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Sudden-Onset Behavioral Disturbance
in a Woman with No Prior Psychiatric,
Medical History
Nilesh S. Tannu, MD; and Olaoluwa O. Okusaga, MD, MScPHR
M
rs. M is a 30-year-old,
married, African-American woman with no prior
history of mental illness who was
initially admitted to a general hospital due to changes in behavior. Mrs.
M’s husband reported that during
the 2 days prior to her admission,
she seemed to have difficulty paying
attention and registering information; she would sometimes talk excessively and at other times would
stare blankly and not engage in any
conversation with her husband. She
also experienced insomnia and was
Nilesh S. Tannu, MD, is a Resident Physician, Department of Psychiatry and Behavioral Sciences, The University of Texas
Medical School at Houston. Olaoluwa O.
Okusaga, MD, MScPHR, is an Attending
Psychiatrist and Assistant Professor, Department of Psychiatry and Behavioral
Sciences, The University of Texas Medical
School at Houston.
Address correspondence to: Nilesh S.
Tannu, MD, The University of Texas Medical School at Houston, Department of
Psychiatry and Behavioral Sciences, 1941
East Road, Houston, TX 77054; email:
[email protected].
Disclosure: The authors have no relevant financial relationships to disclose.
doi: 10.3928/00485713-20140403-02
PSYCHIATRIC ANNALS 44:4 | APRIL 2014
intermittently restless. When she
initially arrived at the general hospital, she was agitated and was given a
one-time dose of ziprasidone 20 mg
orally to calm her down. While at
the general hospital, the patient was
also selectively mute.
The initial medical work-up included a complete blood count,
comprehensive metabolic panel,
thyroid panel, urine drug screen, urinalysis, and serum creatine kinase
(CK); the results were within normal limits except for a white blood
cell count of 13,000/µl, 1+ bacteria
in her urine and CK of 2,252. The
elevated CK was thought to be secondary to agitation and the fact that
she needed physical restraint. She
was started on ciprofloxacin 500 mg
orally for a suspected urinary tract
infection. Quetiapine 25 mg orally
at bedtime was started for agitation
and to target insomnia. She was seen
by a neurologist who felt there was
a low likelihood that Mrs. M.’s presentation was secondary to encephalitis or meningitis. Nevertheless, she
was treated empirically with ceftriaxone, vancomycin, and acyclovir
while the results of cerebrospinal
fluid (CSF) analyses were awaited.
Computed tomography (CT) scan
of the head, magnetic resonance
imaging (MRI) of the brain (with
and without contrast), and magnetic
resonance angiogram (MRA) of the
head and neck (without contrast)
were all negative for any acute findings. Electroencephalogram (EEG)
was negative for any abnormal activity, and the CSF analyses showed
no growth on culture after 72 hours.
The CSF analyses were also negative for Neisseria meningitides
CW135, Escherichia coli K1, Haemophilus influenzae, Streptococcus
pneumoniae, and Group B streptococcus. She was medically cleared
by neurology and internal medicine,
and the psychiatry consult-liaison
team recommended inpatient psychiatric evaluation and treatment.
She was subsequently transferred to
our acute inpatient psychiatric unit
by the fourth day of admission at the
general hospital.
When she arrived in our unit,
Mrs. M was uncooperative, selectively mute, and had significant psychomotor retardation. She appeared
internally preoccupied, would sit
and stare blankly at times with some
inappropriate smiling. She also intermittently exhibited stereotypic
movement and facial grimacing. She
could not answer questions, and the
treatment team was unable to obtain
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any information from her. She required nursing assistance with feeding and other activities of daily living. Her husband confirmed that she
had no past psychiatric history. She
had been her normal self before the
current episode, which started about
7 days prior to her presentation to
our inpatient psychiatric facility. He
was not aware of any hospitalizations, medications, illicit drug use,
or suicide ideations/attempts. He
was also unaware of any family history of mental illness in the patient.
Mrs. M had a normal developmental
history and did not have any delay
in her milestones. She completed
her General Education Development and later went on to graduate
with a diploma in medical billing
and coding. She was employed as a
biller and coder at a doctor’s office.
She had been married for 6 years,
had a 6-year-old child, and did not
have any legal history. There were
no significant findings on physical
examination.
The patient was started on ziprasidone 20 mg twice a day on the day
of admission to our inpatient unit
and by day 2, this was increased to
40 mg twice a day and lorazepam
1 mg three times per day was also
started. Ziprasidone was discontinued on day 3 of admission and
risperidone was started at a dose of
2 mg in the morning and 1 mg at
night. Mrs. M’s Bush Francis Catatonia Rating Scale (BFCRS)1 score
was 25 on the day of admission to
our unit, and during the next 4 days,
she remained selectively mute and
intermittently wandered aimlessly
around the unit. She seemed to also
have minimal choreoathetoid-like
movement, and on day 5 serum
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ceruloplasmin and copper were ordered to rule out Wilson’s disease.
The CK level was also reevaluated.
Ceruloplasmin, copper and CK
were within the normal range. She
started showing some treatment response by day 6, and by the eighth
day, she had improved significantly.
She started showing some
treatment response by day
6 and by the eighth day, she
had improved significantly.
Mrs. M. was no longer having purposeless movements and was able
to engage in an intelligible conversation. She did not have any mood
or psychotic symptoms at the time
of discharge on day 10, and her BFCRS was then zero. We started tapering down the dose of lorazepam
by day 8, and she was discharged on
risperidone 3 mg/day and advised
to follow up with an outpatient psychiatrist within a week. Mrs. M’s
discharge diagnosis was brief psychotic disorder. We recommended
that risperidone be discontinued in
the outpatient if she remained well
during the follow-up appointment.
DIAGNOSIS:
De Novo Catatonia / Brief
Psychotic Disorder (298.8)
De novo catatonia and idiopathic
catatonia are synonymous terms
used when catatonia is the first neuropsychiatric manifestation in an
individual with no previous history
of psychiatric, neurologic, or medical disorder.2-4 De novo catatonia is
not a separate disease entity in the
Diagnostic and Statistical Manual
for Mental Disorders, fourth edition (DSM-IV) or The International
Statistical Classification of Diseases
and Related Health Problems, 10th
edition (ICD-10), and both systems
of classification assume catatonia to
be a subtype of schizophrenia, secondary to a general medical condition, or a specifier for a mood disorder. Currently, the literature on de
novo catatonia is very sparse and
only a few case reports have been
published.3-5 We now report a case
of de novo catatonia that was successfully treated with a combination of risperidone and lorazepam.
We decided to give Mrs. M a final
diagnosis of brief psychotic disorder (298.8) because she had catatonic behavior that lasted less than
1 month and eventual full return to
premorbid level of functioning, and
her condition could not be better accounted for by another psychiatric
condition, substance use, or general
medical condition. The creation of
the new category, “unspecified catatonia (codes 781.99 and 293.89),”
will be very helpful in diagnosing
cases such as this. DSM-V had not
yet been published when we initially
saw this patient.
DISCUSSION
This case illustrates the utility of
the risperidone-lorazepam combination for the treatment of catatonia, a
finding that has been documented in
a number of case reports;6 two of the
previous reports were in individuals
with mood or psychotic disorders,
whereas one was in an individual
with disulfiram-induced catatonia.7
Ours is the first report on the effec-
PSYCHIATRIC ANNALS 44:4 | APRIL 2014
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tiveness of the risperidone-lorazepam combination in an individual
without any apparent psychiatric,
medical, or medication-based cause
of catatonia. We initially started the
patient on ziprasidone but decided
to switch to risperidone based on
the case reports that suggested that
risperidone in combination with
lorazepam was an effective pharmacologic option in the treatment
of catatonia. Though there are no
controlled clinical trials, an increasing body of evidence points to the
clinical effectiveness of second-generation anti-psychotics in non-malignant catatonia.8-13 Some authors
have proposed that the plausible
mechanism of the beneficial effect
of second-generation antipsychotics
in catatonia could be the antagonism
of 5HT2A, thereby increasing the
dopaminergic activity in the prefrontal cortex.14,15
The few studies of de novo catatonia seem to suggest that the condition comprises a significant percentage of all cases of catatonia. For
example, 46.15% of the 65 cases
of catatonia studied by Benegal et
al.3 were classified as idiopathic (de
novo catatonia), and in the sample
studied by Barnes et al.,2 40% were
classified as idiopathic catatonia.
De novo catatonia appears to share
identical clinical features with catatonia that develops in the context
of schizophrenia or mood disorder.
For example in the study by Benegal
et al.3 the distribution of catatonic
symptoms (eg, stupor, posturing,
negativism, etc.) did not differ between subjects with de novo catatonia and those with catatonia on the
PSYCHIATRIC ANNALS 44:4 | APRIL 2014
background of other illnesses. Furthermore, both groups had a good
response to electroconvulsive therapy. In addition, de novo catatonia
was more prevalent among women,
and the illness was of a shorter duration compared to catatonia associated with either schizophrenia or
depression but the difference was
not statistically significant. Similarly, nine of the 10 cases of de novo
catatonia in the study by Barnes et
al.2 were female, and the de novo
catatonia group also seemed to have
higher rates of first-degree relatives
with a history of catatonia.
CONCLUSION
We have presented the case of a
30-year-old woman with de novo
catatonia who was effectively treated with a combination of risperidone
and lorazepam, with the patient having complete recovery and return
to premorbid level of functioning.
The outcome of this case is consistent with the few previous reports
of the effectiveness of risperidonelorazepam combination in treating
catatonic symptoms. Controlled
clinical trials of the effectiveness of
the risperidone-lorazepam combination for de novo catatonia (as well
as catatonia in the context of other
psychiatric and medical conditions)
are needed.
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