Semicircular Canal Dysfunction Research Articles

Posture control in Pusher syndrome: influence of lateral semicircular canals

SummaryPusher syndrome is an interesting disorder of balance in patients with encephalic lesions characterized by the peculiar behavior of actively pushing away from the non-hemiparetic side and resisting against passive correction, with a tendency to fall toward the paralyzed side. The role of vestibular system on the pushing behavior is not clear. Aim: To evaluate horizontal semicircular canal function in patients with Pusher syndrome, using caloric and rotation tests. Study Design: Observational prospective. Material and Method: We evaluated 9 inpatients with stroke and Pusher syndrome at the neurological unit of HCFMRP-USP. We applied neurological and neuropsychological exams, NIHSS, Scale for contraversive pushing (SCP), caloric and rotation tests. Results: We evaluated 9 patients (5 men) with mean age of 71.8 ± 5.9 and mean NIHSS of 18.33. Three patients presented contralateral directional preponderance on caloric test and we found four patients with directional preponderance on analysis of the slow phase velocity of rotation test response. Conclusion: Our findings indicate that a dysfunction of semicircular canals does not seem to be relevant for the clinical manifestations of the Pusher syndrome.

Otolith formation in a mutant Medaka with a deficiency in gravity sensing

Mutant Medaka ha exhibit spontaneous mutation that is characterized by frequent inhibition or perturbation in the formation of utricular otoliths and/or semicircular canals. Three major features of otolith morphogenesis were observed in ha strain: 1) The initial appearance of otoliths was delayed, mispositioned, and malformed compared to normal embryos. 2) No utricular otoliths appeared on macula of any ha fry just after hatching. A symmetric state of otoliths was seen only when saccular otoliths were situated on macula in both inner ears. 3) In some fry, formation of utricular otoliths was observed in their later development. However, no new utricular otoliths appeared after fish were seventy or more days old after hatching. These observations show that otolith morphogenesis in ha is very different from that of wild-type. In this study, we classified adult ha into four different phenotypes using the existence or absence of utricular otoliths as our criteria. We concluded that dysfunction of utricular otoliths and semicircular canals cause a defect that affects the gravity-sensing abilities of medaka ha.

Postural control in horizontal benign paroxysmal positional vertigo.

Sixteen patients affected by benign paroxysmal positional vertigo of the horizontal semicircular canal (BPPV-HSC) were investigated by means of dynamic posturography (DP) and during bithermal caloric stimulation. Data were compared to data from 40 patients with benign paroxysmal positional vertigo of the posterior semicircular canal (BPPV-PSC) and 20 healthy controls. No postural deficit was observed before or after a liberative Lempert's manoeuvre when patients were compared to control subjects. BPPV-PSC postural scores were significantly impaired compared to scores from the BPPV-HSC group. A residual significant postural impairment was also observed after a successful liberative manoeuvre in the BPPV-PSC group. Electronystagmographic recordings before recovery revealed significant hypoexcitability of the affected ear in 8/16 patients of the BPPV-HSC group. After the liberative manoeuvre, a symmetric bilateral response to caloric stimulation was recorded in all patients. Three main conclusions can be drawn from the present data. First, disorders of the horizontal semicircular canal do not change postural control. Second, dynamic posturography can detect the postural imbalance due to posterior semicircular canal dysfunction even after resolution of paroxysmal vertigo attacks. Third, utricular dysfunction can be ruled out as a cause of the residual postural deficit observed in BPPV-PSC patients. Therefore the recovery delay observed even 1 month after the liberative manoeuvre in the BPPV-PSC-group might be due to the persistence of small amounts of residual debris in the canal, to paralysis of ampullar receptors, or to the time needed for central vestibular re-adaptation.