Findings from lesions studies suggest that lesions of the orbital prefrontal regions result in olfactory identification deficits, while olfactory acuity is spared (e.g., Jones-Gotman & Zatorre, 1988). Further, findings of more dramatic olfactory impairment following prefrontal lesions rather than damage to midline structures (e.g., thalamus) are consistent with a hierarchical organization of processing from medio-dorsal thalamic nucleus to entorhinal cortex and then to lateral posterior orbitofrontal cortex (Potter & Butters, 1980).
Studies in temporal lobe epilepsy (TLE) report reductions in olfactory acuity in patients with right temporal lobectomies (Martinez et al., 1993), while olfactory recognition, discrimination, and short-term memory ability are impaired in patients presurgery (Jones-Gotman et al., 1997; Martinez et al., 1993). Discrimination and short-term memory deficits are greater after temporal lobectomy (Martinez et al., 1993). Olfactory identification is relatively preserved in TLE patients presurgery; however, deficits are observed in lobectomized patients with lesions involving the OFC (Jones-Gotman & Zatorre, 1993).
Deficits in olfaction (acuity, memory, and identification) appear early in the course of a number of neurodegenera-tive disorders, including cortical Dementia of the Alzheimer's Type, and some of the subcortical dementias, namely Parkinson's disease, Huntington's disease, and HIV-related dementia. However, such deficits have not been reported in patients with atypical parkinsonian syndromes, including corticobasal degeneration and progressive supranuclear palsy (see Doty, 2001; Pantelis, Brewer, & Maruff, 2000). These findings are consistent with the nature of involvement of the relevant olfactory circuits in these various disorders, and suggest that smell ability may assist in differential diagnosis. Studies have also found deficits in olfactory memory in chronic alcohol abusers and of identification ability in patients with Korsakoff syndrome (Potter & Butters, 1980). Olfactory identification deficits have also been found in motor neuron disease (MND), multiple sclerosis (MS), and Down syndrome (McKeown et al., 1996).
Was this article helpful?