Neurological
Basis of Visual Hallucinations in Individuals with Schizophrenia
This is the first in a three part series
examining the neurological basis of visual hallucinations (VH) in a schizophrenic population. In Carlson’s
classic text, Physiology of Behavior, he provides us with a descriptive account of the human visual
system. The last few pages of chapter six briefly discussed vision deficits and
disorders: achromatopsia, visual agnosia and prosopagnosia, for example. Most
of these conditions typically arise from damage to some specific brain area—achromatopsia,
for instance, occurs after damage to area V8 of the Visual Association Cortex.
I wondered about mental disorders involving perception. For instance, by what neuro-mechanism
of action (or lack thereof) would be involved in a positive symptom of
schizophrenia, such as the visual hallucinations?
No doubt, although the most commonly
reported hallucination experiences are auditory, they can nonetheless manifest
across any senses modality. Indeed, research reveales that the literature on
auditory hallucinations in a schizophrenic population dwarfs research regarding
the same population and visual hallucinations. Nonetheless, Kéri, S. et al. (2010)
provided an interesting study on impaired visual contrast sensitivity and (more
interesting to me) anomalous perceptual experiences in first episode
schizophrenics.
The study had two parts. In the
first, there was an assessment of visual contrast sensitivity biased toward the
processing characteristics of Magnocellular (M) vs. Parvocellular (P) pathways.
The researchers note that current research studying M and P pathways in
schizophrenia indicate the significant impairment of M pathways. And this makes
sense, since M pathways provide extensive input to cortical areas responsible
for spatial location, perception and visio-motor coordination. The second part
of their study focused on investigating the intensity of anomalous subjective
experiences, with the hypothesis that the intensity of anomalous perceptual
experience would be associated with visual contrast sensitivity
alterations.
Although the research was conducted
with a low N of 20 (on the other hand, 20 may be a high sample population of first
episode schizophrenics!), their research showed that schizophrenic patients
displayed “significantly elevated contrast sensitivity values in the
steady-pedestal test for M pathways, F(1, 38) < 14.27, p .001, whereas the patients did not differ from
control participants in the pulsed-pedestal test for P pathways, p > .1.”
Also, interestingly, they found that
their data regarding M pathway expression in schizophrenia was contradicted by prior
research (Javitt, 2009). However, the disparity can most likely be related to
the introduction of dopamine antagonist antipsychotics. Of course this only begs
the questions and highlights the need for further research regarding dopamine
levels and VH in schizophrenia.
It will be interesting to follow the
current research trends on neuropsychology as it relates to schizophrenia. The
cynic in me doubts that a cure will readily be available (especially since we
know schizophrenia to be partially genetic and our current knowledge of genetics
being so limited). Still, current advances in neuroscience may pave the way for
treatments to some positive symptoms of individuals with schizophrenia.
References
Carlson,
N. R. (2010). Physiology of behavior. Boston, MA: Pearson.
Javitt, D. C. (2009). When doors
of perception close: Bottom-up models of disrupted
cognition
in schizophrenia. Annual Review of Clinical Psychology, 5, 249–275.
Kiss,
I., Fábián, Á., Benedek, G., & Kéri, S. (2010). When doors of perception
open:
Visual contrast
sensitivity in never-medicated, first-episode schizophrenia. Journal Of
Abnormal Psychology, 119(3), 586-593. doi:10.1037/a0019610
Prepared
by Phillip J. Kuna for John G. Kuna, PsyD and Associates Counseling
(570)961-3361
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