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No 444: October 10, 2018

Geraghty AWA, Essery R, Kirby S, Stuart B, Turner D, Little P, Bronstein A, Andersson G, Carlbring P, Yardley L. Internet-Based Vestibular Rehabilitation for Older Adults With Chronic Dizziness: A Randomized Controlled Trial in Primary Care. Ann Fam Med. 2017 May;15(3):209-216. doi: 10.1370/afm.2070.

Abstract

PURPOSE: Vestibular rehabilitation is an effective intervention for dizziness due to vestibular dysfunction, but is seldom provided. We aimed to determine the effectiveness of an Internet-based vestibular rehabilitation program for older adults experiencing dizziness in primary care.

METHODS: We undertook a single-center, single-blind randomized controlled trial comparing an Internet-based vestibular rehabilitation intervention (Balance Retraining, freely available from https://balance.lifeguidehealth.org) with usual primary care in patients from 54 primary care practices in southern England. Patients aged 50 years and older with current dizziness exacerbated by head movements were enrolled. Those in the intervention group accessed an automated Internet-based program that taught vestibular rehabilitation exercises and suggested cognitive behavioral management strategies. Dizziness was measured by the Vertigo Symptom Scale-Short Form (VSS-SF) at baseline, 3 months, and 6 months. The primary outcome was VSS-SF score at 6 months.

RESULTS: A total of 296 patients were randomized in the trial; 66% were female, and the median age was 67 years. The VSS-SF was completed by 250 patients (84%) at 3 months and 230 patients (78%) at 6 months. Compared with the usual care group, the Internet-based vestibular rehabilitation group had less dizziness on the VSS-SF at 3 months (difference, 2.75 points; 95% CI, 1.39-4.12; P <.001) and at 6 months (difference, 2.26 points; 95% CI, 0.39-4.12; P = .02, respectively). Dizziness-related disability was also lower in the Internet-based vestibular rehabilitation group at 3 months (difference, 6.15 points; 95% CI, 2.81-9.49; P <.001) and 6 months (difference, 5.58 points; 95% CI, 1.19-10.0; P = .01).

CONCLUSIONS: Internet-based vestibular rehabilitation reduces dizziness and dizziness-related disability in older primary care patients without requiring clinical support. This intervention has potential for wide application in community settings.

PMID: 28483885

Link to Free Article:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5422081/

No 443: October 3, 2018

Popkirov S, Staab JP, Stone J. Persistent postural-perceptual dizziness (PPPD): a common, characteristic and treatable cause of chronic dizziness. Pract Neurol. 2018 Feb;18(1):5-13. doi: 10.1136/practneurol-2017-001809. Epub 2017 Dec 5.

Abstract

Persistent postural-perceptual dizziness (PPPD) is a newly defined diagnostic syndrome that unifies key features of chronic subjective dizziness, phobic postural vertigo and related disorders. It describes a common chronic dysfunction of the vestibular system and brain that produces persistent dizziness, non-spinning vertigo and/or unsteadiness. The disorder constitutes a long-term maladaptation to a neuro-otological, medical or psychological event that triggered vestibular symptoms, and is usefully considered within the spectrum of other functional neurological disorders. While diagnostic tests and conventional imaging usually remain negative, patients with PPPD present in a characteristic way that maps on to positive diagnostic criteria. Patients often develop secondary functional gait disorder, anxiety, avoidance behaviour and severe disability. Once recognised, PPPD can be managed with effective communication and tailored treatment strategies, including specialised physical therapy (vestibular rehabilitation), serotonergic medications and cognitive-behavioural therapy.

PMID: 29208729

No 442: September 26, 2018

Bayer O, Brémová T,  Strupp M, Hüfner K. A randomized double-blind, placebo-controlled, cross-over trial (Vestparoxy) of the treatment of vestibular paroxysmia with oxcarbazepine. J Neurol. 2018 Feb;265(2):291-298. doi: 10.1007/s00415-017-8682-x. Epub 2017 Nov 27.

Abstract

OBJECTIVE: Vestibular paroxysmia (VP) is characterized by short, often oligosymptomatic attacks of vertigo which occur spontaneously or are sometimes provoked by turning the head. Despite the description of the disease almost 40 years ago (first termed "disabling positional vertigo"), no controlled treatment trial has been published to date. The Vestparoxy trial was designed as a randomized, placebo-controlled, double-blind cross-over trial to examine the therapeutic effect of oxcarbazepine (OXA) in patients with definite or probable VP.

METHODS: Patients were recruited from August 2005 to December 2011 in the outpatient Dizziness Unit of the Department of Neurology of the Munich University Hospital, and randomized to receive OXA (first week: 300 mg once per day, second week: 300 mg b.i.d., third week: 300 mg t.i.d. until the end of the third month), followed by placebo or vice versa with a 1-month wash-out period in between. The primary endpoint was the number of days with one or more attacks. Secondary endpoints were the number of attacks during the observed days, and the median (for each day) duration of attacks. All these endpoints were assessed using standardized diaries collected at the end of each treatment phase.

RESULTS: Forty-three patients were randomized, 18 patients provided usable data (2525 patient days) for at least one treatment phase and were included in the main (intention-to-treat) analysis. The most common reasons for discontinuation documented were adverse events. The risk of experiencing a day with at least one attack was 0.41 under OXA, and 0.62 under placebo treatment, yielding a relative risk of 0.67 (95% CI 0.47-0.95, p = 0.025). The number of attacks during the observed days ratio was 0.53 (95% CI 0.42-0.68, p < 0.001) under OXA compared to placebo. Median attack duration was 4 s (Q25: 2 s, Q75: 120 s) under OXA, and 3 s (Q25: 2 s, Q75: 60 s) under placebo treatment. When days with no attacks, i.e., duration = 0, were included in the analysis, these figures changed to 0 (Q25: 0, Q75: 3 s), and 2 (Q25: 0, Q75: 6 s). No serious adverse events or new safety findings were identified during the trial.

CONCLUSIONS: The Vestparoxy trial showed a significant reduction of VP attacks under OXA compared to placebo treatment, confirming the known and revealing no new side effects.

PMID: 29204964

No 441: September 19, 2018

Lehnen N, Langhagen T, Heinen F, Huppert D, Brandt T, Jahn K. Vestibular paroxysmia in children: a treatable cause of short vertigo attacks. Dev Med Child Neurol. 2015 Apr;57(4):393-6. doi: 10.1111/dmcn.12563. Epub 2014 Aug 22.

Abstract

Vestibular paroxysmia due to neurovascular compression is a syndrome consisting of frequent short episodes of vertigo in adults that can be easily treated. Here we describe the initial presentation and follow-up of three children (one female, 12y; two males, 8y and 9y) who experienced typical, brief, vertiginous attacks several times a day. Nystagmus was observed during the episodes. Cranial magnetic resonance imaging revealed arterial compression of the eighth cranial nerve. The attacks ceased after administration of low-dose carbamazepine (2-4mg/kg daily). Vestibular paroxysmia must be considered in the differential diagnosis of children with brief vertiginous episodes.

PMID: 25146998

No 440: September 12, 2018

Strupp M, Lopez-Escamez JA, Kim JS, Straumann D, Jen JC, Carey J, Bisdorff A, Brandt T. Vestibular paroxysmia: Diagnostic criteria. J Vestib Res. 2016;26(5-6):409-415. doi: 10.3233/VES-160589.

Abstract

This paper describes the diagnostic criteria for vestibular paroxysmia (VP) as defined by the Classification Committee of the Bárány Society. The diagnosis of VP is mainly based on the patient history and requires: A) at least ten attacks of spontaneous spinning or non-spinning vertigo; B) duration less than 1 minute; C) stereotyped phenomenology in a particular patient; D) response to a treatment with carbamazepine/oxcarbazepine; and F) not better accounted for by another diagnosis. Probable VP is defined as follows: A) at least five attacks of spinning or non-spinning vertigo; B) duration less than 5 minutes; C) spontaneous occurrence or provoked by certain head-movements; D) stereotyped phenomenology in a particular patient; E) not better accounted for by another diagnosis.Ephaptic discharges in the proximal part of the 8th cranial nerve, which is covered by oligodendrocytes, are the assumed mechanism. Important differential diagnoses are Menière's disease, vestibular migraine, benign paroxysmal positional vertigo, epileptic vestibular aura, paroxysmal brainstem attacks (in multiple sclerosis or after brainstem stroke), superior canal dehiscence syndrome, perilymph fistula, transient ischemic attacks and panic attacks. Current areas of uncertainty in the diagnosis of VP are: a) MRI findings of vascular compression which are not diagnostic of the disease or predictive for the affected side because they are also observed in about 30% of healthy asymptomatic subjects; and b) response to treatment with carbamazepine/oxcarbazepine supports the diagnosis but there are so far no randomized controlled trials for treatment of VP.

PMID: 28262641

No 439: September 6, 2018

Brandt T, Strupp M, Dieterich M. Vestibular paroxysmia: a treatable neurovascular cross-compression syndrome. J Neurol. 2016 Apr;263 Suppl 1:S90-6. doi: 10.1007/s00415-015-7973-3. Epub 2016 Apr 15.

Abstract

The leading symptoms of vestibular paroxysmia (VP) are recurrent, spontaneous, short attacks of spinning or non-spinning vertigo that generally last less than one minute and occur in a series of up to 30 or more per day. VP may manifest when arteries in the cerebellar pontine angle cause a segmental, pressure-induced dysfunction of the eighth nerve. The symptoms are usually triggered by direct pulsatile compression with ephaptic discharges, less often by conduction blocks. MR imaging reveals the neurovascular compression of the eighth nerve (3D constructive interference in steady state and 3D time-of-flight sequences) in more than 95% of cases. A loop of the anterior inferior cerebellar artery seems to be most often involved, less so the posterior inferior cerebellar artery, the vertebral artery, or a vein. The frequent attacks of vertigo respond to carbamazepine or oxcarbazepine, even in low dosages (200-600 mg/d or 300-900 mg/d, respectively), which have been shown to also be effective in children. Alternative drugs to try are lamotrigine, phenytoin, gabapentin, topiramate or baclofen or other non-antiepileptic drugs used in trigeminal neuralgia. The results of ongoing randomized placebo-controlled treatment studies, however, are not yet available. Surgical microvascular decompression of the eighth nerve is the "ultima ratio" for medically intractable cases or in exceptional cases of non-vascular compression of the eighth nerve by a tumor or cyst. The International Barany Society for Neuro-Otology is currently working on a consensus document on the clinical criteria for establishing a diagnosis of VP as a clinical entity.

PMID: 27083889

No 438: August 29, 2018

Naoi T, Morita M, Kawakami T, Fujimoto S. Ipsiversive Ocular Torsion, Skew Deviation, and Hearing Loss as Initial Signs of Anterior Inferior Cerebellar Artery Infarction. Intern Med. 2018 Jul 1;57(13):1925-1927. doi: 10.2169/internalmedicine.0283-17. Epub 2018 Feb 9.

Abstract

A 67-year-old man with hypertension and type 2 diabetes mellitus was admitted to our hospital because of left hearing loss and vertical diplopia. A neurological examination showed ocular torsion, skew deviation, and sensorineural hearing loss in the left ear. Brainstem and cerebellar neurological signs were not observed. Left middle cerebellar peduncle infarction was evident on magnetic resonance imaging. He was treated with antiplatelet, however, the infarct progressed after this administration. Ocular tilt reaction (OTR) involves the triad of ocular torsion, skew deviation, and head tilt. Ipsiversive OTR components associated with hearing loss can be early diagnostic signs of anterior inferior cerebellar artery infarction.

PMID: 29434137

No 437: August 22, 2018

Yang CJ, Cha EH, Park JW, Kang BC, Yoo MH, Kang WS, Ahn JH, Chung JW, Park HJ. Diagnostic Value of Gains and Corrective Saccades in Video Head Impulse Test in Vestibular Neuritis. Otolaryngol Head Neck Surg. 2018 Aug;159(2):347-353. doi: 10.1177/0194599818768218. Epub 2018 Apr 10.

Abstract

Objectives We investigated changes in video head impulse test (vHIT) gains and corrective saccades (CSs) at the acute and follow-up stages of vestibular neuritis to assess the diagnostic value of vHIT. Study Design Case series with chart review. Setting Tertiary medical center.

Subjects and Methods Sixty-three patients with vestibular neuritis who underwent vHIT at an initial presentation and an approximately 1-month follow-up were included. vHIT gains, gain asymmetry (GA), peak velocities of CS, and interaural difference of CS (CSD) were analyzed.

Results Mean vHIT gains increased significantly from the acute stage to the follow-up exam. The mean GA, peak velocities of CS, and CSD had decreased significantly at the follow-up. The incidence of CSs was also significantly decreased at the follow-up. The abnormal rate (87%) considering both gain and CS value was significantly higher than that (62%) considering vHIT gain only at the follow-up, although the abnormal rates did not differ at the acute stage (97% vs 87%).

Conclusion The abnormal rates based on both vHIT gains and CS measurements are similar at the acute stage of VN but are considerably higher at the follow-up stage compared with the abnormal rates based on vHIT gains alone. It is thus advisable to check both CS and vHIT gain while performing vHIT to detect vestibular hypofunction.

PMID: 29631490

No 436: August 17, 2018

Tarnutzer AA, Straumann D1. Nystagmus. Curr Opin Neurol. 2018 Feb;31(1):74-80. doi: 10.1097/WCO.0000000000000517.

Abstract

PURPOSE OF REVIEW: The clinical and laboratory assessment of nystagmus in patients with neurologic disorders can provide crucial elements for a state-of-the-art differential diagnosis. An increasing number of publications in the fields of neuro-otology and neuro-ophthalmology have nystagmus in the center of interest, which makes frequent updates on the diagnostic and therapeutic relevance of these contributions indispensable. This review covers important clinical studies and studies in basic research relevant for the neurologist published from January 2016 to August 2017.

RECENT FINDINGS: Current themes include vestibular nystagmus, positional nystagmus, optokinetic nystagmus and after-nystagmus, vibration-induced nystagmus, head-shaking nystagmus, postrotatory nystagmus, caloric nystagmus, nystagmus in cerebellar disorders, differential diagnosis of nystagmus and treatment approaches (whereas infantile nystagmus syndrome is not addressed in this review). These studies address mechanisms/pathomechanisms, differential diagnoses and treatment of different forms of nystagmus.

SUMMARY: In clinical practice, a structured description of nystagmus including its three-dimensional beating direction, trigger factors and duration is of major importance. The differential diagnosis of downbeat nystagmus is broad and includes acute intoxications, neurodegenerative disorders and cerebrovascular causes amongst others. In patients with positional nystagmus, the distinction between frequent benign peripheral and rare but dangerous central causes is imperative.

PMID: 29120919

No 435: August 8, 2018

Hernowo A, Eggenberger E.  Skew deviation: clinical updates for ophthalmologists. Curr Opin Ophthalmol. 2014 Nov;25(6):485-7. doi: 10.1097/ICU.0000000000000105.

Abstract

Background: Skew deviation can be defined as vertical misalignment of the eyes that does not map to any of cyclovertical muscles, in association with neurologic symptoms and signs and with posterior fossa lesion. It can be differentiated from trochlear nerve palsy by the direction of ocular torsion and the change in the degree of vertical deviation with upright and supine head position. It is commonly caused by ischemia of the posterior paramedian pons, medial thalamus, or cerebellum. Other less common mechanism being demyelinating lesion, mass effect, infection, hemorrhage, or intracranial hypertension. When the vestibular nuclei are involved, skew deviation may occur with acute vestibular syndrome. Ground-in or Fresnel prism may alleviate diplopia in relatively small vertical deviation; however, patient with larger deviation or with the presence of ocular torsion may benefit from surgery of the cyclovertical muscles.

Objective: This article discusses the current approach in diagnosing skew deviation, as well as recent findings in the lesion localization.

Design: Descriptive

Summary: Skew deviation can be appropriately diagnosed from the nature of the ocular torsion and the vertical deviation, along with the presence of lesion involving posterior paramedian pons and/or medial thalamus.

PMID: 25250734

No 434: August 1, 2018

Armstrong RA. Visual problems associated with traumatic brain injury. Clin Exp Optom. 2018 Feb 28. doi: 10.1111/cxo.12670. [Epub ahead of print]

Abstract

Traumatic brain injury (TBI) and its associated concussion are major causes of disability and death. All ages can be affected but children, young adults and the elderly are particularly susceptible. A decline in mortality has resulted in many more individuals living with a disability caused by TBI including those affecting vision. This review describes: (1) the major clinical and pathological features of TBI; (2) the visual signs and symptoms associated with the disorder; and (3) discusses the assessment of quality of life and visual rehabilitation of the patient. Defects in primary vision such as visual acuity and visual fields, eye movement including vergence, saccadic and smooth pursuit movements, and in more complex aspects of vision involving visual perception, motion vision ('akinopsia'), and visuo-spatial function have all been reported in TBI. Eye movement dysfunction may be an early sign of TBI. Hence, TBI can result in a variety of visual problems, many patients exhibiting multiple visual defects in combination with a decline in overall health. Patients with chronic dysfunction following TBI may require occupational, vestibular, cognitive and other forms of physical therapy. Such patients may also benefit from visual rehabilitation, including reading-related oculomotor training and the prescribing of spectacles with a variety of tints and prism combinations.

PMID: 29488253

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