Search PubMed⌕ Search

Biomedical subjects

S Manaka

Publications and source records attributed to S Manaka.

At least 55 records · Page 3Linked to original sources
PubMed1981

The difference between children and adults in the onset of post-traumatic epilepsy.

In order to clarify the difference between children and adults in the onset of post-traumatic epilepsy, 96 outpatients of our clinic were investigated statistically. The subjects comprising 40 children and 56 adults were followed up for more than three years. The latency of the children i.e., the interval between a head injury and the onset of epilepsy, was longer than that of the adults. The 95%-confidential interval classified by age group indicated that the upper limits of latency of the group under the age of two, those between three and 14 and those aged more than 15 were about 13, six and three years, respectively. We concluded that children with a severe head injury should be followed up until age 20 and adults for about three years.

Adolescent↗
PubMed1981

Pituitary apoplexy in acromegaly during bromocriptine therapy.

Two cases of pituitary apoplexy occurring in the course of long-term bromocriptine therapy for active acromegaly are described. Although bromocriptine was effective in lowering serum growth hormone levels and concomitant clinical improvement was achieved, both patients developed an acute episode suggesting pituitary apoplexy when the therapy was continued for 6 and 24 months, respectively. Surgery verified marked haemorrhage and necrosis of an eosinophilic pituitary adenoma in each case. Bromocriptine may have suppressed the growth of these pituitary adenomas resulting in necrosis of the tumour, followed by haemorrhage into the adenoma. Pituitary apoplexy has not been documented as a complication of bromocriptine therapy. This report points out a possible role of bromocriptine in the development of this catastrophe and that careful follow-up is required when long-term treatment with bromocriptine is attempted.

Acromegaly↗
PubMed1981

Changes in extracellular potassium concentration in cortex and brain stem during the acute phase of experimental closed head injury.

A high potassium concentration ([K+]o) in brain tissue impedes neuronal activity, as observed in spreading cortical depression. Experimental studies were performed on mice and rats to determine the role of changes of [K+]o in cerebral concussion. In the first experiment, a 600 gm-cm impact was delivered to the vertex of the mouse skull. This impact induced arrest of spontaneous movement for 465 +/- 55.9 seconds (mean +/- SD), accompanied by apnea, bradycardia, and low-voltage electroencephalographic recordings (EEG). The injury was also frequently followed immediately by epilepsy. This impact induced an increase of cortical [K+]o from the control level of 4.1 +/- 1.8 mM to 20-30 mM, with gradual recovery within 30 minutes to the control level. In the second experiment, an impact of 9000 gm-cm was delivered to the midline parieto-occipital area of the rat and produced concussion-like phenomena similar to those elicited in mice. This level of trauma induced a significant increase of cortical [K+]o from the control level of 4.2 +/- 0.8 mM to 20-50 mM in all of the rats, and also a significant increase of brain-stem [K+]o from 3.9 +/- 0.6 to 20-30 mM in 73% of the rats. In these latter rats, the impact also induced apnea and a transient elevation of blood pressure, and resulted in low-voltage EEG recordings. In 23% of the rats in which [K+]o changes in the brain stem were not significant, the impact caused a transient reduction of blood pressure. The present study disclosed that an increase of [K+]o in the cerebral cortex and also in the brain stem is an important element in the phenomenon of concussion.

Acute Disease↗
PubMed1981

[Changes of extracellular potassium concentration in the cortex and brain stem during the acute phase of experimental closed head injury (author's transl)].

The high concentration of extracellular potassium ((K+)o) impedes neuronal activity by depolarizing the membrane potential and further causing depolarization block or conduction block, and also causes swelling of astrocytes, which may result in narrowing of extracellular space and affect the diffusion of metabolites. Thus, when high concentration of extracellular potassium prolongs, pathological changes of neurons may ensue. In such state as cerebral ischemia, contusion or spreading depression, marked elevation of extracellular potassium was reported by many authors. In order to reveal the changes of extracellular potassium during the acute phase of closed head injury, following experimental studies were performed. In the first experiment, closed head injury model of the mouse was used. Directly after the impact with 600 g.cm, spontaneous movement of the animal disappeared for about 5-6 minutes often accompanied by immediate epilepsy. In this state, cortical (K+)0 increased from the control level of 4.1 +/- 1.8 mM to 20-30 mM. The elevated (K+)0 recovered gradually within 10-30 minutes. Directly after the same impact, apnea, bradycardia and low voltage EEG also appeared. In the second experiment, closed head injury model of the rat was used. With the impact of 9000 g.cm, the same concussion-like symptoms appeared as those of mice. Directly after the impact, (K+)0 in the cortex and brain stem elevated but the change patterns of cortical (K+)0 and brain stem (K+)0 were different. The different patterns in changes of (K+)0 were classified into four types. Type 1. Both cortical and brain stem (K+)0 elevated significantly immediately after the trauma, and recovered to control level within 30 minutes. Type 2. Both (K+)0 elevated significantly as in type 1 but only brain stem (K+)0 recovered within 30 minutes. Type 3. With the exacerbation of vital signs, both (K+)0 elevated over 50 mM, resulting in the death of the animal. Type 4. Although cortical (K+)0 elevated significantly after the impact, the increase of brain stem (K+)0 was below 10 mM. In type 1,2 and 3, blood pressure always elevated and brady- or apnea appeared immediately after the impact. In type 4, blood pressure after the impact showed to become slightly lower transiently as compared to control blood pressure. In control study, spreading depression was elicited by application of KC1-solution on the cortex. Spreading depression caused the elevation of cortical (K+)0 only, and almost no changes of brain stem (K+)0 were observed. The present study suggested that during the acute phase of closed head injury, diffuse neuronal disturbances involving the brain stem existed. And the elevation of brain stem (K+)0 is an important finding of this study because it may affect the level of consciousness directly by the mechanisms as described above.

Animals↗
PubMed1980

[Auditory electroencephalography (author's transl)].

New monitoring method of EEG using auditory expression were proposed; (1) Multification method, (2) Frequency modulation method and (3) Harmonic musical scale method. The first has merit surveying the trend of EEG, the second detecting paroxysm and the third detecting abnormal basic activities.

Biofeedback, Psychology↗
PubMed1979

The role of extracellular potassium in early epilepsy.

Clinical studies indicate that early epilepsy after injury may be associated with some transient and reversible pathophysical processes of the brain. It has been proposed that epileptogenesis in the neocortex and hippocampus may be related to potassium ion accumulation in extracellular spaces. To investigate this hypothesis, we measured [K+]0 using potassium-sensitive microelectrodes in the sensorimotor cortex of cats during early seizures induced by trauma. The [K+]0 increases associated with seizure activity ranged from 14.6 to 25.1 mM, and these were significantly higher than those unassociated with spikes or seizure discharges. Moreover, high K+ solutions (15 mM or more) directly applied to the cortex produced spiking and seizures. These results seem to support the hypothesis that accumulation of [K+]0 is related to development of early epilepsy.

Animals↗
PubMed1978

[Measurement of cerebral blood flow with hydrogen clearance method: technique and a comparative study with the venous out flow method (author's transl)].

Local cerebral blood flow was measured with hydrogen clearance method in fifteen dogs and compared to direct measurement obtained by Michenfelder's venous out flow method. The sagittal sinus was exposed by a midline frontooccipital incision and extensive craniectomy. A tappered catheter was passed in to the superior sagittal. sinus. For measuring hydrogen clearance, platinum wire electrodes with a red tip of 0.5 mm in length and 0.3 mm in diameter were introduced into the parietal and occipital cortex. About ten percent hydrogen gas was given directly into the endotracheal tube for three to five minutes and the obtained clearance curves were transferred to semilog graph papers. Total cerebral blood flow was caliculated by bicompartmental analysis and compared to the two minutes initial slop index. The results are as follows. 1) A linear regression analysis of flows caliculated from the initial slope and bicompartmental analysis shows a high correlation coefficient. 2) There is a high correlation between flows caliculated from electrodes used at the same experiments. 3) Cerebral blood flow from the initial slope measured by hydrogen clearance method shows a high correlation wit flows caliculated from Michenfelder's venous out flow method.

Animals↗