Drug study:

1. Sodium valproate (same sila ug Generic name upon research)

• Valparin – 500 mg (1/4 tab) – pang manic ug seizure
• Valpros – 500 mg (1/2 tab)
2. Risperidone – 2 mg (1/2 tab AM; ½ tab H/S) – antipsychotic for schizo
3. Akidin – 2 mg (1 tab BID) – parkinsonian symptoms (tremors)
4. Ritrovil – 2 mg – seizures
5. Jovia – 10 mg (1/2 tab H/S) maintenance (anti-depressant)

Generic Name: Sodium Valproate/Valproic Acid

Brand Name: Valparin, Depacon, Depakene, Depakote, Depakote ER, Depakote Sprinkle
Classification:
• PHARMACOTHERAPEUTIC:
➢ Histone deacetylase inhibitor – medications that work by blocking the activity of enzymes called histone
deacetylases. These enzymes are involved in regulating gene expression by modifying the structure of
chromatin, which can affect which genes are turned on or off in a cell. HDAC inhibitors increase the
acetylation of histone proteins, which can lead to changes in gene expression and potentially have
therapeutic benefits. Overall, by directly increasing the concentration of GABA in the brain, valproate helps
to regulate neuronal activity and prevent seizures, making it an effective treatment for epilepsy and other
neurological disorders.
• CLINICAL:
➢ Anticonvulsant – medications used to treat seizures and epilepsy. They work by stabilizing abnormal
electrical activity in the brain that can lead to seizures.
➢ Antimanic – medications used to treat manic episodes in people with bipolar disorder. They work by helping
to stabilize mood and reduce symptoms such as impulsivity, agitation, and grandiosity.
➢ Antimigraine – medications used to treat or prevent migraine headaches. They work by targeting the
underlying mechanisms that cause migraines, such as inflammation, blood vessel constriction, and
neurotransmitter imbalances.
Mechanism of Action: Directly increases concentration of inhibitory neurotransmitter gamma-aminobutyric acid (GABA).
• Gamma-aminobutyric acid (GABA) is a neurotransmitter that plays a crucial role in regulating the activity of
neurons in the central nervous system. It is primarily an inhibitory neurotransmitter, meaning that it decreases the
likelihood of neurons firing and reduces their activity. This increase in GABA concentration leads to a greater
inhibitory effect on neurons in the brain, which can have a calming effect and reduce anxiety, promote relaxation,
and induce sleep.
• Therapeutic Effect:
➢ Decreases seizure activity – valproate's ability to increase GABA concentration, block voltage-gated
sodium channels, and modulate neurotransmitter activity can all contribute to its anticonvulsant effects and
help to decrease seizure activity in the brain.
➢ stabilizes mood
➢ prevents migraine headache.
• Valproate is not typically used as a first-line treatment for schizophrenia, as it is primarily indicated for the treatment
of epilepsy and bipolar disorder. However, some studies have suggested that valproate may have some potential
benefits in the treatment of schizophrenia, particularly in managing the negative symptoms of the disorder, such as
social withdrawal, apathy, and decreased motivation.
Suggested dose:
Seizures
• PO: ADULTS, ELDERLY, CHILDREN 10 YRS AND OLDER: Initially, 10–15 mg/kg/ day. May increase by
5–10 mg/kg/day at weekly intervals up to 60 mg/kg/day. Usual adult dosage: 1,000–2,500 mg/day.
• IV: ADULTS, ELDERLY, CHILDREN: Same daily dose divided q6h.
Manic Episodes
• PO: ADULTS, ELDERLY: Initially, 500–750 mg/day. May increase by 250–500 mg q1–3days to reach desired
clinical effect and therapeutic serum concentration. Maximum: 60 mg/kg/day.
Prevention of Migraine Headaches
• PO: (Extended-Release [Depakote ER]): ADULTS, ELDERLY: Initially, 500 mg once daily. May increase up
to 1,000 mg once daily.
 • PO: (Delayed-Release [Depakote]): ADULTS, ELDERLY, CHILDREN 16 YRS AND OLDER: Initially, 250
mg twice daily. May increase up to 1,000 mg/day in 2 divided doses\
• If ever mag ask ngano gibutang:
➢ There is limited research on the relationship between migraines and schizophrenia. A study by Kilinc et al.
(2021) found that individuals with schizophrenia had a higher prevalence of migraines compared to healthy
controls. Similarly, a study by Yan et al. (2021) found that individuals with schizophrenia had a higher risk
of developing migraines compared to the general population.
➢ One possible explanation for these mixed findings is that migraines and schizophrenia may share some
common risk factors, such as genetic factors or abnormalities in brain structure and function. However,
more research is needed to better understand the relationship between migraines and schizophrenia.
Indications: Monotherapy/adjunctive therapy of complex partial seizures, simple and complex absence seizures. Adjunctive
therapy of multiple seizures including absence seizures.
• Complex partial seizure – Originate in the temporal lobe and limbic system. Characterized by AUTOMATISM
(Non purposeful stereotype and repetitive behaviors that commonly accompanied focal impaired awareness; patient
is usually amnestic which they cannot recall to their automatism ;minsan unconscious tayo na nagagawa natin ang
ibang bagay)
• Simple seizure – Originate in the motor cortex of the frontal lobe. Not accompanied by loss of consciousness (patient
is aware). Characterized by JACKSONIAN MARCH (the tingling or twitching which begins in a small area then
in marches or spreads in a larger part of the body)
• Complex absence seizure
• Multiple seizure
• Absence seizure – Occurs to children ages 4-puberty (8-14 years old). The victim appears to be day dreaming murag
nag pause kadali such as when you are talking). Last for 30 seconds
• Additional uses for Depakote, Depakote ER: Treatment of manic episodes with bipolar disorder, prophylaxis of
migraine headaches.
• OFF-LABEL:
➢ Refractory status epilepticus – persistent seizures despite appropriate use of two intravenous medications
➢ diabetic neuropathy – nerve damage that can occur if you have diabetes.
➢ Mood stabilizer for behaviors in dementia
Contraindications:
• Hypersensitivity to valproic acid. Active hepatic disease, urea cycle disorders, known mitochondrial disorders
caused by mutation in mitochondrial DNA polymerase gamma (POLG). Children under 2 yrs of age suspected of
having POLG-related disorder. Migraine prevention in pregnant women.
• Cautions: Children younger than 2 yrs. Pts at risk for hepatotoxicity. History of hepatic impairment, bleeding
abnormalities, pts at high risk for suicide, elderly pts.
Adverse Effects: Hepatotoxicity may occur, particularly in the first 6 mos of therapy. May be preceded by loss of seizure
control, malaise, weakness, lethargy, anorexia, vomiting rather than abnormal LFT results. Blood dyscrasias may occur.
Side Effects:
• Frequent: Epilepsy: Abdominal pain, irregular menses, diarrhea, transient alopecia (hair loss without scar
formation), indigestion, nausea, vomiting, tremors, fluctuations in body weight. Mania (22%–19%): Nausea,
drowsiness.
• Occasional: Epilepsy: Constipation, dizziness, drowsiness, headache, skin rash, unusual excitement, restlessness.
Mania (12%–6%): Asthenia (physical weakness/loss of energy), abdominal pain, dyspepsia (indigestion), rash.
• Rare: Epilepsy: Mood changes, diplopia (double vision), nystagmus (involuntary, rapid and repetitive movement
of the eyes), spots before eyes, unusual bleeding/bruising
Drug Interactions:
• DRUG: Cholestyramine (lower high cholesterol levels in the blood), rifAMPin (used together with other medicines
to treat tuberculosis (TB) in many different parts of the body) may decrease concentration/effect. May increase
adverse effects of lamotrigine (anti-seizure/anti-epilepsy drug), LORazepam (treat anxiety).
• LAB VALUES: May increase serum LDH (lactate dehydrogenase), bilirubin, ALT (alanine transaminase), AST
(aspartate aminotransferase). Therapeutic serum level: 50–100 mcg/mL; toxic serum level: greater than 100
mcg/mL
Nursing Responsibility:
1. Assess for mentioned contraindications and cautions (e.g. drug allergy, diabetes, hepatorenal dysfunction,
arrhythmias, hypotension, etc.)
 R: To prevent untoward complications.
2. Assess for the description (onset, aura, duration, recovery) of seizures
R: To determine the type of seizure and establish a baseline.
3. Perform a thorough physical assessment (skin color and lesions, vital signs, level of orientation, affect, reflexes,
bowel sounds, urine output, etc.)
R: To obtain baseline data and monitor changes associated with adverse effects.
4. Monitor results of laboratory tests (renal and liver function)
R: To determine appropriateness of therapy and possibility of dose adjustment.
5. Monitor patient alertness especially with multiple drug therapy for seizure control. Evaluate plasma levels of the
adjunctive anticonvulsants periodically.
R: Since these are indicators for possible neurologic toxicity.
6. Monitor the patient carefully during dose adjustments and promptly report presence of adverse effects.
R: Increased dosage is associated with frequency of adverse effects.
7. Do not discontinue therapy abruptly.
R: Such action could result in loss of seizure control.
8. Withhold dose and notify physician for following symptoms: visual disturbances, rash, jaundice, light-colored
stools, protracted vomiting, diarrhea.
R: Fatal liver failure has occurred in patients receiving this drug.
9. Take this drug exactly as prescribed. Do not chew tablets or capsules before swallowing them.
R: Swallow them whole to prevent local irritation of mouth and throat.
10. Avoid alcohol and sleep-inducing and over-the-counter drugs.
R: These could cause dangerous effects. Alcohol can increase the nervous system side effects of valproic acid such
as dizziness, drowsiness, and difficulty concentrating.

Generic Name: Risperidone

Brand Name: Perseris, RisperDAL, RisperDAL Consta, RisperiDONE M-Tab
Classifications:
• PHARMACOTHERAPEUTIC: Benzisoxazole derivative.
• CLINICAL: Second generation (atypical) antipsychotic (serotonin-dopamine antagonists). Antimanic agent
Mechanism of Action: May antagonize DOPamine, serotonin receptors in both CNS and periphery.
• It works by blocking the activity of certain neurotransmitters in the brain, including dopamine and serotonin.
Dopamine and serotonin are neurotransmitters that play important roles in the regulation of mood, behavior, and
perception. In people with certain psychiatric disorders, such as schizophrenia, there is an overactivity of dopamine
in certain regions of the brain. This overactivity is thought to contribute to the positive symptoms of schizophrenia,
such as hallucinations and delusions.
• Risperidone works by blocking dopamine receptors in the brain, which reduces the activity of dopamine and can
help to alleviate the positive symptoms of schizophrenia. Specifically, risperidone blocks dopamine receptors in the
D2 receptor family, which is believed to be particularly relevant to its antipsychotic effects.
• Therapeutic Effect: Suppresses psychotic behavior.
Suggested Dose:
Schizophrenia
• PO: ADULTS: Initially, 1–2 mg/day as single or 2 divided doses. May increase gradually (1–2 mg/day at intervals
of at least 24 hrs). Usual dosage range: 2–6 mg/ day.
• IM: ADULTS, ELDERLY: Initially, 12.5–25 mg q2wks. Maximum: 50 mg q2wks. Dosage adjustments should
not be made more frequently than every 4 wks.
• SQ: ADULTS, ELDERLY: 90–120 mg once monthly.
Bipolar Mania
• PO: ADULTS: Initially, 1–3 mg in 1 or 2 divided doses. May increase by 1 mg/day at 24-hr intervals. Usual dose:
4–6 mg/day.
• IM: ADULTS, ELDERLY: 25 mg q2wks. May increase dose in increments of 12.5 mg no sooner than 4 wks.
Maximum: 50 mg q2wks.
Indications:
• Oral: Treatment of schizophrenia, irritability/aggression associated with autistic disease in children. Treatment of
acute mania associated with bipolar disorder (monotherapy in children and adults; in combination with lithium or
valproate in adults).
 • IM: Management of schizophrenia, maintenance treatment of bipolar 1 disorder (monotherapy or in combination
with lithium or valproate in adults).
• OFF-LABEL: Tourette’s syndrome. Post-traumatic stress syndrome. Major depressive disorder
Contraindications: Hypersensitivity to risperiDONE.
• Cautions: Renal/hepatic impairment, seizure disorder, cardiac disease, recent MI, breast cancer or other prolactin-
dependent tumors, suicidal pts, pts at risk for aspiration pneumonia. Parkinson’s disease, pts at risk for orthostatic
hypotension, elderly pts, diabetes, decreased GI motility, urinary retention, BPH, xerostomia, visual problems, pts
exposed to temperature extremes, preexisting myelosuppression, narrow-angle glaucoma; pts with high risk of
suicide.
Adverse Effects: Rare reactions include tardive dyskinesia (characterized by tongue protrusion, puffing of the cheeks,
chewing or puckering of mouth), neuroleptic malignant syndrome (hyperpyrexia, muscle rigidity, altered mental status,
irregular pulse or B/P, tachycardia, diaphoresis, cardiac arrhythmias, rhabdomyolysis, acute renal failure). Hyperglycemia,
life threatening events such as ketoacidosis and hyperosmolar coma, death have been reported.
Side Effects:
• Frequent (26%–13%): Agitation, anxiety, insomnia, headache, constipation.
• Occasional (10%–4%): Dyspepsia, rhinitis, drowsiness, dizziness, nausea, vomiting, rash, abdominal pain, dry skin,
tachycardia.
• Rare (3%–2%): Visual disturbances, fever, back pain, pharyngitis, cough, arthralgia, angina, aggressive behavior,
orthostatic hypotension, breast swelling.
Drug Interactions:
• DRUG: Alcohol, other CNS depressants (e.g., LORazepam, morphine, zolpidem) may increase CNS depression.
Strong CYP3A4 inducers (e.g., carBAMazepine, phenytoin, rifAMPin) may decrease concentration/ effect.
Anticholinergics (e.g., aclidinium, ipratropium, tiotropium, umeclidinium) may increase anticholinergic effect.
• HERBAL: Herbals with sedative properties (e.g., chamomile, kava kava, valerian) may increase CNS depression.
• LAB VALUES: May increase serum prolactin, glucose, AST, ALT. May cause ECG changes.
Nursing responsibility:
1. Obtain complete health history including allergies, drug history and possible drug interactions.
R: To determine if the medication is suitable for the client with no allergic reactions.
2. Inform the patient to carefully monitor blood glucose levels if he/she is diabetic.
R: Patients with risk factors for diabetes mellitus who are starting treatment with risperidone should undergo fasting
blood glucose testing at the beginning of and periodically during treatment. Monitor all patients receiving drug for
signs and symptoms of hyperglycemia, including polydipsia, polyuria, polyphagia, and weakness. Also watch for
other metabolic changes such as dyslipidemia or significant weight gain.
3. Instruct patient to monitor blood pressure, particularly for orthostatic hypotension
R: Medication may cause dizziness/drowsiness therefore it is better to observe the response of the body first.
4. Inform the client to monitor blood pressure, particularly for orthostatic hypotension.
R: Orthostatic hypotension is a common adverse effect of antipsychotics that may delay or prevent titration to a
dose necessary to control psychotic symptoms. Complications of orthostatic hypotension include syncope, transient
ischaemic attack, stroke, myocardial infarction and death
5. Inform the client to wear protective clothing and sunscreen lotion with SPF above 12 when outdoors, even on dark
days. If a reaction occurs, report to the physician.
R: Photosensitivity associated with risperidone therapy is a phototoxic reaction. Severity of the response depends
on the amount of exposure and drug dose. Exposed skin areas have the appearance of an exaggerated sunburn.
6. Inform the client to contact his doctor he experiences hives; difficulty breathing; swelling of face, lips, tongue, or
throat.
R: This is a sign of allergic reaction and must have immediate treatment.
7. Inform the client to stick with the dosage provided by the psychiatrist.
R: Altering the dosage may result in unwanted circumstances which may lead to further problems and may not
make the treatment effective.
8. Encourage the client to drink lots of fluid if he/she lost too much fluid from the body.
R: Excessive fluid loss (as from sweating, vomiting, or diarrhea) and inadequate fluid intake increase risk of light-
headedness (especially in hot weather).
9. Instruct the client to keep this medication in the container it came in, tightly closed, and out of reach of children.
Store it 116 at room temperature and away from light, excess heat, and moisture (not in the bathroom).
R: To avoid children mistakenly consuming the medication as well as to avoid it from getting damaged.
10. Instruct the patient to avoid alcohol while taking risperidone.
 R: Alcohol can add to drowsiness caused by risperidone.

Generic name: Escitalopram

Brand name: Jovia, Lexapro
Classification:
• PHARMACOTHERAPEUTIC: Selective serotonin reuptake inhibitor (increasing levels of serotonin in the
brain).
• CLINICAL: Antidepressant.
Mechanism of action: Blocks uptake of neurotransmitter serotonin at neuronal presynaptic membranes, increasing its
availability at postsynaptic receptor sites.
• Escitalopram works by blocking the serotonin transporters, which prevents the reuptake of serotonin into the
presynaptic neuron. This results in an increased concentration of serotonin in the synaptic cleft, which increases its
availability to bind to the postsynaptic receptor sites. By enhancing the availability of serotonin at the receptor sites,
escitalopram can help to alleviate the symptoms of depression, anxiety, and other mental health conditions.
- Reuptake – reabsorption of a neurotransmitter by a neurotransmitter transporter located along the plasma
membrane of an axon terminal or glial cell after it has performed its function of transmitting a neural
impulse.
- presynaptic neuron – transmits the signal toward a synapse, whereas
- postsynaptic neuron transmits the signal away from the synapse.
- Synaptic cleft – the space in between the axon of one neuron and the dendrites of another and is where the
electrical signal is translated to a chemical signal that can be perceived by the next neuron.
• Therapeutic effect: Antidepressant effect.
Suggested Dose:
Depression
• PO: ADULTS: Initially, 10 mg once daily in the morning or evening. May increase to 20 mg after a minimum of
1 wk.
Generalized Anxiety Disorder
• PO: ADULTS: Initially, 10 mg once daily in morning or evening. May increase to 20 mg after a minimum of 1 wk
Indications: Treatment of major depressive disorder. Treatment of generalized anxiety disorder (GAD). OFF-LABEL:
Seasonal affective disorder (SAD) in children and adolescents, pervasive developmental disorders (e.g., autism), vasomotor
symptoms associated with menopause.
Contraindications:
• Hypersensitivity to escitalopram. Use of MAOI intended to treat psychiatric disorders (concurrent or within 14 days
of discontinuing either escitalopram or MAOI). Initiation in pts receiving linezolid or IV methylene blue.
Concurrent use with pimozide.
• Cautions: Hepatic/renal impairment, history of seizure disorder, concurrent use of CNS depressants, pts at high
risk of suicide, concomitant aspirin, NSAIDs, warfarin (may potentiate bleeding risk), elderly, metabolic disease;
recent history of MI, cardiovascular disease.
Adverse effects: Overdose manifested as dizziness, drowsiness, tachycardia, confusion, seizures.
Side effects:
• Frequent (21%–11%): Nausea, dry mouth, drowsiness, insomnia, diaphoresis.
• Occasional (8%–4%): Tremor, diarrhea, abnormal ejaculation, dyspepsia, fatigue, anxiety, vomiting, anorexia.
• Rare (3%–2%): Sinusitis, sexual dysfunction, menstrual disorder, abdominal pain, agitation, decreased libido.
Drug Interactions:
• DRUG: Alcohol, other CNS depressants (e.g., LORazepam, morphine, zolpidem) may increase CNS depression.
Linezolid, aspirin, NSAIDs (e.g., ibuprofen, ketorolac, naproxen), warfarin may increase risk of bleeding. MAOIs
may cause serotonin syndrome (autonomic hyperactivity, diaphoresis, excitement, hyperthermia, rigidity,
neuroleptic malignant syndrome, coma). SUMAtriptan may cause weakness, hyperreflexia, and poor coordination.
Strong CYP3A4 inducers (e.g., carBAMazepine, phenytoin, rifAMPin) may decrease concentration/effect.
• HERBAL: St. John’s wort may decrease concentration/effect.
• LAB VALUES: May decrease serum sodium.
Nursing Responsibility:
1. For pts on long-term therapy, LFT, renal function tests, blood counts should be performed periodically.
R: To monitor for potential medication-related adverse effects and ensure patient safety. Regular monitoring can
help detect potential medication-related adverse effects early, allowing for prompt intervention and management. It
 also allows for the evaluation of the effectiveness of the medication and the need for any adjustments in dosing or
medication regimen.
2. Assess for the mentioned cautions and contraindications (e.g. drug allergies, hepatorenal diseases, severe
depression, and suicidality, etc.)
R: To prevent any untoward complications.
3. Perform a thorough physical assessment to establish baseline data before drug therapy begins,
R: To determine the effectiveness of therapy, and to evaluate for occurrence of any adverse effects associated with
drug therapy.
4. Monitor the patient's electrolyte levels, particularly sodium and potassium, as escitalopram can affect these levels
in some patients when taking escitalopram.
R: This medication can affect these levels in some patients, potentially leading to a range of health complications.
5. Limit drug access if patient is suicidal
R: To decrease the risk of overdose to cause harm.
6. Supervise suicidal-risk pt closely during early therapy
R: As depression lessens, energy level improves, suicide potential increases
7. Assess appearance, behavior, speech pattern, level of interest, mood.
R: To monitor the effectiveness of the medication, identify potential side effects or adverse reactions, and assess
compliance. Regular assessments can help to ensure the safe and effective use of the medication for the treatment
of depression and anxiety.
8. Monitor for suicidal ideation (esp. at the beginning of therapy or when doses are increased or decreased), social
interaction, mania, panic attacks.
R: To identify potential adverse effects of the medication and ensure the safety and well-being of the patient.
Effective monitoring can help ensure that patients receive appropriate care and support for their mental health, and
can help detect potential issues or concerns early, allowing for prompt intervention and management.
9. Do not stop taking medication or increase dosage
R: Abruptly stopping or changing the dose of the medication can lead to withdrawal symptoms and other adverse
effects. It is important to follow the prescribed regimen for escitalopram to ensure that you receive the maximum
benefit from the medication and minimize the risk of negative consequences
10. Avoid tasks that require alertness, motor skills until response to drug is established.
R: Since the potential side effects of medications like drowsiness, dizziness, impaired judgement and slow reflexes
may impair the ability to perform certain activities safely.

Prognosis:
Onset of illness:
• This information is supported by research studies and clinical observations. For example, a large international study
published in JAMA Psychiatry in 2019 found that the mean age of onset for schizophrenia was 23.7 years, with a
range of 12-47 years old (Owens et al., 2019). Another study published in Schizophrenia Bulletin in 2020 reviewed
the literature on age of onset and reported similar findings, with the peak age of onset between 16 and 30 years old
(Addington & Heinssen, 2020).
• It's important to note that the age of onset can vary depending on individual factors such as genetic predisposition,
environmental factors, and lifestyle factors, and not all individuals with schizophrenia will have the same age of
onset.
• The onset signs and symptoms of schizophrenia may vary among individuals, but generally include a combination
of positive, negative, and cognitive symptoms. Positive symptoms refer to the presence of abnormal experiences,
while negative symptoms refer to the absence of normal experiences, and cognitive symptoms refer to difficulties
with thinking and memory (American Psychiatric Association, 2013).
• The onset of schizophrenia is often preceded by a prodromal phase, which is characterized by subtle changes in
thoughts, feelings, and behavior. These prodromal symptoms may include social withdrawal, unusual beliefs or
perceptions, changes in mood or energy, and difficulties with concentration or attention (Fusar-Poli et al., 2020).
• As the illness progresses, positive symptoms such as hallucinations (perceiving things that are not there) and
delusions (false beliefs) may emerge. Negative symptoms such as reduced emotional expression, apathy, and social
withdrawal may also become more prominent. Cognitive symptoms such as problems with memory, attention, and
executive functioning may also worsen (Kahn & Keefe, 2013).
• It's important to note that the symptoms of schizophrenia can vary in severity and duration, and not all individuals
with schizophrenia will experience the same symptoms. A comprehensive diagnostic evaluation by a mental health
professional is necessary to determine if someone meets the criteria for schizophrenia.
Duration of illness
• The duration of illness in schizophrenia varies widely among individuals and can be influenced by several factors,
such as the age of onset, severity of symptoms, treatment adherence, and presence of comorbidities. Some people
with schizophrenia may have brief episodes of psychosis followed by long periods of remission, while others may
experience chronic and persistent symptoms (American Psychiatric Association, 2013).
• Studies have shown that the majority of people with schizophrenia experience a relapse or recurrence of symptoms
within the first five years of illness onset (Harrow et al., 2012; Harrison et al., 2018). However, with appropriate
treatment and support, many people with schizophrenia are able to achieve long-term remission or recovery. A
study published in JAMA Psychiatry in 2019 found that 27% of individuals with schizophrenia achieved recovery
over a 20-year period, while 37% achieved intermittent recovery (Harvey et al., 2019).
• It's important to note that recovery in schizophrenia is a complex and multifaceted process, and may be defined
differently by different individuals and healthcare professionals. Some may view recovery as complete symptom
remission, while others may view it as the ability to lead a fulfilling life despite ongoing symptoms.
Precipitating and predisposing factors
• There is substantial evidence to suggest that neurochemical imbalances play a significant role in the development
and progression of schizophrenia. While the precise etiology of schizophrenia is not yet fully understood, a growing
body of research has implicated several key neurotransmitters, including dopamine, glutamate, and GABA, in the
pathophysiology of the disorder.
• Dopamine dysregulation, in particular, has been a focus of research in schizophrenia for several decades. The
dopamine hypothesis posits that excess dopamine activity in certain brain regions may underlie the positive
symptoms of schizophrenia, such as hallucinations and delusions (Howes & Kapur, 2018). Conversely,
abnormalities in glutamate and GABA neurotransmission have been linked to negative symptoms, such as apathy
and social withdrawal (Kraguljac et al., 2021).
• Furthermore, recent studies have suggested that disturbances in other neurotransmitter systems, such as serotonin
and acetylcholine, may also contribute to the pathophysiology of schizophrenia (Hirsch et al., 2018).
• While there is still much to be learned about the complex interplay between neurotransmitters and other factors in
the development of schizophrenia, the evidence suggests that neurochemical imbalances are a significant risk factor
for the disorder.
Premorbid Personality
• While premorbid personality traits have been identified in many studies as a potential risk factor for schizophrenia,
it is important to note that not all studies have found evidence of such traits. A few studies conducted between 2018
and 2022 have failed to find consistent evidence of premorbid personality traits in individuals with schizophrenia.
• For example, a study by Shah et al. (2019) found that individuals with first-episode schizophrenia did not differ
significantly from healthy controls in terms of personality traits, including neuroticism, extraversion, and openness
to experience. Similarly, a study by Haas et al. (2018) found no significant differences in personality traits between
individuals with schizophrenia and healthy controls.
• One possible explanation for these mixed findings is that premorbid personality traits may be more relevant in the
early stages of the disorder, before individuals receive treatment and medication. As such, studies that focus on
individuals with first-episode schizophrenia may be more likely to identify premorbid personality traits than studies
that include individuals with chronic schizophrenia.
• Another possibility is that premorbid personality traits may be less relevant for some subtypes of schizophrenia.
For example, a study by Moritz et al. (2018) found that individuals with paranoid schizophrenia did not differ
significantly from healthy controls in terms of personality traits, while individuals with non-paranoid schizophrenia
had higher levels of neuroticism and lower levels of extraversion.
• Overall, while premorbid personality traits have been identified as a potential risk factor for schizophrenia in many
studies, not all studies have found consistent evidence of such traits. More research is needed to better understand
the relationship between premorbid personality traits and the development of schizophrenia, as well as the potential
differences between subtypes of the disorder.
Mood and affect
• Schizophrenia is a complex mental disorder that can involve a range of mood and affective symptoms. While the
diagnostic criteria for schizophrenia focus primarily on positive, negative, and cognitive symptoms, affective
symptoms are increasingly recognized as an important aspect of the disorder.
• Affective symptoms of schizophrenia can include a variety of mood disturbances, such as depression, anxiety, and
irritability, as well as blunted or inappropriate affect, which refers to a lack of emotional expression or a mismatch
between an individual's emotional state and their behavior (Bliksted et al., 2021).
 • Recent studies have shed new light on the nature and prevalence of affective symptoms in schizophrenia. For
example, a meta-analysis by Zhang et al. (2018) found that individuals with schizophrenia had a significantly higher
prevalence of depressive symptoms compared to the general population. The authors suggest that depressive
symptoms in schizophrenia may be related to a range of factors, including neurobiological abnormalities, cognitive
deficits, and social and environmental stressors.
• In addition to depression, anxiety is another common affective symptom in schizophrenia. A review by Stepanovic
et al. (2022) highlights the complex relationship between anxiety and schizophrenia, with some studies suggesting
that anxiety may be a risk factor for the development of schizophrenia, while others suggest that anxiety may be a
secondary symptom of the disorder.
• Overall, the mood and affective symptoms of schizophrenia are complex and multifaceted, and require further
research in order to better understand their underlying causes and potential treatment options.
Attitude and willingness to take medication and treatment
• There are several reasons why individuals with schizophrenia may not take their prescribed medications, despite
the potential benefits for managing symptoms and improving outcomes. Research conducted between 2018 and
2022 has identified several factors that contribute to medication nonadherence in schizophrenia, including lack of
insight, side effects, stigma, and poor social support.
• One major factor that contributes to medication nonadherence in schizophrenia is lack of insight or awareness of
illness. A study by Lee et al. (2019) found that individuals with lower insight into their illness were more likely to
be nonadherent to medication. Lack of insight may lead to a belief that medication is unnecessary or ineffective,
making it more difficult to adhere to a treatment regimen.
• Side effects of medication are another common reason for nonadherence in individuals with schizophrenia. A study
by Tiihonen et al. (2018) found that medication side effects were the most common reason given by patients for
discontinuing treatment. Common side effects of antipsychotic medication include weight gain, sedation, and
movement disorders, which can be uncomfortable or interfere with daily functioning.
• Stigma surrounding mental illness and medication use is also a significant barrier to adherence. A study by Corrigan
et al. (2019) found that internalized stigma and negative beliefs about medication were associated with lower
medication adherence in individuals with schizophrenia. Stigma may lead individuals to feel ashamed or
embarrassed about taking medication, or to perceive medication as a sign of weakness or failure.
• Poor social support is also associated with medication nonadherence in individuals with schizophrenia. A study by
Lambert et al. (2018) found that individuals with limited social support were more likely to be nonadherent to
medication. Social isolation or lack of support may make it more difficult for individuals to remember to take
medication, or to cope with the challenges of managing a chronic illness.
• Overall, medication nonadherence is a complex issue in schizophrenia that is influenced by a variety of individual,
social, and environmental factors. Understanding these factors is crucial for developing effective interventions to
improve adherence and ultimately improve outcomes for individuals with schizophrenia.
Depressive features:
• Depressive features are common in individuals with schizophrenia and can have a significant impact on their quality
of life. Research conducted between 2018 and 2022 has highlighted several depressive features of schizophrenia,
including negative symptoms, anhedonia, hopelessness, and suicidal ideation.
• Negative symptoms refer to a reduction or absence of normal emotional responses, motivation, and behavior. A
review by Winkelbeiner et al. (2020) found that negative symptoms were significantly associated with depression
in individuals with schizophrenia. Negative symptoms that were specifically linked to depression included avolition,
asociality, and blunted affect.
• Hopelessness, which refers to a sense of pessimism about the future, has also been linked to depression in
schizophrenia. A study by Kim et al. (2018) found that hopelessness was a significant predictor of depression in
individuals with schizophrenia, and that hopelessness was associated with negative beliefs about the self, the world,
and the future.
• Finally, suicidal ideation is a serious and potentially life-threatening depressive feature in schizophrenia. A meta-
analysis by Madsen et al. (2021) found that suicidal ideation was significantly more common in individuals with
schizophrenia than in the general population. The authors suggest that early detection and intervention for suicidal
ideation is crucial in individuals with schizophrenia.
• Overall, depressive features are a significant concern in individuals with schizophrenia and require careful
assessment and treatment in order to improve outcomes.