Topographical disorientation was thought to be divided into two groups: scene agnosia and defective route finding. Patients with scene agnosia can morphologically perceive familiar buildings and streets, but cannot identify them. Thy can, however, remember their way around familiar areas. The six patientsin our study all exhibited a common lesion: the posterior part of the right parahippocampal gyrus. We think this region plays an important role in the development of scene agnosia. From the findings of this study, it is suggested that scene agnosia is caused by a disconnection between the visual area that perceives scene and the temporal association areas retaining memories of them. Patients with defective route finding, in contrast to scene agnosia, can identify familiar buildings and streets, but cannot remember their way around well known areas. When we placed them in one spot in an area they were familiar with, they could remember the names and locations of the buildings they could see from that spot; that is, the feature of defective route-finding is the inability to remember the positional relation between two points within a comparatively wide range not surveyable in a single visual experience; in a sense it is a disability in the sense of direction. In four patients ex-hibiting symptoms of defective route-finding, the common lesion was from the right retrosplenial region to the medial part of the parietal lobe, suggesting the association of that region with bearing and orientation functions for navigation over wide spaces.
Recently, many functional areas have been identified in the parietal cortex of the brain in monkeys, and owing to this, cytoarchitectonic subdivision has been elaborated in the monkey parietal cortex. This review deals with sulcal patterns of the parietal lobe in human and monkey brains, and corticocortical connections of both neurophysiologi-cally defined regions and cytoarchitectonic areas of the parietal cortex in monkeys. The author proposes that the transverse occipital sulcus is a boundary between the parietal and occipital cortices in the human brain. A brain map of the monkey is presented. The parietal cortical areas are subdivided into somatosensory, eye movement related, hand or upper limb movement related, vestibular, and auditory areas, according to neu-rophysiologically defined functions of individual cortical areas. The somatosensory system contains areas 3a, 3b, 1, 2, 5, 7b, and SII: S1 projects to motor and premotor areas and somatosensory association areas project to premotor areas, the prefrontal, temporal, and limbic cortices, and the hippocampus. The eye movement system is composed of areas 7a, LIP, and PIP: It receives input from visual and temporal cortices and sends output to premotor areas, the prefrontal cortex, and the hippocampus. Hand movements are mediated in areas AIP, VIP, CIP, MIP, PEc, and V6A: These areas receive afferents from somatosensory areas, visual and temporal cortices and send efferents to the ventral premotor area. The vestibular functions are executed by coordination of areas 3aNV, 3aHV, 2NV, Ri, and VPS: These areas reciprocate with the cingulate cortex and insula and project to the ventral premotor area, SWA, and frontal eye field. The auditory system involves areas VIP and LIP: It receives afferents from the superior temporal sulcal cortex and sends efferents to the premotor area, frontal eye field, and prefrontal cortex.
Spontaneous downbeat nystagmus occurs in patients with lesions involving the caudal midline of the cerebellum and the lower brain stem. However, downbeat nystagmus is also observed in positional and positioning tests. It is speculated that this type differs in origin from spontaneous downbeat nystagmus. This study was designed to investigate the clinical features of positional and positioning downbeat nystagmus. Sixty patients (22males and 38 females) presenting positional and positioning downbeat nystagmus were examined using an infrared CCD camera. The diagnoses of the 60 patients were cerebrovascular disorder in 33, spinocere-bellar ataxia type 6 in 4, multiple systemic atrophy in 3, posterior fossa tumor in 3, Arnold-Chiari malformation in 1, alcohol-induced cerebellar atrophy in 1, arachnoidal cyst in 1, subacute cerebellar ataxia in 1, posttympanoplasty in 4, Meniere's disease in 2, and unknown in 7. We speculated that central positional downbeat nystagmus may be related to imbalance of the sacculo-ocular reflex due to dysfunction of the cerebellar nodulus. Positional and positioning downbeat nystagmus were observed in peripheral lesions besides the central lesions. We speculated that peripheral positional downbeat nystagmus may be caused by dysfunction of the sacculus.
A patient with Meniere's disease demonstrating alternating seesaw-like fluctuation of bilateral hearing loss was treated by intravenous drip injection of glycerol for about 3 years and glycerol test had been performed 59 times. The results showed that the response on the glycerol test was very good even at the advanced stage, but the hearing activity gradually worsened. When the response on the glycerol test was good, his hearing activity recovered quickly after the glycerol test regardless of the hearing level. These results suggest that glycerol is not effective for controlling the hearing loss in Meniere's disease but glycerol might be useful for predicting the recovery of hearing loss or checking the potential of hearing activity.
Treadmill locomotion has become a popular means of indoor exercise. Immediately after stepping off a treadmill following several minutes of exercise, individuals often feel as if the floor on which they are standing carries them forward. After natural running, similar sensations do not occur in healthy subjects. This study was undertaken to explore the nature of impaired postural stability following treadmill exercise. Postural sway was measured in 13 healthy subjects (11 males and 2 females; mean age 21.5 years) after walking with eyes open on a standard treadmill exerciser. The speed of walking was set at 5km/hr, and locomotion was maintained for 2, 4, 8, 16 minutes respectively. The postural sway response was characterized by systematic forward displacement followed by gradual decay to baseline and was accom-panied by perception of motion. Fore back postural sway range (FBPSR) after treadmill walking was significantly greater than FBPSR before treadmill walking. For 2, 4, and 8 minutes of treadmill walking, FBPSR after treadmill walking was greater when the walking time was longer. But for 16 minutes of treadmill walking, FBPSR after treadmill walking was smaller than that after 8 minutes of treadmill walking. For all treadmill walking perception of motion was greater when the walking time was longer. We concluded that treadmill locomotion may cause a visual somatosensory/motor conflict and recalibration of visuomotor control systems may be responsible for the sensation of motion after treadmill walking.
A case of Hunt syndrome with recurrent vertigo and hearing loss is reported. The patient was a 70-year-old male. He complained of oral pain and facial palsy. Vesicles were detected on the left side in his mouth, and audiogram showed sensorineural hearing loss. The serum antibody titer for vallicera zoster virus was significantly elevated. We diagnosed Hunt syndrome, and treated him with intravenous steroid and anti-viral drug administration. He recovered completely without facial nerve palsy, but several weeks later he experienced vertigo. Audiogram showed sensorineural hearing loss again and we diagnosed recurrence of Hunt syndrome.
Down-beat nystagmus is often observed in dizzy patients with a central lesion focus; however, up-beat nystagmus has rarely been noted. A 57-year-old man who com-plained of dizziness was diagnosed as having Wernicke encephalopathy on the basis of neurological findings, an MRI and the past history given at first visit to Aichi Medical University. Up-beat nystagmus was observed under an infrared camera and recorded by electronystagmography (ENG). An eye-tracking test for optokinetic nystagmus showed saccades and ataxia. Vitamin B1 50 mg per day was administered immediately. Although symptoms such as cerebellar ataxia had improved by the third day after administration and were almost absent by the 19th day, saccades and ataxia, recorded by ENG, and up-beating nystagmus remained for more than 4 months.
Benign paroxysmal positional vertigo (BPPV), one of the most common diseases of peripheral vestibular origin, is characterized by transient vertigo accompanied by benign paroxysmal positional nystagmus (BPPN) provoked by turning over in bed, lying down or sitting up. BPPN with a torsional component, short latency and a crescendo-decrescendo mode, is provoked by positional testing and disappears within 30 sec. The direction of the torsional nystagmus, provoked by lying down, reverses by sitting up. The nystagmus may decrease by repeated provocations as an adaptation. Canalolithiasis of the posterior canal is widely accepted as a cause of BPPV, because BPPN is well predicted and BPPV is successfully treated by Epley's canalith repositioning procedure on the basis of this hypothesis. Canalolithiasis of both the horizontal and anterior canals has also been reported as BPPV-variants. In this study, BPPN recorded by an infrared CCD camera and video recorder, and the incidence and meaning of the vertical component of BPPN were investigated in 110 cases of BPPV with torsional BPPN. Out of all 110 cases, up beating vertical component appeared in 39 (35.5%), down beating in 24 (21.8%) and no vertical component in 47 cases (42.7%), when torsional BPPN was provoked by lying down. Horizontal nystagmus of the direction changing type was also observed in 4 cases. According to the canalolithiasis hypothesis, upward and downward vertical components triggered by lying down should occur in the posterior and anterior canal types, respectively. Pure torsional positional nystagmus provoked by positioning was assumed to occur in the crus communis type, in which free-floating endolymph particles remain in the crus communis of the labyrinth.