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Biomedical subjects

Y De Smet

Publications and source records attributed to Y De Smet.

14 recordsLinked to original sources
PubMed1992

[Non-ischemic borderline brachial paralysis].

Non ischemic anterior borderzone brachial paralysis. Anterior borderzone brachial paralysis (ABBP) is a hemodynamic ischemic syndrome of the watershed zone between the anterior and middle cerebral arteries. Two cases of non ischemic reversible ABBP are reported. The first suffered from multiple sclerosis; a CT-scan showed a lesion of the corona radiata, at the level of the anterior hemispheric borderzone. The second suffered from lung adenocarcinoma. A CT-scan showed multiple metastases, one being surrounded with oedema at the level of the anterior borderzone. According to its reversibility, the ABBP was reported to the inflammatory-oedematous reaction and not to a demyelinating or metastatic lesion itself. As ABBP may occur unilaterally, the name "one-armed man syndrome" should be used instead of "man-in-the-barrel syndrome" (which always implies a bilateral paralysis).

Adult↗
PubMed1991

[Acute corticosteroid myopathy in patient with asthma].

A patient, treated by mechanical ventilation with pancuronium or atracurium and with intravenously administered corticosteroid for status asthmaticus, presented with rhabdomyolysis (severe amyotrophy and marked of creatine kinase activity) and acute flacid and areflexic quadriplegia, involving the proximal and distal muscles but sparing the cephalic musculature. After review of the investigations (biochemistry, electromyogram, muscle biopsy), the diagnostic of acute corticosteroid myopathy following status asthmaticus was suggested, and a pancuronium neuromuscular complication or a critically ill polyneuropathy excluded. The non-inflammatory rhabdomyolysis concerned all the fiber types. Predominantly distal weakness resolved six months after the insult, in spite of the laboratory recurrence of the rhabdomyolysis at the time of a new status asthmaticus briefly treated with corticosteroid.

Acute Disease↗
PubMed1990

[Bilateral, symmetrical and simultaneous putamino-capsulo-caudal infarction].

The first case, to our knowledge, of bilateral, symmetric and simultaneous infarction in the basal territory of the middle cerebral arteries is reported. The patient presented with a pseudo-rostral brainstem syndrome, including loss of oculo-vestibular reflexes, severe tetraparesia and akinetic mutism-like disturbance of consciousness. The lesions were due to embolism, caused by atrial fibrillation, occluding the ostium of the lenticulostriate arteries. It involved only the putamino-capsulo-caudal regions, concerning the whole anterior and posterior dorsal capsules. The term tetraparetic mutism is proposed to describe this new clinico-pathological syndrome, which is the sum of a capsular tetraparesia, due to the lesion of the geniculate and cortico-spinal fibres at the level of the genu and posterior limbs, and of a capsular akinetic mutism, due to the lesion of the reticular thalamo-cortical tracts at the level of the anterior limbs. These total capsular infarcts moreover involved all the oculomotor cortico-reticular tracts, which could explain the absence of oculo-vestibular reflexes.

Aged↗
PubMed1987

Cerebrospinal fluid GABA and homocarnosine concentrations in patients with Friedreich's ataxia, Parkinson's disease, and Huntington's chorea.

Free and total gamma-aminobutyric acid (GABA) and homocarnosine concentrations were measured in the lumbar cerebrospinal fluid (CSF) of patients with Friedreich's ataxia, Huntington's chorea, and Parkinson's disease (with and without levodopa treatment), and compared with those determined in control subjects. Values found in Friedreich's ataxia or Parkinson's disease were not significantly different from those in controls. Unexpectedly, in Huntington patients, known to have a characteristic decrease in GABA concentrations in specific brain areas, CSF concentrations of total GABA and homocarnosine were significantly higher, whereas free GABA was not different from controls. These findings indicate that the measurement of CSF GABA and homocarnosine in patients with CNS degenerative diseases should be interpreted cautiously.

Adult↗
PubMed1986

[The thalamic syndrome of Déjérine-Roussy. Prolegomenon].

Predicted by Dejerine and Long in 1898 and formally described by Dejerine and Roussy in 1906, the "thalamic syndrome" corrected the wrong hypothesis of a capsular "sensory cross roads" suggested by Charcot after 1873 and supported in France during 25 years. Both established the "persistent frank organic hemianesthesia" (sensory-sensitive for Charcot, pure sensitive for Dejerine), namely that a sensory deficit, still severe after regression of the early hemiplegia, could be due to focal brain damage. At that time such a clinical concept was hardly acceptable because it opposed the classic greek philosophical idea that sensation and movement should not be separated. Moreover, intelligence was at that time looked as a four-stage process including sensation, imagination, intellect and memory. The very first step began with the "sensus communis", an anteroom-like where all the sensations simultaneously perceived were coordinated to ensure mind unity. This "sensus communis" was given many subcortical seats during the following centuries, such as the trigone (Herophilus), the ventricles (Founders of the Church, Soemmering), the pineal body (Descartes), the striate bodies (Willis) and, finally, the thalamus (Todd and Carpenter's "English theory"). The description by Meynert in 1871 of a transcapsular direct "sensory bundle" and the cases reported by Türck in 1859 of a sensory-sensitive hemianesthesia after a posterior capsular lesion (in fact, thalamo-capsulostriate) led Charcot to develop his theory after 1873. Owing to the new staining methods of Weigert and Marchi introduced around 1885, Dejerine showed in 1895 the route of the medial lemniscus and his arrival in the thalamus, which led him to postulate in 1898 a "thalamic syndrome" and later to demonstrate it.

England↗
PubMedDate not supplied

[Ataxic hemiparesis due to a cerebellar lacuna].

The authors report a case of ataxic hemiparesis (dysarthria-clumsy hand syndrome plus crural hemiparesis with homolateral ataxia), secondary to a single cerebellar lacuna (CT scan), in a left rostral para-vermian position in the vicinity of the peduncle and secondary to arterial hypertension. They discuss the nosological aspects of this recently established entity and the origin of particularly severe and persistent dysphagia in their case (cerebellar dysphagia?)

Aged↗