Milan Dhaniram

1414848

PSYC1009 (SLOT GROUP E)

Tutorial group: T (SH2132)

Schizophrenia can be defined as a “collection of seriously debilitating conditions”
(Carr, 2001) characterized predominantly by hallucinations, delusions and thought
disorder, and the term “Schizophrenia” originates from the Greek word ‘skhizein”
meaning ‘split’ and ‘phren’ which means ‘of the mind’ (Weiten, 2013). Hallucinations
are the sensation experienced when there is an absence of an external stimulus
(Carr, 2001). Delusions refer to the false and/or made-up beliefs of the ill individual,
for example, a person who experiences persecutory delusions can believe that other
people are out to get them/ harm them (Carr, 2001). The last prominent
characteristic of schizophrenia is Thought Disorder, which is referred to as
“disorganized and illogical speech” (Carr, 2001).

In this essay, the symptoms and subtypes of schizophrenia will be described in order
to have a better understanding when discussing the brain structures, as well as the
neurochemistry, that are implicated/involved in Schizophrenia and how they lead to
these symptoms. The medication involved to control these Schizophrenic symptoms
(as schizophrenia cannot be permanently cured) and how they function on the brain
and neurochemistry shall also be discussed.

There are three types of possible symptoms as seen in schizophrenic people:

Positive symptoms, whereby there is an active manifestation of abnormal behaviour,
inclusive of hallucinations and delusions; Negative symptoms, which consists of
deficits in affect (our demeanour), affecting one’s speech and motivation; lastly, the
Disorganized symptoms, being the rambling of speech, erratic behaviour and
inappropriate affect (Weiten, 2013).

Based on possible etiological factors (classified as symptomatology), classification

systems such as ‘ICD 10’ and ‘DSM V’ are used as a tool to subtype schizophrenia
(Carr, 2001). Five subtypes of Schizophrenia have been identified: Paranoid
schizophrenia (prominent delusions and hallucinations but affect is still intact);
Disorganized (marked disruption in speech and behaviour with inappropriate/flat
affect); Catatonic (unusual motor response and over-active); Residual (at least one
episode of schizophrenia and without major symptoms); and Undifferentiated (other
symptoms that don’t fall into the other four categories) (Weiten, 2013).

The major brain regions affected include the prefrontal cortex, the basal ganglia and
the limbic system (Chakraborty, 2014). The prefrontal cortex is the brain region
directly behind the forehead. This brain area is largely accountable for complex tasks
known as ‘executive functions’ (Chakraborty, 2014), like decision-making,
strategizing and adjusting behaviours (mostly social ones or ones based on past
experiences). If the prefrontal cortex experiences malfunctioning, it usually causes a
loss of these capabilities and the distinctive disordered thinking of schizophrenia
(Chakraborty, 2014).

Another brain area that gets affected in schizophrenia and is connected to the
prefrontal cortex, is the basal ganglia (Chakraborty, 2014). This region is known for
producing dopamine and assists in regulating coordinated movement, and the
reward and motivation pathway to make a person feel good (Chakraborty, 2014). It
has been detected that brain imaging studies show increased activity in the basal
ganglia and decreased connectivity between this region and the prefrontal cortex in
people with schizophrenia (Chakraborty, 2014). The results of this sensitive area
being damaged are disordered thinking, as well as psychosis, due to the surplus
release of the neurotransmitter dopamine into the brain (Yoon et al., 2013).

The limbic system consists of brain structures that are predominantly liable for
learning and memory as well as processing emotion (Chakraborty, 2014). Just like
the decrease in connections between the prefrontal cortex and the basal ganglia, a
February 2015 study report published in "European Psychiatry" found alterations in
the connectivity between fragments of the limbic system and the prefrontal cortex in
people with schizophrenia. Furthermore, the limbic system’s abnormal brain-
chemistry is also a factor that contributes to schizophrenia.

According to Yoon (et al.,2013), it is understood that Patients with schizophrenia

experienced excess activity in the substantia Nigra, decreased activity in the
prefrontal cortex, and diminished functional connectivity between these regions of
the brain. This implicates that communication among these regions was out of sync,
and that the higher the level of connectivity between the substantia Nigra and the
striatum, the higher the level of psychosis seen in patients with schizophrenia (Yoon
et al., 2013). These findings show significance in the conversation of schizophrenia
as the prefrontal cortex-basal ganglia circuit is a possible common pathway, linking
cognitive deficits and psychosis (Yoon et al., 2013).
Neurotransmitters i.e. substances that permit nerve cells to communicate between
each other and are known to play a role in the development of schizophrenia (Smith,
2015). There is a strong chance that the disorder is associated with some imbalance
of complex neurotransmitters (Smith, 2015). Recent research has shown that
“glutamate, GABA, acetylcholine and serotonin are also involved in the pathology of
schizophrenia and lead to the high-affinity of the D (2) – receptor” (Brisch 2014).

With regards to the neurochemistry of schizophrenia, there is one neurotransmitter

that is believed to be the most important, namely, dopamine (Brisch 2014). The
production of dopamine occurs in the substantia Nigra and ventral tegmental regions
of the brain. The positive symptoms shown in schizophrenia are due to an increase
release of dopamine, activating D2-receptor. The negative symptoms of
schizophrenia result from reduced D1-receptor activation in the prefrontal cortex
(Brisch 2014). Another neurotransmitter, GABA, has a5 receptors which ameliorates
cognitive deficits in rats. The increase in dopamine is caused by hyperactivity of the
ventral hippocampus (Brisch 2014).

With regards to antipsychotic medications, it tends to operate by hindering a

particular subtype of the dopamine receptor, known as the D2 receptor (Tung, 2007).
‘Conventional antipsychotics’, known to be older and more commonly used
antipsychotic medication, block the D2 receptor and ameliorate one’s positive
symptoms. Although, it is highly unfortunate that these conventional (or ‘typical’)
antipsychotics also block D2 receptors in areas outside of the mesolimbic pathway.
The result of this can lead to the negative symptoms associated with the illness to
worsen. Chlorpromazine, haloperidol, trifluoperazine, perphenazine and
fluphenazine (Tung, 2007) are a few of the first-generation/conventional/typical
antipsychotic drugs used to treat individuals with schizophrenia and other similar
disorders. A second generation of antipsychotics, referred to as the atypical
antipsychotics by many, block D2 receptors as well as a specific subtype of
serotonin receptor, the 5HT2A receptor (Tung, 2007). It has been allegedly
understood that this dual-action at D2 and 5HT2A receptors treats both positive and
negative symptoms. The atypical antipsychotics include clozapine, risperidone,
olanzapine, quetiapine, paliperidone and ziprasidone (Tung, 2007).
Most all medications are known to have their set of side effects, and antipsychotic
mediation is no different: Side effects from blocking the D2 receptor can include
tremors, inner restlessness, muscle spasms, sexual dysfunction and, although an
uncommon case, tardive dyskinesia, a disorder that causes repetitive, involuntary,
purposeless movements (Tung, 2007). These side effects are more often associated
with the conventional (or typical) antipsychotics. The side effects linked to atypical
antipsychotics include weight gain, diabetes and lipid disorders (Tung, 2007). It can
be noted that antipsychotic ‘agents’ can be and have been prescribed to treat other
conditions apart from schizophrenia such as Tourette’s syndrome, substance abuse,
stuttering, obsessive-compulsive disorder, post-traumatic stress disorder,
depression, bipolar disorder and personality disorders (Tung, 2007). Similar to anti-
depressants, antipsychotic medications do not work directly after consumption; it
could lag until the eighth week before noting any therapeutic benefits. And the side
effects of antipsychotics typically occur before symptoms of the illness are bettered.

According to Biomedical research, it has been stated that early detection and
intervention could anticipate later stages of many diseases, one of which being
Schizophrenia. Current medical and scientific research is in the process of
recognizing genes and environmental components in connection with schizophrenia
(Yoon et al., 2013). Evidence shows that the fundamentals of every effective
antipsychotic medication in schizophrenia encompasses dopamine and its
interaction with other neurochemical pathways.

People suffering with Schizophrenia such as Jonathon (individual identified as a

case study as part of the essay topic), who experienced more positive symptoms of
Schizophrenia and is someone who falls under the Paranoid subtype of the illness,
namely auditory hallucinations as well as delusions. With the aid of medication such
as Haldol (known to be a first-generation/typical antipsychotic drug), Jonathon is able
to have his dopamine neurotransmitters rebalanced, and maintain regular and
normal moods and behaviours with psychotic behaviours controlled and inhibited.

To conclude, clearly depression and schizophrenia are very complex and debilitating
disorders (Tung, 2007). Fortunately, medications like antidepressants and anti-
psychotics can help treat the core symptoms. Knowing how these drugs work and
what effects they can have will be an important step in using them properly and
effectively.

Referencing list:

• Carr, Alan. 2001. Psychology Focus: Abnormal Psychology. United Kingdom:

Psychology Press. (Carr 2001)

• Chakraborty, Sudipta. 2015. “Areas of the Brain Affected by Schizophrenia”.

Article taken from Livestrong. Last accessed 20 April 2015. (Chakraborty, 2014)

• Yoon JH, Minzenberg MJ, Raouf S, D’Esposito M, Carter CS. “Biological

Psychiatry: Impaired Prefrontal-Basal Ganglia Functional Connectivity and
Substantia Nigra Hyperactivity in Schizophrenia”. National Institute of Mental Health.
January 14, 2013. (Yoon et al., 2013)

• Smith, Brian. (2015). “What Causes Schizophrenia?”. Psych Central.

Retrieved on May 9, 2016 (Smith, 2015)

• Brisch, Ralf. 2014. “The role of dopamine in schizophrenia from a

neurobiological and evolutionary perspective”. Frontiers in Psychology. Last
accessed 19 May 2014. (Brisch 2014)

• Miyamoto, Seiya, Anthony S. LaMantia, Gary E. Duncan, Patrick Sullivan,

John H. Gilmore and Jeffrey A. Lieberman. 2003. “Recent Advances in the
Neurobiology of Schizophrenia”. Biology Online. last accessed 4 September 2007.
(Miyamoto et al., 2003)

• Weiten, Wayne. 2013. Psychology: Themes and Variations (South African

Ed.). United Kingdom. Cengage Learning, Inc. (Weiten 2013)

• Tung, Anthony. 2007. “How Antidepressant and Antipsychotic Medications

Work”. Taken from "Medications" issue of Visions Journal, pp. 7-8. Last accessed 11
February 2011. (Tung, 2007)