SCHIZOPHRENIA & NON AFFECTIVE PSYCHOTIC DISORDERS

By

Dapap D.D

BHUTH

Psychosis/History

• Greseinger ?? 1860s; Unitary Psychosis
• Morel (1809-1873): Demence Precoce
• Karl Kaulbaum (1828-1899): Catatonia
• Edwold Hacker (1843-1909): Hebephrenia
• Emil Kraeplin (1856-1926): Dementia praecox
• Eugene Bleuler (1857-1939): Schizophrenia

What is schizophrenia?

Schizophrenia is a term used to describe a heterogeneous group of mental illnesses which are diverse in nature and cover a broad range of cognitive, emotional and behavioural disturbances.

Core features of schizophrenia

• Positive symptoms: auditory hallucinations, particularly in the third person; changes in thought construction and form; and bizarre delusions

and/or

• Negative symptoms: such as blunted affect, emotional incongruity, poverty of thought, social withdrawal.

EPIDEMIOLOGY

• Incidence rates: 0.1 and 0.4 per 1000 population (Jablensky et al, 1992). Lifetime risk of developing schizophrenia is 7.0-13.0 per 1000 (Reiger et al 1988) in the US.
• Point prevalence in Europe 2.5-5.3% per 1000 (Jablensky, 1988).
• Prevalence (1%) is the same any where in the world (WHO collaborative study )using Schenider’s first rank symptom diagnostic criteria (Jablensky et al 1992).
• High rates have been reported in Slovenia, extreme north of Sweden, Western Islands, among Catholics in Canada and Tamils of southern India (Cooper, 1978).

……. Epidemiology

• Onset of schizophrenia 15 and 45 years
• Gender: equally in men and women
• Mean age of onset is about five years earlier in men.
• Social Class: Low socioeconomic class

Aetiology (Cooper, 1978)

• Predisposing Factors: Genetic, season of birth. pregnancy and birth complications, personality, substance abuse
• Precipitating Factors: Environmental conditions, stress.
• Perpetuating Factors: poor compliance with medications, substance use, general medical conditions.

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Biological Factors

• Genetic Factors
• Concordance rates of about 50% in monozygotic twins and lifetime risk of about 45% in children of two schizophrenic parents.
• Chromosomal markers: Current approaches using RFLP have identified long arm of chromosome 5, 11, 18, 19 and X. as being associated with schizophrenia.
• Dopamine Hypothesis: Schizophrenia is due to heightened activity of dopamine at one more sites in the brain

Dopamine Hypothesis…………….

• This has dominated biochemical and pharmacological thinking about schizophrenia for decades
• However, it alone cannot significantly explain the full pathophysiology of the illness and moreso, increased dopaminergic activity cannot account for the negative symptoms of schizophrenia (Crow, 1980; Tandon et al, 1995, 1999).
• It is believed nowadays that it is the interactions between dopamine and other neurotransmitter systems that are relevant to the production and expression of the symptoms of schizophrenia

Cholinergic functions in Schizophrenia

• Recent studies over the past few years have shown that muscarinic cholinergic activity is increased in schizophrenia, particularly during psychotic exacerbations (Riemann et al, 1994; Tandon et al, 1991, 1996).
• The researchers suggested that as dopamine increases at the onset of acute psychosis, cholinergic activity increases as well, in an attempt to maintain the dopamine/acetylcholine balance.

Serotonin:

• Hallucinogens that affect the serotonin cause psychosis that resemble schizophrenia.
• Serotonin/dopamine antagonists have powerful antipsychotic properties.
• The dopamine/serotonin antagonists (clozapine, risperidone, ziprasidone, qutepine, sertindole, olanzapine) have varying affinities for the 5HT2 receptors. For example, clozapine binds very tightly to histamine receptors, while qutepine binds very tightly to α 1 adrenergic receptors

Glutamate

• One strong evidence of its importance in schizophrenia is that the blockade of N-methyl-D-aspartate (NMDA), a principal glutamate receptor is associated with psychotic symptoms, and possibly, with psychosis in schizophrenia
• Also, the NMDA antagonist, phencyclidine produces effects in normal persons that some describe as resembling schizophrenia. Phencyclidine also produces an exacerbation or worsening of symptoms when it is administered to patients with schizophrenia

PERINATAL COMPLICATIONS:

• Hypoxia leads to intraventricular or periventricular bleeds, resulting in ventricular enlargement.
• Pyramidal cells in the CA1 region of the hippocampus are among the most vulnerable in the human brain to mild ischaemia.
• Premature birth or LBW
• Complications during delivery; excessive bleeding, prolonged labour
• People born in winter- due to viral infections which could make the mother to develop fever which could lead to brain damage for the foetus even at about 38.5 degrees centigrade

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Maternal Malnutrition: Lines of evidence support this, (Brown et al,1996)

• Leads to IUGR with adverse effects on brain development
• Prenatal malnutrition affects maternal systems critical to the developing foetal nervous system.
• Prenatal/neonatal insults to the CNS due to:
• Poor nutrition during pregnancy e.g.
• During the 2nd world war, children born by pregnant Dutch women who were in the early part of their pregnancy (about 1^st to the 2^nd trimester) who were made to starve by the Germans had a high prevalence of schizophrenia among them.

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Neurodevelopmental hypothesis

• The symptoms of schizophrenia are due to abnormalities in neuronal development with onset during the prenatal/neonatal periods of life. Some aspects of the human brain specifically in the Pre frontal cortex do not fully mature until the periods of late adolescence to early childhood.
• Alternatively it is possible that lesion remains dormant until the normal processes of brain maturation in adolescence lead to the use of neuronal circuits that are not greatly developed in children
• This accounts for the delay in the manifestation of the symptoms of the brain insults

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Neuropathology:

• Anatomical sites: The frontal lobe, limbic system, basal ganglia, thalamus and brain stem.
• The mesolimbic – mesocortical pathways, nigrostriatal pathway, tuberoinfundibular pathways
• Volume reductions:
• Whole Brain (3%)
• Temporal lobe (left 6% right 9.5%)
• Amygdala / hippocampal complex (left 6.5%, right 5.5%)
• Volume is increased in the lateral ventricles (left 44%, right 36%)
• Grey matter is reduced but white matter volumes may be increased

Computerized Tomography:

• Lateral and third ventricular enlargement.
• Reduction in cortical volume.
• Abnormal cerebral asymmetry.
• Reduced cerebellar volume and brain density.
• These CT abnormalities have been reported to correlate with presence of negative symptoms, neuropsychiatric impairments, increased neurological signs, frequent extra pyramidal side effects to antipsychotics.

Magnetic Resonance Imaging:

• Reduction in hypocampal-amygdala complex.
• Reduction in parahypocampal gyrus.
• Difference in T1 and T2 relaxation time

Magnetic Resonance Spectroscopy:

• Reduction in phophomonoesters and inorganic phosphates. Elevated phophodiesters and adenosine triphosphate.
• Positron Emission Tomography: Inability to increase blood flow to the dorsolateral prefrontal cortex while performing a psychological task like the Wisconsin Card Sorting Test. Increased D2 receptors in the basal ganglia.

Electrophysiology:

• Schizophrenics have abnormal EEG records
• Increased sensitivity to activation procedures.
• Decreased α activities.
• Increased θ and δ activities.
• Increased ability to filter irrelevant sounds and to de extremely sensitive to background noise.
• Evoked Potentials
• The P 300 wave which is located in the limbic system is smaller in schizophrenics. The N 100 (a negative wave) and its contingent variation are also abnormal.

PSYCHOIMMUNOLOGY

• Decreased T-cell interleukin production.
• Decreased number and responsiveness of peripheral lymphocytes.
• Abnormal cellular and humoral reactivity to neurons.
• Presence of brain directed antibodies. These findings may suggest the presence a neurotoxic virus or autoimmune disease.

PSYCHOENDOCRINOLOGY

• Decreased concentration of LH/FSH.
• Blunted release of prolactin and growth hormone to GnRH or TRH (among those with negative symptoms).
• Abnormal dexamethasone suppression test (DST).
• Blunted release of growth hormone to apomorphine stimulation.

Psychosocial Factors

Psychoanalytic theory:

• Sigmund Freud postulated that schizophrenia is due to developmental fixation that occurred earlier than those culminating in neurosis.

Psychodynamic theory

• Schizophrenia is a regressive response to overwhelming frustration and conflict with people in the environment.
• conflict between ego and the external world.

Learning theory:

• Children mimic their parents’

Family Theories

• Double bind hypothesis of Gregory Bateson: This is when children receive conflicting parental messages from their parents about their behaviour, attitude and feelings.
• Schisms and Skews hypothesis of Theodore Lidtz: In skews, a parent is overtly close to a child of the opposite sex. In schism, there is power struggle between both parents about a child.
• Pseudumutual and pseudohostile verbal communication of Lyman Wynne: A strange and unique verbal communication within certain families.

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High expressed emotions (Leff and Vaughan, 1976):

• This consists of emotional over-involvement, critical comments, hostility. EE of more than 35 hours a week is high and can precipitate a relapse

Others

• Personality (Kretschmer 1936)
• Personality build (asthenic build)
• Life events (Paykel)

Risk Factors for Poor Outcome of Schizophrenia

• Younger age of onset.
• Male sex
• Poor pre morbid functioning
• Long duration of treated psychosis
• Negative symptoms
• Absence of social support
• Insidious onset

.....Risk Factors for Poor Outcome of Schizophrenia

• Neurological soft signs
• Past psychiatric history
• History of violence
• Poor psychosexual functioning
• No or few affective symptoms
• No identifiable precipitating psychosocial stressor

OTHER PROBLEMS

• Co-morbidity: Substance use, depression, suicide, general medical conditions
• Stigma
• Mortality
• Homelessness
• Unemployment
• Victimization/abuse/injuries
• Violation of rights
• Impact on care givers

ICD 10 diagnostic criteria for schizophrenia

• At least one of the following must be present:
• 1. Thought echo, thought insertion or withdrawal or thought broadcasting.
• 2. Delusions of control influence or passivity, clearly referred to body or limb movements or specific thoughts, actions, or sensations; delusional perception;
• 3. Hallucinatory voices giving a running commentary on the patient’s behaviour, or other types of hallucinatory voices coming from some part of the body.
• 4. Persistent delusions of other kinds that are culturally inappropriate and completely impossible (e.g. being able to control the weather, or being in communication with aliens from another world).

ICD 10 diagnostic criteria for schizophrenia

Or at least two of the following:

• 1.persistent hallucinations in any modality, when occurring everyday for at least 1 month, when accompanied by delusions (which may be fleeting or half-formed) without clear affective content, or when accompanied by persistent overvalued ideas;
• 2.Neologism, breaks, or interpolations in the train of thought, resulting in incoherence or irrelevant speech;
• 3. catatonic behaviour, such as excitement, posturing or waxy flexibility, negativism, mutism and stupor;
• 4. “negative” symptoms, such as marked apathy, paucity of speech, and blunting or incongruity of emotional responses (it must be clear that these are not due to depression or to neuroleptic medication).

Pattern of course

Course should not usually be coded unless there has been a period of observation of at least 1 year.

• Continuous
• Episodic with progressive deficit
• Episodes with stable deficit
• Episodic remittent
• Incomplete remission
• Complete remission

Others

• Course uncertain, period of observation too short

Types (ICD 10)

• Paranoid schizophrenia
• Catatonic
• Hebephrenic
• Undifferentiated
• Post schizophrenic depression
• Residual
• Simple
• Schizophrenia unspecified

MANAGEMENT- Biopsychosocial model

• Biological
• Typical versus atypical antipsychotic
• Use of depot neuroleptic
• Treatment resistant schizophrenia
• Electroconvulsive therapy

Psychological Treatment:

• Behaviour Therapy
• Psychotherapy

Social Treatment: Occupational therapy

DELUSIONAL DISORDERS

• In 1863, Karl Ludwig Kalbaum used the term paranoia, which he characterized as uncommon but distinct.
• Kalbaum referred to the condition as a partial insanity that affect the intellect but not other areas of mental functioning.
• Emil Kraepelin also recognized a condition he called paranoia, characterized by a persistent delusional system in the absence of hallucinations and personality deterioration
• Eugene Bleuler considered paranoia, as distinct from schizophrenia, to be such a rare condition that it did not warrant a separate diagnostic category.
• Sigmund Freud He suggested that paranoid delusions develop from repressed homosexual impulses.

EPIDEMIOLOGY

• Prevalence is lower than that of schizophrenia between 0.02 and 0.03.
• Slightly commoner in females many of them are employed and married.
• May be commoner among low social economy status

Aetiology

• Largely unknown
• Not associated with schizophrenia and also rarely associated with mood disorders
• Biological Factors
• May be associated with neurological conditions of the limbic system and basal ganglia.
• May arise as a normal response to abnormal experiences in the environment.
• Psychodynamic Factors
• Hypersensitive people with specific ego problems like reaction formation, projection, and denial

DSM – 1V Diagnostic Criteria for Delusional Disorder

1. Non bizarre delusions (i.e. involving situations that occur in real life, such as being followed, poisoned, infected, loved at a distance, or deceived by a spouse or lover, or having a disease) of at least 1 month’s duration.
2. Criterion A for schizophrenia has never been met. Tactile and olfactory hallucinations may be present in delusions disorder if they are related to the delusional theme.
3. Apart from the impact of the delusions) or its ramifications., functioning is not markedly impaired and behavior is not obviously odd or bizarre.

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……….. CRETERIA

D. If mood episodes have occurred concurrently with delusions, their total duration has been brief relative to the duration of the delusional periods.

E. The disturbance is not due to the direct physiological effects of a substance (e.g. a drug of abuse, a medication) or a general medical condition.

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Types

• Erotomanic type: delusions that another person, usually of higher status, is in love with the individual
• Grandiose type: delusions or inflated worth, power, knowledge, identity, or special relationship to a deity or famous person.
• Jealous type: delusions that the individual’s sexual partner is unfaithful.
• Persecutory type: delusions that he person for someone to whom the person is close) is being malevolently treated in some way.
• Somatic type: delusions that the persons has some physical defect or general medical condition
• Mixed type: delusions characteristic of more than one of the above types but no one theme predominates

Treatment

• low dose of antipsychotic like haldol, pimozide, may be used.
• Psychotherapy and family therapy are also very important.
• Social support is also helpful

THANK YOU AND GOD BLESS