The neural mismatch hypothesis in the development of motion sickness is widely accepted. Essential to the neural mismatch hypothesis of motion sickness is the neural mismatch signal encoding spatial disorientation. We examined the neurochemical response to caloric stimulation with hot or cold water in the rat brain. Caloric stimulation with hot or cold water induced biphasic release of glutamate in the vestibular nucleus, indicating that the vestibular input is directly transmitted from the inner ear to the vestibular nucleus. However, hot or cold caloric stimulation induced monophasic release of histamine and acetylcholine in the hypothalamus and hippocampus respectively, suggesting that the neural mismatch signal, but not vestibular input itself, is transmitted to these regions. Our previous study showed that the hypothalamus plays an important role in the vestibulo-autonomic reflex. Since the hippocampus has a "spatial map", the possibility was examined that the hippocampus generates the neural mismatch signal. In our lesion study using a rat model, hippocampal lesion aggravated motion sickness, suggesting that the hippocampus counteracts spatial disorientation. The cerebellar lesion has no effect on the development of motion sickness, suggesting that the cerebellum is not the region generating the neural mismatch signal.
The vestibulo-ocular reflex (VOR) generates smooth eye movements that are compensatory for head movements to ensure gaze stabilization during head rotation. The VOR, which consists of semicircular-ocular reflex (ScOR) and otolith-ocular reflex (OOR), is adaptively controlled to correct VOR performance when visual-vestibular mismatch arises during head movement. Most studies have investigated horizontal ScOR gain adaptation after exposure to enhanced, reduced, or direction-reversed visual surround motion produced either by optical devices or by coupling altered visual surround motion with head movement in such a way as to reduce or eliminate retinal image slip during head movement. In natural head movement, not only the ScOR, but also the OOR must be used to keep the line of sight stationary in space. It remains unclear how human subjects combine input from the semicircular canals and otolith organs to establish spatial orientation. To investigate the synergy of the ScOR and the OOR, we examine the plasticity of the OOR using visual-vestibular interaction and the effect of adaptive plasticity in the OOR upon ScOR. We demonstrated a reason-ably consistent effect of adaptation of OOR sensitivity on the ScOR using a visual magnification paradigm. Our data suggest that the OOR and the ScOR partly share common neural pathways in such a way that a change in the synaptic efficacy of one pathway is accompanied by a change in the other. Recent data have also suggested the existence of a convergent neuron that receives input from both the semicircular canals and otolith organs in the cat. The role of a neural store that receives input from both the semicircular canals and the otolith organs to maintain a spatial orientation is discussed.
We report a patient with Neurovascular Compression Syndrome (NVC) who felt solo vertigo. A 48-year-old male with a history of asthma, complained of vertigo without cochlear symptoms. On brain MRI and MRA, he was found to have "dolichoectasia" in his left vertebral artery. We suspected that dolichoectasia induced his vertigo, speculating that his left vertebral artery (VA) compressed his left vestibular nerve (VN). Pre-operative examination of neurotology showed normal values except for VEMP (vestibular-evoked-myogenic-potentials). In operation for microvascular decompression (MVD), we confirmed left VA and that the posterior-inferior cerebellar artery compressed his left inferior vestibular nerve. MVD was successfully performed. Post-operative examination of neurotology showed all normal, including VEMP. The diagnosis of NVC and the indication of MVD for NVC were decided carefully, and we confirmed that VEMP was very useful for the diagnosis of NVC.
We compared the results of analysis of vestibulo-ocular reflex (VOR) obtained by manual rotation with those of a caloric test performed at the interval of one hour, and examined the validity and limitations of VOR analysis as a test for the estimation of vestibular function and imbalance in routine vestibular clinical practice. VOR response was recorded by a manually rotating standard clinical chair for approximately 40 s. VOR gain was slightly, but significantly, correlated with the peak slow phase velocity of caloric response (r=0.253, p<0.05). However, patients with poor caloric response failed to exceed the range of two standard deviations of the mean value of normal subjects, indicating that it is clinically difficult to use VOR gain alone as an estimate of unilateral vestibular function. VOR directional preponderance (VOR-DP%) correlated well with caloric canal paresis (CP) (CP%; r=0.605, p<0.001). VOR-DP% was within the normal range in patients with caloric CP%<20 and exceeded the normal range in most subjects with caloric CP%>50. VOR-DP% varied widely when caloric CP% ranged between 20 and 50. Visual suppression in VOR(VSrot)correlated well with that in caloric test (VScal)(r=0.460, p<0.05). In all cases with VScal<40, VScal exceeded the normal range. These results indicate that determination of VOR-DP% and VSrot should contribute to the early diagnosis of fresh vestibular disorder, especially in daily clinical practice.
Benign Paroxysmal Positional Vertigo (BPPV) is a common vestibular disorder, and the symptoms are well controlled by physical maneuvers. However, some patients suffer relapse. We examined the prognosis of BPPV after the canalith repositioning procedure (CRP). CRP was effective in about 95.1%, but 13% relapsed. All relapsed cases were women aged over 40 years, however, no factor responsible for the relapse was identified. Disturbance of Ca metabolism in the otoconia due to aging or menopause may be involved in the relapse. CRP is effective, but we must always be aware of the possibility of relapse.
Intracranial hypotension, caused by lumbar puncture, spinal anesthesia, arachnoidal cyst, and arterio venous malformation, has become increasing common. Symptoms vary including vertigo, tinnitus, hearing loss, headache, photophobia, and nausea. These are relieved upon reclining and are worsened by sitting or standings. We treated a patient in whom dizziness and tinnitus were evoked after anesthesia, and downbeating vertical nystagmus, was recorded by infra-red CCD camera. Our findings suggested this patients nystagmus was caused by downward displacement of the cerebellum due to intracranial hypotension.
Periodic alternating nystagmus (PAN) is defined as abnormal horizontal eye movements whose directions periodically alternate. It is an unusual finding, except in congenital nystagmus, but has manifested in various disorders. Despite the many reports about PAN, the length of the cycles has not been discussed. In this paper, we report two cases of PAN, and demonstrate that there are two types of PAN which are de-fined by the length of cycle. One type is symmetric, the length of the cycle toward the right and/or left is regular, and the other is asymmetric, the cycle is irregular and the direction changes at random. Case 1 was a 38-year-old man with spinocerebellar ataxa 6 (SCA6) showing symmetric PAN. Brain MRI showed atrophy of the cerebellum. He suffered from oscillopsia and his cerebellar disequilibrium was severe. Case 2 was a 21-year-old man with congenital nystagmus showing asymmetric PAN. Because he was negative for CNS lesions, and specific nystagmus of pendular jerking type was seen, his disease was diagnosed as congenital nystagmus. The direction and cycle of PAN was irregular. The diseases and mechanism of PAN in these two patients may differ. PAN caused by central nervous disorders is strictly symmetric, while others are asymmetric.