Schizophrenia Presentation 2

SCHIZOPHRENIA
DR PHINIUS MAKUBI • PGY-3 IMED

OBJECTIVES
• Description of the syndrome
• Epidemiology, etiology and pathophysiological

mechanisms
• Management – psychopharmacology and

cognitive behavioral approaches
Definition
❖A spectrum of disorders characterized by
severely impaired cognitive processes ,
personality disintegration, affective disturbances
and social withdrawal.
Schizophrenia occurs in:

❖All races
❖All cultures
❖All social classes
❖Both sexes
HISTORY
• The ancient Greek and Roman literature showed
that although the general population probably had
an awareness of psychotic disorders,there was
no condition that would meet the modern
diagnostic criteria for schizophrenia in these
societies.
• Early theories supposed that mental disorders

were caused by evil possession of the body, and
the appropriate treatment was then exorcising
these demons, through various means (music,
drilling holes)
HISTORY
Dr. Emile Kraepelin (1856- 1926)
• Believed the chief origin of psychiatric disease to

be biological and genetic malfunction.
• “Dementia praecox" (early dementia) – 1893
• Kraepelin is specifically credited with the classification

of the unitary concept of psychosis, into two distinct
forms (Kraepelinian dichotomy):
Dementis praecox.
Manic depression.
HISTORY
Dr. Eugen Bleuler (1857 – 1939)
• Coined the term, "schizophrenia" in 1911.
• The first to describe the symptoms as "positive" or "negative."
Eugen Bleuler—4 A’s
• Disturbance of Associations —Thought disorder.

• Affective blunting — Inappropriate emotional response.
• Ambivalence — holding of conflicting attitudes and emotions towards
others and self
• Autism —social withdrawal- preferring to live in a fantasy world rather
than interact with the social world appropriately.
HISTORY
Kurt Schneider (1887 -1967)
• First-rank symptoms
ABCD:
• Auditory hallucinations (3rd person)
• Broadcasting of thought
• Controlled thought (delusions of control)
• Delusional perception.
Schneiderian first-rank symptoms
Epidemiology
• Lifetime prevalence 0.3%-0.7% of population world
wide (variation race , ethnicity, geographical origin
e.t.c.)
• Males = females
• Females have later onset , better functional outcome

and
display a bimodal age distribution
• Onset :- male (10-25 years)

female (1st peak 25-35yrs ,2nd peak
>40yrs)
ETIOLOGY
The specific etiology of schizophrenia is not known. Its origin is thought

to be multifactorial:
1. Genetics factors
2. Biochemical factors
3. Neuropathology
Genetics
• Highly heritable
• Risk increases with relationship e.g. 10% for 1st degree relative
or fraternal twin, 50% concordance for monozygotic twin
• Environmental factors certain but poorly characterized

(season of birth , intrauterine malnutrition, viral illness,
perinatal insults, drug exposure)
Genetics
• Like most medical disorders non- mendelian, multiple risk genes of
small effect and variable penetrance
• Recent advances shows that, a number of candidate genes are

involved in a range of neurodevelopmental and neuromodulatory
processes
• Opens the possibility for understanding molecular pathways to

schizophrenia and for screening and intervention
Biochemical factors
Dopamine hypothesis (influential)
• The classical dopamine hypothesis (too much dopamine in

schizophrenia) rested on the observation that DA releasing drugs can
cause psychosis and the discovery that antipsychotics were dopamine
antagonists.
• Increased subcortical DA related to psychosis
• Decreased prefrontal DA related to impaired cognition
• Decreased prefrontal activity ( DA based or otherwise) may lead to

subcortical DA dysregulation and psychosis
Dopamine Theory
of Schizophrenia
Hyperdopaminergic Hypodopaminergic
pathways pathways
Positive symptoms Negative symptoms

Biochemical factors
Serotonin hypothesis
It has been shown that serotonin excess results in both

positive and negative symptoms.
The robust serotonin antagonist activity of clozapine and

other 2nd generation antipsychotics to decrease positive
symptoms in chronic patients has contributed to the
validity of this preposition.
Biochemical factors
Glutamate hypothesis
Glutamate is the major CNS excitatory neurotransmitter.
Hypofunction of the N-methyl-D-aspartate (NMDA)
glutamate receptor has been hypothesized to contribute to
the pathology of schizophrenia
Neuropathology
• Neurodevelopmental model supposes that in

schizophrenia there is a “silent lesion” in the brain,
• It does not interfere too much with the basic brain

functioning in early years, but expresses itself in the
time, when the subject is stressed.
Neurodevelopment and schizophrenia
Diagnostic criteria (DSM V)
Two (or more) of the following, each present for a significant portion of time
during 1 month period. At least one of these must be (1),(2) or (3) :-
Active – phase symptoms

1. Hallucinations.
2. Delusions.
3. Disorganized speech (e.g. frequent derailment or incoherence).
4. Grossly disorganized or catatonic behavior.
5. Negative – passivity , avolition , blunted affect.
• Minimum duration of 6 months of continuous signs of
illness associated with functional decline.
• All other differentials should be ruled out.
• The disturbance should not be attributed to a substance

(drug abuse or medication)
• If there is history of autism spectrum disorder or

communication disorder of childhood onset , the additional
diagnosis of schizophrenia is made only if the patients
symptoms fit the above mentioned criteria.
Only Specify the course after 1 year:
• First episode, currently in acute episode.

• First e episode, currently in partial remission.
• First e episode, currently in full remission.
• Multiple episodes, currently in acute episode.
• Multiple episode, currently in partial remission.
• Multiple episode, currently in full remission.
• Continuous.
• Unspecified.
• Specify if with catatonia
• Specify the current severity ……

Investigations
• NO gold standard test
• Screen for drugs of abuse (urine)

• Bloods for fbc, biochemistry, blood glucose, TFTs, TPHA and
VDRL
• EEG
• ECG
• CT and MRI brain
Course of schizophrenia
After 10 years, of the people diagnosed with schizophrenia:

• 20% Completely Recover
• 25% Much Improved, relatively independent
• 30% Improved, but require extensive support network
• 15% Hospitalized, unimproved
• 10% Dead (Mostly Suicide)
Good prognostic factors
• Female
• Older age of onset
• Married
• Living in a developing (as opposed to developed) country
• Good premorbid personality
• No previous psych history
• Good education and employment record
• Acute onset, affective symptoms, good compliance with
meds
Poor prognostic factors
• Early age of onset
• Male sex
• Lower educational achievements
• More prominent negative symptoms
• More prominent cognitive impairments

Comorbidity
• High comorbidity with substance-related disorders (1/2 smoke
cigarettes and tobacco)
• Anxiety disorders
• Increased rate of obsessive-compulsive disorder and panic

disorder.
• Schizotypal or paranoid personality disorder may sometimes

precede the onset of schizophrenia.
• 80% of all persons with schizophrenia have significant concurrent

medical illnesses (DM, CVS , pulmonary diseases e.t.c.)
Management
• Early intervention important for improving functional outcome –

psychoeducation and family involvement
• Medication treatments
• Psychosocial treatments
Antipsychotic medications
• All are dopamine D2 receptor antagonists
• First generation or typical medications
• Have high affinity for D2
• Extra pyramidal side effects (EPS), galactorrhoea and tardive

dyskinesia common
• Clozapine (old atypical) for treatment resistant patients
• 1% prevalence of agranulocytosis – hypersalivation and

sedation can occur with the use of clozapine.
Antipsychotic medications
• Second generation or atypical drugs – dopamine

stabilizers)
• Less EPS, less affective blunting, less

depression/sedation, less cholinergic side effects
• Highly variable side effects main factor in long term

medication choice
• Once daily dosing
• Weight gain and impaired glucose tolerance

Summary of medication
• Psychopharmacology of schizophrenia is effective

• Side effects can be significant
• Individual patient response is variable
• Combine with antidepressants and mood stabilizers
• Residual cognitive deficits

Respond poorly to current medications and Strongly
predicts functional disability
ECT - Catatonic type

Psychosocial treatments
• Education of parents and carers
• Cognitive behavioral therapy
• Individual psychotherapy
Insight orientation
supportive
• Rehabilitation
• Group psychotherapy
Psychosocial treatments
COGNITIVE- BEHAVIORAL THERAPY (CBT)
Techniques :-
• modeling (learning by observing)
• Assertiveness and social skills training
• Emphasis on moving from unrealistic thoughts to realistic ones

Future directions in the treatment of schizophrenia
• Much stronger focus on early intervention and

prevention e.g. early psychosis clinics and prodromal
studies
• Specific treatments for cognition in schizophrenia
• As molecular pathways associated with neural

phenotypes become understood new, non dopamine
based therapies
• Renewed emphasis on rehabilitation

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SCHIZOPHRENIA

DR PHINIUS MAKUBI • PGY-3 IMED

• Epidemiology, etiology and pathophysiological

• Management – psychopharmacology and

Schizophrenia occurs in:

• Early theories supposed that mental disorders

• Believed the chief origin of psychiatric disease to

• “Dementia praecox" (early dementia) – 1893

• Kraepelin is specifically credited with the classification

• Coined the term, "schizophrenia" in 1911.

• The first to describe the symptoms as "positive" or "negative."

Eugen Bleuler—4 A’s

• Disturbance of Associations —Thought disorder.

• Females have later onset , better functional outcome

• Onset :- male (10-25 years)

The specific etiology of schizophrenia is not known. Its origin is thought

• Environmental factors certain but poorly characterized

• Recent advances shows that, a number of candidate genes are

• Opens the possibility for understanding molecular pathways to

• The classical dopamine hypothesis (too much dopamine in

• Increased subcortical DA related to psychosis

• Decreased prefrontal DA related to impaired cognition

• Decreased prefrontal activity ( DA based or otherwise) may lead to

Positive symptoms Negative symptoms

It has been shown that serotonin excess results in both

The robust serotonin antagonist activity of clozapine and

• Neurodevelopmental model supposes that in

• It does not interfere too much with the basic brain

Active – phase symptoms

• All other differentials should be ruled out.

• The disturbance should not be attributed to a substance

• If there is history of autism spectrum disorder or

Only Specify the course after 1 year:

• First episode, currently in acute episode.

• Specify if with catatonia

• Specify the current severity ……

• NO gold standard test

• Screen for drugs of abuse (urine)

After 10 years, of the people diagnosed with schizophrenia:

• Early age of onset

• Lower educational achievements

• More prominent negative symptoms

• More prominent cognitive impairments

• Increased rate of obsessive-compulsive disorder and panic

• Schizotypal or paranoid personality disorder may sometimes

• 80% of all persons with schizophrenia have significant concurrent

• Early intervention important for improving functional outcome –

• All are dopamine D2 receptor antagonists

• First generation or typical medications

• Have high affinity for D2

• Extra pyramidal side effects (EPS), galactorrhoea and tardive

• Clozapine (old atypical) for treatment resistant patients

• 1% prevalence of agranulocytosis – hypersalivation and

• Second generation or atypical drugs – dopamine

• Less EPS, less affective blunting, less

• Highly variable side effects main factor in long term

• Once daily dosing

• Weight gain and impaired glucose tolerance

• Psychopharmacology of schizophrenia is effective