Schizophrenia disorder
is depicted as a long-term, destructive brain disorder that begins during
neural development. Individuals with this disorder tend to have delusions, are
socially awkward, and have progressive deterioration of their cognitive abilities.
Dr. John G. Csernansky, from Northwestern University Feinberg School of
Medicine, presented his research regarding neural adaptation and the long-term
course of schizophrenia. Csernansky referred to people with schizophrenia as
having a broken mind and created his own model for the brain disorder. His
model explained the origin of the schizophrenic biological process occurring in
neural development along with the tendency of children to be shy, troublesome
making friends, and problem with fine motor skills. After this premorbid state,
until around fourteen or fifteen years of age, the teenager enters a prodromal
state characterized by the onset of psychosis. The affected person typically
starts to lose friends, develop more distractions, hear their thoughts spoken
aloud, and find special meaning in ordinary objects. In addition, Csernansky
distinguished positive symptoms of schizophrenia as experiences that normal
people do not have for example, thought disorganization. Negative symptoms were
described as social withdrawal, social awkwardness. After the onset of
psychosis, the neurodegenerative disorder enters a progressive state involving
delusions and paranoid themes. I found it particularly interesting that
Csernansky mentioned the content within the delusions and paranoia often
reflects the cultural upbringing of the individual. In the progressive state,
usually schizophrenics start to receive treatment, but the treatment only seems
to better the negative symptoms of the disorder while psychosis is still
evident throughout their lifetime. The human brain physically grows until
around fourteen years of age. Csernansky said that white matter continues to
grow, further developing the brain and basically fills in the spots where the
grey matter eventually thins out. Previous work indicated that grey matter
decline is more exacerbated in schizophrenia. Csernansky provided neuroimaging
evidence of anatomical progression involving changes in the anterior regions of
the caudate and thalamus. Thus, he focused on the frontal and temporal cortical
structures where he found cortical thinning and associated the increase in grey
matter decline with a more disturbed thalamus. Csernansky concludes with saying
that schizophrenic patients require more cognitive activation in dorsolateral
prefrontal cortex to fulfill tasks as opposed to normal people. Furthermore,
there is a possible adaptive mechanism that can compensate for the
neuroanatomical changes in cognitive function in people with schizophrenia.
The long-term course of
schizophrenia is extremely difficult to deal with. Whether it’s the
deterioration in cognitive deficits, or detrimental effects of psychosis,
finding ways to communicate with people in regards to this neurodegenerative
disorder is an obstacle that many people face. Columbia University Medical
Center offers evidence in improving hearing with their journal, Hearing
deficits in schizophrenia tied to specific brain receptor, with the
utilization of D-serine and auditory training exercises. Dr. Joshua T. Kantrowitz,
assistant professor of clinical psychiatry at CUMC, explaining the essence of
voice tone, “ This inability to detect subtle changes in pitch can also make it
difficult to "sound out" words while reading, with over 70 percent of
patients meeting criteria for dyslexia and further exacerbating communication
problems in social and work situations.” Kantrowitz and his research team chose
40 schizophrenic patients and 42 healthy patients who had to listen to multiple
tones and indicate which tone was higher. The pitch difference of the tones
decreased as the test went on, and once the subjects were not able to pick the
higher pitch, researchers would increase the pitch difference again. Kantrowitz
says, “People with normal auditory plasticity usually get better at
discriminating between the two tones as the test progresses, reflecting the
ability to learn”. The results showed he was correct because non-schizophrenic
subjects distinguished tones with a different in pitch of 3%, while
schizophrenic patients averaged 16%. Thus, the auditory plasticity of
schizophrenic subjects is impaired and the CUMC research team proposed that an
NMDA receptor abnormality could play a part in this deficit. The NMDA receptor
is crucial for long-term potentiation in both memory and learning and its
activation involves binding of both glutamate and glycine. Researchers gave
some schizophrenic subjects the amino acid glycine, or D-serine, one time a
week up to three weeks, while other schizophrenic subjects were given a placebo.
Results showed that schizophrenic individuals who took D-serine for two
consecutive weeks improved tone detection, but schizophrenic patients who took
D-serine for only one week did not see improvement. Understanding that D-serine
with different auditory training exercises improves pitch detection in
schizophrenia, researchers can test the use of different glycine and glutamate
agonists to see if they make NMDA activity more efficient. Both
glycine and glutamate binding are needed in order for the NMDA channel to open
and allow an influx of calcium to rush into the cell. The controlled activation
and deactivation of NMDA receptors ultimately determines the effectiveness of
synaptic plasticity, memory, and learning. Learning from Csernansky’s presentation
that psychosis, cognitive deficits, and the miscommunication that
schizophrenics experience on a daily basis, finding the most effective
learning-enhancing drug can possibly improve the long-term auditory deficits in
schizophrenic patients. Moreover, making the NMDA receptor more functional
would help alleviate the negative symptoms of schizophrenia including social
awkwardness, inability to act, and thought disorganization that causes
confusion/delusions in schizophrenics. Csernansky’s research should also be
followed up on because identifying a possible adaptive, compensatory mechanism
would spark methods to counteract the deterioration of cognition seen in
schizophrenia.
Works Cited
Columbia University Medical Center. "Hearing
deficits in schizophrenia tied to specific brain receptor." ScienceDaily.
ScienceDaily, 2 December 2016.
<www.sciencedaily.com/releases/2016/12/161202150855.htm>.
Northwestern University. "Map Of Your Brain May Reveal
Early Mental Illness." ScienceDaily. ScienceDaily, 10 July 2009.
<www.sciencedaily.com/releases/2009/07/090709095431.htm>.
No comments:
Post a Comment