Visual hallucinations, thalamocortical physiology and Lewy body disease: A review

• Published in: Neuroscience and biobehavioral reviews 2019-08, Vol.103, p.337-351
• Main Authors: Esmaeeli, Shooka, Murphy, Kathleen, Swords, Gabriel M., Ibrahim, Baher A., Brown, Jeffrey W., Llano, Daniel A.
• Format: Article
• Language: English
• Subjects: Acetylcholine; Acetylcholine - metabolism; Cerebral Cortex - metabolism; Cerebral Cortex - physiopathology; Dementia; Hallucination; Hallucinations - etiology; Hallucinations - metabolism; Hallucinations - physiopathology; Humans; Lewy body; Lewy Body Disease - complications; Lewy Body Disease - metabolism; Lewy Body Disease - physiopathology; Thalamic reticular nucleus; Thalamus; Thalamus - metabolism; Thalamus - physiopathology; Visual Perception - physiology
• ISSN: 0149-7634; 1873-7528
• DOI: 10.1016/j.neubiorev.2019.06.006

•Mechanisms of visual hallucinations in Dementia with Lewy Bodies (DLB) are unknown.•We hypothesize that changes in thalamocortical circuits underlie these hallucinations.•Here, we review the literature concerning thalamic pathology in DLB.•DLB involves dramatic loss of α7 nicotinic receptors in the thalamic reticular nucleus.•We provide a model whereby α7 nicotinic receptor loss promotes DLB hallucinations. One of the core diagnostic criteria for Dementia with Lewy Bodies (DLB) is the presence of visual hallucinations. The presence of hallucinations, along with fluctuations in the level of arousal and sleep disturbance, point to potential pathological mechanisms at the level of the thalamus. However, the potential role of thalamic dysfunction in DLB, particularly as it relates to the presence of formed visual hallucinations is not known. Here, we review the literature on the pathophysiology of DLB with respect to modern theories of thalamocortical function and attempt to derive an understanding of how such hallucinations arise. Based on the available literature, we propose that combined thalamic-thalamic reticular nucleus and thalamocortical pathology may explain the phenomenology of visual hallucinations in DLB. In particular, diminished α7 cholinergic activity in the thalamic reticular nucleus may critically disinhibit thalamocortical activity. Further, concentrated pathological changes within the posterior regions of the thalamus may explain the predilection for the hallucinations to be visual in nature.