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Benign Paroxysmal Positional Vertigo (BPPV) is a very common cause of vertigo that can affect any of the semicircular canals. Posterior canal BPPV, by far the most frequent form of BPPV, can be effectively treated by a number of different physical methods. During the last few years the diagnosis and treatment of BPPV became so popular that in our tertiary referral Dizziness Clinic we encounter many cases of over-diagnosis, misdiagnosis and maltreatment. This review describes the various types of BPPV and the appropriate diagnostic work-up and treatment, emphasizing the adequate management of uncommon presentations. All physicians who receive appropriate training in BPPV should be able to accurately diagnose posterior canal BPPV by performing the Dix-Hallpike positional test and treat it immediately by one of the physical maneuvers with a success rate of 70%-90%. Futhermore, appropriately trained physiotherapists should be able to treat these cases. Repeated physical maneuvers during a single treatment session seem to be clinically superior to a single maneuver. The published post-treatment measures are inconvenient and should be abandoned. Patients who fail to respond to a single treatment session or with frequent recurrences of BPPV can be instructed to perform a "self-treatment" maneuver. The diagnosis of the different subtypes of horizontal canal BPPV (geotropic and apogeotropic nystagmus) requires special skill since cerebellar and brainstem disorders might also cause horizontal positional nystagmus. Two methods of treatment are commonly used: a rolling maneuver of 270 degrees or 360 degrees ("barbecue maneuver") and the "forced prolonged position" with a success rate of about 70% after a few maneuvers. About 20% of cases of horizontal BPPV fail to respond to these treatments. The anterior canal variant of BPPV characterized by torsional downbeat nystagmus is very rare. In such cases a detailed neurological examination is mandatory in order to rule out other causes of downbeat nystagmus. The authors recommend that patients with suspected horizontal or anterior canal BPPV should be immediately examined by a neurologist and if no other neurological abnormality is found a referral to a specialized dizziness clinic should follow.

Background: Although head trauma is considered a common cause of benign paroxysmal positional vertigo (BPPV), clinical presentation and outcome of traumatic BPPV (t-BPPV) have not been systematically evaluated., Objectives: To compare the clinical presentation, patient's response to physical treatment, and outcome of patients with t-BPPV with those with the idiopathic form (i-BBPV)., Setting: Tertiary referral neuro-otology outpatient clinic., Methods: We reviewed the clinical records of 247 consecutive patients with posterior canal BPPV during the years 1997 to 2000. All patients were diagnosed using the Dix-Hallpike test and treated using the particle repositioning maneuver. Patients with an onset of positional vertigo within 3 days of well-documented head trauma were included in the t-BPPV group. The outcome was compared with the outcome of 42 patients with i-BPPV who were similarly treated and followed up., Results: Twenty-one (8.5%) of the 247 patients with BPPV fulfilled the diagnostic criteria for t-BPPV. The most common cause of head trauma was motor vehicle crash, documented in 57% of the cases; half of the patients additionally suffered from a whiplash injury. While the other causes were diverse, common falls were predominant. Only 2 of the patients involved in motor vehicle crashes experienced brief loss of consciousness. Sixty-seven percent of patients with t-BPPV required repeated physical treatments for complete resolution of signs and symptoms in comparison to 14% of patients with i-BPPV (P<.001). During a mean +/-SD follow-up of 21.7 +/- 9.7 months, 57% of t-BPPV patients and 19% of i-BPPV controls had recurrent attacks (P<.004)., Conclusions: The nature and severity of the traumas causing t-BPPV are diverse, ranging from minor head injuries to more severe head and neck trauma with brief loss of consciousness. It appears that t-BPPV is more difficult to treat than i-BPPV, and also has a greater tendency to recur.

Although head trauma is the cause of Benign Paroxysmal Positional Vertigo (BPPV) in about 15% of cases, the clinical features and response to treatment in this particular group of patients was not previously evaluated. We present 20 cases of traumatic BPPV: 12 cases identified from 150 consecutive BPPV patients diagnosed in our Dizziness Clinic; and 8 cases diagnosed from 75 consecutive head trauma patients seen in the Emergency Room. In all patients the clinical diagnosis was confirmed by the Dix-Hallpike maneuver and all were treated by the Epley procedure. Treatment results were compared to those of 40 consecutive patients with idiopathic BPPV. There was a wide spectrum and severity of head trauma including road accident (7), different falls (5), blow to the head (5) and miscellaneous (3). Two patients experienced brief loss of consciousness. Only two patients were diagnosed as BPPV before referral to our clinic. When presented to our Dizziness Clinic the patients were diagnosed as follows: unspecified dizziness (7), cervical vertigo (4) and transient ischemic attack (1). Five patients (25%) had bilateral BPPV. Eight patients (40%) had complete resolution of symptoms and signs following a single treatment while 12 patients (60%) required additional physical treatments until complete resolution of BPPV was achieved. During follow-up, 11 patients (55%) had recurrent attacks of BPPV. Thirty-four patients with idiopathic BPPV (85%) had a single successful treatment session while the others required repeated physical treatments until complete resolution of BPPV. We conclude that traumatic BPPV is probably under-recognized or misdiagnosed in clinical practice. Response to a single physical treatment seems to be less favorable than in idiopathic BPPV. The Dix-Hallpike maneuver is mandatory in all patients with dizziness and vertigo following head trauma.

BACKGROUND: Machado Joseph Disease (MJD) is an autosomal dominant neurodegenerative disease. In previous studies, we described significant bilateral horizontal Vestibulo-Ocular Reflex (VOR) deficit within this population without any reference to the presence of vestibular symptomatology. OBJECTIVE: To evaluate whether, beyond cerebellar ataxia complaints, MJD patients have typical vestibular symptomatology corresponding to the accepted diagnostic criteria of Bilateral Vestibulopathy (BVP) according to the definition of the International Barany Society of Neuro-Otology. METHODS: Twenty-one MJD, 12 clinically stable chronic Unilateral Vestibulopathy (UVP), 15 clinically stable chronic BVP, and 22 healthy Controls underwent the video Head Impulse Test (vHIT) evaluating VOR gain and filled out the following questionnaires related to vestibular symptomatology: The Dizziness Handicap Inventory (DHI), the Activities-specific Balance Confidence Scale (ABC), the Vertigo Visual Scale (VVS) and the Beck Anxiety Inventory (BAI). RESULTS: The MJD group demonstrated significant bilateral vestibular impairment with horizontal gain less than 0.6 in 71% of patients (0.54±0.17). Similar to UVP and BVP, MJD patients reported a significantly higher level of symptoms than Controls in the DHI, ABC, VVS, and BAI questionnaires. CONCLUSIONS: MJD demonstrated significant VOR impairment and clinical symptoms typical of BVP. We suggest that in a future version of the International Classification of Vestibular Disorders (ICVD), MJD should be categorized under a separate section of central vestibulopathy with the heading of bilateral vestibulopathy. The present findings are of importance regarding the clinical diagnosis process and possible treatment based on vestibular rehabilitation. [ABSTRACT FROM AUTHOR]

Psychiatric Depersonalization/Derealization (DPDR) symptoms were demonstrated in patients with peripheral vestibular disorders. However, only semicircular canals (SCCs) dysfunction was evaluated, therefore, otoliths' contribution to DPDR is unknown. Also, DPDR symptoms in patients with central vestibular dysfunction are presently unknown. DPDR was also studied in the context of spatial disorientation and anxiety, but the relation of these cognitive and emotional functions to vestibular dysfunction requires clarification. We tested patients with peripheral Bilateral Vestibular Hypofunction (pBVH), Machado Joseph Disease (MJD) with cerebellar and central bilateral vestibular hypofunction, and healthy controls. Participants completed the video Head Impulse Test (vHIT) for SCCs function, cervical Vestibular Evoked Myogenic Potentials test (cVEMPt) for sacculi function, Body Sensation Questionnaire (BSQ) for panic anxiety, Object Perspective-Taking test (OPTt) for spatial orientation and Cox & Swinson DPDR inventory for DPDR symptoms. pBVH patients showed significant SCCs and sacculi dysfunction, spatial disorientation, elevated panic anxiety, and DPDR symptoms. MJD patients showed significant SCCs hypofunction but preserved sacculi function, spatial disorientation but normal levels of panic anxiety and DPDR symptoms. Only pBVH patients demonstrated a positive correlation between the severity of the DPDR and spatial disorientation and panic anxiety. DPDR develops in association with sacculi dysfunction, either with or without SSCs dysfunction. Spatial disorientation and anxiety seem to mediate the transformation of vestibular dysfunction into DPDR symptoms. DPDR does not develop in MJD with central vestibular hypofunction but a normal saccular response. We propose a three-step model that describes the development of DPDR symptoms in vestibular patients. • Spatial disorientation and anxiety mediate the transformation of vestibular dysfunction into Depersonalization/Derealization. • Depersonalization/Derealization develops in peripheral Bilateral Vestibular Hypofunction and is associated with sacculi dysfunction. • Depersonalization/Derealization does not develop in Machado Joseph Disease with normal saccular response. [ABSTRACT FROM AUTHOR]