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Authors: Perminder S. Sachdev

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Steroids, antimalarials, isoniazid
Careful medication history; trial off the offending
agent

Cerebrovascular

Small strokes in association cortices or subcortical
MRI/CT/EEG

regions

Space occupying lesions

Cerebral tumors

MRI/CT/EEG

Metabolic

Metachromatic leucodystrophy

Arylsulphatase – A levels, copper, and
Wilson’s disease

ceruloplasmin levels

Dietary

Pellagra, B12 deficiency

B12, Folate levels

Sepsis

Neurosyphilis, Toxoplasmosis, HIV disease
RPR to rule out syphilis (rapid plasma reagin) HIV

antibody titres; lumbar puncture (glucose, protein
in CSF)

Unknown/Degenerative/

Lewy body dementia, Parkinson’s disease
MRI, CT, EEG, Evoked potentials

Demyelinating

Seizures

Partial complex seizures

EEG, including sleep deprivation; telemetric EEG as
indicated

Endocrine

Hyper, or hypothyroidism; hyperparathyroidism
Serum calcium


The mnemonic “TACTICS MDs USE” can be useful in clinical practice.

Table 1.3
Workup to rule out secondary schizophrenia
A. First line assessments in every new patient with psychosis:
1. Neuropsychiatric and medical history
2. Neurological /physical exam

3. Neuropsychological testing

4. Laboratory investigations: complete and differential blood count, erythrocyte sedimentation rate, glucose, electrolytes, thyroid
function tests, liver function tests, electroencephalography, urinary drug screen
B. Second-line assessments in patients with high index of suspicion
1. Blood: Rapid Plasma Reagin (RPR) to rule out syphilis; HIV testing; serum heavy metals; copper and ceruloplasmin levels, serum calcium
levels, autoantibody titres (e.g. antinuclear antibodies for lupus); B12, folate levels; arylsulphatase – A levels
Karyotyping
2. Urine: culture and toxicology; urine drug screen; heavy metal screen
3. Imaging: MRI/CT/ PET/ SPECT of the brain
4. Electrophysiological studies: EEG, polysomnography; evoked potentials
5. Cerebrospinal fluid analyses: glucose, protein cultures; cryptococcal antigen
10

Chapter 1 – Neurobiology and etiology of primary schizophrenia: current status

studies, especially in those in their earlier years of
psychosis
[96]
, such findings are rare. Thus, in the
the disease, those with atypical presentations, and
absence of quantitative analysis, routine brain imag-those in whom there is reason to suspect a primary
ing cannot aid in the differential diagnosis of psy-disorder. Even in those with an established diagnosis
chosis without considering the clinical presentation
of schizophrenia, a neurocognitive examination can
[97].

be of value in characterizing the deficits and setting
treatment goals and priorities that address the con-cerns of the patients and their caregivers. In future
Conclusions

neurocognitive examinations and neuroimaging,
The contemporary view of schizophrenia as a neu-assessments are likely to emerge as valuable parame-ropsychiatric disorder has been shaped by converg-ters to predict and monitor treatment response for all
ing data from multiple lines of research. The paradigm
patients with schizophrenia.

shift was hastened by the availability of newer inves-No clinical feature, singly or as part of a clus-tigational tools such as neuroimaging, as well as
ter of features, reliably distinguishes between pri-advances in histopathological and gene analysis tech-mary and secondary schizophrenia. Early studies,
niques. The old distinction between organic (or struc-many flawed in design by contemporary standards of
tural) and functional (purely psychological) disease
research methodology, suggested that catatonic symp-misled the field and stunted systematic investigation
toms, altered states of consciousness (i.e. confusional
in the disorders that were earlier deemed purely psy-or “dream-like” states), and visual hallucinations are
chological. Classification of psychiatric disorders into
more frequent in secondary schizophrenia, which also
those with or without identifiable etiology has been
tended to have later age of onset. Certain delusions
more meaningful clinically. Even in those without an
such as those involving beliefs of mistaken iden-identifiable etiology, multiple lines of investigation
tity of others (i.e. Capgrass delusions) are thought
provide robust evidence of diffuse alterations in brain
to be more common in secondary than in primary
structure and connectivity. Many of these abnormal-schizophrenia.

ities are also evident in asymptomatic individuals at
Whether to conduct a brain scan in a patient with
genetic predisposition to the disorder, and often evolve
schizophrenia on a routine basis is debatable. When
during the prodromal phase of the illness –sometimes
brain scans (commonly structural, e.g., MRI or CT)
progress early in the illness – and are usually more
have been used clinically as part of the workup of a
prominent in early onset forms of the disorder. A
psychotic patient, the purpose is to rule out a space-greater understanding of the trait and state-related fea-occupying lesion or developmental malformation as
tures of schizophrenia raises the hope of development
the potential cause of the psychosis. Although inci-of successful early interventions that stop or slow, and
dental findings have been reported in MRI studies of
possibly reverse, the progression of disease pathology
even healthy people
[95]
and patients who present with
in schizophrenia.

11

Introduction – Section 1

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