Neurobiology of Mental Health Disorders

This assignment delves into the complex relationship between the brain and various mental health disorders. It examines the role of neurotransmitters such as dopamine and glutamate in conditions like depression and addiction. The impact of genetic predispositions and environmental factors on these disorders is also explored. Students are tasked with analyzing research papers that shed light on the neurobiological underpinnings of mental health, ultimately gaining a deeper understanding of how brain function contributes to these complex conditions.

Running head: NURSING
Nursing
Name of the student:
Name of the University:
Author’s note

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Answer 1
a) Signs and symptoms of severe depressive episodes: David Wilson, a 38 year old man
working as a mechanical fitter for mining company has been diagnosed with Major
Depression (ICD10 diagnosis F32.2 severe depressive episode without psychotic
symptoms). In the category of depressive episodes, his condition comes under F32.2. A
severe depressive episode without psychotic symptoms is one where symptoms like
fatigue, tiredness, lowering of mood, decreased concentration, low capacity for
enjoyment, decreased appetite and sleep disturbance are present at extreme level and
patient develop distressing experiences in life. In patients with F32.2 severe depressive
episodes, the continuous presence of such symptoms results in loss of self-esteem and
feeling of worthlessness (ICD-10 Version: 2016, 2017). This was also seen in case of
David, as his performance at workplace decreased due to poor concentration and he kept
ruminating over negative events resulting in poor self-esteem. Such patients generally
have suicidal feelings and somatic symptoms like unusual waking hours, weight loss, loss
of appetite, psychomotor and loss of libido. As majority of these symptoms were present
in Mr. David Wilson, he has been diagnosed with Major Depression.
b) Pathophysiology of depression: The difficulty faced by Mr. David Wilson is clearly an
indication of severe depression. Major depressive disorder is medical condition in which
feeling, thinking and activities of a person is negatively affected. This leads to feelings of
sadness, loss of interest in activities, guilty feeling, loss of energy, change in appetite and
sleeping patterns and difficulty in concentration. People may experience single or
multiple episodes of depression. The examination of neurobiological theories elucidating
the pathophysiology of depression suggest that depletion of neurotransmitters like

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dopamine and serotonin in the central nervous system results is the underlying factor
behind the pathophysiology of depression (Hasler, 2010).
While considering the pathophysiology behind the condition, it can be said that
neurotransmitters, the brain chemicals plays a major role in depression. Sperner-Unterweger,
Kohl, & Fuchs, (2014) has shown that changes in function of neurotransmitters affect their
interaction with neurocircuits and this in turns results in development of depression as
neurocircuits are mainly involved in maintaining mood stability. Hence, mood stability is
severely affected by the biological changes in neurotransmitters. Links has been found
between inflammatory pathways and neurocircuits in the brain as the mechanism of
interactions of the immune system with the neurotransmitters and neurocircuits affects the
risk for depression. The activation of inflammasome results in release of stress induced
inflammatory signals such as increased expression of pro-inflammatory cytokines. The
inflammatory cytokines consequently has an impact on monoamines, noradrenaline and
dopamine. Neurotransmission plays a role in mood regulation and through several
mechanism, inflammatory cytokines reduces the availability of monoamines which
contributes to the pathophysiology of depression. In case of dopamine, they play a role in
motivation and motor activity and cytokines decreases the release of dopamine leading to
poor mood and depression (Miller & Raison, 2016). Hence, activation of inflammasome
leads to release of inflammatory cytokines and this affects the function of neurotransmitters
and neurocircuits resulting to unsuitable behavior in affected person.
c) There is ambiguous evidence on the specific causes of depression. However, a
combination of biological factors as well as environmental stressors might play a role in
the onset and diagnosis of depression (Uher, 2014).. While reviewing the case of David

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Wilson, it has been found that his mother, Michelle, 69 years old had a history of
depression and currently she was also suffering from early onset of Alzheimer’s
dementia. This is an indication that David may have hereditary links to depression as
blood relatives with history of depression are known to increase the risk of developing
depression. Research has shown that genetics has a role in the development of depression
and as it mainly runs in families, it is highly regarded as hereditary (Flint & Kendler,
2014). In case of David, his mother has been found to have a history of depression and in
such case he is 1.5 to three times more likely to suffer from the condition. Hence,
hereditary factors may have contributed to David’s depression.
Other biological factors that might be the cause of depression in David include the
abnormal brain structure and brain chemistry. For instance, the parts of brain involved in
regulating mood, thinking and behavior might be affected and the imbalance in
neurotransmitters leads to the progression of depression (Kemp, Lickel & Deacon, 2014).
Due to such imbalance, David might be suffering from low moods and other symptoms
of depression.
As David has been working as a mechanical fitter on the Pilmara mines since the
last 7 years, it is also possible that his work environment might have increased the risk of
depression in him. This is said because research has pointed out that mining industry
workers often develops mental health problems like depression and anxiety. The
lifestyles, work characteristics and attitudes influences the mental and psychological
health and well-being of workers (Liu,Wang, & Chen, 2014). Hence, work environment
and occupational factors might be cause of depression in David.

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d) For patients like David, who is suffering from major depressive disorder, two types of
medications can be given to treat him. The first is the selective serotonin reuptake
inhibitors (SSRIs) like Fluoxetine (Prozac) and this is the first medication which is
initially started in patients. However, medications needs to be taken with caution as
Prozac may result in common side effects of skin rashes, restlessness, fever as well as
severe side effects of anxiety, joint pain, seizures and diarrhea. The main cause side
effects in Prozac is that the drug has long half life and this results in slow processing of
drugs in the body (Prozac Oral: WebMD 2017). The function of SSRIs is to prevent the
serotonin neurotransmitter from being reabsorbed into the nerve cells. This results in
lightening of mood effect. Antidepressants are often linked to severe side effects of first
time seizures and SSRIs was found to be associated with the worse odds of having first
time seizures. This was seen mainly because overdose of the drug and timing of taking
medicines (Schloesser et al., 2015).
Another medication that can be given to Mr. David Wilson for treating depression is
tricyclic antidepressants like Clomipramine (Anafranil) if the above medication does not
work on the patient. The drug acts by increasing the level of norepinephrine and serotonins
and blocking the action of acetylcholine. This helps to restore the balance in
neurotransmitters and it alleviates depressive symptoms in patient. However, the
consumption of the medication is associated with many side-effects. Common side effects
include dry mouth, fatigue and constipation whereas serious side effects include low blood
pressure, seizures and irregular heart rate in patients (Annette (Gbemudu) Ogbru, 2017). The
heart rate variability is mostly seen during treatment of patients with tricyclic antidepressants
because of dose variability and abrupt discontinuation of drugs. Evidence by van Zyl,

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Hasegawa & Nagata, (2008) also proved that tricyclic antidepressants lead to the increase in
heart rate of patients.
Answer 2:
a) When David’s employer presented him to the local hospital, he was found in an
intoxicated state. His employer also reported that he is not able to work due to increased
consumptions of alcohol and poor concentration in work. Increased consumption of
alcohol might also be a reason for depressive symptom in patients because alcohol is
found to have an impact on adult brain. Evidence has mainly showed that alcohol has
damaging effects on the brain. Consumption of alcohol results in blurred vision, impaired
memory and slow reaction time. The PET imaging of brains in people with heavy alcohol
consumption has indicated that alcohol influences the function of the neurotransmitter
system, the brain cell mechanism as well as the blood flow within the brains. The
changes in function have been found mainly in frontal lobes which is involved with
learning and memory and the cerebellums involved in controlling movements and
coordination (Hermens et al., 2013). This discussion clearly explains why alcohol
consumption results in impaired memory, difficulty in walking and concentrating. The
dependence and overuse of alcohol can also be regarded as a pathway to depression in
Mr. David because of its link with neuropsychological impairment. The controlled
process of attention and memory and mental flexibility of student is affected by the
overuse of alcohol.
Alcohol has been found to influence neurotransmitter pathway too as evidence has shown
that it activates neuro-immune signaling and persistent neuoroimmune-gene induction leads to

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continuous neurodegeneration and loss of behavioral flexibility in person (Crews et al., 2015).
This has been also support by another research study which has explained that the effect of
alcohol on disrupting dopamine receptor activity. The dopamine receptors in the medial
prefrontal cortex control the cognition process by balancing the excitatory and inhibitory
transmission. The impact of alcohol on dopamine mediated neurotransmission in rats has shown
that behavioral flexibility decreased in rats with alcohol exposure. This confirms that cognitive
function is seriously affected by alcohol exposure due to its impact on dopamine receptor
signaling (Trantham-Davidson et al., 2014). For this reason, cognitive disruption has been seen
in David as he has isolated him from others and shows poor concentration.
b) Pathophysiology of alcohol withdrawal: During admission to the hospital, David came in
an intoxicated state. While staying at the hospital, he is likely to go into alcohol
withdrawal state. Going into the phase of sudden reduction in alcohol use following a
period of excessive consumption may result in alcohol withdrawal symptoms like
vomiting, fever, and increase in heart rate, anxiety and shakiness. In severe cases, people
may also suffer from seizures (Mirijello et al., 2015). In case of people consuming excess
alcohol, ethanol interacts with gamma-aminobutyric acid (GABA) type A receptor and
the N-methyl-D-aspartate (NMDA) receptor. Ethanol targets GABA type A leading to the
downregulation of GABA type A receptors. However, in contrast to the stimulation of
GABA type A receptor, ethanol inhibits function of NMDA receptor and causes
compensatory upregulation of NMDA receptor. Hence, adaptive mechanism in
neurotransmitter-receptor interaction promotes development of alcohol tolerance in
people. In case of alcohol withdrawal in the alcohol-dependent patient, sudden reduction
in alcohol use results in imbalance between the GABA receptor Type A function and the

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NMDA receptor. Due to the decrease in the alcohol level in blood, the inhibitory activity
of GABA is reduced and symptoms of hallucination seizures, tremors and hyperactivity
is seen in affected person (Yanta, Swartzentruber, & Pizon, 2015).
The severity of symptoms in alcohol withdrawal increases because of kindling phenomena.
This is a process where low electrical stimulus leads to changes in behavioral response and
symptoms of seizures. Evidence proves that this phenomena deteriorates the withdrawal
symptoms (Mainerova et al., 2015).
c) In patients with alcohol withdrawal syndrome, many mild to severe symptoms can be
seen which can be mistaken for other clinical condition. It is critical that nurses
effectively manage alcohol withdrawal patients in hospital setting. Common withdrawal
symptoms may include nausea, vomiting and insomnia, whereas severe symptoms
include hallucination, disorientation and agitation. While caring for alcohol withdrawal
patients, the nurse must understand the time at which the symptoms manifest in patients
and the time at which the symptoms must terminate. Alcohol withdrawal patients are
often very agitate and they show behaviors of violent outburst and verbal abuse. In such
situation, the nurse needs to prioritize patient safety and injury. As family members are
going to face problem due to abusive behavior of patient, the role of nurse is to educate
family members regarding withdrawal symptoms and being empathetic and non-
judgmental with patient during this period. Providing relaxing environment to patient is
also important (Mirijello et al., 2015). The nurse must also take caution while interacting
with patients and if they become extremely aggressive, then visitors or nurse must stay
away from them. Observing facial signs and body language of patient can also support a
nurse in keeping patient calm and compliant with treatment process. In case of severe

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withdrawal symptoms, nurse can also provide medications like Benzodiazepines to
control agitation and treat such behavior of patients. Meeting their nutritional needs will
also be important in such situation (Jarvis & Blad, 2010).
Answer 3
Biological link between alcohol and depression
Mr. David Wilson has been diagnosed with Major Depression and considering the impact of
alcohol on neurotransmitter pathways, it can said that his condition has deteriorate even more by
excessive use of alcohol. This explanation points out to the facts that there is biological link
between alcohol and depression. This link is described in detail by the use of different biological
factors which are as follows:
Genetics: The study by Mayfield, Harris & Schuckit, (2008) gives the implication that alcohol
abuse and alcohol independence has relation with genetics and gene expression. For instance,
genetic predisposition and genes increase the impaired controls towards many behavior such as
alcohol use or drug use. This is also proved by the facts that relatives of alcoholics and twins of
alcohol dependent person have fourfold higher risk of alcohol dependence. Secondly, specific
genes like GABA A receptor, alpha 2 gene on chromosome 4 has been found to influence
phenotypes of impulsivity and disinhibition (Dick et al., 2008). A study investigating about
genetic relationship between alcoholism and depression has shown that combination of both
alcoholism and depression run in families and this is most common in first degree relatives. The
study showed that both alcoholism and depression were linked to specific chromosome region of
chromosome 1. Hence, genes present on this region may predispose or increase risk of
alcoholism and depression in different people. The importance of the research was that it

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reinforced the idea that heavy drinkers are genetically vulnerable to depression and
antidepressant treatment on alcoholic depressed patients improves both depression as well as
alcohol consumption symptoms (Nurnberger et al., 2002).
Changes in neurotransmitter pathways: The biological link between alcohol and depression is
also proved in many research as both the condition has been found to lead to changes in
neurotransmitter pathways. This is also evident from the above discussion regarding the
pathophysiology of depression and alcohol withdrawal. A recent study highlighted the fact that
various neurotransmitters are involved in the pathway towards alcohol addiction. This is said
because alcohol exposure has an impact on function and balance of various neurotransmitters in
the brain (Banerjee, 2014). Many studies done in patients with alcohol dependence has shown
that the brain’s neurobiology is permanently changed by effect of alcohol. Alcohol has been
found to particularly influence many neurobiological pathways like dopaminergic, GABA,
serotoninergic and glutamate pathway (Yanta, Swartzentruber, & Pizon, 2015). Alcohol interact
with these transmitters and produce reinforcing affects resultsing in changes in neuronal function
and development of alcoholism. The research by Zuo et al., (2017) investigated particularly
about the effect of ethanol on dopamine and glutamate receptors. The study gave the insight that
ethanol stimulates the release of presynaptic glutamate mediated by the activation of dopamine
subtype receptors and the cAMP dependent metabolic pathways. Hence, this evidence is useful
to manipulate glutamate receptor while planning treatment of alcohol abuse.
The impact of alcohol and depression on neurotransmitter pathway is again understood from
the research by Heberlein et al., (2014) and this again established the biological link between
alcohol and depression. Both depression and alcoholism are associated with morbidity,
impact on quality of living and mortality. While discussing the physiological impact of

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alcoholism and depressions, the researcher showed that chronic alcohol consumption reduces
the availability of dopamine and influences mood and memory of affected person Similarly,
Yin et al., (2016) showed changes in GABA and neurotransmitter system resulting in suicide
behavior and major depressive order. Both GABA and glutamate are major inhibitory and
excitatory neurotransmitters and they are associated with suicidal behavior and major
depressive disorder too. They have the capability to changes the normal function of brain in
the area of cognition, mood regulation, memory and learning. This is reason for
manifestation of symptoms like poor concentration, low esteem, feelings of guilt and social
isolation. As GABA affects the concentration of monoamines in brain which reduced stress,
this mechanism is often exploited for the delivery antidepressant therapy too. Hence,
biological link between alcoholism and depression is proved through the changes in
neurotransmitter system.
Brain dysfunction: Alcoholism and depression is also found to have association with brain
and neurobehavioral functions. For instance, excessive alcohol use has been found to lead to
brain damage and this has been mainly proved by neuro-imaging studies in animals or
deceased patients. The alcohol related brain damage is also affected by age, history of
drinking and risk to specific regions of brain. The regions that are most likely to be damaged
by alcohol exposure includes neurotransmitter system, entire brain, frontal lobe system,
limbic system, thalamus and hypothalamus (Shokri-Kojori et al., 2016). The study regarding
brain development in heavy drinking adolescents have also showed that trajectory of normal
brain development is altered due to excessive consumption of alcohol. The specific brain
region that is affected includes regional cortical volumes and white matter structures. The

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longitudinal analysis of brain structure in adolescents mainly showed heavy decline in frontal
and temporal cortical volumes (Squeglia et al., 2015).
Just like the connection between brain damage and alcoholism, the connection between
depression and brain dysfunction has also been established. The biological link is close
because alcoholism itself is known trigger depression and deteriorates symptoms of
depression. They intensify the effects of GABA leading to sedative effects and this result in
poor concentration in people with depression. Similarly, imbalance in function of
neurotransmitters in both conditions results in depressive symptoms in people. In addition,
the dopamine and the endorphin pathway is also affected by the conditions. Alcohol also
damages the area of brain involved in non-verbal emotional stimuli thus resulting in social
withdrawal and inappropriate behavior in patients (Joseph, 2017).
Vitamin deficiency: The study also showed that vitamin deficiency in people also contributes
to brain damage and results in severe cognitive deficits in person with alcohol use and those
with Major depression (Shokri-Kojori et al., 2016). Nutritional deficiencies are also known to
cause depression and anxiety in people. Certain vitamins like Vitamin B12, B-complex and
Folate are known to delay depression (Rao, et al., 2008).

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