Auditory hallucinations rooted in aberrant brain connectivity
Schizophrenia symptom may be the result of increased connections between sensory and language-processing brain areas
Date:
June 30, 2020
Source:
Elsevier
Summary:
A study reports that auditory hallucinations, a phenomenon in
which people hear voices or other sounds, may arise through altered
brain connectivity between sensory and cognitive processing areas.
FULL STORY ========================================================================== Auditory hallucinations, a phenomenon in which people hear voices or other sounds in the absence of external stimuli, are a feature of schizophrenia
and some other neuropsychiatric disorders. How they arise in the brain has
been unclear, but new research indicates that altered brain connectivity between sensory and cognitive processing areas may be responsible.
==========================================================================
The study from researchers led by Stephan Eliez, MD, PhD, at Geneva
University, Switzerland, appears in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, published by Elsevier.
"Our results demonstrate aberrant development of the thalamic
nuclei involved in sensory processing and [an] immature pattern of thalamo-cortical connectivity to the brain's auditory regions," said
lead author Valentina Mancini, MD.
Using magnetic resonance imaging (MRI), the researchers compared brain structures and their connectivity in 110 healthy control subjects and in
120 subjects with a genetic disorder, named 22q11.2 deletion syndrome,
or DS.
People with 22q11.2 DS are at far higher risk than the general public
to develop schizophrenia and to experience sensory hallucinations. An
estimated one percent of people with schizophrenia have this disorder.
Abnormalities in the thalamus, a brain region recognized as the "gateway"
for sensory information coming into the brain, had already been implicated
in schizophrenia and hallucinations. In the current study, the authors
sought to parse more specifically how the thalamus and its connections
to other brain areas differed in people with 22q11.2 DS -- with and
without auditory hallucinations (AH) -- from the control group. For
this longitudinal study, the researchers collected brain scans every
three years from subjects aged 8 to 35, with each receiving between 1
and 4 scans.
While neither the total volume of the thalamus nor its developmental
growth trajectory differed between 22q11.2 DS and control subjects,
the researchers found differences in specific thalamic sub-nuclei. The
medial and lateral geniculate nuclei (MGN, LGN), which are involved in
relaying auditory and visual sensory information, were smaller in people
with 22q11.2 DS. In contrast, thalamic nuclei that communicate with the
frontal cortex, which is involved in higher cognitive functions, were
larger in 22q11.2 DS subjects than in healthy controls. In addition,
other thalamic nuclei developed differently in the two groups.
When comparing 22q11.2 DS subjects with and without AH, those with AH
had a smaller volume of MGN and a different developmental trajectory.
Upon assessing functional connectivity within the brain, the authors also
found that subjects with AH had greater connectivity between MGN with the auditory cortex and other language-processing areas. They postulate that
such hyper- connectivity might underlie the activation of such auditory
areas at rest, leading to hallucinations.
"These findings provide a mechanistic explanation to the extreme
likelihood of hallucinatory phenomena in youths prone to psychosis due to 22q11.2 deletion syndrome," Dr. Mancini added. "Further, the investigation
of the developmental interactions between the thalamus and the cortex may
help to identify new targets for intervention aimed at preventing the
emergence of psychotic symptoms in individuals at-risk due to genetic conditions or clinical ultra- high-risk status." Cameron Carter, MD,
Editor of Biological Psychiatry: Cognitive Neuroscience and Neuroimaging
added: "This study of individuals with 22q11 may provide a unique window
into the alterations in brain development that underlie the development
of psychotic symptoms, as well as other developmental and cognitive
problems in these young people."
========================================================================== Story Source: Materials provided by Elsevier. Note: Content may be edited
for style and length.
========================================================================== Journal Reference:
1. Valentina Mancini, Daniela Zo"ller, Maude Schneider, Marie Schaer,
Stephan Eliez. Abnormal Development and Dysconnectivity of
Distinct Thalamic Nuclei in Patients With 22q11.2 Deletion
Syndrome Experiencing Auditory Hallucinations. Biological
Psychiatry: Cognitive Neuroscience and Neuroimaging, 2020; DOI:
10.1016/j.bpsc.2020.04.015 ==========================================================================
Link to news story:
https://www.sciencedaily.com/releases/2020/06/200630111442.htm
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