During the treatment process for benign paroxysmal positional vertigo (BPPV) using the canalith repositioning procedure, the otolith can inadvertently enter the semicircular canal instead of the utricle. Canal conversion refers to the situation where the otolith enters a different semicircular canal, while reentry occurs when the otolith returns to the same semicircular canal. The occurrence of a canal conversion can complicate the accurate diagnosis and treatment of BPPV, potentially leading to misdiagnosis and unsuccessful results in the canalith repositioning procedure. In this review, we aim to summarize the incidence, clinical features, and associated risk factors of canal conversion and reentries.
Benign paroxysmal positional vertigo (BPPV) is the most common cause of positional vertigo and nystagmus. Direction-changing positional nystagmus (DCPN), which refers to the change in the direction of nystagmus with different head positions, is a well-known characteristic of horizontal semicircular canal BPPV. The supine head roll test is commonly used to diagnose horizontal canal BPPV. However, persistent geotropic DCPN observed during this test cannot be explained by conventional mechanisms of canalolithiasis or cupulolithiasis. The concept of a “light cupula” has been proposed to account for this unique nystagmus. In this review, we summarize the historical background, clinical features and diagnostic methods, presumed mechanisms, and treatment approaches of the light cupula phenomenon based on the available literatures up to date.
Benign paroxysmal positional vertigo (BPPV) is the most common etiology of benign vestibulopathy. Various treatments for BPPV have been developed, and appropriate treatments for each subtype of BPPV have been provided and used in accordance with clinical practice guidelines published by the American Academy of Otorhinolaryngology-Head and Neck Surgery in 2008 and 2017. Although many therapeutic maneuvers have been reported to show high success rates in the treatment of BPPV patients, some cases are not effective even by appropriate therapeutic maneuvers. This article reviews various factors affecting the successful treatment of BPPV patients.
Vestibular migraine (VM) is a variant of migraine resulting in vestibular symptoms in addition to symptoms typical of migraine. However, without a biomarker or a complete understanding of the pathophysiology, VM remains underrecognized and underdiagnosed. Therefore, the diagnosis of VM is still challenging. Meanwhile, VM should be clearly differentiated from other similar diseases. Here, we highlight these challenges, discuss common vestibular symptoms and clinical presentations in VM, and review the current aspects of its clinical diagnosis and evaluation. The concepts related to the treatment of VM are also discussed.
Anxiety, depression, or other psychiatric symptoms can be the primary cause of dizziness and the secondary complication of dizziness. Regardless of precedence or consequence, dizziness is closely associated with the psychiatric problem. On this ground, this chapter reviews the association between dizziness and anxiety and the treatment for dizziness with psychiatric symptoms.
As the first audiovestibular medicine physician in the University of Port Harcourt Teaching Hospital, Nigeria, a keen observation revealed that a sizeable proportion of the adult patients presenting to our audiovestibular medicine clinic with vertigo are either known hypertensives, or hypertensives yet to have a formal diagnosis. This aroused an ardent curiosity to find the raison d’être, and to shed light on this pathological association between vertigo and hypertension. In line with this, it became imperative to highlight the dynamics of interaction, and pathophysiology behind the role of hypertension in vertigo.
Postural orthostatic tachycardia syndrome (POTS) is a cerebrovascular autonomic dysfunction that is common in young women. POTS can cause dizziness due to orthostatic intolerance. In patients with orthostatic intolerance, it can be diagnosed when the heart rate increases by more than 30 beats per minute within 10 minutes of standing up through the head-up tilt test. However, even a neuro-otologist has difficulty in diagnosing POTS due to the high possibility of misdiagnosis if not paying attention. In this paper, the clinical symptoms, pathophysiology, diagnosis, and treatment of POTS are investigated. In addition, the latest knowledge of POTS is searched to help diagnose and treat POTS.
Vestibular schwannoma (VS) is commonly encountered in the cerebellopontine angle and benign neoplasms that arise from Schwann cells of the eighth cranial nerve, which can show not only hearing loss but also various vestibular symptoms. Dizziness is the symptom causing significantly negative effect on quality of life in patients with VS. Here, we will review the dizziness in VS.
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The velocity-storage circuit comprised of bilateral vestibular nucleus complexes, commissural fiber, and nodulus and uvula functions in refining the raw vestibular signal to estimate rotational velocity, gravity direction, and inertia. In this review, we pursued the functional significance of this velocity-storage circuit and how this physiologic knowledge could help us understand the clinical symptoms and signs of patients with vestibular disorders.
Central vertigo is the common symptom resulting from abnormalities in the central nervous system, caused by various diseases, which include neurodegenerative, vascular, inflammation, infection, tumor, paraneoplastic, toxic, or metabolic disorders. Since the treatment of central vertigo depends on the causes, an accurate diagnosis should be preceded the treatment through a detailed neurotologic examination and laboratory evaluation. Also, it is important to identify and document the neurologic findings accompanied by central vertigo, because some medication focuses on the ocular motor abnormalities as nystagmus or saccadic intrusion. Here, we will review the medical treatment for central vertigo.
The wide availability of next-generation sequencing has enabled a rapid progress in the discovery of genetic variants associated with many disorders. However, the contribution of genetic factors in vestibular disorders is largely unknown due to the low prevalence of familial disorders and the clinical diversity. A detailed clinical characterization of patients and a choice of proper genetic tests are required to identify the genetic contribution in vestibular disorders. In this review, we will introduce a genetic approach for vestibular disorders and update the evidences to support the genetic contribution in vestibular disorders.
Acute vestibular syndrome refers to the rapid onset of vertigo, nausea, vomiting, and unsteady gait. Acute unilateral vestibular neuritis is the most common cause of acute vestibular syndrome. However, vascular lesions involving the brainstem and cerebellum also produce acute vestibular syndrome even without other neurologic deficits. The vestibular nucleus or nucleus prepositus hypoglossi in the dorsal portion of the brainstem, cerebellar structures including flocculus, tonsil, and nodulus, and cerebellar peduncle can produce isolated vertigo and imbalance when damaged. Early recognition of the pseudo-vestibular neuritis of the vascular etiology is warranted for clinicians.
Various neurotologic findings can be observed in stroke involving the brainstem. Analyses of the neurotologic findings are important in brainstem stroke since it can have negative diffusion-weighted image, as well as, presenting with acute vestibular syndrome in isolation without any associated neurologic deficits. In this review we discuss the neurotologic findings from lesion involving (1) the medial vestibular nucleus, (2) nucleus prepositus hypoglossi, (3) inferior cerebellar peduncle, (4) medial longitudinal fasciculus, (5) rostral interstitial nucleus of the medial longitudinal fasciculus, (6) interstitial nucleus of Cajal, and (7) middle and (8) superior cerebellar peduncles. It is important to recognize these specific neurotologic findings depending on the neural structures involved that may guide early detection and proper management.
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Benign paroxysmal positional vertigo (BPPV) is the most common cause of recurrent vertigo that is characterized by sudden onset of vertigo elicited by positional change. American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) and American Academy of Neurology provided clinical practice guideline for BPPV in 2008. Since then, Bárány Society has published BPPV diagnostic criteria in 2015, and AAO-HNS has revised BPPV clinical practice guideline in 2017 to publish update version. This article reviewed recent diagnostic criteria for BPPV included in the International Classification of Vestibular Disorders of Bárány Society and updated practice guideline in the BPPV diagnosis presented by AAO-HNS.
Persistent postural perceptual dizziness (PPPD) is a chronic functional vestibular disorder that manifests with 3 or more months of dizziness, nonspinning vertigo, and unsteadiness. These main symptoms are exacerbated by upright posture, active or passive self-motion, and exposure to visual stimuli. PPPD is usually precipitated by illnesses that cause vertigo, dizziness, or unsteadiness. The common precipitants are acute or episodic peripheral vestibular diseases including vestibular neuritis, Meniere disease, or benign paroxysmal positional vertigo. PPPD is not a diagnosis of exclusion. An abnormal finding on examination or laboratory testing does not necessarily exclude a diagnosis of PPPD. This article reviewed the Bárány Society’s diagnostic criteria for PPPD in detail and discussed directions of future investigations.