Secondary Schizophrenia (20 page)

over-interpreted as an isolated sign. In our experience,
ized laboratories. Elevated blink rates have long been
false positive results can result from a painful shoul-reported in schizophrenia but have no definite diag-der. The forearm rolling sign uses less time and may be
nostic utility, due partly to numerous other factors that
more sensitive and specific
[45].

can influence blinking
[51, 52].

Marked failure of convergence was present in 6%

Cranial nerves

of never-treated schizophrenic patients compared with
1.2% of healthy controls
[8].
In chronic patients, con-The trigeminal/facial corneal reflex was found reduced
vergence difficulties have been found in 18% to 24% of
in 30% and absent in 8% of chronically hospitalized
patients with schizophrenia
[15,
53, 54].

schizophrenic patients. If one excludes the catatonic
Nystagmus was found in only 1.9% of schizo-group, still 5% had no corneal reflex in this series
phrenic patients and 0.14% of healthy students
[3]

[29].

but elsewhere it was found in 3.3% of schizophrenic
Facial asymmetry was found in 3% of schizo-patients
[33].
Early studies found less nystagmus in
phrenic patients and 0.4% of a comparison group
[30].

response to rotation among schizophrenic patients
Similarly, cranial nerve palsies were found in 5% of a
than was found in healthy subjects
[55].
Among ado-schizophrenic sample and none of the control sample
lescent state hospital inpatients, nystagmus was more
[34].
Braun and colleagues noted facial asymmetry in
common in one group diagnosed organic (30%) than
3.2% of their patient sample
[33].

schizophrenic (5%)
[31].
Phencyclidine intoxication,
Impaired gag reflex has been found consistently in
which can strongly resemble idiopathic psychosis,
schizophrenia. In one study, it was found reduced in
presents with nystagmus in more than 50% of acute
29% and absent in 24%
[29],
whereas in another it was
cases
[56].
Optokinetic nystagmus was abnormal in
found impaired in 31.3% of unmedicated patients with
2 of 21 subjects with schizophrenia, compared with
schizophrenia
[46].

none of 20 healthy controls
[19].

Strabismus was found to be more frequent in
Pupils

one sample with schizophrenia (13% of 475) than
Earlier studies on neurological findings included
in healthy controls (4.4% of 697); this was particu-numerous observations on pupil size, including reac-larly true of continuous (as opposed to intermittent)
tions to psychological stimuli. Such studies are now
exotropia (8.2% vs. 0.5%)
[57].

generally conducted using tightly controlled conditions and instrumented measures that cannot be
Motor coordination

matched in usual clinical settings. Irregular pupils
were found in 25% and unequal pupils in 11% of
The testing of motor coordination roughly checks for
a group of patients preselected for having abnormal
the integrity of the cerebellum and associated cir-neurological examinations
[28].
Anisocoria was found
cuits. These include Romberg and other tests of bal-in 5.6% of patients with schizophrenia and 0.4% of
ance; tandem and other variations on gait; finger-healthy university students
[30].
Pupillary findings in
nose, heel-shin, and other tests of motor accuracy;
general were no more prevalent in first admission
and tasks intended to elicit intention tremor. Peculiar-schizophrenia (15.6%) than in healthy controls
[47].

ities of spontaneous movement and examination find-Abnormal pupillary responses were noted in 9.7% of
ings characteristic of cerebellar disease were noted in
a group of schizophrenic patients
[33].
Anisocoria in
schizophrenia by many early authors
[58],
including
the alert patient can reflect any of several problems,
Kraepelin (1919), who even wrote of a “cerebellar form
including intracranial pathology
[48].

of dementia praecox”
[26].
Somewhat in this vein,
numerous investigators of the early twentieth century
[59]
found that patients with schizophrenia showed
Oculomotor

less response to caloric or rotatory vestibular stimula-Smooth pursuit abnormalities have been studied for
tion than do healthy controls. A failed attempt to repli-the past century
[49]
, more actively in recent decades
cate such findings
[50]
triggered modern smooth pur-

[50].
One occasionally notes jerky saccades during
suit eye movements research (discussed above).

unaided observation
[1, 22,
32, 34]
, but smooth pursuit
Subsequent study of cerebellar examination items
49

eye movements are now usually the domain of special-has yielded variable results, but individual cerebellar
The Neurology of Schizophrenia – Section 2

Table 4.1
Rates (%) of cerebellar signs in groups with schizophrenia and in healthy persons
Tandem

Romberg

Finger-nose

Reference

Patient control (p)

Patient control (p)

Patient control (p)

Buchanan & Heinrichs (1989)
∗
(53) 18.4

4

p
=
.003

7.1

0

45–49

18–26

p < .0005

Griffiths
et al.
(1998)
∗
(34)
5

0

5

0

3.3

0

Mohr
et al.
(1996)
∗
(54)
13

3.5

3

0

16–32

8.8–15.8

Shibre
et al.
(2002)
∗
(8)
5

0

1.5

0

4

0

Lawrie
et al.
(2001)
∗
(15)
6.7

14.3

0

2.9

13.3

14.3

Krebs
et al.
(2000) (62)

44.2

12.5

p
=
0.006 28.4

8.3

p
=
0.001 43.2

18.8

p
=
.004

Chen
et al.
(1995) (22)

9.7

1

p
=
.018

1.6

0

Ho
et al.
(2004) (60)

7.7

0.5

p
−
.002

9.7

0.6

p
=
.003

3.9

0.5

NS

Braun
et al.
(1995) (33)

35.5

0

0

∗
Studies using the Neurological Evaluation Scale (53).

signs are fairly common in schizophrenia and usually
included in neuropsychological
[65]
and neurological
found to be at least somewhat more common than
[19,
53,
66]
batteries. Motor sequencing can be quite
in healthy comparison groups
(Table 4.1).
Addition-severely impaired in primary psychosis, enough that
ally, the heel-shin test was found abnormal in 1.9% of
testing cannot be completed. Even cooperative sub-schizophrenic subjects compared with 0.5% of healthy
jects can become quite frustrated by these tasks, which
subjects
[60]
. Abnormal heel-shin performance was
include the fist-ring, the fist-edge-palm, and the alter-found in 3.2% to 6.5% of an uncontrolled series of
nating fist-palm. These are perhaps the most consistent
patients
[33].
One finds that abnormal performance on
and striking deficits in the psychotic disorders
[67].

these tests often bears no resemblance to frank ataxia.

Motor-sequencing deficits should not point to a sec-One group distinctly specified “gross ataxia” in 5.1%

ondary schizophrenia.

of schizophrenic subjects during the Romberg and in
Motor inhibition deficits, indicated by inappropri-1.7% during tandem gait
[61].

ate responses to nontarget stimuli, are also common in
One group
[10]
found that cerebellar signs sep-the primary psychotic disorders. A common example
arated from other neurological signs in a principal
is the Go–No Go test, which has often been studied in
component analysis, and that this factor distinguished
schizophrenia
[68, 69].
Similarly, impersistence, indi-schizophrenic subjects from other subjects. Another
cated by failure to maintain an unnatural position past
group
[11]
found that the posture and oculomotor suba few seconds, is represented in some soft sign batter-scores of an ataxia assessment instrument, but no other
ies
[22,
53].
Neither of these can be expected to reliably
summary scores of neurological performance, pre-distinguish primary from secondary psychosis.

dicted a diagnosis of schizophrenia. Cerebellar signs
are present in a substantial minority of patients with
schizophrenia; gross ataxia is uncommon in both pri-Hypokinetic (Parkinsonian) motor findings
mary schizophrenia and in most cases of secondary
Roughly 10% to 20% of recent-onset, never medicated
schizophrenia.

patients with schizophrenia have Parkinsonian signs
Often linked to cerebellar dysfunction is hypo-

[70, 71, 72].
These most often include diminished
tonia, a finding that is observed periodically in
spontaneous movement of the face and arms, short
schizophrenia
[63].
Observed hypotonia was found in
steps, and diminished arm swing while walking,
a stunning 63% of subjects in one series, more than
and “lead pipe” rigidity (that is, a similar degree of
50% of each subtype
[29].

resistance throughout the range of motion) of the
Motor Sequencing tests were developed by Luria
joints during passive manipulation. When mild and
50

(1966)
[64]
to test prefrontal integrity. They were then
isolated (e.g., when not accompanied by impaired
Chapter 4 – The neurologic examination in schizophrenia

upgaze or overt rest tremor), they have no diagnostic
dromes, Tourette disorder, and a number of uncom-implications, although there may be prognostic
mon disorders
[79].

significance
[71].
Marked or numerous Parkinsonian signs in a person never exposed to dopamine
Gait

antagonists (or at least 3 months free of oral and 6

Gait has not been well studied as such in schizophre-months free of depot agents), calcium blockers, or
nia but can include signs of hemiparesis and hypoki-valproate, is quite uncommon in youth
[73].
The most
netic and hyperkinetic movement disorders, as already
common hypokinetic condition of young adulthood
mentioned. Among other potential information, a
associated with psychosis is Wilson disease, and it is
wide base is indicative of brain damage, particularly
around 300 times less common than schizophrenia.

of the hindbrain. A tendency to minimize or not lift
Other conditions are even less common, including
feet off the floor (“magnetic gait,” now more inclu-the Westphal variant of Huntington disease, spinocere-sively termed apraxic gait), is traditionally linked to
bellar ataxia (Friedreich’s ataxia, with conspicuous
normal pressure hydrocephalus but is also found in
ataxia, usually childhood onset, frequently accompa-several other conditions, many of which can produce
nied by psychosis) and neuroacanthocytosis (more
psychosis and call for neuroimaging
[48,
80].

often chorea than Parkinsonism, psychosis not
common.).

In later life, Parkinson disease and similar move-Sensory exam
ment disorders will naturally be considered in the
Sensory acuity deficits have been consistently linked
differential of Parkinsonian signs, but psychosis is
to psychosis, first in clinical samples of the elderly
rarely prominent in patients with these entities. In
[81]
and more recently in epidemiologic samples of
catatonia, rigidity to passive movement is sometimes
the young
[82, 83, 84].
It is uncertain whether the link
observed, but the overall setting will generally point
between sensory deficits and psychosis may be due to
to the correct diagnosis. Gegenhalten (i.e. seeming
reduced or distorted sensory input, or whether sensory
opposition to all passive movement) is sometimes
disability is a less specific marker of neurologic hand-observed in severely disorganized subjects, and spas-icap. Sensory deficits should be considered together
ticity (velocity-dependent resistance to passive move-with any other findings as part of a possible neurologic
ment) may be seen in patients with impaired gross
syndrome, and should be corrected if possible.