J.Jpn. Surg. Soc.. 78(9): 756-768, 1977
Original article
THE CLINICAL AND EXPERIMENTAL STUDY ON THE PATHOGENESIS OF THE CERVICAL VERTIGO
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Department of Neurosurgery, Juntendo University, School of Medicine Yosuke Imai |
Truncal ataxia thus induced was enhanced by the administration of barbiturate of CO- inhalation.
In contrast, the infiltration with procaine to the deep occipito-atlantal region or intravenous administration of the centrophenoxin blocked the induction of staggering.
In the experimental model using dog, it was found that the regional CBF measured in the posterior fossa was reduced after the electrical stimulation to the neck muscles.
In other series of experiments, the monosynaptic reflex (H-Reflex) was examined to ellucidate the effect of neck stimulation on the spinal motor neurons and their rostral control.
The results obtained were, (1) H-Reflex or MSR was either supressed of fluctuated during the vibratory stimulation, (2) After the decerebellation or the transection at the level of the pons or medulla oblongata, the inhibition of H-Reflex by the vibratory stimuli became less marked than that of control, (3) After the transection of the upper cervical spinal cord, inhibitory effect was no longer noticeable.
From these experimental results, the pathogenetic mechanism of the cervical vertigo is presumably caused by the neurogenic factor, i.e. by the abnormal neck reflex. This reflex is probably concerned with muscle afferent, the brain stem, the cerebellum, the hypothalams and the spinal cord. At the same time it is assumed that abnormal vasomotor reflex related with sympathetic system is playing a concomitant role in the development of the cervical vertigo.
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