[Chronic dizziness in elderly people: its clinical characteristics and magneto-encephalographic findings]

Hiroaki Naritomi
Rinshō Shinkeigaku, Clinical Neurology 2008, 48 (6): 393-400
Many elderly people complain dizziness which may continue occasionally for months or years. According to epidemiological studies, 25-29% of subjects with more than 60 years of age have the experience of dizziness. Dizziness occurs most commonly during head positional changes or walking. Clinical studies have indicated that causes of dizziness are nonspecific and multi-factorial; cerebrovascular diseases, cervical spondylosis, depressive state, poor vision, orthostatic hypotension, whiplash injury, or low cerebrospinal fluid syndrome may play a role in the development of dizziness. Patients with dizziness commonly have neck/shoulder pain, insomnia, left-right imbalance of visual acuity, scoliosis, white matter lesions on head MRI. Little, however, has yet been known as to how these symptoms and radiological findings are related to mechanisms of dizziness. During the last several years, we performed cerebral functional studies using auditory-evoked magneto-encephalography (MEG) in elderly people with chronic dizziness. Two types of functional abnormalities were found in dizziness patients. One is a rotational abnormality of MEG signals at the temporal cortex (Type A) which can be detected by current arrow mapping analysis. This abnormality is similar to that detected by non-evoked MEG in temporal lobe epilepsy patients. In patients with Type A abnormality, administration of anticonvulsants brought about dramatic improvement of dizziness in association with disappearance of rotational abnormalities. The other is abnormal prolongation of interhemispheric neural conduction time (INCT) between the left and right temporal cortices (Type B) which can be estimated from the difference of left and right N100 m peak latencies. The INCT was found to be prolonged correlating with the grade of white matter lesions on MRI. The INCT also seems to be prolonged by lack of sleep. Patients with Type B abnormality commonly have the asymmetry of body, such as left-right imbalance of visual acuity, left-right neck pain, or remarkable scoliosis, in association with insomnia and/or depressive state. According to the study of Penfield, dizziness or vertigo is manifested by stimulation of upper temporal cortex and lower parietal cortex. Mechanisms of dizziness can be hypothecated on the basis of MEG findings as follows: Presumably, there are head-position recognizing (HPR) centers in the left and right cerebral hemispheres. The HPR centers may correspond to the vestibular cortex or the combined system of vestibular, visual and somatosensory cortices. The HPR centers in two hemispheres are receiving head-position signals from vestibular, visual and somatosensory corices and are readjusting the dissociation of information which may exist between each other through rapid interhemispheric neural conduction. In patients with Type A abnormality, dizziness may be caused by abnormal neuronal excitements in left or right HPR center. In patients with Type B abnormalities, dizziness may be caused by the combined factors, one the abnormal prolongation of INCT between left and right HPR centers and the other the large dissociation of head position signals between the left and right HPR centers due to the body asymmetry, such as scoliosis or left-right neck pain imbalance.

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