BYBoche f ontaine reported for the first time pupillary dilatation evoked by electrical stimulation of the cerebrum Since then many investigations were made with regard to almost all cortical areas in concern with this matter. Pupillary dilatation can equally be found through stimulation of amygdala and neighboring cortex, as recently pointed out by Okinaka (1952), Gastaut (1952) and W i l s o n (1952). Purporting to establish exact loci of origin of this function in the nuclear subdivisions of the amygdaloid complex, experiments were performed with electrical and chemical stimuli on 48 cats, 5 dogs and 2 Japanese monkeys (Macacus fuscatus).In the course of these experiments, movements of the eyelids, the eyeballs and the nictitating membranes were frequently observed.Necessary anesthesia was induced by injection of ethylurethane for cat and dog and by inhalation of ether for monkey. Electrical stimulus derived from Porter's inductorium and bipolar silver electrodes as described in the previous paper of Takahashi (1951) and Koikegami and Fuse (1952) were employed. As chemical stimulus, 0.05-O.lcc of 1 mol solution of sodium glutaminate was injected into the amygdaloid complex directly. The pupillary diameter was measured before and during stimulation. The difference between two was utilized as indicative of degree of pupillary response with f, + and tt, roughly corresponding to those in the recent report of W i l s o n (1952), that is, mild (2 to 3mm). moderate (3 to 5 mm), and marked (5 to 8 mm) respectively. Stimulated portion, fixed in alcohol, was examined histologically through Nassl S p i e Irneyer's staining method. Result o f stimulation 0.f the medial principal nucleus TUpon stimulation, mostly by 2 volts and 8cm coil distance, pupils both sides get dilated accompanied by abduced eyeballs, retracted nictitating membrmes and exophthalmus. These phenomena become more and more evident during the stimulation time, in which nystagmus appeam the soonest (fig. 2 b). With the stimulus interrupted, retraction of nictitating membranes and nystagmus disappear a t first, then the pupillary dilatation and exophthalmus of Vblsclt.

No abstract

No abstract

No abstract

The A3243G mutation of the mitochondrial gene is a cause of maternally inherited diabetes and deafness. The aim of this study was to evaluate the frequency and clinical features of this mutation in patients with sensorineural hearing loss (SNHL) in otorhinolaryngic clinics. The frequency of the A3243G mutation in 230 patients with SNHL was 1.74% (4/230). Three of the four patients had diabetes mellitus (DM) and were already aware that they had the mutation. The other had cardiomyopathy but not DM, and proved to have the mutation in this study. The frequency of the mutation was 12.9% (4/31) in patients with a family history of possible maternal inheritance of SNHL, 10.3% (3/29) in patients with DM, and 50% (3/6) in patients with both. The age of onset of SNHL in these patients and their families was between their teens and their forties. The chance of diagnosing the A3243G mutation in patients with SNHL in otorhinolaryngic clinics is probably less than 1%. Association of DM, cardiomyopathy, a family history of possible maternal inheritance of SNHL, and an onset of SNHL between the teens and the forties are signs suggesting the mutation. These signs provide us with a reason for genetic testing for the mutation.