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Biomedical subjects

N Carrera

Publications and source records attributed to N Carrera.

36 records · Page 2Linked to original sources
PubMed1981

[Conduction and origin of evoked potentials in the somesthetic pathway (author's transl)].

In 24 normal subjects, sensory conduction velocity increased progressively from the distal to the proximal segments of the peripheral nervous system. In the central somatosensory pathway, sensory impulses slowed down at a rate much greater than what could be expected from just the three known synaptic delays (1 ms each) in medulla, thalamus and somatosensory cortex. The present data point to the special characteristic of conduction in the thalamo-cortical axons as the main cause for the deceleration observed in the central somatosensory pathway. A conduction velocity of 14 m/s has been calculated for this last segment. However it is also possible that sensory conduction in the medial lemniscus might be reduced in relation to the conduction values in the peripheral segments.

Adult↗
PubMed1980

[Alterations of previous potentials of somatosensory cerebral evoked potential after lesions of the brain-stem (author's transl)].

The characteristics of previous potentials of somatosensory evoked potential in 12 patients with lesions of the brain-stem and in 24 normal individuals have been studied. Lesions of the brain-stem were confirmed by means of computerized axial tomography, arteriography or necropsy. According to data reported by other authors somatosensory evoked potential is anteceded by three previous potentials with central latencies of 10, 12, and 14 milliseconds. Brain-stem lesions which do not involve the medial lemniscus showed normal potencials, while extensive lesions of the protuberance abolish P-12 potential and increase central latencies of P-14 and somatosensory evoked potential. P-12 potential originates in the medial lemniscus and P-14 potential in the thalamic nuclei. The present results confirm the interest of previous potentials of somatosensory evoked potential, as well as other neurophysiologic techniques, in the evaluation of lesions of the brain-stem.

Brain Neoplasms↗
PubMed1980

[Medullar and supraspinal conduction in multiple sclerosis: localization value (author's transl)].

Spinal cord and central conduction velocities were studied in 12 patients with multiple sclerosis and in 20 healthy volunteers using an indirect method (Dorfman's) that includes the determination of the somatosensory evoked potentials by median and posterior tibial nerves stimulation, latency of the F-waves and motor and sensory conduction velocities in the wrist-elbow segment of the median nerve. Patients with symptoms and signs of demyelination showed very altered conductions in both of the segments studied, but five patients without clinical suspicion of sensory alteration showed normal spinal cord and supraspinal conduction time just in the limit of normality. The physiopathologic aspects of the demyelination lesions in the central nervous system that determine a block in the condution are discussed.

Adult↗
PubMed1980

Somatosensory evoked potentials: abnormalities with focal brain lesions remote from the primary sensorimotor area.

Somatosensory evoked potentials (SEPs) were recorded in 41 patients with focal brain lesions recognized by computerized tomography. 21 patients presented damage of the primary sensorimotor area (PSMA), and their SEPs were reduced in amplitude and increased in latency for the two early components (N-22 and N-39), in accordance with previous evidence. The other 20 patients pesented lesions remote from the PSMA, 15 (71%) showing abnormal SEPs mainly characterized by increment in amplitude and duration of N-22 and N-39. Abnormalities of the N-70 and later waves were not specific for any type of lesion. SEPs appeared more sensitive than the EEG for detecting brain dysfunction. The physiopathological and clinical importance of these findings are discussed.

Adult↗
PubMed1980

Neurophysiological assessment of alpha pattern coma.

Somatosensory evoked potentials, blink reflexes, and H wave reflexes, were recorded on several days from three patients with alpha pattern coma. Coma was secondary to cardiac arrest in two cases and to brainstem infarction in one. Results are compatible with damage to the brainstem reticular formation with sparing of thalamo-cortical circuits as the main physiopathological characteristic of alpha pattern coma. This condition should not be regarded as a discrete entity when establishing the prognosis of patients in coma, since they only differ from other patients in coma from the point view of the EEG record.

Aged↗
PubMed1979

[Guillain-Barré syndrome associated to a type B acute hepatitis (author's transl)].

A 42-year-old male patient suffers an acute hepatitis with positive HBs Ag and approximately 2 months after its onset, an acute polyneuritis with lessening of conduction velocity and albumino-cytologic dissociation appeared. Both conditions recuperated synchronously in a few months. This association has been only slightly referred to previously, and the majority of cases lacked facts important to the establishment of a diagnosis. The polyneuritis is possibly secondary to the viral alteration, either directly or due to an ensuing immunological alteration. Besides, there is the possibility that a clinical or sub-clinical demyelinizing neuropathy that does not fill the criteria of a Guillain-Barré syndrome may complicate a hepatitis, or that an acute polyneuritis may associate itself to an autoimmune hepatitis.

Acute Disease↗
PubMed1979

Conduction velocity through the somesthetic pathway in chronic renal failure.

The latencies of evoked potentials recorded at different levels of the peripheral and central nervous system by median nerve stimulation were measured before and after dialysis, and compared with similar recordings in normal volunteers. Abnormally slow conduction velocity was more often found in proximal rather than in distal segments of the peripheral pathway in patients with chronic renal failure. This abnormality was not correlated with the presence of clinical signs of neuropathy or low values of motor conduction velocity, neither was it affected by dialysis. These findings support the hypothesis of peripheral nerve dysfunction secondary to metabolic derangement in uraemic patients.

Adult↗