Vestibular Function Impairment in Alzheimer's Disease.

BACKGROUND: Falls and fractures due to impaired balance in patients with Alzheimer's disease (AD) have an adverse effect on the clinical course of the disease. OBJECTIVE: To evaluate balance impairment in AD from the viewpoint of vestibular functional impairment. METHODS: The subjects were 12 patients with AD, 12 dementia-free elderly adults, and 12 younger adults. Vestibular function was assessed using a stepping test, caloric nystagmus, and a visual suppression (VS) test. RESULTS: The stepping test was abnormal in 9 of the 12 patients in the AD group. An abnormal stepping test was not associated with self-reported dizziness or tendency to fall. Significant VS abnormalities were present in the AD group. The suppression rate of VS was lower in AD patients with either a tendency to fall or constructional apraxia than in AD patients without either. The velocity of the rapid phase of caloric nystagmus before the VS test was similar in the AD group and the elderly control group. Significant abnormalities of both caloric nystagmus and VS were not present in either the elderly or the younger control groups. CONCLUSION: AD could involve impairments in the vestibular control of balance. The VS test is useful for assessing the tendency to fall in AD. Impairment of VS in AD might arise from cerebral vestibular cortex impairment rather than comorbid peripheral vestibular disorders.

Residual central nervous system damage due to organoarsenic poisoning.

BACKGROUND: Drinking well water contaminated with the organoarsenic compound diphenylarsinic acid (DPAA) causes central nervous system (CNS) disorders that improve within several years after last drinking such water. Subjective symptoms such as lightheadedness and dizziness appear to persist, however, suggesting CNS damage. We evaluated CNS damage due to DPAA by detecting abnormal eye movements. METHODS: Subjects comprised 29 victims of exposure to DPAA in whom this substance had been detected in the nails. Investigations were performed more than 3years following cessation of DPAA exposure. Abnormal eye movements were monitored using electronystagmography. We analysed unpaired t-test between exposure subjects who exhibited upbeat nystagmus and those who did not. Upbeat nystagmus parameters were measured, and mean values were calculated. Associations between the properties of upbeat nystagmus and maximum concentrations of DPAA among DPAA exposure were also investigated. RESULTS: Upbeat nystagmus was common among exposure victims, occurring in 23 of 29 subjects (79.0%). The subjects with upbeat nystagmus had significantly higher ratio than those without upbeat nystagmus in the points of subjective symptoms and DPAA concentration of drinking water (p<0.01). The slow-phase amplitude of upbeat nystagmus enlarged with increasing DPAA concentrations, showing a significant positive correlation (p<0.05). These findings suggest that the level of exposure to DPAA affects the properties of nystagmus. High-frequency pathological square-wave jerks (SWJ) were seen in 14 of 29 patients (48.0%), and mean SWJ frequency was 112.4±16.7/min. CONCLUSIONS: Detection of abnormal ocular movements may be useful in evaluating residual/persistent/chronic CNS damage due to organoarsenic poisoning.

Downbeat nystagmus associated with damage to the medial longitudinal fasciculus of the pons: a vestibular balance control mechanism via the lower brainstem paramedian tract neurons.

The paramedian tract (PMT) neurons, a group of neurons associated with eye movement that project into the cerebellar flocculus, are present in or near the medial longitudinal fasciculus (MLF) in the paramedian region of the lower brainstem. A 66-year-old man with multiple sclerosis in whom downbeat nystagmus appeared along with right MLF syndrome due to a unilateral pontomedullary lesion is described. In light of these findings, a possible schema for the vestibular balance control mechanism circuit of the PMT neurons via the flocculus is presented. Damage to the PMT neurons impaired the elective inhibitory control mechanism of the anterior semicircular canal neural pathway by the flocculus. This resulted in the appearance of anterior semicircular canal-dominant vestibular imbalance and the formation of downbeat nystagmus. From the pathogenesis of this vertical vestibular nystagmus, the action of the PMT neurons in the vestibular eye movement neuronal pathway to maintain vestibular balance was conjectured to be as follows. PMT neurons transmit vestibular information from the anterior semicircular canals to the cerebellum, forming a cerebellum/brainstem feedback loop. Vestibular information from that loop is integrated in the cerebellum, inhibiting only the anterior semicircular canal neuronal pathway via the flocculus and controlling vestibular balance.