Progressive supranuclear palsy (PSP) has been reported as a disorder mainly characterized by a tendency to fall, vertical supranuclear gaze palsy, and constriction of the body axis, akinesia, and cognitive impairment. Patients presenting with these typical clinical features are diagnosed as having the PSP-Richardson syndrome (PSP-RS). Electronystagmography (ENG) is useful for the detection of ocular motility disorder, which is the main feature of PSP. In cases of PSP, ocular motility disorder in the vertical direction occurs from the initial stage of the disease, and is characterized by prolonged latency and reduced velocity of the saccadic eye movement in the vertical direction. Horizontal saccadic eye movement disorder also occurs after the intermediate stage. Square wave jerks (SWJ) are often recognized from the initial stage of the disease. In terms of nystagmus, the quick phase is impaired due to impaired saccadic eye movements, and impairment of optokinetic nystagmus also starts from the quick phase movements. Pursuit (smooth) eye movement may also be impaired as the disease progresses. On the other hand, the vestibulo-ocular reflex is maintained even after disease progression to a late stage.

　Benign paroxysmal positional vertigo (BPPV) is the most common cause of peripheral vertigo, and most types of BPPV are treatable. Apogeotropic horizontal semicircular canal BPPV (AH-BPPV) is a syndrome characterized by apogeotropic horizontal direction-changing nystagmus found on the supine-roll test; it is a rather intractable type of BPPV, and while various otolith repositioning procedures have been proposed, there is no established treatment method such as the Epley maneuver used to treat the posterior semicircular canal type of BPPV. Gufoni and Appiani have proposed otolith repositioning procedures for AH-BPPV; the two maneuvers appear to be close, but are actually different. Gufoni et al. first described using the new repositioning maneuver in Italians in 1998 for both horizontal semicircular canal-type BPPV, namely AH-BPPV, and geotropic horizontal semicircular canal-type BPPV (GH-BPPV). The Gufoni maneuver was modified by Appiani in 2005, and Appiani used the Gufoni maneuver for GH-BPPV after using the Appiani maneuver for treating AH-BPPV when the otolith detached from the cupula. These maneuvers used to treat AH-BPPV were complicated, so that there has been confusion in the naming of and methods used to perform these maneuvers. Some authors have described the Gufoni maneuver as the modified Semont maneuver, and other authors have described the Appiani maneuver as the Gufoni maneuver.

　Herein, we would like to summarize the transition of the otolith repositioning procedures for AH-BPPV over time and in the naming of the procedures.

　Cognitive behavior therapy (CBT) is a recommended treatment option for persistent postural-perceptual dizziness (PPPD). However, evidence of its efficacy is insufficient. This study examined the therapeutic effects of CBT for PPPD. We conducted the study from October 2020 to September 2021. The subjects were 13 patients who had been diagnosed as having PPPD (aged 20 years or older; mean age 45.5 years; range 20 to 78 years) and who wished to undergo CBT because conventional medical treatments and vestibular rehabilitation had been ineffective. Seven patients had preceding vestibular disorders. Four had taken selective serotonin reuptake inhibitors (SSRI) for comorbid psychiatric disorders before their first visit to our hospital. We designed a CBT intervention for PPPD that consisted of eight sessions. A clinical psychologist conducted the intervention once or twice a month for approximately 40 minutes a session. We compared the patients’ scores on the Dizziness Handicap Inventory (DHI), the Hospital Anxiety and Depression Scale (HADS), the State-Trait Anxiety Inventory (STAI), and the Cognitive Bias Scale (CBS) before and after the eight CBT intervention sessions. The DHI-P (physical) and STAI scores improved significantly after CBT. Among the six CBS items, fortune teller error, should thinking, mind reading, and personalization improved significantly after CBT. We concluded that CBT is effective for PPPD and reduces patients’ coexisting anxiety.

　To the best of our knowledge, upbeat nystagmus (UBN) has not been reported before in patients with Parkinson's disease (PD). There are also very few reports of cerebellar atrophy in patients with PD. A-60-year-old woman with a 10-year history of PD visited our hospital for deep brain stimulation therapy for her camptocormia. Neurological examination revealed not only the core signs of PD (rigidity, resting tremor, postural instability), but also UBN. ¹²³I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy revealed markedly diminished uptake of MIBG, strongly supporting the clinical diagnosis of PD. Brain MRI revealed prominent cerebellar atrophy, while the brainstem was preserved. ENG showed that the UBN was observed at the primary eye position and enhanced during upward gaze in the light, but not during downward gaze. In addition to UBN, several other abnormal ENG findings were also observed, including horizontal gaze-evoked nystagmus and rebound nystagmus. Secondly, both horizontal and vertical pursuits were disturbed and horizontal OKN was poorly induced. Lastly, the horizontal saccade was relatively hypometric, while the upward saccades were slight hypermetric. Although the pathogenesis of UBN in this patient still remains unclear, UBN is known to be mainly caused by dysfunction of the velocity-to-position integrator caused by pontomedullary lesions or pontomesencephalic lesions. Alternatively, cerebellar control over this integrator is presumably disrupted by lesions in the cerebellum itself or lesions in the cerebellar neural circuits. As for the pathogenesis of UBN in our case, pontomedullary lesion was first suspected, because, besides the abovementioned ENG findings, most cases of UBN reported in the literature are caused by medullary lesions, including lesions of both the medial vestibular and prepositus hypoglossi nuclei, which play an important role as the velocity-to-position integrator. In addition, dysfunction of the vestibular cerebellum was also suspected as a cause, judging from the cerebellar atrophy and other abnormal ENG findings. In conclusion, it is necessary to consider dysfunction of the vestibular cerebellum as a cause of abnormal eye movements in PD, not to mention dysfunction of the brainstem.

　Vertigo and dizziness are known to be associated with comorbid psychological conditions such as anxiety and depression. In cases with dizziness persisting even after the near-disappearance of objective findings, such as nystagmus, the comorbid psychological condition could be conceived as being the cause of the chronic dizziness. Chronic dizziness may reduce a patient's social activities and deteriorate their quality of life. The Dizziness Handicap Inventory (DHI) is widely used in Europe and the United States as a measure of the degree of disability in daily life associated with subjective dizziness. The purpose of this study was to investigate the factors that affect the scores on the DHI, especially focusing on the psychological characteristics, in order to improve the deterioration of the quality of life caused by dizziness. This study was conducted in 211 patients diagnosed as having benign paroxysmal positional vertigo (BPPV), Meniere's disease (MD), vestibular migraine (VM), or vestibular neuritis (VN). The caloric test was used as the vestibular function test, and Self-rating Depression Scale (SDS), Geriatric Depression Scale-15 (GDS) and State-Trait Anxiety Inventory (STAI) were used as the questionnaires for the psychiatric assessments. In this study, we found no significant differences in the scores on the DHI or prevalence of depressive/anxiety tendencies depending on the causative disease underlying the dizziness. In patients with BPPV and MD, the high scores on trait anxiety and SDS increased the overall score on the DHI. The high scores on state anxiety and vestibular dysfunction also affected the overall DHI score in patients with MD. On the other hand, in patients with VN and VM, the psychiatric conditions had no effect on the overall DHI score. We consider that in vertigo patients with BPPV and MD, early evaluation of anxiety tendencies in patients of all ages and of depressive tendencies in those under the age of 65, and provision of psychological support to patients with depressive tendencies and characteristic anxiety tendencies may contribute to improving the QOL of the patients.

　Electrophysiological measurement of the eye rotation axis using stimulation of a single semicircular canal nerve showed that the eye rotated around the axis perpendicular to the plane of the stimulated semicircular canal. Therefore, the affected semicircular canal can be identified by analyzing the eye rotation axis in cases of abnormal nystagmus. When the main component of the abnormal nystagmus is horizontal, the origin of the nystagmus is the lateral semicircular canal. When the main component of the abnormal nystagmus is torsional, the origin of the nystagmus is the anterior and/or posterior semicircular canal. The eye rotation axis in cases of excitatory nystagmus is quite the same as that in cases of inhibitory nystagmus, although the direction of eye rotation is opposite between cases of excitatory and inhibitory nystagmus. Vestibular neuritis mostly involves the superior vestibular nerve. The superior vestibular nerve transmits sensory information transmitted by from the vestibular hair cells located in the anterior and lateral semicircular canals. Therefore, patients with vestibular neuritis exhibit nystagmus with both horizontal and torsional components caused by inhibition of both the anterior and lateral semicircular canals. In patients with Ménière's disease, during a vertigo attack, excitatory nystagmus of anterior and/or posterior and/or lateral semicircular canal origin can be seen. Because the involving ratio of each contributing ratios of the three semicircular canals to nystagmus can vary, the ratio of the torsional component of the nystagmus to the horizontal component also varies. While nystagmus is purely horizontal in some cases, it is purely torsional in others. In the posterior canal type of BPPV, during the Dix-Hallpike maneuver, transient torsional nystagmus with the torsional component directed toward the affected side can be seen. In the lateral canal type of BPPV (canalolithiasis), geotropic positional nystagmus can be seen when the patient is supine. In the lateral canal type of BPPV (cupulolithiasis), apogeotropic positional nystagmus can be seen when the patient is supine.

　Differentiation of central from peripheral lesions is important when examining patients with dizziness or vertigo. Nystagmus is one of the most important clues to the differential diagnosis between central and peripheral lesions. It is not rare in patients with central lesions to have no neurologic symptoms other than nystagmus in the acute phase. Direction-changing gaze-evoked nystagmus, upbeat nystagmus, downbeat nystagmus and direction-changing apogeotropic positional nystagmus are known as characteristic findings of central vertigo. In this article, we report a case with direction-changing gaze-evoked nystagmus, a case with upbeat nystagmus, a case with downbeat nystagmus, and a case with direction-changing apogeotropic positional nystagmus, and explain/speculate on the mechanism of nystagmus in each case.