Picture Source

Have you ever heard about Schizophrenia? I'm sure some of you have. It is a group of illnesses which is associated with personality changes, poor judgement and deterioration in cognitive function. People who have been diagnosed with schizophrenia has some kind of disturbances in affect, behaviour, emotion, mood, perception and thought. The word affect here refers to the expression of emotion. For example, when you're happy, the affect would be smiling. Any abnormalities in the expression of emotion are described as disturbance of affect. It can be a flat affect, meaning there is no expression of emotion or inappropriate affect; for example, you're laughing when you're sad. Schizophrenia is often disabling especially in the area where stigma towards mental health patient is prominent. They are often robbed of any job opportunities, appropriate social conduct and safe housing.

This illness was first described by a German psychologist named Emil Kraepelin in 1890. Back in the day before Kraepelin, this particular illness was thought to be caused by an evil spirit/demon who possessed the human's body. You can guess by now for every human who is supposed to be treated as schizophrenia was exorcised in order to expel this demon, back in the day. There was even a procedure to drill a hole in the patient's skull to release this evil spirit from someone's head. When Kraepelin stumbled upon this illness, he coined the term "dementia praecox" or premature madness to describe an individual who has symptoms relatable to schizophrenia such as catatonia (abnormality of movement) or disorganization of multiple domains that is needed for a proper social interaction.

In 1911, a Swiss Psychiatrist named Eugen Bleuler identified the pattern of symptoms in this disorder. Fundamentally, this illness can be explained through 4 themes of disorganization:

• Ambivalence
• Autism
• Inappropriate Affect
• Looseness of Association

This concept expands and specifies the description of dementia praecox in early adulthood and eventually, Bleuler coined the term schizophrenia which comes from a Greek word meaning split mind to describe the nature of thinking in this kind of illness.

In 1959, all of the symptoms in schizophrenic patients were classified into 5 group of symptoms:

• Auditory Hallucination
• Passivity phenomenon
• Somatic passivity
• Thought possession
• Delusional perception

This is called Schneiderian's First Rank Symptoms of Schizophrenia developed by Kurt Schneider. We can see that, there are multiple criteria and screening processes being speculated by different scientist back in the day. Each and every assessment has their own merits and eventually, all of the features described by Bleuler, Kraepelin and Schneider are incorporated into standardized guidelines which are being used today.

Epidemiology and Etiology of Disease

In the United State of America, the prevalence ranging from 0.6% to 1.9%, while in Malaysia, the prevalence stays at 1%. This illness usually is detected in young adult or late adolescence which cause a considerable impact on the individual's education, personality and social interaction. This is because, during the period of adolescence, from a psychological perspective, it is the time for them to learn to be independent, searching for their identity, moulding their own personality and ultimately developed a mature heterosexual relationship in the community. People who are diagnosed with schizophrenia are often single and unemployed which make it difficult for them to function socially. Men generally have an earlier onset than women but the prevalence rate seem to be equal in both gender.

Picture Source

A couple of years ago, it is thought that schizophrenia is affected by geographical location, but the research carried out in the past found inconclusive result to the hypothesis being made. It is the stigma towards schizophrenic patient which is varied according to geographical location.

Even though this illness has been around since the ancient Egyptian, the precise cause is still unknown. Genetic predisposition is a strong risk factor that can make an individual vulnerable to get schizophrenia but usually, whether or not this vulnerability being triggered will depend on psychosocial factors such as domestic and substance abuse. There are multiple factors that can affect gene expression and mutation and usually, this requires interaction between them such as biological, psychosocial and social factors.

Biological factors

Genetic Factors

Picture Source

This factor is apparent, especially in the twins. A study which is conducted to identify the familial aggregation of schizophrenia in adopted children and twins has found a strong correlation between schizophrenia and genetic predisposition.

• The risk of schizophrenia in general population is 1%
• The risk of schizophrenia among first-degree relatives is 10%
• The risk of schizophrenia among second-degree relatives is 3%
• If both of parents have schizophrenia, the risk escalates to 40%
• The risk of schizophrenia among twins either monozygotic or dizygotic twins were 50% and 10% respectively if the other has this illness.

In a study conducted among adopted children to investigate whether environmental factor overrides the genetic predisposition from affected biological parents has found that, the environment does not play any role in reducing the risk of the children getting schizophrenia. It's further supported by a study which is conducted in 2014, which concluded, a child with schizophrenic siblings will experience the onset of illness at the same age as their siblings.

Biochemical Factors

There are few theories which could explain schizophrenia which include:

• Dopamine theory: This is the most popular theory which is speculated based on the evidence shown by the patients who are on schizophrenic medications. Most of the antipsychotic medication prescribed for this condition act as a dopamine receptor antagonist. The efficacies of the medication would depend on the ability of it to block the dopamine receptor. Amphetamine abuse, on the other hand, could accentuate schizophrenia by over-released of the dopamine in the brain. Both of this conditions show a possible link between dopamine and schizophrenia.
• Serotonin theory: This theory was made based on the action of hallucinogen which could increase serotonin activities and eventually lead to symptoms that mimic schizophrenia. The latest type of antipsychotic called atypical antipsychotic block both dopamine and serotonin receptors which gives a much better outcome in a patient with schizophrenia. Both of this evidences shown the role of serotonin in causing schizophrenia.
• Glutamate theory: Even though more research is needed to strengthen this theory, glutamate, a neurotransmitter (excitatory) in the brain, was found to have a toxic effect which can lead to the development of schizophrenia.
• Gamma-aminobutyric acid (GABA) theory: This theory bolsters the dopamine theory in causing schizophrenia. GABA is an inhibitory neurotransmitter in the brain which is correlated with the level of dopamine. If the level of GABA reduces, the level of dopamine will spike up hence causing schizophrenia.

Neuropathology

Brain abnormalities often lead to various consequences which can include schizophrenia. In the schizophrenic patient, the most common findings that could be contemplated was sulcus and ventricular enlargement associated with brain atrophy and sometimes small thalamus. These changes usually followed by an increase in cerebrospinal fluid in the ventricles. Schizophrenic patients usually associated with hypofrontality, a state of decreased blood flow to the prefrontal cortex which is usually associated with negative symptoms such as decreased cognitive function.

Pre and Perinatal Complications

Picture Source

In a review journal written in 1999 about schizophrenia entitled "The neuropsychopharmacology of phencyclidine: from NMDA receptor hypofunction to the dopamine hypothesis of schizophrenia", the author points out the pre and perinatal complications as one of the most important causes of schizophrenia. Any birth trauma or obstetrical complications can increase the risk of an individual to develop schizophrenia later in life such as:

• Emergency lower segment cesarean section (ELSCS).
• Birth asphyxia
• Low birth weight
• Gestational diabetes
• Maternal haemorrhage

Infections, stress and any disturbances during the second trimester have been linked to a higher risk of developing schizophrenia later in life.

Substance Abuse

This is rather a controversial topic. It's unknown whether the act of drug abuse is the result of schizophrenia or the cause of it. However, there are some drugs which could mimic the symptoms is schizophrenic patient such as hallucination.

Psychosocial Factors

The episode of schizophrenia is usually preceded by a stressful life event such as abuse, divorce or being fired from a job. It seems normal but the experiences are usually more adverse than the normal population.

There are two types of conditions which could predispose an individual to schizophrenia:

• Problems in the social relationship
• Pathological family relationship

In a social relationship, people with schizophrenia might feel comfortable living in an area where social demand is less. They're started to be isolated from the community and anything that can aggravate their anxiety which is related to social interaction demands can aggravate their symptoms. This is called as social drift or social selection.

In another situation called social causation or social breeder, an adverse living situation such as poverty can cause schizophrenia for those who are genetically predisposed.

Picture Source

Overprotective, overcritical, overinvolvement of parents in their children's affair can also lead to the development of schizophrenia. This pathological relationship in a family is common among single child. This behaviour is termed high express emotion behaviour.

References

• Lavretsky H. History of Schizophrenia as a Psychiatric Disorder. In: Mueser KT, Jeste DV, editors. Clinical Handbook of Schizophrenia. New York, New York: Guilford Press; 2008. pp. 3–12.
• Crismon L, Argo TR, Buckley PF. Schizophrenia. In: DiPiro JT, Talbert RL, Yee GC, et al., editors. 1Pharmacotherapy: A Pathophysiologic Approach. 9th ed. New York, New York: McGraw-Hill; 2014. pp. 1019–1046.
• Jentsch JD, Roth RH. The neuropsychopharmacology of phencyclidine: from NMDA receptor hypofunction to the dopamine hypothesis of schizophrenia. Neuropsychopharmacology. 1999;20(3):201–225.
• McDonald C, Murphy KC. The new genetics of schizophrenia. Psychiatr Clin North Am. 2003;26(1):41–63.
• Van Os J, Kapur S. Schizophrenia. Lancet. 2009;374(9690):635–645.