The most representative BPSD for DLB is visual hallucination. This is described as a core symptom in the revised clinical diagnosis guidelines [2] published by the Consortium on Dementia with Lewy Bodies (CDLB). McKeith et al. reported that 80 % of DLB cases involved visual hallucination [3], which could be one factor leading to caregiver breakdown even for patients with relatively intact cognitive function.

The CDLB guidelines describe concrete and vivid, repeated visual hallucination. These are highly varied and may range from small animals (“the wall is covered with small bugs moving around”) to people (“there is a woman with red lipstick in the bathroom staring at me”) to fantasy-based images (“there are dwarves walking around my bed”). Here we would like to focus on both the characteristics of visual hallucinations in DLB cases as well as their mechanism of occurrence. As described by Harding et al. [4] and Yamamoto et al. [5], visual hallucination in cases of DLB resulted from neuropathological factors such as Lewy pathology in areas of the visual cortices such as the amygdaloid nucleus and ventral visual pathway; these were also factors responsible for pareidolia. Nagahama et al. [6] also provided further neuropathological findings in their report of decreased cerebral blood flow in the dorsal and ventral visual pathway according to single photon emission computed tomography (SPECT) imaging of cases of DLB with visual hallucination.

Regardless of specific mechanism, it is significant that DLB-related visual hallucination fundamentally differ from those due to schizophrenia with no organic abnormalities. One good example is a DLB patient with visual hallucination of “men in white clothes dancing and singing in the garden.” In this case, the visual hallucination was thought to be caused by motion of the white lace curtains in the patient’s room; the visual hallucination ceased rapidly when the room’s lights were brightened and the curtains were removed. This patient’s specific visual hallucination was a result of adding a layer of meaning from inner experience to the pareidolia caused by the moving white curtains. The background described above provides a good explanation for the particular usefulness of acetylcholinesterase inhibitors for DLB-related visual hallucination [7], as well as the mitigation of symptoms possible by altering the patient’s physical environment.

The category of visuoperceptual disorders also includes other symptoms, such as illusory perception, for example, perceiving stains on the wall as bugs; metamorphosis, in which perceived objects appear to distort or move; and the sensed-presence effect (leibhaftiges Bewußtsein) of feeling the presence of somebody who is not really there.

The CDLB guidelines describe nonvisual types of hallucination as additional indications for DLB, but the incidence of these is low compared to visual hallucination. Some patients present with auditory hallucination, but often it should properly be classified as delusional misidentification. For example, a woman with jealous delusion of her husband having an affair reported hearing her name mentioned in a television program in the form of “Mrs. A [patient name], whose husband is cheating on her…” It has been reported [3] that about 45 % of DLB patients experience auditory hallucination (including musical), but lack of follow-up study means that actual incidence rates remain unknown.

Delusions occur more frequently in DLB, compared with Alzheimer’s disease (AD) [3]. However, rather than being typified by delusions of theft, these are characterized by delusional misidentification either as a continuation of visual hallucinations or related to delusions resulting from visual misidentification of places, people, or surroundings [8]. Representative examples include putting snacks out for nonexistent children who have come over to play, phantom boarders, or believing that one’s spouse has been replaced by an impostor (Capgras syndrome). Ellis et al. [9] have proposed an interesting hypothesis for mechanisms underlying Capgras syndrome: they hypothesize that faces are recognized normally, but lack of affect usually associated with those individual faces (feelings of affinity, like, or dislike) lead to the conclusion that while the perceived appearance is the same, the person inside must be different. Based on a meta-analysis, Collerton et al. considered DLB a form of visual-perceptual and attentional-executive dementia, which always exhibited frontal lobe function disorders such as attention disorders and executive function disorders [10]. This view also fully supports the hypothesis of Ellis et al. [9] in explaining the mechanism behind delusional misidentification of people: patients are unable to reflect on their own erroneous cognition and come to conclusions such as “this person has my wife’s face, but inside they are somebody else.”

Nagahama et al. [11] reported findings using SPECT that symptoms related to delusional misidentification of people were correlated with reduced cerebral blood flow in the bilateral opercular parts of the inferior frontal gyri, the left insular cortex, the hippocampus, and the nucleus accumbens. Finally, delusions in the usual sense of the word, such as delusions of theft, are also observed in DLB patients, although not as frequently as in AD.

Depression is one of the first symptoms of DLB and is listed in the CDLB guidelines as one of the supportive features. There was the interesting report on the symptoms of DLB in pre-dementia phase that Fujishiro et al. [12] retrospectively investigated the clinical courses, including olfactory dysfunction, dysautonomia, depression, and rapid eye movement sleep behavior disorder, of 90 patients with probable DLB. According to this report, Lewy body-related symptoms were present in 79 of 90 patients (87.8 %) with probable DLB before or at the time of memory loss onset, and they concluded that one of the LB-related symptoms was depression. Some researches indicate a higher frequency of depression for DLB than for AD, while some reports have described major depression episodes in 40 % of DLB patients [8, 13, 14]. Delving into the neuropathological background behind Parkinson’s disease (PD), Frisina et al. [15] describe significant neuronal cell loss in the ceruleus nucleus, the substantia nigra pars compacta, and the dorsal nucleus of the vagal nerve in patients exhibiting depressive symptoms. Furthermore, in their study of correlation of affected sites between PD and depression using [18F]-fluorodeoxyglucose-positron emission tomography (PET), Mentis et al. [16] conclude that glucose metabolism is reduced in the lateral frontal and anterior limbic cortices of PD patients exhibiting depression. In addition, Remy et al. [17] report that depression in PD patients is related to the loss of dopamine and noradrenaline innervation in the limbic system in their study using [11C]RTI-32 PET. These findings suggest that the dysfunctions of the fronto-subcortical and catecholaminergic system are related to PD-related depression. In a study of the selective 5-HT1A serotonin receptor agonist such as [(3)H]8-hydroxy-2-dipropylaminotetralin in 10 patients with DLB, 17 patients with PD with dementia (PDD), and 9 control patients, there was a relationship between depression and increased serotonin 1A receptor in the Brodmann area 36. These findings are relevant for the serotonergic system, which has been considered a significant factor behind major depression. Such results implicate raphe nucleus degeneration and dysfunction as underlying mechanisms for DLB-related depression [18]. Given the neuropathological homologies between PD and DLB [19, 20], the same mechanisms are likely responsible for depression due to both conditions.