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Nuno Canas

Publications and source records attributed to Nuno Canas.

4 recordsLinked to original sources
PubMed2005

[Thyrotoxic periodic paralysis: a case report].

Thyrotoxic periodic paralysis (TPP) is characterized by recurrent episodes of muscle weakness and hypokalemia associated with thyroid hyperactivity. Reported predominantly among individuals of Asian descent, TPP is a rare manifestation of hyperthyroidism in western populations. We describe a typical case of TPP in a 33-year-old portuguese male, who presented with acute tetraparesis associated with hypokalemia (K+ 2.6 mEq/L). The patient had a 8-week history of several episodes of paraparesis of variable intensity; these attacks were usually nocturnal, preceded by strenuous exercise and resolved spontaneously after a few hours. The presence of tachycardia, weight loss, and goiter led to the diagnosis of Graves's disease. The correction of the hyperthyroid function with metimazol and propranolol prevented further episodes of muscle weakness. Thyrotoxic periodic paralysis should be considered in the differential diagnosis of acute episodes of motor paralysis in young patients. The maintenance of a euthyroid status is an essential part of management as this prevents the paralytic episodes.

Adult↗
PubMed2005

Sudden psychotic episode probably due to meningoencephalitis and Chlamydia pneumoniae acute infection.

BACKGROUND: Since 9% to 20% of all cases of acute psychosis presenting to an Emergency Department (ED) are due to a general medical condition, cautious medical workup should be mandatory in such patients. Differential diagnosis must consider conditions as diverse as renal failure or CNS infection. Acute Chlamydia pneumoniae infection usually causes a self-limited respiratory syndrome. Rarely, acute neurological complications occur, with acute meningoencephalitis most frequently reported. Diagnosis requires a high level of suspicion and is difficult to confirm. CASE REPORT: We describe a 22 year-old female Caucasian who, three days after a mild pharingitis, developed an acute psychosis with exuberant symptoms interspersed with periods of lucidity, in a background of normal consciousness and orientation. Initial medical and imagiological workup were inconclusive. After 20 days of unsuccessful treatment with antipsychotics she developed a high fever and was re-evaluated medically. Lumbar puncture revealed an inflammatory cerebrospinal fluid. MRI showed irregular thickening and nodularity of the lateral ventricles' lining. An anti-Chlamydia pneumoniae IgM antibody titter of 85 IU/ml was detected. All symptoms cleared after treatment with antibiotics and corticosteroids. CONCLUSION: This is, to our knowledge, the first reported case of acute CP-associated meningoencephalitis manifesting as an acute psychotic episode. It illustrates the principle that non-organic psychiatric syndromes must remain a diagnosis of exclusion in first-time acute psychosis.

Journal Article↗
PubMed2004

Brain-derived neurotrophic factor facilitates glutamate and inhibits GABA release from hippocampal synaptosomes through different mechanisms.

Brain-derived neurotrophic factor (BDNF) has an acute excitatory effect on rat hippocampal synaptic transmission. To compare the action of BDNF upon the release of excitatory and inhibitory neurotransmitters in the hippocampus, we studied the effect of acutely applied BDNF on the K+-evoked glutamate and on the K+-evoked gamma-aminobutyric acid (GABA) release from rat hippocampal nerve terminals (synaptosomes). The acute application of BDNF (30-100 ng/ml) enhanced the K+-evoked [3H]glutamate release. This effect involved tyrosine-kinase B (TrkB) receptor phosphorylation and Ca2+ entry into synaptosomes through voltage-sensitive calcium channels, since it was abolished by K252a (200 nM), which prevents TrkB-mediated phosphorylation, and by CdCl2 (0.2 mM), a blocker of voltage-sensitive calcium channels. In contrast, BDNF (3-100 ng/ml) inhibited K+-evoked [3H]GABA release from hippocampal synaptosomes. This action was also mediated by phosphorylation of the TrkB receptor, but was independent of Ca2+ entry into synaptosomes through voltage-sensitive calcium channels. Blockade of transport of GABA with SKF 89976a (20 microM) prevented the inhibitory action of BDNF upon GABA release, indicating that BDNF influences the activity of GABA transporters. It is concluded that BDNF influences in an opposite way, through distinct mechanisms, the release of glutamate and the release of GABA from hippocampal synaptosomes.

Analysis of Variance↗