, 2005a; Stackman et al , 2002; Taube et al , 1996)) Vestibular

, 2005a; Stackman et al., 2002; Taube et al., 1996)). Vestibular lesioned rats demonstrate impairments in spatial learning (Ossenkopp and Hargreaves, 1993) and spatial navigation in the absence of visual cues (Stackman and Herbert, 2002). The spatial memory and navigation deficits are unlikely to be attributable to motor impairment (Stackman et al., 2002) or anxiety (Machado et al., 2012 and Smith et al., 2013) and have also been described as long term or permanent deficits (Baek et al., 2010 and Zheng KU-60019 research buy et al., 2009b). There are also limited reports to suggest that cognitive deficits

following bilateral vestibular deafferentation in rats extend beyond spatial memory, with reports of deficits in object recognition memory (Zheng et al., 2004), and attention (using a 5-choice serial reaction time task (Zheng et al., 2009a)). The first human clinical paper to link vestibular dysfunction to cognition impairment (Grimm et al., 1989) reported on 102 patients with perilymph fistular syndrome click here (a rupture in the labrynth, resulting in leakage of perilymphatic fluid) who experienced vestibular symptoms (e.g. vertigo), as well as a range of cognitive and emotional symptoms. Results suggested that while these patients

demonstrated a normal level of global intellectual functioning, their performance on several areas of cognition was impaired. This included psychomotor speed (digit symbol), visual construction

abilities (block design), verbal learning (paired associate learning) and visual sequencing (picture arrangement). Since this initial report, there have been several Reverse transcriptase human studies in patients with differing levels of vestibular loss that have reported deficits in path navigation, spatial memory, spatial perception and attention (Brandt et al., 2005, Caixeta et al., 2012, Cohen, 2000, Grabherr et al., 2011, Guidetti et al., 2008, Peruch et al., 1999 and Schautzer et al., 2003). Spatial memory deficits have been reported in a series of studies assessing patients with bilateral vestibular loss due to neurofibromatosis type 2 after bilateral vestibular neurectomy as compared to age- and sex-matched controls on a human adaptation of the Morris water task, a spatial navigation/maze task initially designed for rat experiments (Brandt et al., 2005 and Schautzer et al., 2003). Results in 12 patients, compared to 10 healthy controls showed impaired performance when patients were required to recall a navigation path in the absence of a visible target. Furthermore, Brandt et al.

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