ObjectiveTo provide a systematic review of the clinical and radiological features of lesion-induced central positional nystagmus (CPN) and identify salient characteristics that differentiate central from peripheral positional nystagmus (PN).MethodsSystematic literature search according to the preferred reporting items for systematic reviews and meta-analysis.ResultsA total of 82 patients from 28 studies met the participants intervention, comparison, outcomes, and study designs criteria for inclusion. An atypical direction of nystagmus for the stimulated canal was reported in 97.5% patients during Dix–Hallpike (D–H) and 54.5% upon supine roll testing. Five types of CPNs were identified during positional testing: positional horizontal nystagmus (pHN) (36.8%), positional downbeating nystagmus (pDBN) (29.2%), positional torsional nystagmus (pTN) (2.1%), positional upbeating nystagmus (pUBN) (2.1%), and a combination of the four profiles (29.9%). CPN was paroxysmal (<60 s) in 85% patients on straight head hanging (SHH), 63.9% on D–H, and 37.5% on supine roll, and had a latency <3 s upon positioning in 94.7% patients in which it was reported. Concurrent vertigo was reportedly present in 63.4% patients and 48.8% demonstrated other neurological signs. Radiologically, in 74.4%, there was mention of cerebellar involvement, isolated brainstem involvement in 8.5%, and 14.6% involved the fourth ventricle.ConclusionCurrently, there is a lack of robust data on the clinical and radiological characteristics of CPN highlighting the need for better phenotyping of CPN to help differentiate this entity from peripheral causes of PN. With increased awareness of CPN, particularly in the acute setting, we may see a change in the estimated prevalence of CPN and improved clinical markers to promptly identify the frequently sinister underlying causes.

BackgroundBalance problems are caused by multiple factors and often lead to falls and related fractures, bringing large socio-economic costs. The complexity of balance control mechanisms, the lack of medical expertise, and the absence of specialised equipment contribute to the delayed or incorrect diagnosis and management ofthese patients. Advances in computer science have allowed the development of computer systems that support clinical diagnosis and treatment decisions based on individualised patient data. The aim of the EMBalance decision support system (DSS) is to support doctors facing this clinical challenge, to make a definitive diagnosis and implement an effective management plan. The EMBalance study will determine the accuracy of this supportive tool when used by non-specialist doctors. This study is funded by the European Union’s Seventh Framework Programme.Methods/designEMBalance is a proof-of-concept study designed as a non-commercial, international, multi-centre, single-blind, parallel-group randomised controlled trial to be carried out at four clinical sites in the United Kingdom, Germany, Greece and Belgium. The study is comprised of three stages: internal pilot, phase I (diagnosis) and stage II (management). For this purpose, 200 patients presenting with persistent dizziness (>3 months’ duration) to primary care services will be randomised to either the intervention group (diagnostic assessment with the DSS) or a control group (diagnostic assessment without the DSS). Patients allocated to the intervention group will be assessed by a doctor with the support of the EMBalance DSS, while patients allocated to the control group will receive a visit as per standard practice. Ultimately, all patients’ diagnoses and management plans will be certified by a consultant in neuro-otology.DiscussionEMBalance is the first trial to test the accuracy of a DSS in both the diagnosis of and the management plan for vestibular disorders across the healthcare systems of four different countries. The EMBalance study is the result of a combined effort of engineers and physicians to develop an accurate tool to support non-specialist doctors, with no risk for the patient. This trial will provide reliable information about the benefits of implementing DSSs in primary care while supporting the feasibility of testing the EMBalance algorithms in further research.Trial registrationClinicalTrials.gov NCT02704819. Registered 29 February 2016.Electronic supplementary materialThe online version of this article (doi:10.1186/s13063-016-1568-x) contains supplementary material, which is available to authorized users.

Objective: To provide a systematic review of the clinical and radiological features of lesion-induced central positional nystagmus (CPN) and identify salient characteristics that differentiate central from peripheral positional nystagmus (PN).Methods: Systematic literature search according to the preferred reporting items for systematic reviews and meta-analysis.Results: A total of 82 patients from 28 studies met the participants intervention, comparison, outcomes, and study designs criteria for inclusion. An atypical direction of nystagmus for the stimulated canal was reported in 97.5% patients during Dix-Hallpike (D-H) and 54.5% upon supine roll testing. Five types of CPNs were identified during positional testing: positional horizontal nystagmus (pHN) (36.8%), positional downbeating nystagmus (pDBN) (29.2%), positional torsional nystagmus (pTN) (2.1%), positional upbeating nystagmus (pUBN) (2.1%), and a combination of the four profiles (29.9%). CPN was paroxysmal (<60 s) in 85% patients on straight head hanging (SHH), 63.9% on D-H, and 37.5% on supine roll, and had a latency <3 s upon positioning in 94.7% patients in which it was reported. Concurrent vertigo was reportedly present in 63.4% patients and 48.8% demonstrated other neurological signs. Radiologically, in 74.4%, there was mention of cerebellar involvement, isolated brainstem involvement in 8.5%, and 14.6% involved the fourth ventricle. Conclusion:Currently, there is a lack of robust data on the clinical and radiological characteristics of CPN highlighting the need for better phenotyping of CPN to help differentiate this entity from peripheral causes of PN. With increased awareness of CPN, particularly in the acute setting, we may see a change in the estimated prevalence of CPN and improved clinical markers to promptly identify the frequently sinister underlying causes.

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