Evaluation of vestibular function in young children

Phillips, James O.; Backous, Douglas D.

doi:10.1016/s0030-6665(02)00062-2

Cited by 31 publications

(53 citation statements)

References 64 publications

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“…Parents may have to be present to decrease fear and anxiety, and smaller children, or those under three years of age, may actually have to sit on their parents laps to be tested in special equipment such as the rotational chair (6). The testing environment must not be overly colourful or busy, although a picture of a child undergoing the same type of testing may be helpful (6,7).…”

Section: Differential Diagnosismentioning

confidence: 99%

“…Testing static visual acuity can include a review of cranial nerves, especially optic, oculomotor and auditory nerves, and vestibuloocular reflex testing, usually through playful games like peek-a-boo and gaze fixation and gaze shifts (7). Dynamic visual acuity, also an indirect measure of vestibular function, commonly includes the head-shaking nystagmus test in which a child can say "no" as fast as he or she can (7). Frenzel lenses can be added for older children (6,7).…”

Section: Differential Diagnosismentioning

confidence: 99%

“…Dynamic visual acuity, also an indirect measure of vestibular function, commonly includes the head-shaking nystagmus test in which a child can say "no" as fast as he or she can (7). Frenzel lenses can be added for older children (6,7).…”

Section: Differential Diagnosismentioning

confidence: 99%

“…Third, children may have less facility in describing (articulating) their symptoms (5,6). Finally, children require different approaches to testing where fear-and ageappropriate needs are considered, and the results of these tests must be adjusted for a younger population to be fully reliable (1,3,7). This is a review of the literature on benign paroxysmal vertigo of childhood (BPVC), a peripheral vestibular disorder reputedly similar to benign paroxysmal positional vertigo (BPPV) in adults.…”

mentioning

confidence: 99%

“…Supporters of the diagnosis of BPVC consider it a relatively rare peripheral vestibular disorder that is commonly misdiagnosed or overlooked (7,22) and whose clinical picture is similar to adult BPPV but with several additional distinctive features. In both BPPV (adult) and BPVC, the short duration of the attack, latent period before the onset of vertigo, fatigability of the signs and symptoms, kind of nystagmus and periods of exacerbation-remission have rendered this disorder a peripheral end-organ disturbance (3,5,6).…”

mentioning

confidence: 99%

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Benign paroxysmal vertigo of childhood: A review of the literature

Batson

2004

Paediatrics &Amp; Child Health

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Section: Differential Diagnosismentioning

confidence: 99%

Section: Differential Diagnosismentioning

confidence: 99%

Section: Differential Diagnosismentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Benign paroxysmal vertigo of childhood: A review of the literature

Batson

2004

Paediatrics &Amp; Child Health

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A novel DFNA9 mutation in the vWFA2 domain of COCH alters a conserved cysteine residue and intrachain disulfide bond formation resulting in progressive hearing loss and site‐specific vestibular and central oculomotor dysfunction

Street

Kallman

Robertson

et al. 2005

American J of Med Genetics Pt A

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Mutations within the COCH gene (encoding the cochlin protein) lead to auditory and vestibular impairment in the DFNA9 disorder. In this study, we describe the genetic mapping of progressive autosomal dominant sensorineural hearing loss first affecting high-frequency auditory thresholds within a human pedigree to the long arm of chromosome 14 in band q12. A maximal pairwise LOD score of 7.08 was obtained with marker D14S1021. We identified a c.1625G > T mutation in exon 12 of COCH that co-segregates with auditory dysfunction in the pedigree. The mutation results in a predicted p.C542F substitution at an evolutionarily conserved cysteine residue in the C-terminus of cochlin. The c.1625G > T transversion in COCH exon 12 represents the first reported mutation outside of the LCCL domain which is encoded by exons 4 and 5. The 542F mutant cochlin is translated and secreted by transfected mammalian cells. Western blot analysis under non-reducing and reducing conditions suggests that the 542F mutation alters intramolecular cochlin disulfide bond formation. In the vestibular system, a progressive horizontal canal hypofunction and a probable saccular otolith challenge were detected in family members with the c.1625G > T COCH alteration. Abnormal central oculomotor test results in family members with the c.1625G > T COCH alteration imply a possible central nervous system change not previously noted in DFNA9 pedigrees harboring mutations within the LCCL domain.

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