Vertigo and dizziness in children.

Vertigo and dizziness in children.

Handb Clin Neurol. 2016;137:353-63

Authors: Jahn K

Abstract
Vertigo and dizziness of at least moderate severity occur in >5% of school-aged children and cause considerable restrictions in participation in school and leisure activity. More than 50% of dizzy children also have headache. Vestibular migraine and benign paroxysmal vertigo as a migraine precursor are the most common diagnoses in dizziness clinics for children and adolescents. They account for 30-60% of diagnoses. Other common causes are somatoform, orthostatic, or posttraumatic dizziness. All other disorders that are known to cause vertigo and dizziness in adults also occur in children, but incidence rates are usually lower. The vestibular and balance systems are largely developed after 1 year of age. Therefore, clinical and laboratory testing is reliable. Brain magnetic resonance imaging to exclude severe conditions, such as a brainstem tumor, is necessary only if clinical - in particular, ocular motor - testing is abnormal. Most conditions causing vertigo and dizziness in childhood and adolescence are treatable. Nonpharmacologic prophylaxis should always be recommended in vestibular migraine. Behavioral support is useful in somatization. Evidence for the effectiveness of drug therapy is largely based on experience in adult populations. High-quality controlled studies in childhood cohorts are sparse. It is important to make a correct diagnosis early on, as counseling and appropriate treatment may avoid chronic illness.

PMID: 27638083 [PubMed - in process]

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Vestibular migraine.

Vestibular migraine.

Handb Clin Neurol. 2016;137:301-16

Authors: von Brevern M, Lempert T

Abstract
During the last decades a new vestibular syndrome has emerged that is now termed vestibular migraine (VM). The main body of evidence for VM is provided by epidemiologic data demonstrating a strong association between migraine and vestibular symptoms. Today, VM is recognized as one of the most common causes of episodic vertigo. The clinical presentation of VM is heterogeneous in terms of vestibular symptoms, duration of episodes, and association with migrainous accompaniments. Similar to migraine, there is no clinical or laboratory confirmation for VM and the diagnosis relies on the history and the exclusion of other disorders. Recently, diagnostic criteria for VM have been elaborated jointly by the International Headache Society and the Bárány Society. Clinical examination of patients with acute VM has clarified that the vast majority of patients with VM suffer from central vestibular dysfunction. Findings in the interval may yield mild signs of damage to both the central vestibular and ocular motor system and to the inner ear. These interictal clinical signs are not specific to VM but can be also observed in migraineurs without a history of vestibular symptoms. How migraine affects the vestibular system is still a matter of speculation. In the absence of high-quality therapeutic trials, treatment is targeted at the underlying migraine.

PMID: 27638080 [PubMed - in process]

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Posttraumatic dizziness and vertigo.

Posttraumatic dizziness and vertigo.

Handb Clin Neurol. 2016;137:295-300

Authors: Szczupak M, Hoffer ME, Murphy S, Balaban CD

Abstract
Traumatic brain injury is an increasingly common public health issue, with the mild variant most clinically relevant for this chapter. Common causes of mild traumatic brain injury (mTBI) include motor vehicle accidents, athletics, and military training/deployment. Despite a range of clinically available testing platforms, diagnosis of mTBI remains challenging. Symptoms are primarily neurosensory, and include dizziness, hearing problems, headaches, cognitive, and sleep disturbances. Dizziness is nearly universally present in all mTBI patients, and is the easiest symptom to objectify for diagnosis. Aside from a thorough history and physical exam, in the near future specialized vestibular function tests will be key to mTBI diagnosis. A battery of oculomotor (antisaccade, predictive saccade) and vestibular tasks (head impulse test) has been demonstrated to sensitively and specifically identify individuals with acute mTBI. Vestibular therapy and rehabilitation have shown improvements for mTBI patients in cognitive function, ability to return to activities of daily living, and ability to return to work. Dizziness, as a contributor to short- and long-term disability following mTBI, is ultimately crucial not only for diagnosis but also for treatment.

PMID: 27638079 [PubMed - in process]

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Otologic disorders causing dizziness, including surgery for vestibular disorders.

Otologic disorders causing dizziness, including surgery for vestibular disorders.

Handb Clin Neurol. 2016;137:279-93

Authors: Bertholon P, Karkas A

Abstract
This chapter will focus on vertigo/dizziness due to inner-ear malformations, labyrinthine fistula, otosclerosis, infectious processes, and autoimmune inner-ear disorders. Inner-ear malformation due to dehiscence of the superior semicircular canal is the most recently described inner-ear malformation. Vertigo/dizziness is typically induced by sound and pressure stimuli and can be associated with auditory symptoms (conductive or mixed hearing loss). Labyrinthine fistula, except after surgery for otosclerosis, in the context of trauma or chronic otitis media with cholesteatoma, still remains a challenging disorder due to multiple uncertainties regarding diagnostic and management strategies. Otosclerosis typically manifests with auditory symptoms and conductive or mixed hearing loss on audiometry. Vertigo/dizziness is rare in nonoperated otosclerosis and should draw clinical attention to an inner-ear malformation. Computed tomography scan confirms otosclerosis in most cases and should rule out an inner-ear malformation, avoiding needless middle-ear surgical exploration. Labyrinth involvement after an infectious process is unilateral when it complicates a middle-ear infection but can be bilateral after meningitis. Labyrinth involvement due to an inflammatory disease is a challenging issue, particularly when restricted to the inner ear. The diagnosis relies on the bilateral and rapid aggravation of audiovestibular symptoms that will not respond to conventional therapy but to immunosuppressive drugs.

PMID: 27638078 [PubMed - in process]

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Menière's disease.

Menière's disease.

Handb Clin Neurol. 2016;137:257-77

Authors: Espinosa-Sanchez JM, Lopez-Escamez JA

Abstract
Menière's disease (MD) is a chronic multifactorial disorder of the inner ear characterized by episodic vestibular symptoms associated with sensorineural hearing loss, tinnitus, and aural pressure. Epidemiologic and genomic evidence supports a genetic susceptibility with multiple biochemical pathways involved, including the endocrine system, innate immune response, and autonomic nervous system. Allergens, infectious agents, vascular events, or genetic factors could modify inner-ear homeostasis and trigger MD. The diagnosis of MD is based on clinical criteria and requires the observation of an episodic vertigo syndrome associated with low- to medium-frequency sensorineural hearing loss and fluctuating aural symptoms (hearing loss, tinnitus, and/or fullness) in the affected ear. Headache is also found during the attacks and bilateral involvement is found in 25-40% of cases. Audiologic and vestibular assessment is recommended to monitor the clinical course. The treatment of MD is symptomatic to obtain relief of vestibular episodes and preventive to limit hearing loss progression. Treatment options include sodium restriction, betahistine, intratympanic gentamicin, or steroids and eventually surgery, such as cochlear implantation.

PMID: 27638077 [PubMed - in process]

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Benign paroxysmal positional vertigo and its variants.

Benign paroxysmal positional vertigo and its variants.

Handb Clin Neurol. 2016;137:241-56

Authors: Nuti D, Masini M, Mandalà M

Abstract
Benign paroxysmal positional vertigo is a common labyrinthine disorder caused by a mechanic stimulation of the vestibular receptors within the semicircular canals. It is characterized by positional vertigo and positional nystagmus, both provoked by changes in the position of the head with respect to gravity. The social impact of the disease and its direct and indirect costs to healthcare systems are significant owing to impairment of daily activities and increased risk of falls. The first description of a patient with benign paroxysmal positional vertigo is from Robert Bárány in 1921, but the features of the syndrome and the diagnostic maneuver were well described by Dix and Hallpike in 1952. Since then, the gradually increasing interest of otolaryngologists and neurologists has led to a progressive advance in the knowledge of this labyrinthine disorder with regard to its epidemiologic, pathophysiologic, clinical, and therapeutic aspects. Despite the often effective diagnosis and treatment of most cases of benign paroxysmal positional vertigo, the physiopathologic explanations of the disease are mainly speculative. In this chapter, we describe the epidemiologic, pathophysiologic, clinical, and therapeutic aspects of benign paroxysmal positional vertigo.

PMID: 27638076 [PubMed - in process]

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Bilateral vestibulopathy.

Bilateral vestibulopathy.

Handb Clin Neurol. 2016;137:235-40

Authors: Strupp M, Feil K, Dieterich M, Brandt T

Abstract
The leading symptoms of bilateral vestibulopathy (BVP) are postural imbalance and unsteadiness of gait that worsens in darkness and on uneven ground. There are typically no symptoms while sitting or lying under static conditions. A minority of patients also have movement-induced oscillopsia, in particular while walking. The diagnosis of BVP is based on a bilaterally reduced or absent function of the vestibulo-ocular reflex (VOR). This deficit is diagnosed for the high-frequency range of the angular VOR by a bilaterally pathologic bedside head impulse test (HIT) and for the low-frequency range by a bilaterally reduced or absent caloric response. If the results of the bedside HIT are unclear, angular VOR function should be quantified by a video-oculography system (vHIT). An additional test supporting the diagnosis is dynamic visual acuity. Cervical and ocular vestibular-evoked myogenic potentials (c/oVEMP) may also be reduced or absent, indicating impaired otolith function. There are different subtypes of BVP depending on the affected anatomic structure and frequency range of the VOR deficit: impaired canal function in the low- and/or high-frequency VOR range only and/or otolith function only; the latter is very rare. The etiology of BVP remains unclear in more than 50% of patients: in these cases neurodegeneration is assumed. Frequent known causes are ototoxicity mainly due to gentamicin, bilateral Menière's disease, autoimmune diseases, meningitis and bilateral vestibular schwannoma, as well as an association with cerebellar degeneration (cerebellar ataxia, neuropathy, vestibular areflexia syndrome=CANVAS). In general, in the long term there is no improvement of vestibular function. There are four treatment options: first, detailed patient counseling to explain the cause, etiology, and consequences, as well as the course of the disease; second, daily vestibular exercises and balance training; third, if possible, treatment of the underlying cause, as in bilateral Menière's disease, meningitis, or autoimmune diseases; fourth, if possible, prevention, i.e., being very restrictive with the use of ototoxic substances, such as aminoglycosides. In the future vestibular implants may also be an option.

PMID: 27638075 [PubMed - in process]

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An overview of vestibular rehabilitation.

An overview of vestibular rehabilitation.

Handb Clin Neurol. 2016;137:187-205

Authors: Whitney SL, Alghwiri AA, Alghadir A

Abstract
Data related to the efficacy of vestibular rehabilitation and its evolution as an intervention are provided. Concepts and various treatment strategies are described, with explanations of why people with uncompensated peripheral and central vestibular disorders might improve with rehabilitation. Various tests and measures are described that are commonly used to examine patients and determine their level of ability to participate in their environment. Factors that affect recovery, both positively and negatively, are described in order to better prognosticate recovery. A case utilizing many of the principles discussed is included to provide insight into how to utilize vestibular rehabilitation with a person with an uncompensated peripheral vestibular loss.

PMID: 27638071 [PubMed - in process]

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Bedside examination.

Bedside examination.

Handb Clin Neurol. 2016;137:91-101

Authors: Straumann D

Abstract
In most dizzy patients a limited selection of bedside tests, together with the history, is adequate to establish a differential diagnosis and select the next diagnostic and therapeutic procedures. A set of basic bedside tests that should be applied in every patient with vertigo or imbalance allows identifying: (1) patients who need immediate referral for further assessment and treatment; (2) patients with nonthreatening disorders for which treatment can be started without more detailed testing; (3) patients with benign paroxysmal vertigo, in whom a detailed work-up is not required and who can immediately be treated with an appropriate particle-repositioning maneuver; and (4) patients who need a comprehensive neuro-otologic and neurologic work-up. Additional neuro-otologic bedside tests help to further refine the differential diagnosis.

PMID: 27638065 [PubMed - in process]

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Multisensory integration in balance control.

Multisensory integration in balance control.

Handb Clin Neurol. 2016;137:57-66

Authors: Bronstein AM

Abstract
This chapter provides an introduction to the topic of multisensory integration in balance control in, both, health and disease. One of the best-studied examples is that of visuo-vestibular interaction, which is the ability of the visual system to enhance or suppress the vestibulo-ocular reflex (VOR suppression). Of clinical relevance, examination of VOR suppression is clinically useful because only central, not peripheral, lesions impair VOR suppression. Visual, somatosensory (proprioceptive), and vestibular inputs interact strongly and continuously in the control of upright balance. Experiments with visual motion stimuli show that the visual system generates visually-evoked postural responses that, at least initially, can override vestibular and proprioceptive signals. This paradigm has been useful for the study of the syndrome of visual vertigo or vision-induced dizziness, which can appear after vestibular disease. These patients typically report dizziness when exposed to optokinetic stimuli or visually charged environments, such as supermarkets. The principles of the rehabilitation treatment of these patients, which use repeated exposure to visual motion, are presented. Finally, we offer a diagnostic algorithm in approaching the patient reporting oscillopsia - the illusion of oscillation of the visual environment, which should not be confused with the syndrome mentioned earlier of visual vertigo.

PMID: 27638062 [PubMed - in process]

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