The blink reflex elicited by auditory stimulation was studied electrophysiologically in rabbits. It was recorded as the microvibration of the eyelid, and called auditory-evoked eyelid microvibration (AMV).
1) Three or more peaks were observed in AMV. The latency of AMV, which was measured from the stimulation point to the first deflection, was 14.64±4.14 msec. And the amplitude, which was represented by the peak-to-peak amplitude, was 0.120±0.089 G.
2) The maximum amplitude was obtained by the stimulation sound of 1,000 Hz in almost all cases. The bigger the sound pressure was, and the shorter the rise time was, the greater the amplitude became. There was no significant difference of amplitude with the change of the duration of the stimuli or the interstimulus interval. So we used a binaural auditory stimulation comprising; a repetition of 1,000 Hz tone bursts,109 dB HL intensity, with a duration of 10 msec without rise time, and 3 seconds interstimulus interval.
3) AMV was obtained from both ipsi- and contralateral eyelids when the stimulation was applied monoaurally.
4) In travenous administration of pancuronium bromide, a kind of muscle relaxant, caused the disappearance of AMV. This result demonstrates that AMV is myogenic in origin.
5) Barbiturate, chlorpromazine and diazepam decreased the amplitude of AMY, while amphetamine and cardiazol increased it. As the brainstem reticular formation (RF) is thought to be the common action point of these drugs, the data suggests a close relation between AMV and the function of RF.

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Electrophysiological studies on the effect of stimulation of the nucleus ventralis anterior (VA)and nucleus reticularis (RET) of the thalamus were conducted in the rabbit. The following results were obtained.
1) The ave rage spike and wave pattern appearing in the cerebral cortical EEG on stimulation of the VA with 3 Hz and that induced by a similar stimulation of the RET was calculated by use of the digital computor (Nihon Kohden ATAC-201) and a comparison of the patterns showed that spikes predominated when the VA is stimulated and waves predominated when the RET is stimulated.
2) Late components N6 and N7 of the average evoked potential appearing in the cerebral cortex on stimulation of the sciatic nerve are suppressed by 3Hz stimulation of the VA and intensified by stimulation of the RET.
3) Late components HN5 and H N6 of the average evoked potential of the hippocampus elicited by stimulation of the sciatic nerve are at times intensified by stimulation of the VA and RET with 3 Hz and suppressed at other times but a trend for intensification was greater with stimulation of the RET.
4) The integratin g value of the evoked muscular discharge, appearing in the fore-and hindlimbs on stimulation of the cerebral cortex, increased or decreased with stimulation of VA (3,8Hz) and RET (3,8 Hz) but a greater trend for decrease was observed with VA atimulation compared to RET stimulation.
5) The integratin g value of the evoked muscular discharge, appearing in the fore- and hindlimbs on stimulation of the hippocampus, increased or decreasad with stimulation of VA (3,8 Hz) and RET (3,8 Hz).
6) A trend for decrease in the carotid blood flow was noted on stimulation of the VA (3,100Hz) but there was little change on RET stimulation (3,100 Hz).
7) The frequency of spontaneous discharges of the cervical sympathetic trunk increased with VA stimulation (3,100 Hz) but decreased with RET stimulation (3,100 Hz).
8) The arrest reaction in the behavior of the rabbit with both VA stimulatio n (3,100 Hz)and RET stimulation (3,100 Hz) but a trend for a lower threshold was noted with VA stimulation.
9) The effect of drugs (morphine, barbiturate, chlorpromazine, tridion) on the spike and wave pattern elicited by 3 Hz VA and 3 Hz RET stimulation was studied using the digital computor (ATAC-201) and it was found that tridion had a suppressive action on the spike induced by stimulation of both VA and RET.
The findings suggest that VA is involv ed in the appearance of petit mal symptoms and spikes are more closely related than waves. It can also be said that drugs like tridion, which show a suppressive action on spikes rather than on waves, will be more effective in the petit mal patient.

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It has been suggested that from Lee's and other investigator's light microscopical studies necrogenic changes may play an important role in the ceroidogenesis.
An attempt was made to develop a diet-induced hepatic necrosis in JCL/ICR strain mice. One group of mice was fed on Sigma-made dried baker's yeast (Type I) diet, a modified vitamin-E deficient for 21-560 days (A group). Another group was fed on 0.06% DAB diet for 3-520 days (B group).
Light microscopical exam inations of the liver from the both A and B groups revealed hepatocytes undergoing “shrivelled necrosis” (Takagi,1964) in the early experimental stage, and in the later stage ceroid coexisting with hemosiderin granules was found in the Kupffer cells. Intra-nuclear inclusion bodies in the hepatocytes also were occasionally visible.
Electron microscopically the hepatocytes showing cytoplasmic condensation w ere accompanied by various degeneration, i. e., an increased matrical density, extreme mitochondrial swelling and soon. The above changes similar to those observed in “dark cells” might shift to “shrivelled necrosis”.
These degenerated hepatocytes showed all stages of focal cytoplasmic degradation and autophagic vacuoles including denatured cellular organelle. Occasionally Councilman-like bodies were fou nd within the cytoplasm of the degenerated hepatocytes as well as in the sinusoid. The findings corresponding with “apoptosis” (Kerr et al.,1972) also were found in some cases.
Alternatively, fragments of cellular debris probably derived from necrotizing liver cells were found to be ingested by Kupffer cells, which included acid-phosphatase-positive phagolysosomes (pigment bodies) constituting the ultrastructure of ceroid. Besides, these phagolysosomes contained, in addition to membranous structures, multivacuolar structures, osmiophilic structures with large or small vacuoles and innumerable ferritin particles.
These findings suggest that the phagocytosis by Kupffer cells of disintegrated liver cells or their cellular debris plays an important role in the ceroidogenesis in the Kupffer cells.
It is noted that the A group disclosed hemoglobinuria suggesting elevated hemolysis and crystal-like structures measuring 5μ in length, possibly derived from erythrocytes in the pigment bodies.
These findings similar to those peculiar to vitamin-E-deficient animals may have been induced, due to the dietary components given the same group.
Moreover, intranuclear inclusion bodies in the hepa tocytes and the findings suggesting “apoptosis” (Kerr et al.,1972) between Kupffer cells and necrotic material were found in both the A and B groups.
The likelihood th at a cellular immunity might be involved in the occurrence of ceroid in hepatic necrotic lesions also is discussed.

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Atrial fibrillation is a common arrhythmia in Wollf-Parkinson-White (WPW) syndrome and the QRS complex during atrial fibrillation (Af) is usually wide due to delta wave. In the patient with WPW syndrome described here, the QRS complex was wide during normal sinus rhythm (NSR) and was normal during Af.
case report
A 40-year-old businessman complained of a ten-year history of occasional bouts of palpitation.
No abnormalities were detected on physical examination.
The chest X-ray and laboratory data were wi thin normal limits. The 12-lead electrocardiogram during Af showed normal QRS complexes (0.08 sec.) but during NSR. (79 beats/min.) QRS complexes (0.13 sec.) were wide with delta wave and P-R interval of 0.09 sec. which was typical typical type B WPW syndrome.
His bundle electrogram sho wed H-V interval of 50.0 msec. during Af. During NSR A-H interval was 86.2 msec and H-V interval 39.6 msec. Right atrial pacing with progressive reduction in the cycle length resulted in A-H prolongation. H deflection was buried in V deflection at a pacing rate of 128.4/min. and 3: 1 or 4: 1 A-V block occured at 167.8/min.
The atria were stimulated with the basic cycle length of 810.8 msec. LBBB like p attern occured at A₁-A₂ intervals of 410.0 msec. H deflection was buried in V defletion at 370.0msec and QRS was normalized at 325.0 msec. An effective refractory period (ERP) of accessory pathway (AP) and AV node was 353.0 and less than 315 msec., respectively.
AV-A conduction time during ventricular pacing remained constant.
A reciprocating tachycardia could not be induced during the electrophysiological study.
comment
Conduction of the Af impulses to the ventricules occures through normal conduction pathways and/or AP. In most cases A-V conduction occures through AP and QRS complexes are wide with delta wave. The QRS complex is entirely normal when A-V conduction occurs only through normal conduction pathways. However this phenomenon is very rare and only few cases have been reported. Although 'the mechanism is not fully understood, it may be partly explained by: 1) ERP_AP>ERP_{AV node} 2) retrograde concealede conduction to AP were postulated. There are several other possible mechanisms. Due to various direction, rhythm or strength of fibrillation impulse, the fibrillation impulses: 1) cannot input into the AP; 2) are blocked within the AP and 3) cannot stimulate the large ventricular muscles (mismatch impedance). However, more studies are required to corroborate them.

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