A CASE OF
ATYPICAL TARDIVE DYSKINESIA COMPLICATED WITH DIABETES
*Ganesh Shanker, **Jai Singh
Yadav, ***Maheshwar Nath Tripathi
*Junior Resident Department of Psychiatry , IMS,
**Assitant Professor Departmnet of Psychiatry,
***Senior Resident, Departmnet of Psychiatry,
Place of the Study: Department of Psychiatry,
Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005.
A case of 41
year old male was admitted from psychiatry OPD with complaints of excessive
sleep, laziness, decreased activities, jerky movements of the whole body,
difficulty in walking and sitting down for two months. One year back, he had
features suggestive of psychosis lasted for 2 months since then he was on
typical antipsychotics. Medications were stopped one month before onset of
present complaints. He was known diabetic for more than a year and had erectile
dysfunction with tingling and numbness of the limbs. Scales used were
Brief-Psychiatric Rating Scale (BPRS) for symptoms rating, Clinical Global
Improvement (CGI) /Quality of Life Scale (QLS) for general condition and
Modified AIMS (abnormal involuntary movement scale) for movement rating.
Patient was put on quetiapine 200mg/day, pregabalin 75mg/day in divided doses
and injection insulin 2ml/day s/c. Modified AIMS regularly administered at two
weeks interval during treatment and BPRS were applied. The reduction of AIMS
score 60% and BPRS score 28% were noticed during initial 2 weeks of treatment.
The 2% and 6% further improvement in respective scores were noticed after 4
weeks. These improvements were reflected in enhanced social functioning,
quality of life and good compliance.
The first case
of Tardive dyskinesia in year 1964 it has always been a matter of concern for
patient on neuroleptic medication.
dyskinesia most commonly occurs in patients with psychiatric conditions who are
for many years. One study reported that within the first four years of using
antipsychotic medications, 18.5 percent of young adults develop symptoms.
Furthermore, 31 percent of those over 55 years of age develop tardive
dyskinesia symptoms in the same time frame. Other estimates suggest that it
occurs in 15-30% of patients receiving treatment with antipsychotic neuroleptic
medications for 3 months or longer. Other estimates suggest that with each
year of neuroleptic use, 5% of the patients will show signs of tardive
dyskinesia, i.e., 5% after one year, 10% after two years, 15% after three years
with no clear upper limit. Eventually, according to these estimates, if on
the drugs long enough, the majority of patients will develop the disorder.
of tardive dyskinesia varies with the type of neuroleptic (e.g., haloperidol
more often than
perphenazine , daily dose
and duration of treatment (the higher the daily dose and the longer the
duration of treatment, the higher the risk). The D2 hypersensitivity hypothesis
is also supported by evidence of a dose-response relationship, withdrawal
effects, studies on D2 agonists and antagonists, animal studies and genetic
polymorphism research. Hyperinsulinemia and hyperglycemia associated with
insulin resistance may potentially contribute to the pathogenesis of tardive
Patient Mr. a
41 year old male admitted in the psychiatry ward with complaints of excessive
sleepiness, laziness, reduced activities of daily life and odd behaviour for
last one year. He used to fall asleep during short travels in the auto-rickshaw
or during conversation. His energy level decreased significantly and he
was not taking interest in outdoor activities like marketing. One day he
started behaving strangely in the form of taking off his clothes and running
around in nude condition. He also become restless and wanted to go outside with
which he was refrained. He was not following command of his relatives and he
was not listening to them. There were no features of aggressiveness or abusive
language towards others or suspiciousness.
admitted under a general practitioner for around 2 weeks and was discharge with
advice to take haloperidol 15mg/day, trifluperazine 10mg/day and
trihexiphenidyl 6mg/day in divided doses. His behavioural symptoms improved at
the time of discharge. He was diagnosed diabetes mellitus type-II with
psychosis. He took consultation of an endocrinologist who prescribed him tab
metformin 500 mg one tab twice daily. He was very irregular to take treatment.
During follow up for diabetes mellitus his blood sugar was found uncontrolled
on many occasion, but insulin was never started. After six months of
antipsychotic treatment patient started complaining of rigidity of whole body.
He used to walk in stooped posture, for this complaint he consulted the same
physician. The drugs were adjusted but his problem not relieved, he was even
not able to go to toilet. The problem in maintaining of posture, standing and
walking aggravated to such an extent that patient was not able to stand without
support for little moment. Medicine and neurology consultation was made, but
during his two week treatment as indoor patients in the medicine ward very
minimal improvement was reported. With controlled sugar patient was transferred
to psychiatry ward in the same institute. Although his blood sugar was under
control with the start of insulin, but it was noticed that patient was unable
to manage himself while walking. As he initiates walking he develops trembling,
prominent jerky movement in thorax and after few steps whole body starts
shaking vigorously which led him to stop walking and made to sit.
There was no
history of developmental delay. Pre morbidly he was introvert in nature. There
was no habit of psychoactive substance use in the history. No history of trauma
in the past.
like electroencephalography (EEG) and Computed tomography (CT) of brain were
found to be within normal limit. Magnetic resonance imaging (MRI) showed mild
cerebral atrophy. Thyroid profile (T3, T4, and TSH) normal and testing for the
human immunodeficiency virus (HIV) 1 and 2 were found negative. On insulin
blood glucose level was controlled.
combined approaches with other specialty and diagnosed the patient as a case of
tardive dyskinesia. Neurologist ruled out the relations of organicity and
clinical presentations. Patient was put on quetiapine 200mg/day, pregabalin
75mg/day in divided doses and injection insulin 2ml/day s/c. Modified AIMS
(abnormal involuntary movement scale) regularly administered at two weeks
interval during treatment, the time course of abnormal movements regularly
recorded and BPRS were applied. The reduction of AIMS score 60% and BPRS score
28% were noticed during initial 2 weeks of treatment. The 2% and 6% further
improvement in respective scores were noticed after 4 weeks. These improvements
were reflected in enhanced social functioning, quality of life and good
estimated that at least 10-20% of patients and perhaps as high as 50% of
patients treated with neuroleptic drugs for more than a year exhibit some
tardive dyskinesia. 
tardive dyskinesia is usually associated with facial tics and movement of jaw,
lips and tongue, it can also affect other parts of the body such as the torso,
hips and legs. In the February 2008 issue of clinical Neurology and Neurosurgery,
two researchers at the Bayor College of Medicine in Houston, Texas published a
report identifying three patients who had been exposed to neuroleptic drugs
designed to block dopamine receptors and as a result, had developed “tardive
gait”. This was the first time “tardive gait” (which the researchers
described as “Duck-like”) had actually been documented and described. Their
conclusion was that the dysfunctional walk of these patients should in fact be
classified as a symptom of tardive dyskinesia. 
In our case
report we found very prominent trunk movement associated with walking
difficulties which came out to be an atypical and rare presentation of tardive
dyskinesia, not noticed in previous studies. Tardive gait is characterized by-
in changing direction
uncontrolled manner of sitting down
no apparent reason
when attempting to go through a door or ascend/descend a staircase
and female patients are more prone to develop tardive dyskinesia. It is
very hard to treat, although switching anti-cholinergic anti-Parkinsonian
agents to amantidine has been found useful. Also, if the patient is on a
traditional anti-psychotic, switching to an atypical anti-psychotic often helps.
Vitamin E has been widely used and some research suggested it might be mildly
effective. Other natural remedies include melatonin, B-6, CoQ10 etc. The
main advantage to atypical anti-psychotics is their lower rate of tardive
dyskinesia. Single RCTs demonstrated a lack of evidence of any effect for
bromocriptine, ceruletide, clonidine, estrogen, gamma linolenic acid,
hydergine, lecithin, lithium, progabide, seligiline and
tetrahydroisoxazolopyridinol. The meta-analysis found that five interventions
were effective: L-dopa, oxypertine, sodium valproate, tiapride and vitamin E;
neuroleptic reduction was marginally significant.
the advantage of atypicality we started quetiapine. We find that when patient
was given pregabalin (150mg/day) for the diabetes associated neuropathy,
features of tardive dyskinesia improved significantly.
“tardive gait” ware misdiagnosed because their symptoms closely resemble those
of Parkinson’s disease. So, there was need to look into this, rather unexplored
domain of atypical presentation of tardive dyskinesia for its better
management, with the possible use of pregabalin.
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