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Biomedical subjects

P Barreiro

Publications and source records attributed to P Barreiro.

At least 19 recordsLinked to original sources
PubMed1995

Hypersomnia after tegmental pontine hematoma: case report.

We describe polysomnographic studies of a 44 years-old man who showed a defect in the central nervous regulation of the sleep-waking cycle (SWC), hypoventilation and cardiovascular hyperactivity after a right-sided tegmental pontine hematoma. A significant increase in total sleep time mainly depending upon stage 1 + 2 was observed. Predominant unilateral damage to the medial and central region of the reticularis pontis oralis (Poo) nucleus, extending into the central part of the rostral reticularis pontis caudalis (Poc) nucleus, was presumably responsible for the hypersomnia in this patient.

Adult↗
PubMed1994

Benign mitochondrial myopathy with decreased succinate cytochrome C reductase activity.

In most of the cases previously described, the defect on complex II was suggested by low activity of succinate cytochrome C reductase (SCCR). The clinical pattern of the previous 10 cases is heterogeneous and may be limited to one particular tissue or be of a more general nature. We report a 22-year-old-woman, daughter of consanguineous parents, with generalized muscle weakness, easy fatigability and benign course, who showed a decrease of SCCR activity in mitochondria of muscle fibers. Free carnitine (FC) concentration was decreased in muscle as well. The muscle biopsy showed a mild variation in fiber size, with fiber type I predominance, subsarcolemmal oxidative DPNH accumulations, excess of neutral lipids and abnormally large mitochondria with paracrystalline inclusions. A possible inheritance pattern is discussed. Coenzyme Q10 therapy in this patient induced a significant increase of global MRC index score and a decrease of the turns-mean amplitude ratio in the automatic analysis of the EMG.

Adult↗
PubMed1994

[Clinical and investigative approaches in mitochondrial diseases. A review of 15 cases].

The results of laboratory investigations in concerning 15 patients suspected of mitochondrial disease (MD) are presented. Our purpose is to provide an outline of the investigative modalities that support the clinical suspicion and have been found to be useful in the diagnosis. Five clinical groups were studied including 5 exercise intolerances (2 with inflammatory myopathy), 3 with myopathies (1 with dilated cardiomyopathy), 2 with progressive external oftalmoplegia (1 associated with cerebellar ataxia+epilepsy+hypertrophic cardiomyopathy+pes cavus), 4 with encephalopathies (3 with myoclonic encephalopathies with ataxia and dementia and 1 with epilepsy and tremor), and 1 with metabolic acidosis and cardiomyopathy. We used the following categories of investigative procedures: clinical phenotype analysis including pedigree study, neurophysiological tests, bicycle ergometric evaluation, neuroimaging, microscopic study of skeletal muscle biopsy, post-mortem examination, biochemical assays and molecular genetic studies. EMG showed myopathic changes in 5 cases, features of neuropathy in 2, mixed myopathic and neuropathic pattern in 1 and nonspecific changes in 3. EMG was normal in 3 patients. The most common skeletal muscle abnormalities were variation in fiber size (60%), lipid inclusions (33.3%), oxidative subsarcolemmal aggregates (26.7%) and ragged-red fibers (26.7%). Electron microscopy revealed mitochondrial abnormalities in 8 out of 14 patients' muscle biopsies, and in myocardiac and hepatic tissues of another. Site of biochemical defect was located in 12 patients. Complex I defect in 6, complexes I+IV deficiencies in 3, complex II defect in 1, complex IV deficiency in 1, complexes II+IV deficiencies in 1, and complex III defect in 1. In 2 patients the biochemical defect was not located. Mitochondrial DNA alterations were not found in 7 investigated patients. The clinical spectrum of MD has become increasingly wider. After the clinica suspicion, the diagnosis depends up on the appropriate use of skeletal muscle biopsy, biochemical investigations and molecular genetic techniques. Conventional EMG and automatic measurement of the electromyogram are particularly helpful in confirming the clinical suspicion in patients with predominantly central nervous system disease or in cases in which clinical signs are few.

Adolescent↗
PubMed1994

[Idiopathic granulomatous angiitis of the central nervous system].

We diagnosed idiopathic granulomatous angiitis of the central nervous system in a 51-year-old man by leptomeningeal and cortical biopsy. The patient's disease was prolonged, with symptoms recurring over a period of 15 years. Treatment with prednisone and cyclophosphamide produced total remission after a follow-up of 22 months. Computerized tomography was less sensitive and revealed fewer lesions than did magnetic resonance imaging. Angiography was not sensitive and leptomeningeal and cortical biopsy were essential for diagnosis in this patient.

Age of Onset↗
PubMed1990

[Wilson's disease: computed tomography and magnetic resonance imaging].

Wilson's disease is an autosomal recessive hereditary disease in which the capacity of biliary copper excretion is reduced, resulting in a toxic accumulation of this metal in the liver, brain and other organs. The neuroimaging techniques, computed tomography (CT) and nuclear magnetic resonance (NMR), have been incorporated to the diagnostic workup in patients with suspected Wilson's disease (WD). We report two patients with WD in whom CT and NMR were carried out for the evaluation of the central nervous system (CNS). The lesions appeared as hypodense areas in CT or signal abnormalities in NMR over the involved structures: putamen, caudate nucleus, cerebellar dental nucleus, red nucleus and subcortical white matter. In one of the patients, hypointense signal areas were found over both putamen nuclei in T-2 times of NMR, which might correspond to cavitary necrosis or copper deposition. The lesion distribution suggests that vascular lesions might play a role in the mechanisms of tissue damage. These findings show that CT and NMR are very helpful to evaluate WD. NMR images are quite characteristic of this disorder.

Adolescent↗
PubMed1989

Differentiation of smooth muscle in the genital tract of the female mouse and its temporal relation with the development of the Wolffian nerve.

The development of the smooth muscle in the genital tract of the female mouse was studied by light and electron microscopy before and after birth. These studies showed that: a) between 13 days of fetal development and 2 days after birth the cells surrounding the Mullerian duct were undifferentiated and showed a fibroblast-like appearance; b) between 3 and 10 days after birth the cells acquired several characteristics of smooth muscle but they did not seem fully mature; c) between 30 and 180 days after birth the cells acquired a mature appearance; and d) the Wolffian nerve reached the Mullerian duct surrounding tissue before the start of smooth muscle differentiation.

Animals↗
PubMed1989

[Recurrent Miller-Fisher syndrome associated with brachial neuritis].

The clinical and electrophysiological evolution of a 24-year-old patient with Miller-Fisher's syndrome and findings of mild peripheral neuropathy in the electromyographic study is reported. The patient had been treated six years previously for a similar disease and he recovered in 2 months. During the plasmapheresis therapy of the second episode he developed pain and weakness of the left shoulder girdle, and the EMG was consistent with bilateral brachial neuritis. The disease had improved clinically after 6 weeks, except for supracapsular brachial neuropathy; this territory remained denervated after 3 months of evolution. A diagnosis of Crohn's disease had been made between both episodes. The discussion focuses on the rarity of recurrent forms of Miller-Fisher's syndrome and the association of the reported case with brachial neuritis and Crohn's disease.

Adult↗
PubMed1978

[Modifications of insulin and growth hormone after medium chain triglycerides ingestion (author's transl)].

Authors determined the variation of glucose, ketone bodies (KB), free fatty acids (FFA), insulin and growth hormone (HGH) in blood produced by the ingestion of 1.5 g./kg. of medium chain triglycerides (MCT) in 10 healthy children between 5 and 11 years. Blood values were determined starting 30 minutes before the MCT ingestion and at 30 minutes intervals until 120 minutes post ingestion and a final determination at 180 minutes. The glucose did not change. The KB were increased (p less than 0.01) from 30 to 120 minutes and the FFA from 90 (p less than 0.01) to 120 minutes (p less than 0.001) after ingestion. Insulin secretion was elevated between 30--90 minutes with a peak value at 60 minutes (p less than 0.001). HGH began to increase at 60 minutes, remaining elevated at the last determination at 180 minutes. The HGH basal value was 0.5 +/- 0.2 ng./ml.; began to increase at 60 minutes and reached the value of 3.9 +/- 1.06 ng./ml. and 4.8 +/- 2.04 ng./ml. at 90 and 120 minutes respectively (p less than 0.001). We do not know the origin of the HGH increase. The changes may explain FFA elevation and other metabolic actions of MCT. The glucose-insulin ratio showed that the hyperinsulinemia was not caused by an increased glucose level.

Administration, Oral↗