If the patient is convinced of the presence of what is in fact a hallucination and also gives it personal origin, the symptom assumes the status of a delusion (a fixed false belief). The combination of olfactory hallucinations and delusions of this type signifies a psychiatric illness. Zilstorff wrote informatively on this subject. There is often a complaint of a large array of odors, most of them noxious and seemingly emanating from the patient (intrinsic hallucinations); in others, they are attributed to an external source (extrinsic hallucinations). Both types vary in intensity and are remarkable with respect to their persistence. They may be combined with gustatory hallucinations. According to Pryse-Phillips, who took note of the psychiatric illness in a series of 137 patients with olfactory hallucinations, most were associated with endogenous depression or schizophrenia. In schizophrenia, the olfactory stimulus is usually interpreted as arising externally, and as being induced by someone for the purpose of upsetting the patient. In depression, the perception is of the stimulus being intrinsic. The patient may go to great lengths to rid himself of the perceived odor, the usual ones being excessive washing and use of deodorants; the condition may lead to social withdrawal. There is reason to believe that the amygdaloid group of nuclei is the source of the hallucinations, as stereotactic lesions here have reportedly ameliorated both the olfactory hallucinations and the psychiatric disorder (see Chitanondh).
Olfactory hallucinations and delusions may occur in conjunction with Alzheimer dementia, but one should also consider the possibility of a late-life depression.
Loss of Olfactory Discrimination (Olfactory Agnosia)
Finally, one must consider a disorder in which the primary perceptual aspects of olfaction (detection of odors, adaptation to odors, and recognition of different intensities of the same odor) are intact, but the capacity to distinguish between odors and their recognition by quality is impaired or lost. In the writings on this subject, this deficit is usually referred to as a disorder of olfactory discrimination. In dealing with other sense modalities, however, the inability to identify and name a perceived sensation would be called an agnosia. To recognize this deficit requires special testing, such as matching to sample, the identification and naming of a variety of scents, and determining whether two odors are identical or different.
Such an alteration of olfactory function has been shown to characterize patients with the alcoholic form of Korsakoff psychosis; this impairment is not attributable to reduced olfactory acuity or to failure of learning and memory (Mair et al). As indicated previously, the olfactory disorder in the alcoholic Korsakoff patient is most likely caused by lesions in the medial dorsal nucleus of the thalamus; several observations in animals indicate that this nucleus and its connections with the orbitofrontal cortex give rise to deficits in odor discrimination (Mair et al, Slotnick and Kaneko). Eichenbaum and associates demonstrated a similar impairment of olfactory capacities in a patient who had undergone extensive bilateral medial temporal lobe resections. The operation was believed to have eliminated a substantial portion of the olfactory afferents to the frontal cortex and thalamus, although there was no anatomic verification of this. In patients with stereotactic or surgical amygdalotomies, Andy and coworkers noted a similar reduction in odor discrimination. Thus it appears that both portions of the higher olfactory pathways (medial temporal lobes, and medial dorsal nuclei) are necessary for the discrimination and identification of odors.