SCHIZOPHRENIASchizophrenia is a clinical syndrome of variable, but profoundly
disruptive, psychopathology that involves cognition, emotion,
perception, and other aspects of behavior. The expression of these
manifestations varies a cross patients and over time, but the effect of
the illness is always severe and is usually long -lasting.
Schizophrenia is the most common psychotic illness and characterised by
two sets of symptoms; symptoms present during the acute phase; and
those present when the illness is well established (chronic).
Symptoms of the acute phase (positive symptoms) include
hallucinations, delusions, disturbance of thinking, and perplexity
(muddled, wondering, uncertainty, vagueness).
Chronic symptoms develo p insidiously and are more damaging to
performance and social functioning. Chronic symptoms include loss of
soc ial drive (loss of volition, abu lia), blunted emotions and affect, odd
behaviour, and apathy (negative symptoms).
Schizophrenia is a leading worl dwide public health problem that exacts
enormous personal and economic costs. Schizophrenia affects just less
than 1 percent of the world’s population.
World Health Organisation (WHO) studied of 10 countries estimated an
annual incidence 0.07 to 0.14 per 1000 population. Schizophrenia occurs
most often between the ages of 15 and 45 years. Variation of incidence
and prevalence rates may reflect differences of diagnostic criteria and
The incidence is equal in men and women but the mean age of onse t is
earlier in men.
The lifetime risk of developing schizophrenia is probably between 7.0
and 13.0 per 1000.
Using similar diagnostic criteria, WHO studies showed similar
prevalence in different countries.
In the acute phase (syndrome), the patient fee ls unjustly treated
(persecuted), not understood, misunderstood, and usually offers no
explanation to what he is going through.
He becomes suspicious and withdraws mentally and physically frompeople around him and absorbed and preoccupied with his own th oughts.
Mood fluctuates between anger, irritability, anxiety, and depression.
Affect may become blunted or inappropriate (incongruous) to the
The patient may giggle or laugh for no apparent reason, probably
responding to his own thoughts or ha llucinations.
Thought become muddled and difficult to convey to others because of
vagueness (circumstantial, tangential), poor connection to each other
(loose association), or muddled (incoherent).
Auditory hallucinations present as single wards, phrases , or conversation,
and sometimes as noises or music.
The voices may be of people known to the patient, belong to strangers, of
males or females, or of one or more persons.
Voices may directly address the patient (your are a bastard, homosexual),
talk abo ut him in the third person (he is a bastard, homosexual), comment
on his actions and behaviour, (running commentary), or give him
commands (do this, do not do that).
The voices are initially distressing, but they may become familiar and
ignored by the pat ient.
Other types of hallucinations as visual, tactile, somatic, olfactory, and
gustatory (taste) are less frequent.
Although persecutory delusions are common in schizophrenia, they are
not diagnostic because they are also present in other psychotic diso rders.
Delusions of control (by outside power, person, police), delusions of
reference (personalisation of events, TV programmes, news), and
delusions about possession of thoughts (thoughts withdrawal, insertion,
and broadcast) are less common but are more diagnostic of schizophrenia.
Culture, traditions, and religious beliefs flavour the contents and context
of the delusions and hallucinations.
Cognitive functions of memory, intelligence, and orientation remain
Judgement and reasoning in matters not incorporated by the delusions
However, the ability to interpret proverbs and extract concepts fromgeneral themes (abstract thinking) may become impaired.
The patient interprets ideas and images literally and unable to appreciate
the hid den meaning behind them (concrete thinking). Insight is most
often impaired or lost.
The chronic phase (syndrome) is characterised by the presence of
negative symptoms as well as some of the positive symptoms.
The patient gradually becomes reluctant to g o to school or work and
withdraws from social activities.
Performance and functioning deteriorate.
More time is spent at home and in bed virtually doing nothing and signs
of self -neglect become evident.
Peculiar postures and movements as stereotype, ma nnerism, catatonia,
and waxy flexibility may occur.
The patient may remain immobile, mute, and unresponsive (catatonic
stupor) for hours or days without food and drink.
The patient is conscious, and after recovery, some patients report that
they aware of the surrounding.
Sometimes catatonic stupor changes to unprovoked and uncontrolled
motor activity and aggression (catatonic excitement).
Delusions, in contrast to the acute phase, cause little or no emotional
distress (blunted or flat affect).
In both the acute and the chronic syndromes, the constellation of
symptoms and their severity may vary in different patients.
Symptoms of thought disorder are prominent in young patients, whereas
paranoid symptoms are prominent in older patients.
Depressive symp toms may be present early at onset of the disease,
during its course, or after recovery.
It is not clear whether the depressive symptoms are part of the disease,
side effects of the drugs, or a reaction to recovery and regain of insight.
A rare and unexp lained phenomenon of excessive water drinking that
may lead to intoxication may occur in schizophrenia. Schneider’s first
rank symptoms (SFRS) are incorporated in the ICD -10 and DSM1Vdiagnostic criteria of schizophrenia.
These symptoms include hearing ow n thoughts spoken loud; third -person
hallucinations; hallucinations in the form of commentary; somatic
hallucinations; thoughts withdrawal or insertion; thoughts broadcasting;
delusional perceptions; and feelings ,impulses and actions are experienced
as mad e by or influenced by external agents.
ICD -10 requires that the symptoms are present for one month, whereas
DSM1V requires six months.
Some SFRS are present in some patients with mania.
Subtypes of schizophrenia include hebephrenic, catatonic, paranoid, and
Hebephrenic (disorganized) type shows silly and childish behaviour with
affective symptoms, thought disorder, and fragmented delusions and
Catatonic symptoms are prominent in the catatonic type.
Paranoid schizop hrenia is characterised by well -organised and elaborate
delusions (systematised, there is a theme) and a relatively normal affect
and thought process.
Simple schizophrenia develops insidiously and presents as gradual
deterioration of functioning in school , work, and socially. Positive
symptoms are absent.
AETIOLOGY : The aetiology of schizophrenia is not well understood,
but the available evidence indicates a strong genetic predisposition. The
average lifetime risk is about 5 percent among first -degree rel atives of
schizophrenics compared with 0.2 -0.6 percent among first -degree
relatives of control. Family studies showed that 16.2 percent of children
of schizophrenic mothers developed schizophrenia compared with 1.9 per
cent among controls.
There is also e xcess (21.3%) of children with schizoid, schizotypal, and
paranoid personality disorders than among controls (5%).
Twin studies showed higher concordance for schizophrenia in
monozygotic twins (about 50%) than in dizygotic twins (about 10%).
The offsprin g of the healthy twin carry the same degree of risk to
develop schizophrenia as the affected twin.Adoption studies showed that there is excess of schizophrenia,
schizoaffective psychosis, and schizotypal personality disorders in the
biological relatives of schizophrenic probands.
Hebephrenic and catatonic schizophrenia carry a higher genetic loading
than paranoid type.
There is no agreement about the mode of inheritance of schizophrenia
and three theories are proposed.
The monogenic theory suggests a s ingle gene of variable penetrance to
account for the variable degree of risk in the relatives of the proband
(first -degree, second -degree).
The polygenic theory suggests that schizophrenia is the result of the
cumulative effect of several genes and is exp ressed when a certain
threshold of susceptibility is exceeded.
Whereas the monogenic and polygenic theories suggest that
schizophrenia is a single disease, the heterogenic theory suggests that
schizophrenia is a group of disorders.
These disorders have d ifferent genetic make -up and this may account for
the difference in the expression of this disease.
Molecular genetic studies so far did not locate a gene or genes linked to
Gross examination of the brain of schizophrenics showed smaller w eight,
enlarged lateral ventricles, and reduced volume of the hippocampus and
These changes tend to be more evident on the left side of the brain.
Histopathological examination showed disturbance of cytoarchitecture in
the hippocamp us, frontal cortex, cingulate gyrus, and entorhinal cortex.
MRI studies showed reduced temporal lobe volume and abnormalities in
the frontal lobe, basal ganglia, and thalamus.
Enlargement of the lateral ventricles is associated with male sex, early
age of onset, neuropsychological impairment, and poor response to
MRI changes are associated with poor response to treatment and
Studies showed that schizophrenic patients often have some softneurological signs. Soft neurological signs are not associated with
neurological deficit and include minor changes in the EEG, balance, eye -
tracking movements, tendon reflexes, stereognosis, proprioception, and
Studies of brain functions with PET and SPET showed reduced blood
flow in the frontal and prefrontal cortex (hypofrontality) during tasks
(Wisconsin Card sorting Test) that require participation of these areas.
A study of monozygotic twins discordant for schizophrenia showed that
affected twins had reduced prefrontal blood flow and reduced
These findings suggest that symptoms of schizophrenia are associated
with abnormal function of the temporal and frontal lobes.
It is suggested that disorders of attention and conscious awareness, or the
breakdown of internal representation of mental events predispose to the
development of psychotic symptoms.
It is also suggested that symptoms of frontal lobe lesions resemble the
negative symptoms of schizophrenia.
BIOCHEMICAL CHANGES IN SCHIOPHRENIA: The dopamine
hypothesis suggests that schizophrenia result from excessive activity at
This hypothesis is based on the following observations.
(1) Amphetamine and cocaine (psychostumulants) abuse may produce a
psychotic disorder indisti nguishable from schizophrenia and worsen or
cause relapse of the disease.
(2) The therapeutic effect of antipsychotic drugs is by blocking
postsynaptic dopamine receptors.
Amphetamine and cocaine release monoamines, particularly dopamine
and noradrenaline , at the synapses in the brain and increase their
The precursor of dopamine , L-dopa and the directly acting dopamine
agonist bromocriptine may cause psychosis in patients taking these drugs.
However, these observations do not necessarily prove that the
abnormality in schizophrenia is primarily in the dopamine transmission
The therapeutic potency of antipsychotic drugs correlate with theiraffinity to bind to and block dopamine D 2 receptors.
These drugs are also effective in mania.
Pos t-mortem biochemical studies of brains of schizophrenic patients
revealed increased dopamine receptor density in the caudate nucleus,
putamen, and nucleus accumbens.
There is also increased concentration of dopamine in the amygdala of the
left hemisphere and caudate nucleus.
Treatment with antipsychotic drugs may increase the density of dopamine
Recent studies examined the role of the excitatory amino acid
neurotransmitter glutamate. Glutamate has extensive interactions with
Phencyclidine (angle dust) and ketamine are glutamate receptor
antagonists and produce delusions and hallucinations as well as negative
ENVIRONEMENTAL AETIOLOGICAL FACTORS: Studies of birth
complications in schizophrenic and controls are in inc onsistent.
An older study found more obstetric complications in schizophrenics than
in controls, but a recent study did not confirm this finding.
However, in the presence of family history of schizophrenia, obstetric
complications may increase the risk o f developing schizophrenia and
lateral ventricle enlargement.
Studies of the season of birth showed that more schizophrenics were
born in winter than in summer.
Viral infections are more frequent in winter months and it is suggested
that prenatal exposur e to infection increase the incidence of
This suggestion has not been confirmed.
The association between personality disorders and schizophrenia is not
clear, but studies suggested that abnormal premorbid personality is more
common in schi zophrenics.
The incidence of schizophrenia is about equal in both sexes.However, males have earlier age of onset, poor premorbid personality,
more frequent severe relapses, and more evidence of structural brain
Schizophrenic women have lat er -onset, more affective and paranoid
symptoms, and better prognosis.
PSYCHODYNAMIC THEORIES: Freud’s theory on the development of
schizophrenia states that mental energy (libido) is withdrawn from
external objects and becomes attached to the ego.
This w ithdrawal from the external world leaves the patient mentally
isolated, and to cope with this isolation, a world of fantasy and unreality
is created (delusions and hallucinations).
Melanie Klein believed that schizophrenia starts in infancy.
At an early stage of development (paranoid -schizoid position), the infant
deals with innate (instincts) aggressive impulses by splitting both his own
ego and his representation of his mother into two conflicting parts, one
wholly good and the other wholly bad.
During normal development, the child resolves the conflict by realising
that himself and his mother can be good at one time and bad at another.
Failure to resolve this conflict forms the basis for future development of
Hartman suggested that the basic psychopathology is ego defect that
resulted in abnormal defence mechanisms to neutralise the libido and
FAMILY THEORIES: These propose that schizophrenia is the result of
abnormal relationship (deviant role relationship) or abno rmal
communication (disordered communication) in the family.
Two family patterns are described; marital skew where one parent was
dominant and the other submissive; and marital schism where parents
maintained contrary view and the child is caught in the m iddle.
Abnormal communication between the child and the parents sends
contradictory signals (love and rejection, double bind) to the child who
learns to respond ambiguously.
Disordered social communication (vague, lose, indefinite, fragmented)
also occ urred between the parents and affected the child.SOCIAL FACTORS: Culture is unlikely to play a role in the aetiology
of schizophrenia because the incidence rates of the disease are similar in
countries with different cultures. However, cultural factors ( religion,
traditions, custom) may influence the contents of delusions,
hallucinations, and thought disorder. The higher incidence and prevalence
of schizophrenia in lower social class is probably the result of the disease
rather than the cause of it. The e ffects of the disease on schooling and
occupation lower social status. Schizophrenics are over -represented in
inner -city areas, but whether this is because of social and occupational
decline (drifting), or because of environmental etiological factors is n ot
clear. Studies showed that the incidence of schizophrenia is higher among
migrants compared to the incidence in their native country and in the
native population of the host country. The roles of premorbid personality,
stress of migration, social isolat ion, and racial discrimination are not
clear. Psychological life stresses appear to increase the risk of developing
first episodes and precipitating relapses of schizophrenia. Severity of
symptoms of chronic patients correlated with stressful life event. I n
summary, the aetiology of schizophrenia is not clear, but the available
knowledge favours a strong genetic predisposition with contribution from
DIFFERENTIAL DIAGNOSIS: The positive symptoms are the
hallmark of the acute phase of schizophrenia and are usually present with
the negative symptoms in the chronic phase. For the purpose of diagnosis,
these symptoms should be present with intact consciousness and
clinically normal cognitive functions. Other disorders that may present
with positive symptoms are organic and mood disorders. Acute brain
syndromes as herpes simplex encephalitis, delirium, and drugs
intoxication (amphetamine, LSD) often present with delusions and
hallucinations. Complex partial seizure may present with psychotic
symptoms. Diffuse brain diseases as dementia, systemic lupus
erythematosus, general paralysis of insane, and AIDS may present with
psychotic symptoms. Alcohol abuse may be associated with psychotic
symptoms during intoxication, withdrawal, and in korsakov -Wernicke
syndrome. Organic brain disorders are often associated with cognitive
impairment, clouding of consciousness, and abnormal neurological
findings. Mood disorders with psychotic symptoms are differentiated
from schizophrenia by the dominance of affe ctive symptoms, delusions
and hallucinations confirm guilt, worthlessness or grandiosity, and the
contents are accepted by the patient. Patients with schizophrenia reject
the contents of their delusions and hallucinations. Schizophrenia with
dominant negat ive symptoms may be confused with personalitydisorders.
TREATMENT OF SCHIZOPHRENIA
ANTISPYCHOTIC DRUGS: The antipsychotic drugs are the backbone
of any treatment regime for schizophrenia. Regimes that include
rehabilitation and social support are only he lpful after the florid
symptoms have subsided. Interpretative psychotherapy and emotionally
and socially demanding programmes are inappropriate and worsen the
symptoms. Most antipsychotic drugs are lipophilic (lipid -soluble) and
easily absorbed from the gu t to reach liver through the portal circulation.
They undergo first -pass metabolism (before reaching the blood
circulation) which reduces the amount of the parent drug in the blood.
The plasma level of any drug depends on the amount absorbed, the rate of
m etabolism (individual variation), and interaction with other drugs. Some
drugs are liver enzyme induces (speed metabolism) whereas others are
enzyme inhibitors (retard metabolism). Some drugs induce their own
enzymes and lower their blood level. Some drugs have pharmacologically
active metabolites whereas others have inactive metabolites. In the
plasma, antipsychotic drugs are bound to plasma proteins and only a
fraction is free and pharmacologically active. They are lipid -soluble and
readily cross through the lipid membrane of the blood -brain barrier. They
are also stored in body -fat. Excretion of these drugs is mainly through the
kidney, and some re -enter the intestine with the bile and reabsorbed.
Following a single dose, plasma concentration of a drug r ises to a
maximum and then gradually declines. The rate of decline depends on the
rate of metabolism and elimination. Plasma half -life of a drug is the time
taken for the concentration to fall to half the maximum concentration.
The rate of elimination decl ines as the plasma concentration falls, and for
some drugs, it takes days or weeks (about five times the plasma half -life)
to washout the drug. Elimination -time is important when prescribing
drugs of known interaction. Combining interacting drugs may incre ase
the plasma concentration causing toxicity, or decrease it causing poor
response. With regular dosing, the rates of absorption and elimination
become about equal and the concentration in the plasma remains within
the therapeutic range (steady state). Th e time that is required for a drug to
reach a steady state is about five times its half -life. Drugs with long and
medium half -life are given once or twice a day, whereas those with short
half -life require frequent dosing. In general, younger patients metab olise
and excrete drugs more efficiently and require higher doses. Elderly
patients, because of renal and hepatic impairment, require lower doses.
Antipsychotic drugs block dopaminergic receptors (D receptor
antagonists), and some of which have selective a ffinity to a particulartype of receptors. It is noted that their therapeutic potency is related to
their affinity to block D 2 receptors. D 2 type dopamine receptors are also
found presynaptically on dopamine neurones. These act as autoreceptors
and inhibit the release of dopamine (negative feedback). Antipsychotic
drugs also block D 2 autoreceptors. Antipsychotic drugs also block
noradrenergic and cholinergic receptors causing autonomic nervous
system side effects. Dopaminergic receptors blockade in the basa l ganglia
produces extrapyramidal side effects. Antipsychotic drugs include
phenothiazines, thioxanthines, butyrophenones, substituted benzamides,
butylpiperidines, and the atypical antipsychotics. There are three
phenothiazine groups of drugs, which vary in their sedating and
extrapyramidal side effects. Aminoalkyl compounds represented by
chlorpromazine are the most sedating and have moderate extrapyramidal
and marked anticholinergic side effects. Their effective dosage is the
highest in the group. Piperi dine compounds represented by thioridazine
are moderately sedating and have marked anticholinergic and weaker
extrapyramidal side effects. Their effective dosage is moderate.
Piperazine compounds represented by trifluoperazine are the least
sedating and ha ve the weakest anticholinergic and strongest
extrapyramidal side effects. Their effective dose is small. The
thioxanthines are represented by flupenthixole and clopenthixole and are
similar in structure and properties to the phenothiazines. The
butyropheno nes represented by haloperidol are potent antipsychotic with
marked extrapyramidal and very little sedating side effects. The
butylpiperidines represented by pimozide are structurally related to the
butyrophenones but have longer half -life to be given once daily. The
substituted benzamides represented by sulpride and remoxipride are
highly selective D 2 receptors antagonist. They are less likely to cause
extrapyramidal disorders and have no sedating and anticholinergic side
effects. The therapeutic effects a nd the extrapyramidal side effects of the
antipsychotic drugs are presumably related to their antidopaminergic
properties. The atypical antipsychotics are so called because although
they block D 2 dopaminergic receptors are less likely to cause
extrapyramid al side effects. Atypical antipsychotics currently include
amisulpride, clozapine, olanzapine, quetiapine, respiridone, and
sertindole. Their main therapeutic advantage is their presumed efficacy
on the negative as well as the positive symptoms of schizoph renia. The
relapse rate is lower in patients on antipsychotic medications. Depot
preparations (long acting) as fluphenazine decanoate and haloperidol
decanoate are used when compliance to take the medication is a problem.
Intramuscular injection of chlorpr omazine, droperidol, or haloperidol is
used to quickly sedate a disturbed patient. The extrapyramidal side effects
include parkinsonian syndrome, acute dystonia, akathisia, and tardivedyskinesia (TD). Parkinsonian syndrome is the most common side effect
and is clinically similar to Parkinson disease. It presents as bradykinesia
(reduced mobility) or akinesia (no mobility), slowness of movements,
rigidity, and tremor. Symptoms appear a few months after starting
treatment. It responds to dose reduction and a nticholinergic
antiparkinsonian drugs (benzhexol, procyclidine). Acute dystonia
(abnormal posture of parts of the body) is more common in young males,
and appears early in treatment and sometimes after a single dose. It may
involve the tongue (painful prot rusion), twisting and retraction of the
neck and head (torticollis), upward and sideways rolling of the eye balls
(oculogyric crisis), or twisting and arching of the trunk (opisthotonus).
Acute dystonia responds promptly to intravenous anticholinergic
anti parkinsonian drugs and antihistamines. Akathisia (motor restlessness,
fidgeting) is an uncontrolled urge to change body -posture and position. It
may appear early or late after starting treatment and may respond to dose
reduction and antiparkinsonian drugs. Tardive (late to develop)
dyskinesia is more common among women and elderly patients and
usually appear after long -term treatment with antipsychotic drugs. . Risk
factors for the development of TD include older age, diffuse brain
damage, and the presence of affective disorder. It is suggested that after
long -term blockade of the dopaminergic receptors, these become
supersensitive to the effect of dopamine causing TD. TD may present as
chewing and sucking movements, facial grimacing, and choreoathetosis.
TD may worsen or improve after withdrawal of the antipsychotic drugs.
Treatment with anticholinergic antiparkinsonian drugs (benzhexol), and
dopamine agonist drugs (apomorphine, bromocriptine, L -dopa) may
aggravate TD. Well -established TD is resistant to tre atment. Drugs used
for the treatment of TD include lithium, carbamazepine, sodium
valproate, Atypical antipsychotic, tetrabenazine (depletes dopamine), and
-blockers. Most patients taking antipsychotic drugs either have tolerable
or no extrapyramidal side effects and the routine prophylactic use of
antiparkinsonian drugs is not justified. Other side effects of
antipsychotics include anti -adrenergic symptoms (postural hypotension,
tachycardia, nasal congestion, delayed or no ejaculation), and
anticholinergic symptoms (dry mouth, reduced sweating, constipation,
blurred vision). Patients with hypertrophy of the prostate may have
urinary hesitation or retention because of the anticholinergic side -effects
(poor bladder contraction). Uncommon side effects include hypothermia,
cardiac arrythmias, galactorrhoea, seizures in epileptic patients,
photosensitivity and pigments accumulation (skin, eye lens, cornea),
retinal degeneration, blood dyscrasias, and cholystatic jaundice.
A rare, but serious complication of anti psychotic treatment, is theneuroleptic malignant syndrome (NMS).
NMS usually occur during the first 10 days of treatment and the onset is
usually rapid (1to 3 days). The clinical picture includes hyperpyrexia, and
muscular, mental, and autonomic symptoms . Generalised muscular
rigidity may involve the muscles of swallowing causing dysphagia, and
the intercostal muscles causing dyspnoea. Muscular rigidity may cause
muscle damage with raised creatine phosphokinase plasma level and
myoglobinurea. Severe case s may present with impaired consciousness,
stupor, or akinetic mutism. The patient is aware of the surroundings but
does not communicate or moves. Patients who recover report that they
attempted to speak but were unable to vocalise. Milder cases may stutte r.
Autonomic disturbance cause excessive sweating and salivation, unstable
blood pressure, tachycardia, and urinary incontinence. Complications
include cardiovascular failure, renal failure, pneumonia, and
thromboembolism. NMS has a course of 1 to 2 weeks and a mortality rate
of about 10 percent. Patients who survive have complete recovery.
Management includes stopping the antipsychotic drugs, measures to
lower body temperature, and maintenance of fluid balance and blood
pressure. Diazepam and dantrolene ar e given to reduce muscular rigidity.
Combined treatment with lithium and antipsychotic drugs may predispose
the patient to develop NMS. There are reports of unexplained sudden
death of patients taking antipsychotic drugs.
COURSE AND PROGNOSIS: Schizophren ia is a serious mental illness
often associated with occupational and social decline. Earlier long -term
follow up studies (M. Bleuler, Ciompi, Huber) showed that about one
third of patients had good or fair recovery and social adjustment. Full
recovery usu ally occurred in the first two years of the illness and seldom
after five years. Patients with first admission generally did better and
symptoms became less severe during the later years of life.
The clinical features of relapses are usually similar to th ose of the first
attack. Some recent studies showed better outcome (Johnston), whereas
others showed similar (Tsoi and Wong) or worse outcome (Carone), but
the general trend agrees with earlier studies.
Severe disability occurred in about 20 percent of pa tients. Schizophrenia
carries a substantially higher mortality rate than the general population
both from natural causes and suicide. Long -term follow up studies show
that up to 10 percent of schizophrenics die by suicide. Some of the factors
that may pred ict good prognosis include sudden onset, positive
symptoms, and older age at onset, significant affective symptoms,
paranoid type illness, and good social and occupational premorbidadjustment. The opposite of these factors may predict poor outcome.
Studie s in developed and developing countries showed that the outcome
is better in the latter where complete recovery is more likely. Studies of
the effects of the environment on the symptoms showed that under -
stimulating environment was associated with worseni ng negative
symptoms and over -stimulating and demanding environment can
precipitate positive symptoms and lead to relapse. Schizophrenics have
limited resources to cope with excessive social demands and emotional
involvement. The term “high expressed emoti ons” includes critical
comments, expressed hostility, and emotional over -involvement. Studies
had show that relapse rate is higher in families where relatives show high
◗ CLIENT AND FAMILY TEACHING:
• How to manage illnes s and prevent relapse
• Importance of maintaining prescribed medication regimen and regular
• Avoiding alcohol and other drugs
• Self -care and proper nutrition
• Teaching social skills through education, role modeling, and practice
• Counseling a nd education of family/significant others about the biologic
causes and clinical course of schizophrenia and the need for ongoing
• Importance of maintaining contact with community and participating in
supportive organizations and care