Cardiac arrhythmia is an uncommon cause of faintness and presyncope. Both bradycardia and tachycardia may induce a transient drop of blood pressure followed by reduction of cerebral blood flow, which evokes faintness and presyncope. The most frequent cause of faintness/presyncope is a neurally mediated reflex, and cardiac arrhythmia is the second common cause in the general population. Since several severe types of arrhythmias may induce sudden death, it is important to recognize faintness and presyncope as a warning sign for further potentially lethal arrhythmic events in selected patients. Taking a detailed medical history and recognition of the accompanied symptoms allows the practitioner to distinguish cardiogenic faintness/presyncope from a neurally mediated one. A definitive diagnosis of cardiogenic faintness/presyncope should be performed by clarifying the direct relationship between the symptoms and documented arrhythmia. However, conventional 12-lead electrocardiography (ECG) and ultrasound echocardiography are useful for risk stratification of faintness/presyncope even after disappearance of the symptoms. Holter ECG and event recorders are widely used for detection of arrhythmic events related with faintness/presyncope. Bradycardia may evoke faintness. However, bradycardia without significant cardiac pause usually accompanies shortness of breath, but not faintness or presyncope. Sudden cardiac pause, with or without preceding tachycardia, is a major cause of faintness/presyncope. Tachycardia is the most important cause of faintness and presyncope. Both supraventricular tachycardia and ventricular tachycardia can cause faintness/presyncope. Of note, faintness and presyncope related with ventricular tachycardia in patients with impaired cardiac function should be evaluated carefully by assessing the risk of sudden cardiac death. Several types of ventricular tachycardia and fibrillation, including Brugada's syndrome, also may cause sudden death. A thorough examination must be performed to clarify the risk of sudden death in patients having these conditions. In conclusion, careful evaluation of faintness and presyncope taking possible involvement of arrhythmia into consideration is important to predict and prevent sudden cardiac death.
Many patients who have been receiving treatment for dizziness in our clinic complained of some worsening of their symptoms or changing of their usual problems after the “Mega-quake” of 11, Mar. 2011, i.e. the Higashi-Nihon Daishinsai earthquake (Magnitude: 9.0). In order to elucidate the influence of the Mega-quake on patients with dizziness, we assessed 235 subjects within 2 weeks after the `quake' with a questionnaire. The number of new patients within the 2 weeks before and after the earthquake rose from 19 to 29. The response rate from the questionnaire was 59%, and the three most serious symptoms were as follows, “horizontal swinging of the earth”, “vertical movement of the earth”, “nausea sensation similar to motion sickness”, rather than the usual symptoms such as vertigo or blackouts. As objective findings, spontaneous and positional nystagmus was encountered 27% of the respondents and one in 5 patients showed a larger area of body sway in the Gravicorder Recording. Some of the neurological considerations were discussed based on the results of our investigation regarding the earthquake and body equilibrium.
A study was conducted on children and adolescents complaining of vertigo, dizziness and equilibrium disturbance who were examined at the Department of Otorhinolaryngology of Mie University Hospital from August, 2000 to July, 2010. Of the 673 patients who visited our vertigo clinic, 22 (3.3%) were 18 years of age or under. Their equilibrium and neurological status were examined. They consisted of 7 boys and 15 girls and their ages ranged from 5 to 18. Of the 22 patients, 9 had orthostatic dysregulation, 8 had peripheral vestibular disorders and 3 had benign paroxysmal vertigo of childhood. In the vestibular diseases of peripheral origin, there were Ménière's disease, bilateral vestibular dysfunction, vestibular neuritis and large vestibular aqueduct syndrome. Regarding the characteristics of vertigo, 8 (35%) complained of rotatory vertigo and 15 (65%) non-rotatory vertigo. Eight (36%) had some kind of hearing loss. The long term clinical course of a 5-year-old girl with Ménière's disease and the clinical course of 9-year-old girl with benign paroxysmal vertigo of childhood are explained in detail.
Objectives: The purpose of this study was to assess the diagnostic accuracy of foam posturography for peripheral vestibulopathy. Methods: Two-legged stance tasks were conducted in patients with peripheral (n=94) vestibulopathy and healthy controls (n=193), under four conditions; eyes open with and without the foam rubber, and eyes closed with and without the foam rubber. We examined 6 parameters: the velocity of movement of the center of pressure, the envelopment area determined by tracing the movement in the eyes closed/foam rubber condition, Romberg's ratio of velocity and area with foam rubber, and the foam ratios (ratios of a measured parameter with and without the foam rubber) of velocity and area with eyes closed. Results: All the 6 parameters were significantly higher in peripheral vestibulopathy patients compared with the controls (p<0.0001). The area under the receiver operating characteristic curve for the Romberg's ratio of velocity with the foam rubber was 0.888, which was the largest, and was not influenced by age in healthy controls. Conclusions: Foam posturography is useful for preliminary assessment of peripheral vestibulopathy. From a practical standpoint, the Romberg's ratio of velocity with the foam rubber seems the most suitable parameter for assessment of patients with peripheral vestibulopathy.
Care seeking behavior in dizziness was analyzed with a questionnaire survey. A quarter of the respondents who experienced dizziness did not consult a medical institution because of slight or transient symptom. Respondents who consulted a medical institution were divided into two groups, the group consulting their family doctor and the group consulting a specialized institution. Thirty-four-point-eight of them had a history of multiple visits. The most common dissatisfaction with medical care for dizziness was poor improvement in the condition. The most common reason for multiple visits was also poor improvement in the dizziness. The recognition rate of the dizziness specialist was the highest in the multiple visits group. Common recognition means were the media and the internet. The dizziness specialist was asked to perform appropriate care on the correct understanding of care-seeking behavior of patients with dizziness.
We report herein on a case of unique head position-induced dizziness and nystagmus. A 64-year-old man complained of recurrent dizziness during head shaking following hair washing for over 20 years. Because a medullary lesion was suspected at another clinic, he was referred to our university hospital. He showed no cochlear or abnormal neurological symptoms. Routine equilibrium function and neurological tests showed unremarkable findings. A T2-weighted image on brain MRI revealed a high-intensity signal area on the ventral medullary surface. No abnormalities of the vertebral artery were found on MRA imaging and transcranial ultrasonography, namely disappearance, meandering, malformation, or stoppage. On examination, the patient showed down beating nystagmus and dizziness when he bent forward swiftly and shook his head in a sitting position. His nystagmus had a small amplitude and lasted for a few seconds during dizziness. From the MRI findings and a history of Fallot's tetralogy, he was diagnosed as having a congenital neuroenteric cyst. He was followed without any conservative management and surgery because his symptoms disappeared by avoidance of the dizziness-inducing head position. Downbeat nystagmus typically occurs in patients with lesions involving the caudal midline of the cerebellum and the lower brain stem. A distinct vertical head-shaking nystagmus suggests the existence of a central lesion. It is speculated in our case that the unique head position and head shaking caused temporary circulatory disturbance of the cerebellum and the lower brain stem systems.