In order to estimate the familial morbidity risk of schizophrenia, parents and siblings of 1,691 inpatients meeting the DSM‐III criteria for schizophrenia were investigated on the basis of a review of medical records, family history data and/or personal interviews. The morbidity risks of schizophrenia to parents and siblings of the schizophrenic probands were 4.0% and 4.1%, respectively, which were greater than the morbidity risk in the general population. Siblings of 118 probands whose parents suffered from schizophrenia were at a significantly greater risk of schizophrenia than siblings of 1,493 probands whose parents did not have schizophrenic illness. These findings support thenotion of familial transmission of schizophrenia. A total of 16.4% of the schizophrenic probands had at least one first‐degree relative with schizophrenia. This is significantly greater in the female probands than in the male probands.

Summary Sleep was induced in dogs by a repetitive stimulation of low frequency (about 5C./sec.) low voltage (3 V.) current on the animal's thalamic inkgrating system. This experimental sleep is termed “thalamogenic sleep”. By taking simultaneous records of both cortical and subcortical EEG during the experimental sleep and giving it an electroencepha‐lographic interpretation, and further comparing it with the EEG patterns of the normal sleep and of that under barbiturate narcosis, the following results were obtained: 1. The EEG records of a wake and resting animal consist of irregular patterns of low voltage (7–15C./sec.) waves showing no such rhythm resembling the aL rhythm in man. The EEG pattern from 20 th sec. after the beginning of stimulation gradually gets increased in the amplitude, and turn to slow waves. This change is more marked in the subcortex. From about 30 th sec. on, spindle bursts of about 12C./sec. appear synchronously at relatively regular intervals in the cortical motor area and somato‐sensory area. As a rule, spindle bursts are not detectable in the subcortical record, only occasionally accompanied by some superposing slow waves. With the advance of sleep, appearance of the spindle bursts gets rarer and, instead, high voltage slow waves of 1–3C./sec. predominate. These slow waves come out again more marked in the sulxortical EEG, wherein there are seen the succession of the voltage waves with amplitude often raised up to 330μV. The cessation of the stimulation at this moment does not cause the slow waves to disappear. 2. The changes in the animal's behavior go nearly parallel with those in the EEG pattern. Particularis noticeable is the coincidence of both features under wake state. When the thalamic integrating system is activated with a stimulation of high frequency (30–90C./sec.), the animal wakes up and the EEG begins to show the arousal waves with that. 3. With pulse duration kept constant, the factor which determines the variance between sleep and activating reactions is represented by frequency. By altering the frequency we are able to obtain both the sleep reaction as well as the activation reaction from the same portions at will. 4. Dog's EEG and the process during the sleep induced by an electrical stimulation on thalamus agrees with the KEG and the process seen in the natural sleep, but different from those under barhiturate narcosis. Consequently, it is reasonable to regard the sleep caused by electrical thalamic stimulation as an induced form of the natural sleep, judged both from the clinical and the electroencephaloyraphic findings. 5. At present we interpret the mechanism of thalamogenic sleep as follows: It is no other matter than synchronization of the diffuse cortical activity originated in the thalamic integrating system. This synchronization of the thalamic integrating system goes propagated not only to the cerebral cortex but also to the various sukortical regions, namely; striatum, hypothalamus and midbrain. This agrees with the fact that sleep is a functional depressi...

The relation between age at onset of schizophrenia diagnosed using DSM-III criteria and the presence or absence of this illness among first-degree relatives was investigated in 2417 patients. The mean age at onset among those with a family history of schizophrenia was slightly and nonsignificantly earlier than that of schizophrenic patients without a positive family history. The former developed their illness before the age of 25 years more frequently than did the latter.

A handedness questionnaire which was given to 1774 schizophrenic inpatients was identical to that employed in our previous study on healthy students. Information was obtained on forced conversion of hand usage in childhood and the occurrence of left-handedness in their families. Family history of schizophrenia was also investigated. There were no significant differences in the prevalence of left-handedness or non-right-handedness (i.e., left-handedness and ambidexterity combined) between schizophrenic patients and normal subjects. However, the rate of converted right-handedness in schizophrenics was higher than that in normal people. The incidence of original non-right-handedness (i.e., present non-right-handedness and converted right-handedness combined) in schizophrenics was greater than that in normal controls.

The age at onset of schizophrenia was investigated in 2,417 inpatients (1,433 males and 984 females) meeting the DSM-111 criteria for schizophrenia. About 80% of the patients became schizophrenic before the age of 30. The mean age at onset of the male patients was slightly earlier than that of the female patients. There was a higher cumulative percentage of the male patients who became affected at each age quinquennium. More men than women became schizophrenic before the age of 30.