Secondary Schizophrenia (22 page)

light response and other findings in

neurosyphilis; unequal pupils may reflect
ocular/brainstem pathology

Anosmia

Hyposmia seen in small proportion

Consider Parkinson disease/dementia, head
injury

Eye movements

Saccadic/smooth pursuit abnormalities,

Nystagmus in drug toxicity (barbiturate,

not obvious at bedside; nystagmus

benzodiazepine, PCP); paresis in Wernicke
uncommon

encephalopathy

Visual field/visual acuity

Normal

Consider contribution of visual deficit to
psychosis

Auditory acuity

Normal

Consider contribution of auditory deficit to
psychosis

Parkinsonian (hypokinetic) signs

Rigidity in catatonia; mild rigidity in

Consider Parkinson disease, Wilson’s Disease
schizophrenia

Dyskinetic (hyperkinetic) signs

Mild findings occasional in never-treated
Lond differential; tardive dyskinesia, Sydenham
schizophrenia

or Huntington chorea, Tourette Syndrome

Vibration/position sense

Normal

Consider B12 deficiency; diabetes mellitus;
neurosyphilis

Cerebellar signs (Romberg, finger-nose,

Common in schizophrenia when mild

Consider cerebellar disease; Wernicke

heel-shin, tandem gait)

encephalopathy or other toxic-metabolic

problem

Apraxic gait

Not seen

Structural neuroimaging indicated, often

frontal lobe disease

in schizophrenia adds little or no additional cerebellar
[113].
These are by no means specific findings, though,
or other motor impairment to that seen in schizophre-and are more helpful if kept in mind as one explanation
nia without alcoholism
[54,
60,
108, 110, 111].
Existing
for such movement disturbances if observed.

studies suggest that the neurological examination will
probably not be helpful in distinguishing schizophre-

Conclusion

nia from the psychotic disorders secondary to alcohol.

Nearly a century of study yields fairly consistent results
Among acute intoxications, phencyclidine (PCP)
with respect to the prevalence of the diagnostically
may most closely resemble schizophrenia. Nystagmus
important “hard” signs in schizophrenia. Based on this
is the most common neurologic sign; extrapyramidal
work, a neurologic assessment of patients with psy-motor signs such as rigidity and dystonia are seen
chosis should include:

occasionally
[56]
. PCP should be considered in the
r

differential for acute or even subacute psychosis with
Gait
∗

r

nystagmus.

Arm circling or drift

r

Intoxication with stimulants, such as amphe-Face hand test
r

tamines and cocaine, can simulate schizophrenia. Par-Symmetric double simultaneous stimulation,
ticularly in the acute (intoxicated) phase, one may
including feet

r

observe pupillary dilation and hyperkinetic motor
Muscle stretch reflexes

r

signs that may resemble tardive dyskinesia or akathisia
Babinski

[112].
In withdrawal, there is some tendency for
r
Visual fields

54

patients to develop hypokinetic (Parkinsonian) signs
r
Visual acuity screening

Chapter 4 – The neurologic examination in schizophrenia

r
Auditory acuity screening

The second, which would only be feasible in referral
r
Vibratory sensation

centers, would compare the examinations of primary
r
Involuntary movements (chorea, athetosis, tic)
∗

schizophrenia with a group with a schizophrenia-r
Parkinsonian signs
like psychosis of a particular etiology. For example, a
r
Motor asymmetries (gait, face, limbs)
∗

group of patients with epilepsy and psychosis could be
compared with a group with primary schizophrenia,
(
∗
May be observed without specific formal elicitation).

matched demographically and perhaps for severity
Table 4.2
provides a quick guide to interpreting
of psychosis, with examiner blinding. Another feasi-results of the examination to rule out a secondary
ble study would compare primary schizophrenia with
schizophrenia.

stimulant-induced psychosis.

Although the research cited herein is diverse and
It is doubtful, though, that research will remove
interesting, it has severe limitations in helping us dis-the need for clinician judgment in interpreting the
tinguish primary from secondary schizophrenia. What
results of an individual’s neurologic exam. Routinely
we clearly need are studies directly addressing the
performing the examination (rather than delegating to
use of the neurologic exam in detecting secondary
an extender or to a consultant) is invaluable, as one can
schizophrenia. These studies should take two forms:
then readily distinguish typical from atypical perfor-one, better conducted among representative clinical
mance for a schizophrenia patient. Finally, the exam
samples, would investigate the yield of a structured
should be considered as a whole and in light of all other
examination in detecting neuropathology of poten-available information (history, mental state, diagnostic
tial etiologic significance among psychotic patients.

studies, etc.).

55

The Neurology of Schizophrenia – Section 2

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Chapter 4 – The neurologic examination in schizophrenia