple areas of calcifications and a left capsulostriatal lucency. Gadolinium enhanced MRI disclosed significant abnormalities surrounding the left middle cerebral artery in the sylvian fissure. The titers of anticysticercian antibodies were highly positive in the serum and the CSF. The investigations in search of another cause of the stroke were negative. The outcome was good after a treatment associating albendazole and methylprednisolone. The increasingly recognized links between neurocysticercosis and stroke, especially in endemic areas are reviewed. Neurocysticercosis is an exceptional cause of ischaemic stroke in non endemic areas. In non-endemic areas, this cause of stroke has to be systematically suspected in patients coming from endemic areas. The diagnosis is based upon MRI, CT scanner and serologic tests. Treatment requires anti-parasitic drugs. The role of the corticosteroids is discussed.

Adult↗

[Frontal cerebral abscess, a rare complication of nasosinusal polyposis. Apropos of a case].

Sinusonasal polyposis is frequent but usually benign. A 77-year-old woman with an history of sinusonasal polyps, presented with fever and neurologic impairment. Radiologic imaging showed a polypoïd mass filling the nose and sinuses, eroding the ethmoïd bone, progressing intracranially, and causing brain abscess. The literature is reviewed, according to the relations between brain abscess development and nasal polyposis, with emphasis on intracranial extension of sinusonasal polyps. Treatment of the nasal polyps, usually based on the use of local or general corticosteroïds, can avoid this serious complication.

Aged↗