Brain Deficits in Visual Hallucinations

One the early things I was taught in my neuroscience training was that new-onset visual hallucinations need to be assessed for medical or "organic causes".

Auditory hallucinations were felt to be more characteristic of schizophrenia.

One medical disorder linked to visual hallucinations is dementia with Lewy bodies (DLB). 

DLB is second to Alzheimer's disease in producing neurodegenerative dementia. Visual hallucinations is a hallmark of DLB and is found in up to 70% of clinical samples with the disorder.

A recent study from France provides insight into the neuroanatomical correlates of visual hallucinations in DLB.

Researchers in this study used single-photon emission computed tomography (SPECT) in a group of 36 subjects with DLB who reported visual hallucinations.

This group of cases was compared to 30 subjects with DLD who did not report visual hallucinations.

Specific differences in blood flow were noted with visual hallucinations. Visual hallucinations subjects had diminished cerebral perfusion in the following regions.

• Left anterior cingulate cortex
• Left orbitofrontal cortex
• Left cuneus

Deficits in regional cerebral perfusion in several areas correlated with the severity of visual hallucinations:

• Bilateral anterior cingulate cortex
• Left orbitofrontal cortex
• Right parahippocampal gyrus
• Right inferior temporal cortex
• Left cuneus

The authors note the cuneus (also known as Brodmann's area 18). This region is known as a secondary visual integration area. Reduced blood flow to this region may contribute to visual processing errors and the subjective sensation of visual hallucinations. Perfusion deficits in more anterior regions may contribute to inability to recognize the visual hallucinations as abnormal.

This study is one of many emerging showing specific clinical features of neuropsychiatric disorders may relate to specific neuroanatomical deficits and impairment.

Readers with more interest in this topic can access the free full-text manuscript by clicking on the citation below.

Image of left cingulate cortex is an iPad screen shot from the app 3D Brain from the author's files.

Follow the author on Twitter @WRY999

Heitz C, Noblet V, Cretin B, Philippi N, Kremer L, Stackfleth M, Hubele F, Armspach JP, Namer I, & Blanc F (2015). Neural correlates of visual hallucinations in dementia with Lewy bodies. Alzheimer's research & therapy, 7 (1) PMID: 25717349

The Neurocircuitry of Anorexia Nervosa

Walter Kaye, M.D., Director of the Eating Disorders Treatment and Research Program at the University of California, San Diego presented a Frontiers in Neuroscience  lecture on September, 14, 2010.   The presentation was titled: “ Is anorexia nervosa an eating disorder? New insights into puzzling symptoms”.  The presentation highlighted some his recent research that has been summarized in the manuscript cited at the end of this blog post.

Dr. Kaye noted that eating disorders characterized by a phenotype of several continuous behavioral traits that appear to have some genetic contributions.  Childhood temperamental and characterological traits associated with anorexia nervosa include:

• Drive for thinness
• Perfectionism
• Harm avoidance
• Negative emotionality
• Altered interoceptive awareness
• Inhibition
• Obsessive-compulsive personality traits

Interoreceptive awareness includes a variety of body sensations such as gastric fullness, hunger and satiety.  The insular brain cortex is being recognized as a crucial brain structure in interoceptive awareness and it's integration with other brain functions. 

Some of the imaging research in anorexia nervosa (the condition’s medical coding number is 307.1) focuses on abnormalities involving appetite.  Underweight patients with anorexia nervosa appear to have altered appetite or an ability to suppress appetite to an unusually large degree.  Appetite dysregulation in anorexia nervosa includes a dislike for high-fat foods, failure to rate food as positive when hungry and a reduced aversive response to sucrose during satiation.   Several brain circuits appear to contribution to appetite and food consumption regulation including the hypothalamus, the ventral (limbic) neurocircuit and the dorsal neurocircuit.

Dr. Kaye and colleagues have performed a series of imaging studies examining appetite in those with anorexia nervosa.   He feels the anterior insula cortex might play a key role in anorexia nervosa.  This brain structure integrates with the cortex region involved in taste.  The insula also projects and interacts with key limbic structures including the amygdale, the anterior cingulated cortex and the orbitofrontal cortex.  These regions may interpret taste in a manner that integrates affective relevance, conflict monitoring and incentive learning. 

Kaye summarized that dysregulation in both the dorsal and ventral neurocircuits may contribute to anorexia nervosa.   Cortical circuits (top-down) are overengaged in anorexia nervosa resulting in high anticipatory reactivity, behavioral rigidity, and excessive worry.  This top-down overengagement is implemented through the interoceptive pathways, insular cortex amydala and anterior cingulated cortex.  The neural information  converges in the straitum where food delay receives priority over eating.

Dr. Kaye summarizes “..future imaging studies should focus on characterizing neural circuits, their functions and their relationship to anorexia nervosa.  Genetic studies might shed light on the complex interaction of molecules within these neural circuits.”

Dr. Kaye’s Eating Disorders Treatment and Research Program website is here.

Link to full pdf of the citation noted below and other UCSD publications is here.  This has several excellent figures explaining issues in neurocircuitry in anorexia nervosa.

Photo above of limbic system with cingulate cortex in pink, amygdala in blue, and hippocampus in green from 3D Brain iPad screen shot.  Courtesy of Yates Photography

Kaye WH, Fudge JL, & Paulus M (2009). New insights into symptoms and neurocircuit function of anorexia nervosa. Nature reviews. Neuroscience, 10 (8), 573-84 PMID: 19603056