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Biomedical subjects

Andrew H Clarke

Publications and source records attributed to Andrew H Clarke.

5 recordsLinked to original sources

Dynamic pitch rotation affects eye torsion.

CONCLUSION: Most of the subjects studied had eye torsion responses to pitch, although the direction of torsion varied between subjects. Opposite responses may be the result of individual variation in anatomical or physiological vector orientations of hair cells in the anterior or posterior utricle or in the saccule. OBJECTIVE: This study aimed to determine whether systematic changes in eye torsion occur when subjects are rotated in forward and backward pitch. MATERIALS AND METHODS: Twenty-one normal subjects were seated in a dual axis human rotator, positioned so that the interaural axis was aligned with the axis of pitch rotation. Fixation LED suppressed vertical or horizontal eye movement. Recordings were carried out in darkness apart from the fixation LED, using a three-dimensional eye tracker based on CMOS image sensors. Subjects were twice tilted from upright to 90 degrees occiput down, then forward to 45 degrees face down. RESULTS: Most subjects had eye torsion changes in response to pitch, with mean amplitudes of approximately 2 degrees to 90 degrees backward tilt and 1 degree to 45 degrees forward tilt. Ten subjects had clockwise torsion to backward pitch and counterclockwise to forward pitch; six subjects had the opposite responses. Statistical testing of the distributions of the regression slopes between these two groups were significant (p<0.001). Five subjects had unclear responses.

Acceleration↗

Utricular dysfunction in patients with benign paroxysmal positional vertigo.

OBJECTIVE: The objective of this study was to test the hypothesis that utricular function is impaired in patients with idiopathic benign paroxysmal positional vertigo. STUDY DESIGN: Prospective cohort study. SETTING: Tertiary dizziness clinic and vestibular research laboratory. PATIENTS: Twelve patients with unilateral idiopathic benign paroxysmal positional vertigo were examined 1 week and 1 month after successful treatment with positioning maneuvers and compared with 24 healthy subjects. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Otolith function was assessed with estimation of the subjective visual vertical and analysis of the torsional otolith-ocular reflex. Unilateral stimulation of the utricle was performed on a rotator that allowed eccentric lateral displacement of the patient during earth-vertical rotation with constant velocity. The otolith-ocular reflex was recorded with three-dimensional video-oculography. RESULTS: There was no difference in the estimation of the subjective visual vertical between patients and controls. The peak-to-peak amplitude of the otolith-ocular reflex torsional eye position was smaller in patients than in the control group. The gain of the unilateral otolith-ocular reflex was reduced in patients on both sides on first testing. After several weeks, only the affected labyrinth showed a reduced otolith-ocular reflex gain. CONCLUSION: Our findings document otolith dysfunction in patients with idiopathic benign paroxysmal positional vertigo possibly secondary to degeneration of the utricular macula. This finding may account for the transient mild imbalance and dizziness that some patients with benign paroxysmal positional vertigo experience even after resolution of positional vertigo.

Adult↗

Otolith mass asymmetries in the utricle and saccule of flatfish.

The otolith mass of the saccules and utricles of plaice, Pleuronectes platessa (n = 39) and turbot, Psetta maxima (n = 21) was measured using an electronic microbalance. In the right-eyed plaice, the left utricular otoliths were found to be significantly heavier than the right (p < 0.0001), whereas no significant difference was found between left and right saccular otoliths (p < 0.751). In the left-eyed turbot, both the right utricular and saccular otoliths were found to be significantly heavier (in both cases, p < 0.0001). While the gene and regulative protein responsible for the peripheral biomineralisation process have been identified, it remains unclear how the symmetry between the right and left otoliths in fish species is regulated. Here it is likely that an additional central mechanism is involved. It must be assumed that similar processes govern the systematic asymmetry observed in flatfish such as the plaice and turbot. Taken together these findings are strongly suggestive of concomitant CNS modification and metamorphic plasticity, presumably represented in genetic code.

Animals↗

Acute migrainous vertigo: clinical and oculographic findings.

Migrainous vertigo (MV) is an increasingly recognized cause of episodic vertigo. However, the pathophysiology of MV is still a matter of speculation and it is not known to what extent the dysfunction is located in the central or peripheral vestibular system. The aim of this prospective study was to describe the clinical spectrum of acute MV and to clarify which structures of the vestibular system are involved. Testing of 20 patients with acute MV included neuro-otological examination, recording of spontaneous and positional nystagmus with 3D video-oculography, and audiometry. Pathological nystagmus was observed in 70% of patients during acute MV: six had isolated spontaneous nystagmus, five had isolated positional nystagmus and three had a combination of the two. Only a few patients showed additional ocular motor deficits. Imbalance was observed in all patients except one. Hearing was not affected in any patient during the attack. The findings during acute MV point to central-vestibular dysfunction in 10 patients (50%) and to peripheral vestibular dysfunction in three patients (15%). In the remaining seven patients (35%) the site of involvement could not be determined with certainty. MV should be considered in the differential diagnosis of vertigo with spontaneous and positional nystagmus and can present both as a central and a peripheral vestibular disorder.

Acute Disease↗

Migrainous vertigo presenting as episodic positional vertigo.

Migraine can cause vestibular symptoms including positional vertigo. Of 362 consecutive patients presenting with positional vertigo, 10 with migrainous vertigo mimicking benign paroxysmal positional vertigo (BPPV) were identified. The following factors help to distinguish migrainous positional vertigo from BPPV: short-duration symptomatic episodes and frequent recurrences, manifestation early in life, migrainous symptoms during episodes with positional vertigo, and atypical positional nystagmus.

Age of Onset↗