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Biomedical subjects

M Lousa

Publications and source records attributed to M Lousa.

At least 19 recordsLinked to original sources
PubMed2002

Event-related evoked potential P300 in frontotemporal dementia.

There are no studies on event-related cognitive potentials in frontotemporal dementia (FTD). In order to evaluate the aptitude and usefulness of the event-related P300 potential in this disease, we prospectively examined 60 cases: 11 patients with FTD diagnosed according to the Lund and Manchester criteria and Neary consensus criteria, 33 patients with a probable Alzheimer's disease diagnosis following NINCDS-ADRDA criteria, and 16 normal controls. P300 latency, amplitude and reaction time were recorded using an auditory oddball paradigm. In this sample, P300 potential could be reliably performed by 10/11 FTD patients, notwithstanding their language or executive function deficiencies. The FTD group P300 mean latency was midway between the normal controls and the Alzheimer's disease group (ANOVA F(2, 74199) = 16.5; p = 0.00003). The latency range of the FTD patients were within normal values (average plus 1.96 standard deviation of the values of the control group), except for one case with a latency of 448 ms. Post hoc Newman-Keuls analysis showed that the P300 latencies of the control and FTD groups did not differ significantly (p = 0.15) and that the Alzheimer's disease group had a delayed P300 latency that differed significantly from that of the FTD (p = 0.002) and control group (p = 0.0002). However, there was overlapping in P300 latency values of the three groups. Despite these differences in latencies, the reaction time was significantly increased in the FTD and the Alzheimer's disease groups. These findings indicate that the P300 potential is less affected in patients with FTD than those with Alzheimer's disease. This fact could aid in FTD diagnosis, differential diagnosis with Alzheimer's disease and possibly its clinical management.

Aged↗
PubMed2001

Study of antiphospholipid antibodies in patients treated with antiepileptic drugs.

BACKGROUND: Antiphospholipid antibodies (lupus anticoagulant and anticardiolipin antibodies) are associated with a variety of clinical situations, including drug-intake, but their relationships with antiepileptic drugs have been scarcely investigated. OBJECTIVE: To determine the prevalence of antiphospholipid antibodies in patients treated with antiepileptic drugs and the associated risk of thrombotic events. PATIENTS AND METHODS: We performed the serologic study of thirty-six consecutively prospectively recruited epileptic patients treated with diverse antiepileptic drugs during 44.38 +/- 8.08 months (mean +/- SD) in which antiphospholipid antibodies were determined using cardiolipin and a mixture of phospholipid from rabbit brain as antigen for detection of cardiolipin and lupus anticoagulant by ELISA and in addition lupus anticoagulant was carried out also using coagulometric assays. A clinical evaluation was done in order to determine the presence of thrombotic events in the following five years. RESULTS: Antiphospholipid antibodies were detected in 43% of these patients, in most of them as anticardiolipin antibodies (IgM subtype). The patients did not present thrombotic events during the time of the study. CONCLUSION: Antiphospholipid antibodies are positive in a high proportion of these patients but thrombosis were not found during the study duration. This may be explained by the fact that the profile of aCL positivity not associated to positive LA observed in these patients does not confer a risk for thrombotic events.

Adolescent↗
PubMed2000

Status epilepticus with neuron-reactive serum antibodies: response to plasma exchange.

The authors report a patient with partial and secondarily generalized status epilepticus who required 70 days of general anesthesia for seizure control. Although antiepileptic medications failed to control the seizures, they resolved with plasma exchange. The patient's serum reacted with rat cerebral cortex, hippocampus, and cerebellum, but not with cells expressing the glutamate receptor GluR3. These findings suggest an immune response against neuronal antigens other than GluR3.

Adolescent↗
PubMed1997

Isolated pontine infarctions with prominent ipsilateral midfacial sensory signs.

BACKGROUND: Pontine infarctions may produce combined motor, sensory, cerebellar, and cranial nerve dysfunction. Midline sensory complaints and facial pain are uncommon. CASE DESCRIPTIONS: Three patients are described with hypoesthesia and numbness of the midline facial area associated with dysarthria and contralateral hemiparesis due to pontine strokes. MRI demonstrated isolated ipsilateral ischemic infarctions of the ventral pons. CONCLUSIONS: Pontine infarctions can produce diverse sensory features. Ipsilateral midfacial sensory defect has been rarely reported. The clinicoanatomic basis for the ipsilateral midfacial sensory defect described is unknown. Involvement of the dorsal trigeminothalamic tract or fiber tracts related to central regions of the face, located in the medial part of the midbrain, could help to explain these data. The symptoms could be due to direct damage or to edema resulting from the infarct. In some patients, midfacial sensory complaints, particularly of the ala nasi, could be an early sign of major pontine deficits and may be important to determine appropriate treatment.

Aged↗
PubMed1994

Study of antiphospholipid antibodies in a patient with Sneddon's syndrome and her family.

BACKGROUND: Sneddon's syndrome is a disease characterized by livedo reticularis and cerebrovascular lesions, with a hereditary transmission and unknown etiopathogenesis. A number of reports have documented a link between antiphospholipid antibodies and Sneddon's syndrome with different results. The present work was designed to sequentially study antiphospholipid antibodies in a patient with Sneddon's syndrome and her family and their potential role in thrombotic events. We used cardiolipin and a mixture of phospholipids from rabbit brain as antigen for antiphospholipid assays to determine diagnostic usefulness. CASE DESCRIPTIONS: A patient with Sneddon's syndrome and 12 available family members belonging to three generations were evaluated to determine the presence of antiphospholipid antibodies (lupus anticoagulant and anticardiolipin antibodies) during vascular thrombotic events and asymptomatic periods. CONCLUSIONS: Our results support a temporal relation between thrombotic events in Sneddon's syndrome and lupus anticoagulant; anticardiolipin antibodies remained invariable. Our index case patient and her father could be diagnosed as having primary antiphospholipid antibody syndrome. Aspirin was not effective in preventing thrombosis. After the onset of oral anticoagulant therapy, no recurrences were seen. The use of a mixture of phospholipids as antigen could present some advantages in serological studies performed in antiphospholipid syndromes.

Adolescent↗
PubMed1984

Mitochondrial defects in Lowe's oculocerebrorenal syndrome.

We performed biochemical studies on isolated mitochondria from a muscle biopsy specimen in a patient with Lowe's syndrome. Respiratory controls of mitochondrial preparations with substrates reducing nicotinamide adenine dinucleotide and with a flavoprotein-linked substrate were markedly diminished, but the oxygen consumption was normal with ascorbate and tetramethylphenylenediamine as substrates, which suggested a defect in electron transport prior to the cytochromes. The organelles also showed decreased adenosine diphosphate phosphorylate-oxygen ratio, indicating a partial uncoupling. These findings suggest that Lowe's syndrome could be considered a mitochondrial disease.

Adenosine Diphosphate↗
PubMed1983

Mitochondrial function in myasthenia gravis.

We determined the respiration rate, respiratory control and ADP/O ratios, with different substrates in mitochondria isolated from 2 patients with myasthenia gravis and compared them with normal human muscle. In all cases studied, a severe alteration of the respiratory control with variable derangement of oxidative phosphorylation was found. This abnormality of mitochondrial metabolism was referred to by Luft as 'loosely coupled' and was reported in other neuromuscular diseases. In our opinion this defective oxidative metabolism is nonspecific.

Adenosine Diphosphate↗
PubMed1982

Bilateral optic nerve meningioma. Case report.

A case of bilateral optic nerve meningioma is reported. The onset of the clinical symptoms, at age 27, resembled unilateral optic neuritis with papilledema, leading to bilateral amaurosis with optic atrophy 4 years later. Skull X-ray revealed a "blistering' type of bone reaction. In the carotid angiogram, the ophthalmic artery appeared quite enlarged and displaced. The CT scan showed a fusiform enlargement of both optic nerves. Pathological diagnosis was based upon an optic nerve biopsy. Including the present case, only 12 instances of bilateral optic nerve meningioma have been reported.

Adult↗
PubMed1981

Intracerebral arachnoidal cyst containing choroid plexus. Case report.

A case of an intracerebral "primary" arachnoidal cyst of the left fronto-parietal region is reported. No communication with the ventricular system or with subarachnoidal space was found at the first surgical procedure. It contained genuine choroid plexus and clinically behaved as an expansive intracranial mass.

Arachnoid↗
PubMed1980

Mitochondrial functions in chronic spinal muscular atrophy.

We determined the respiration rate, respiratory control and ADP/O ratios, with different substrates in mitochondria isolated from seven patients with chronic spinal muscular atrophy and compared them with normal human muscle. In all cases studied, a severe alteration of the respiratory control with variable derangement of oxidative phosphorylation was found. Similar findings have been described in other neuromuscular disorders including the so-called "mitochondrial myopathy". We believe that this disturbance of mitochondrial function is non specific and only the hypermetabolic syndrome of Luft could be considered biochemically as a "mitochondrial myopathy", a disorder selectively involving mitochondria of skeletal muscle.

Adolescent↗