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Biomedical subjects

K Sainio

Publications and source records attributed to K Sainio.

101 records · Page 6Linked to original sources

Electroencephalographic changes during experimental hangover.

The EEG was recorded in 27 subjects during hangover. Male healthy volunteers drank 1.75 g/kg body weight of ethanol in 3 h and the EEG was recorded 14-16 h later when the degree of hangover was highest. For control purposes a second EEG was recorded after a similar session when subjects drank water instead of ethanol. A third record was taken in normal laboratory conditions. T5-A1 and O1-A1 derivations were subjected to computer analysis from which spectral and frequency parameters were calculated. Visual analysis of the EEG during hangover showed a decrease and slowing of alpha activity and an increase in theta activity. Spectral analysis of the EEG gave a statistically significant increase in 7-8 c/sec activity during hangover. The EEG change could not be explained in terms of blood alcohol level, hypoglycaemia or acidosis. Also fatigue could be excluded as a cause of EEG change by means of "water controls". The conclusion is that the slowing of the EEG during hangover is caused by the depressant action of ethanol, or its metabolites, on cortical function.

Adolescent↗

Sleep-waking cycle in rabbits after cerebral ischemia.

In rabbits experimental cerebral ischemia of 4-6 min was followed by degradation of the electroencephalographic sleep-waking cycle, as determined from 3 h afternoon records: I. Hyposomnia i.e., reduction of slow wave and paradoxical sleep lasting for about 2 days, was seen, with gradual normalization in case of survival. II. In the first postischemic days abundant 14-17 c/sec spindles appeared in the motor cortex against a low voltage desynchronized background, making the EEG of waking qualitatively different from control records. The results are discussed with reference to polygraphic studies in comatose patients, EEG phenomenology of drowsiness, and cerebral monoamines.

Animals↗

Event-related brain potential of human newborns to pitch change of an acoustic stimulus.

We report here event-related potentials (ERPs) of human newborns to occasional pitch changes in a repetitive sequence of tone pips. These pitch changes elicited a large slow negative ERP component which resembles the mismatch negativity (MMN) generated by the adult brain under similar conditions. This MMN-type of negativity in newborns suggests that already at this early ontogenetic stage the brain monitors the acoustic environment for a possible change in any of its repetitive aspects. Apart from its theoretical interest, this finding might provide a new way to test the development of the central nervous system and to diagnose cerebral dysfunction at a very early stage.

Acoustic Stimulation↗

Ocular findings in muscle-eye-brain (MEB) disease: a follow-up study.

We present ocular findings of 20 patients with the recessively inherited muscle-eye-brain (MEB) disease, characterised by severe visual failure, mental retardation, a pachygyria-polymicrogyria type neuronal migration disorder and congenital muscular dystrophy. The ocular findings consisted of myopia ranging from -6 to -27 D, retinal degeneration and optic atrophy. Five infants had congenital glaucoma, and juvenile cataracts developed in 9 children. The visual evoked potentials were abnormally high (> 50 microV) and delayed in 70% of patients. The electroretinogram was abolished in 12 patients. The changes were progressive during the follow-up time, which was up to 20 years.

Adolescent↗

Epilepsy and the electroencephalogram in progressive encephalopathy with edema, hypsarrhythmia, and optic atrophy (the PEHO syndrome).

Progressive encephalopathy with edema, hypsarrhythmia, and optic atrophy (PEHO) syndrome) is an apparently autosomal recessive disorder manifested by infantile spasms, severe hypotonia, and early arrest of psychomotor development. Subcutaneous edema in the limbs, typical facial features, and blindness with optic atrophy are also present. Neuropathologic and radiographic studies show progressive brain atrophy, which is accentuated infratentorially. We recorded 85 EEGs from 10 patients between the ages of 3 weeks and 12.7 years; follow-up ranged from 7 months to 12.1 years. The infantile spasms were preceded by other neurological symptoms in all patients. Seven of nine patients showed focal or generalized epileptiform activity or abnormal EEG background. All patients developed hypsarrhythmia, first recorded between 3 and 11 months of age, that was resistant to therapy with ACTH and antiepileptic drugs. After the hypsarrhythmia disappeared, five patients showed slow spike-wave activity generally seen in the Lennox-Gastaut syndrome, and three patients showed background EEG abnormality with generalized or diffuse paroxysmal activity. There were no specific EEG features that could help in the diagnosis of PEHO. The PEHO syndrome should be borne in mind in the diagnostic work-up of patients with infantile spasms, so that potentially harmful treatment can be avoided, and the parents can be counseled about the inheritability of the disorder.

Age Factors↗