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A CASE OF ATYPICAL TARDIVE DYSKI

A CASE OF ATYPICAL TARDIVE DYSKINESIA COMPLICATED WITH DIABETES

 *Ganesh Shanker, **Jai Singh Yadav, ***Maheshwar Nath Tripathi

*Junior Resident Department of Psychiatry , IMS, BHU

**Assitant Professor Departmnet of Psychiatry, IMS, BHU

***Senior Resident, Departmnet of Psychiatry, IMS, BHU

Place of the Study: Department of Psychiatry, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005.

 

Abstract:

 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.

 

Introduction:

 

The first case of Tardive dyskinesia in year 1964 it has always been a matter of concern for patient on neuroleptic medication.

Tardive dyskinesia most commonly occurs in patients with psychiatric conditions who are treated with antipsychotic medications 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.[1] 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.[2] Eventually, according to these estimates, if on the drugs long enough, the majority of patients will develop the disorder.[3]

 

The incidence 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.[4] Hyperinsulinemia and hyperglycemia associated with insulin resistance may potentially contribute to the pathogenesis of tardive dyskinesia.[5]

 

Case summary:

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.

He was 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.

Investigation 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.

We made 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 compliance.

 

Discussion:

It is 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. [6]

Although 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.[7] 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”.[8] 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. [9]

 

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-

·                 Short, quick "stutter steps"

·                 Difficulty in changing direction

·                 An uncontrolled manner of sitting down

·                 Falling for no apparent reason

·                 Stopping when attempting to go through a door or ascend/descend a staircase

 

The elderly 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.[10] The meta-analysis found that five interventions were effective: L-dopa, oxypertine, sodium valproate, tiapride and vitamin E; neuroleptic reduction was marginally significant.

 

Considering 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.

 

Patients with “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.

 

References:

1.        Saltz BL, Woerner, MG, Kane JM, et al.. Prospective study   of   tardive dyskinesia incidence in the elderly. JAMA 1991; 266 (17): 2402–6.

2.        Jeste DV, Caligiuri MP. Tardive Dyskinesia.  Schizophr Bull 1993; 19 (2): 303–315.

3.        Robert W.  Mad in America: Bad Science, Bad Medicine, and the Enduring Mistreatment of the Mentally Ill, Perseus Pub 2002.

4.        Michael H. The primacy of neuroleptic-induced D2 receptor hypersensitivity in tardive dyskinesia. Psychiatry Online 2007; 13 (12): 18–26.

5.        Schultz SK, Arndt S, Andreasen NC, et al. Impaired Glucose Tolerance and Abnormal Movements in Patients with Schizophrenia. Am J Psychiatry 1999; 156: 640-642.

6.        Sadock BJ, Sadock VA. Tardive dyskinesia. In: Kaplan and Sadock's Synopsis of Psychiatry. Ed.10th; 2007.

7.        Kuo S, Janlovic J. "Tardive Gait" Clinical Neurology and Neurosurgery2008; 110: 2.

8.        Ralph A. "Tardive Dyskinesia : A Side Effect of Antipsychotic Medications That Can Be Understood and Treated." The Madison Doctrine; 2009.

9.        Putzhammer A,  Perfahl M, Pfeiff L, Hajak G. "Gait Disturbances in Patients with Schizophrenia and Adaptation to Treadmill Walking." Psychiatry and Neurosciences 2005; 59:3.

10.     Soares KV, McGrath J. The treatment of tardive dyskinesia-A systematic review and meta-analysis. Affiliations Schizophrenia Research 1999; 39:1-16