Vertebrobasilar insufficiency (VBI) is caused by transient ischemia in the brainstem including the vestibular nucleus due to impaired vertebrobasilar arterial flow. The most common causes of VBI are atherosclerosis, which can block posterior circulation supplying the brain stem, and embolisms which arise from the heart and proximal vertebral and basilar arteries due to arrhythmia, as well as hemodynamic disorders associated with changes in blood pressure. VBI is frequently associated with vertigo and disequilibrium as primary symptoms accompanied by neurologic symptoms and signs involving double vision, loss of vision, gait ataxia, face and limb numbness, weakness, dysarthria and oropharyngeal dysfunction. Posterior circulation strokes may induce fluctuating symptoms and signs with time depending on which area is ischemic. It is crucial to examine the pathological condition of the vessels in the vertebrobasilar system to evaluate blood flow hemodynamics and vascular morphology in patients experiencing episodes of VBI with Doppler ultrasonography and a vascular imaging technique such as (Magnetic Resonance) MR and (Computed Tomography) CT angiography. Cerebrovascular circulation and metabolism-improving agents, antiplatelet agents, etc., are usually used to treat VBI. VBI should be considered during the differential diagnosis of patients with recurrent vertigo and require an early detection. Therefore, VBI might require careful follow-up and treatment for preventing the progression of vertigo and other neurological deficits in the vertebrobasilar arterial region.
In a previous report, we proposed a method for the frequency analysis of sway of the center of gravity in a standing posture. The method evaluated power-law distribution of the peak-area values in the spectrum from the frequency range 0.01Hz to 5Hz in. In this study, we improved this technique as a method to estimate a high frequency band (1-5Hz) and a low frequency band (0.01-1Hz) separately. Using our improved method, the body sway of 8 healthy adults and 10 healthy elderly people was examined. The elderly subjects showed the following results in comparison with the younger adults. 1) The first was a disorder of the power-law distribution in the low frequency band. This disorder suggests a failure of the interaction between the visual and vestibular systems on the maintenance of the standing posture. 2) The second results was an increase in value of the scaling exponent of power approximation indicating flattening of the power-law distribution curve. The flattening indicates an increase of random tendency of the sway. 3) The third was an increase of the peak-area values in the high frequency band. This finding indicates a failure of fine control of muscle activity by the proprioceptive system.
A 53-year-old man with an esophageal ulcer, mediastinal emphysema, and diabetic ketoacidosis who was highly malnourished developed Wernicke's encephalopathy. He showed lateral gaze-evoked nystagmus and disturbance of gait. A caloric test showed bilateral canal paresis, but cervical and ocular vestibular-evoked myogenic potentials (c-VEMP, o-VEMP) were present. The brain MRI demonstrated a high intensity signal in the bilateral medial thalamic region on T2 weighted images and diffusion weighted images. These findings suggest involvement of the medial vestibular nucleus and the medial thalamic region. Thiamine was administered, but the nystagmus remained. Persisted diet lacking thiamine possibly made the brain lesion irreversible.
Most animals including humans can judge whether an approaching object will hit them, but neural correlates for time-to-collision estimation in primates are still unknown. A previous model study suggested that time-to-collision estimation could be derived in MST using optic flow. In this study, we searched for neural correlates in the dorsal MST and caudal FEF. We examined discharge of single neurons using a Julesz pattern (20° × 20°) combined with a 0.5° single spot. For collision stimuli, a Julesz pattern of 5° × 5° visual angles was first presented on a computer display placed 50cm ahead of the monkeys' eyes. After 0.5-1s, the pattern expanded to simulate its approach to the monkeys at constant velocities of 13-120cm/s from a simulated distance of 75cm for MST neurons (100cm for FEF neurons) until the collision, while the monkeys fixated on a stationary spot on the screen center. We recorded 25 neurons in the dorsal MST that responded to collision stimuli. Of these, 13 neurons responded continuously during collision stimuli indicating that they simply responded to components of the optic flow (group A). The remaining 12 neurons exhibited peak discharge before the time of collision (group B). Time-to-collision of group B neurons depended on the approaching pattern velocity, whereas distance-to-collision was nearly constant, suggesting that group B neurons signaled distance-to-collision. In contrast, most caudal FEF neurons that responded to collision stimuli (8/11) exhibited peak discharge almost at the time of collision, and the peak discharge time remained constant irrespective of the approaching pattern velocity. Most of these neurons (7/8) were pursuit-related. These results suggest that dorsal MST and caudal FEF have different roles in estimating time-to-collision from visual motion.
I analyzed 33 patients with mal de debarquement who visited my clinic in the past 7 years and 8 months. The ratio of female to male patients was 3: 1; 78.8% of the patients who became sick were in their 20s to 40s; 45.4% of the patients had suffered longer than a year. Symptoms were first provoked following travelling on ships in 10 patients, boarding airplanes in 5, taking trains in 3, getting on vehicles in an amusement park in 2, getting in high-speed elevators in 1 (all the above comprised 63.6% of the patients), huge earthquakes in 3, shaking in the building in 1, and giving shows with a grampus dolphin in an amusement aqua-park in 1. Excepting sensuous or visible continuous body sways, patients often complained of brain fatigue, photophobia, having sleepiness in the daytime, headache, and discomfort related with changes in the atmospheric pressure and temperature. Past histories such as dropping, falling down or heavy brows on the neck were found in 48.5% of the patients. Since 4 patients were finally diagnosed to have suffered from cerebrospinal fluid hypovolemia, patients who are suspected as having mal de debarquement should be examined to rule out this disease. The peculiar phenomena associated with the syndrome may be explained by supposing that the brain maintains the illusion of existing in a moving space even after the body has returned to a standstill, or to terra firma, because the brain had been in anomalous or exhausted states.
After the huge earthquake in Japan on March 11th 2011 (magnitude 9.0), many people in the eastern area of Japan close to the epicenter felt dizziness, as if they were rocking at a time when no aftershocks were actually occurring. There are a few reports about dizziness after major earthquakes in the world, but there has been no study so far with analysis of large numbers of cases of earthquake sickness. We conducted an epidemical clinical study and called those symptoms “post earthquake dizziness syndrome; PEDS.” Affected subjects became aware of the rocking feeling within a minute especially when indoors and seated. A significant difference was found with respect to gender, with a prevalence of females, and with the people who were prone to suffer from motion sickness. Otherwise, there was no relationship with case histories of vertigo-related diseases. On the other hand, anxiety and social stress from the disaster seemed to be contributory factors. The underlying mechanism is associated with stimuli to the vestibular and equilibrium balance systems. Emotional disorders such as post-traumatic stress disorder (PTSD) were added to the etiology. For the prevention and treatment, maintaining fitness in daily life and avoiding anxiety caused by reports in the media seemed to be important. Physiotherapy and medication also proved important to prevent symptoms from getting worse.
Postural, tension-type headache is the most prominent symptom of cerebrospinal fluid leakage. However, in otoneurological practice, dizziness and not headache is the most frequent presenting symptom in patients with this disorder. Affected patients usually describe their dizziness as a floating sensation. Rotatory vertigo occurs quite rarely. Their complaint is substantiated by high degrees of postural unsteadiness. Some patients cannot stand still even with their eyes open. They stumble and totter while walking. In contrast to such high degrees of postural ataxia, oculomotor disorders such as nystagmus, saccadic pursuit, and decrease of oculomotor nystagmus are not seen. As with other symptoms, dizziness and postural unsteadiness are influenced by the weather, and get worse when the weather is bad. The authors speculate that unsteadiness in both peripheral and central nervous systems involved in spatial orientation (integration of visual, vestibular, and proprioceptive input) underlies the dizziness, postural unsteadiness, and a variety of other symptoms of cerebrospinal fluid leakage.