Abnormal autonomic function has a significant impact on the appearance and severity of dizziness. Therefore, it is important to evaluate the autonomic nervous system function in clinical practice. While the autonomic nervous system is anatomically classified as a peripheral nervous system, it is innervated by a higher central nervous system that is associated with psychological factors such as stress and emotion. Abnormal autonomic function has both organic and functional aspects, and both often coexist and are difficult to categorize clearly. However, the degree of dysfunction perceived by the patients themselves can be assessed by means of several questionnaires. The Toho Medical Index consists of 43 questions on symptoms related to autonomic dystonia and 51 questions on psychological symptoms, which can be answered with a “yes” or “no”. The index can be classified into four patterns, such as “Vegetative syndrome,” by answering “yes” or “no” to questions consisting of 43 autonomic nervous system-related symptoms and 51 mental symptoms. Another method is to observe autonomic dysfunction indirectly by evaluating the effects of the central nervous system, known as central sensitization. The Central Sensitization Inventory is used internationally to evaluate central sensitization. The Somatic Symptom Scale-8 is a questionnaire that assesses the burden caused by physical symptoms, including dizziness, through eight questions. In our previous study, we were able to extract the effects of central sensitization in somatic symptom disorder with high accuracy by utilizing this questionnaire. In the clinical evaluation of dizziness, it is necessary to evaluate not only organic abnormalities of the autonomic nervous system but also functional disorders of the autonomic nervous system, and the questionnaires mentioned above may serve as simple screening tools.

Herein, we present the case of a patient with dizziness who presented with various clinical findings associated with lithium toxicity. The patient, a man in his 40s, had been receiving treatment for bipolar disorder, depression, and delusional disorder for four years. Shortly after he started receiving lithium carbonate (200 mg/day) for bipolar disorder, he developed dysarthria and an unsteady gait. Two weeks thereafter, he developed consciousness disturbance and was transported to the emergency room of a nearby hospital. Based on the high blood concentration of lithium (2.19 mEq/L), the patient was diagnosed as having lithium toxicity. His systemic symptoms improved with hemodialysis; however, he continued to suffer from dizziness episodes, prompting referral to our department for further examination. At our department, gaze testing with the patient sitting upright revealed spontaneous nystagmus on lateral gaze. Positional testing in the supine position showed a downbeat nystagmus. An eye tracking test demonstrated a saccadic pattern, and optokinetic nystagmus testing indicated poor nystagmus development. Additionally, caloric testing showed reduced vestibular response and impaired visual suppression. A brain MRI showed no abnormalities. Based on these findings, we concluded that the patient’s dizziness could be attributable to cerebellar dysfunction caused by lithium toxicity. Despite treatment, however, the dizziness failed to improve. Lithium carbonate has a narrow therapeutic index, necessitating careful monitoring during administration. Notably, in patients receiving diuretics, ACE inhibitors, NSAIDs, or metronidazole, drug-drug interactions are associated with a higher risk of lithium toxicity. Furthermore, patients taking psychotropic medications, phenothiazines, or butyrophenones are at a higher risk of developing irreversible cerebellar or extrapyramidal symptoms associated with lithium toxicity. Therefore, frequent monitoring of serum lithium levels should be ensured in patients receiving treatment with lithium carbonate.

We report a case of a 79-year-old man who presented with positional vertigo and spontaneous downbeat nystagmus and was diagnosed as having vertebrobasilar insufficiency. Magnetic resonance angiography (MRA) and ultrasonographic evaluation of the vertebral artery revealed hypoplasia of the left vertebral artery. Caloric testing did not reveal canal paresis, but visual suppression was weakened, suggesting the presence of cerebellar and brainstem dysfunction. The video head impulse test revealed increased vestibulo-ocular reflex (VOR) gain in the anterior canal and decreased VOR gain in the left posterior canal, which was thought to be due to disinhibition of the VOR of the anterior canal due to damage to the floccules, and impairment of the VOR of the posterior canal due to damage to the pons. This led to hyperfunctioning of the anterior canal, with formation of an upward slow phase followed by a downward fast phase, resulting in the appearance of spontaneous downbeat nystagmus. The downbeat nystagmus was observed in the right lateral decubitus position in the absence of cervical twisting, but disappeared during the supine roll test in the right-head-down position with cervical twisting. This disappearance was due to a decrease in blood flow in the left vertebral artery caused by rightward twisting of the neck, which led to dysfunction of the midbrain-pontine junction and disappearance of hyperfunctioning of the VOR of the anterior canal.

Vestibular rehabilitation (VR) for patients with bilateral vestibular dysfunction is considered, in general, to be less effective as compared with that for those with unilateral vestibular dysfunction. Herein, we report the case of a patient with bilateral vestibular dysfunction in whom VR was associated with marked improvement of the vestibular symptoms.

The patient was a 67-year-old man who primarily communicated through writing because of severe bilateral sensorineural hearing loss and speech impairment since childhood. He presented with a 2-year history of dizziness and increasing unsteadiness, particularly during movements and in dark environments. Vestibular function testing led to the diagnosis of bilateral vestibular dysfunction, and VR was prescribed.

Over a three-month period, the patient underwent seven 40-minute VR sessions with a physical therapist and performed exercises at home for at least 20 minutes daily. The VR program included gaze stability exercises, habituation exercises, and substitution exercises. Since verbal communication was not possible, alternative communication strategies, such as instructions displayed on a tablet screen and gestures, were employed during the VR sessions. The patient successfully completed the three-month VR program without any adverse events.

The dizziness severity, as assessed by the Dizziness Handicap Inventory (DHI), improved, with the score decreasing from 24 to 12. Motion sensitivity, measured by the Motion Sensitivity Quotient (MSQ), improved, with a reduction of the score from 28.3 to 4.7. Gait function, evaluated by the Functional Gait Assessment (FGA), improved, with the score increasing from 22 to 27. Static balance, measured by total path length in the eyes-closed without rubber condition of posturography, improved, with decrease of the path length from 472 cm to 267 cm in 60 seconds. The patient continues to visit our otolaryngology department and is now able to carry out daily activities without difficulty.

Despite the patient being unable to communicate verbally, the implementation of alternative communication methods allowed effective VR to be implemented, leading to symptom improvement.

The utility of balance function tests in the diagnosis of vertigo was retrospectively evaluated using paper-based data (1996–1998) and digitally collected data (2023–2024). Data of a total of 1,392 cases from the paper dataset and 182 cases from the digital dataset were analyzed by logistic multivariate analysis for major vertigo disorders. The diagnostic value of individual tests varied by disorder, and the incorporation of newer testing modalities appeared to enhance the diagnostic accuracy. While data entry from paper records was time-consuming, the digital dataset allowed for efficient data capture and reliable storage, underscoring its potential usefulness for the development of AI-based automated diagnostic systems.

Relapsing polychondritis (RP) is a rare, progressive systemic inflammatory disorder that targets the cartilage and proteoglycan. While occurrence of audiovestibular symptoms has been reported in 20%–50% of cases of RP, reports of detailed vestibular assessments remain limited. This study was aimed at clarifying the characteristics of audiovestibular dysfunction in patients with RP through comprehensive neuro-otological evaluations.

We retrospectively reviewed the data of five patients diagnosed as having RP based on the clinical symptoms and results of cartilage biopsy between 2009 and 2025. All the patients were evaluated by pure-tone audiometry and vestibular testing, including caloric testing, cervical vestibular evoked myogenic potential (cVEMP), and ocular VEMP (oVEMP), and their clinical omit outcomes were evaluated.

All five patients exhibited bilateral sensorineural hearing loss. Although only two patients reported dizziness or imbalance, vestibular function testing revealed moderate to severe bilateral canal paresis and VEMP abnormalities in all five cases. All the patients received steroid therapy, and while the hearing improved in two cases, vestibular dysfunction persisted in all three cases in whom the treatment outcomes were evaluated.

This study showed that detailed neuro-otologic evaluation frequently reveals the presence of asymptomatic vestibular dysfunction in patients with RP, which tends to be refractory to treatment. Therefore, potential balance impairments should be taken into consideration when managing patients with RP.

Managing acute vertigo in the emergency department (ED) presents several challenges: (1) emergency physicians must differentiate dangerous cases of vertigo; (2) determining the appropriate department to admit the patient to for undiagnosed, but admission-requiring vertigo can be difficult; (3) contacting and calling the on-call physician responsible for the hospitalized patient is necessary; and (4) significant time is required to manage cases where medically stable patients refuse to go home due to anxiety or social reasons. These issues place a heavy burden on the ED staff.

To address these challenges, we introduced a clinical pathway for the hospitalization of patients with acute vertigo. Dangerous causes of vertigo, such as cerebral infarction, are ruled out by obtaining brain MRI with diffusion-weighted imaging. The designated admitting department is otolaryngology. Emergency physicians can apply the pathway at their discretion without consulting an otolaryngologist. Eligible patients include those experiencing continuous vertigo for more than one hour. Additionally, patients who request hospitalization, even for social reasons, are also eligible.

The implementation of this pathway not only reduced the burden on the ED staff but also led to positive outcomes, including an increase in the number of hospitalized patients.

To differentiate dizziness of central origin, it is necessary to focus on neurological signs and symptoms other than dizziness. However, the pathology of dizziness cannot be determined from neurological signs/symptoms other than dizziness.

Like peripheral dizziness, central dizziness is often caused by vestibular imbalance, more precisely, a disruption of the central vestibular pathway, which includes not only the horizontal, but also vertical and rotational directions. Vestibular imbalance is reflected in eye deviation and nystagmus. Therefore, even in cases of central dizziness, the pathology causing the dizziness can be identified by using Frenzel glasses to evaluate eye deviation and nystagmus. Actually, in clinical practice, it is much more useful to use Frenzel goggles to correctly evaluate vestibular imbalance, the main cause of dizziness, rather than engage in a systematic differential diagnosis of dizziness in a broad sense, including circulatory insufficiency and anemia.

When differentiating central dizziness, it is not sufficient to look for neurological signs/symptoms other than dizziness. It is also necessary to identify the underlying pathology of the dizziness using Frenzel goggles.

Videooculography (VOG) enables evaluation of three-dimensional eye movements, including horizontal, vertical, and torsional components. Recent technological advances have further enhanced VOG as both a research and clinical tool. Developments include quantitative analysis of nystagmus, examinations using visual stimuli, integration with filing systems, and high-speed video recording. High-speed VOG allows for more detailed capture of rapid eye movements as compared with conventional systems. We recorded eye movement responses to galvanic vestibular stimulation (GVS) using our VOG system. Horizontal and torsional nystagmus was observed, with responses depending on the polarity and intensity of the stimulation.