Secondary Schizophrenia (21 page)

motor control, but these phenomena are distinct from
lead-pipe Parkinsonian rigidity.

Visual

Visual acuity problems are of course quite common
Hyperkinetic (including choreoathetotic or
in the general population, so are unlikely to shed
Huntingtonian) motor findings

light on differential diagnosis. Visual fields have not
been found impaired in schizophrenia
[19].
No visual
Although even less common than Parkinsonism in
field deficits were found in routine confrontation test-a never-medicated adult subject with schizophrenia,
ing of younger schizophrenia patients
[33].
In the
“tardive-like dyskinesia”
[74]
may be observed in mild
elderly, psychosis is associated with visual impairment,
form in acute subjects
[71, 72, 75]
and more promi-or at least uncorrected visual impairment
[81].
Stud-nently in older and more chronic (but still never-ies comparing elderly patients with schizophrenia-like
medicated) subjects
[76, 77],
as well as some normal
disorder to those with dementia and other organic
persons, especially the immature
[78]
and the elderly
mental disorders have not found differences in visual
[79].
Diagnostically, such movements (particularly
acuity
[85, 86]
, although certain other differences in
chorea) raise the possibilities of Huntington disease
ocular health were noted.

(often distinguishable by its precarious gait, the “milk-maid’s grip,” and definitively by genetic testing). Involuntary movements are very often traceable to drugs,
Auditory

such as the chronic use of dopamine-blocking agents,
Assorted acoustic and related abnormalities have
to cocaine and other stimulants, and occasionally to
occasionally been associated with schizophrenia
prescription drugs that are not dopamine antagonists.

[87],
but studies of patients with schizophrenia
[88,

51

A lengthy differential includes post-infectious syn-

89]
have found no abnormalities on basic acuity
The Neurology of Schizophrenia – Section 2

measures. In two studies
[85, 86],
elderly patients with
occipital association areas) include visuospatial, com-schizophrenia-like disorders had less auditory deficits
plex tactile information, and sensory input from mul-than those with dementia and other organic mental
tiple modalities. These tests (including right-left ori-disorders.

entation, audiovisual integration, graphesthesia) are
almost always labeled soft signs. They are found fre-Olfactory
quently in schizophrenia and have little known significance in diagnosing secondary psychoses. The
Olfactory identification is impaired in schizophrenia
face-hand test, a form of asymmetric double simul-but also in a wide array of other conditions such as
taneous stimulation
[96, 97]
has a long history of
ageing, movement disorders, and at least some demen-study in schizophrenia, dementia, and other types of
tias
[90]
. This parameter has been studied more than
brain injury. After minimal instruction, the subject
simple olfactory sensitivity, which is intact in
is touched simultaneously on each of four asymmet-schizophrenia
[91, 92].

ric combinations of face and hand. In schizophrenia,
there may be an increased tendency to neglect the hand
Tactile

stimulus in the first or second of these initial trials
In many studies, subjects with schizophrenia have
[9].
The four asymmetric stimuli are followed by two
been asked to perform tasks involving the sense of
symmetric stimuli, to both sides of the face and to
touch, but few of these studies have been of the basic
both hands. If, after reporting only the face stimulus
tactile functions. One study using electric stimuli with
on the first four trials, the subject reports the sym-schizophrenia subjects and healthy controls found ele-metric stimuli correctly, the asymmetric trials can be
vated tactile thresholds in subjects but no differences
repeated. Continuing to report only the face stimulus
in pain thresholds
[93].
Bilateral symmetric double
at this point is indicative of an “organic” mental disor-simultaneous stimulation is accepted as a subtle test
der, rather than schizophrenia
[96, 97].

for unilateral sensory loss. One small study found frequent extinctions in several psychiatric groups, includ-Neurologic exam as an aid in detecting
ing 29% in the schizophrenia group; this was not statistically greater than the 5% in the healthy control group
neuromedical etiologies

[19].
Some studies
[94]
list “extinction” among their
Specific neurologic exam items most likely to be of
neurologic tests but are unclear as to whether they refer
value in a “rule-out” exam are those that are least com-to this test or the face-hand text (discussed later).

mon in (primary) schizophrenia, those that are sensitive and at least moderately specific for particular
Dorsal column sensory tests

fairly common causes of secondary schizophrenia, and
The dorsal column carries vibratory sensations and
those that predict a high yield for more expensive or
position sense. Deficits in these may increase suspi-time-consuming diagnostic procedures. Existing stud-cion of B

ies suggest that the following neurological findings
12 deficiency or CNS syphilis, which are today
uncommon mimics of schizophrenia but also can
are infrequent in primary schizophrenia and are more
reflect common comorbid problems such as diabetes
common in secondary schizophrenia:

mellitus. In a sample of schizophrenic subjects it was
1. Asymmetry of muscle strength reflexes (unless
found that at least 50% had impaired vibratory sensa-isolated to a single joint)
tion in their hands, but statistically significant group
2. Absent muscle stretch reflexes, except in the
differences from healthy controls were found only in
elderly
[48]

frequencies of at least 200 Hz (higher than those usu-3. Babinski reflex (upgoing toe)
ally tested at the bedside)
[95]
. We find no data on the
4. Hemiparesis (possibly excepting the flattened
prevalence of abnormal vibratory or position sense, as
nasolabial fold or mild isolated paresis)
clinically assessed, in primary schizophrenia.

5. Absent corneal reflex

6. Nystagmus without other explanation, such as
Higher order sensory tests

toxicity

Sensory information processed in the posterior asso-7. Marked hearing deficit
52

ciation areas of the cortex (temporal, parietal, and
8. Anosmia or marked insensitivity to smell
Chapter 4 – The neurologic examination in schizophrenia

9. Persistent extinction of hand on face-hand test
Detecting specific etiologies of

10. Marked chorea or athetosis without other
secondary schizophrenia

explanation (e.g., prior drug treatment)

11. Marked ataxia without toxic explanation (current
There are essentially no neurologic data comparing
drugs or toxins)

groups with schizophrenia to those with any particular types of secondary schizophrenia. Certain forms
of epilepsy can mimic schizophrenia, but there are no
Neurologic examination abnormalities are rou-known characteristic neurologic findings. Ischaemic
tinely considered in the aggregate, on an informal basis
or neoplastic lesions can produce psychosis and in so
in clinical practice but can also be aggregated for-doing tend to produce findings in accordance with
mally. For example, we derived a summary “hard” (i.e.

lesion location or by increasing intracranial pressure.

localizing) sign index from a neurologic battery con-Velocardiofacial syndrome affects approximately
structed for a family study
[98],
including the follow-2% of those diagnosed with schizophrenia, can be
ing: Romberg sway, Babinksi reflex, extinctions dur-specifically tested if suspected, and carries with it sig-ing symmetric double simultaneous light touch, hemi-nificant family-planning implications. It has no spe-paresis evident during the arm circling test, facial
cific neurologic examination profile
[104].

asymmetry noted at rest, and lateralizing dysgraphes-Metachromatic leukodystrophy is a rare white
thesia.

matter disease famous for close simulations of schizophrenia. Adult-onset cases have been divided into
cases with quite distinct motor and psychiatric pre-

The significance of global impairment

sentations. The psychiatric subgroup presents with
Like general cognitive impairment, the presence of a
a schizophrenia-like illness in adolescence or young
variety of neurologic signs, even if individually non-adulthood, with no frankly abnormal neurologic
specific, increases the likely yield of an organic workup
findings
[105].

[99].
The overall severity of impairment in a neuro-Psychotic disorders resembling schizophrenia can
logic examination
[54,
61]
, specifically impairment on
complicate chronic alcoholism. These usually feature
perceptual tests
[100, 101],
may predict impairment in
nonbizarre delusions or hallucinations. There are no
a neuropsychological battery. Supporting the impor-known characteristic neurologic features, but chronic
tance of “nonspecific” neurologic findings are some
alcoholism tends to carry with it findings of polyneu-studies of imaging in routine general psychiatric prac-ropathy and cerebellar injury
[106].
As with any delir-tice. In one series of 150 head CT scans
[102]
neurolog-ium, the alcoholism-related Wernicke’s syndrome can
ical examinations were globally abnormal in 15 of 16

superficially resemble psychosis and has characteristic
subjects for whom abnormal CT results had an impact
extraocular paresis and ataxia. Complicating this issue
on treatment. Neurologic findings were localizing in
(and complicating the recent interest in “cerebellar”

only 8 of the 15 cases. A set of neurologic “soft” signs
deficits in schizophrenia), schizophrenic brains may
and cognitive tests, previously found to predict perfor-have an increased incidence of subtle Wernicke pathol-mance on a neuropsychological battery
[99]
admin-ogy, perhaps due to the toxic-metabolic extremes to
istered to a group of patients referred for MRI, pre-which they may be prone
[107].

dicted periventricular white matter lesions. Using step-Comorbid substance use disorders can also cause
wise multiple regression, a motor sequencing task and
diagnostic confusion, by raising the question of
visual tracking were highly efficient in predicting this
substance-induced psychotic disorder, and by poten-result
[103].
Thus, nonspecific and nonfocal signs may
tially contributing additional neurologic impairment.

prove predictive of imaging results in schizophrenia.

Alcohol is the only popularly abused substance for
One may wonder that there are not more studies rel-which there is a significant body of neurologic exam-evant to the question of whether the neurologic exam
ination research in schizophrenia. There is some evi-is helpful in selecting psychotic patients for imaging.

dence for increased impairment in higher-order per-Although there are many series of research subjects
ceptual functioning in schizophrenia with comorbid
involving both neurologic and imaging studies, cases
alcoholism
[108, 109],
but this effect is probably not
of secondary schizophrenia are routinely screened out,
dramatic enough to be of advantage in clinical diag-

53

so that most studies are of little use for our purpose.

nosis. Surprisingly, most studies found that alcoholism
The Neurology of Schizophrenia – Section 2

Table 4.2
Guide to interpreting results of the examination to rule out a secondary schizophrenia
Neurologic sign

Findings in primary schizophrenia

If abnormal, consider

Muscle stretch reflexes

Occassionally exaggerated or diminished

Asymmetry in focal lesions; diminished or
delayed relaxation in hypothyroidism;

exaggerated in white matter disease

Babinski (upgoing toe)/hemiparesis

Rare

Focal lesions; white matter disease

Pupils /cornea

Unequal pupils rarely seen; may have

Dilated in PCP/stimulant psychosis; absent
diminished corneal reflex