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Neurology India
Medknow Publications on behalf of the Neurological Society of India
ISSN: 0028-3886 EISSN: 1998-4022
Vol. 51, Num. 2, 2003, pp. 254-256

Neurology India, Vol. 51, No. 2, April-June, 2003, pp. 254-256

Case Report

Akathisia - diagnostic dilemma and behavioral treatment

S. K. Mattoo, G. Singh, A. Vikas

Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh-160012, India.

S. K. Mattoo
Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh-160012, India.

Accepted on 24.01.2002.

Code Number: ni03079


Akathisia, an involuntary movement disorder resulting from exposure to antipsychotics, is characterized by subjective restlessness and a strong desire to move about. The diagnosis is often complicated by the overlapping symptoms of pseudoakathisia, chronic akathisia and tardive dyskinesia. This report deals with a patient with schizophrenia who developed akathisia after exposure to antipsychotics. Later, she developed movements that were more like pseudoakathisia and tardive dyskinesia rather than acute akathisia. On failure of anti-akathisia medication, she was treated with a behavioral regime to which her akathisia responded. This behavioral regime used the technique of distraction as a primary tool. This case report highlights the diagnostic difficulties in akathisia and the application of behavioral treatment for akathisia that is non-responsive to anti-akathisia medication.

Key Words: Akathisia, Movement disorder, Antipsychotics, Behavioral management.

Introduction of antipsychotics in the 1950s revolutionized the treatment of schizophrenia. Soon the patients on these drugs were noted to be experiencing serious neurological side-effects.1 Akathisia is one such frequently recognized side-effect.2 Diagnosis of akathisia often becomes difficult due to the existence of confusing and overlapping concepts of pseudoakathisia and chronic akathisia.3 More recently, researchers have also tried to establish a relationship between akathisia and tardive dyskinesia.4 Even though akathisia is an extremely distressing condition, its pharmacotherapy often produces only modest results.1 There is no literature available regarding the use of behavioral methods in the treatment of akathisia and related conditions.

We describe here a case of a middle-aged woman with schizophrenia who developed akathisia following antipsychotics. The diagnostic difficulties and the behavioral techniques used in her treatment are highlighted.


A 42-year-old graduate housewife from a middle socio-economic status Hindu nuclear family of urban background, presented with an illness characterized by hearing voices and abnormal involuntary movements of legs of about one year duration. She complained of her thoughts becoming known to others. She was frequently noted to be muttering and smiling and at times, clapping and bursting into laughter for no apparent reason. After about 2 months of these symptoms she was brought to our psychiatric outpatient department. A diagnosis of paranoid schizophrenia was made and she was started on Risperidone 4 mg per day. Within 1 month, as her presenting symptoms improved significantly, she started showing `negative' symptoms in the form of disinterest in self-care and household work. She would keep lying in bed, lost to herself for most part of the day. Also, gradually she stopped socializing. Significantly, there was no evidence of any depressive symptoms during this period.

About 1 month after starting Risperidone, the patient started complaining of anxiety-restlessness on sitting down. It would decrease partly only if she would get up and pace around. After a few weeks, she also started complaining of anxiety-restlessness while standing at a place for a long time. Hence, she would keep shifting her weight from one leg to another—as if walking at a spot. A provisional diagnosis of akathisia was made. Initially, Risperidone was gradually withdrawn and replaced with olanzapine 10 mg per day. Later, as there was no improvement in her movements, propranolol 50 mg per day and lorazepam 8 mg per day were tried for a period of 4 weeks. She started having constant tapping movements of her feet while sitting. She would be markedly distressed due to these movements and hence, became totally dysfunctional. As a result she was admitted to our inpatient unit after about 8 months of the onset of illness.

During the hospital stay, routine investigations including hemogram, blood biochemistry and urine examination revealed no abnormality. She was observed to be making constant shuffling movements while standing, shifting weight between the two feet, as if walking at a place. These movements occurred at a frequency of 40-45 per minute. She regarded these movements to be happening on their own and claimed to have no control over these. In a sitting position she would complain of inner restlessness and stand up immediately which would partially relieve her restlessness. Also, while sitting she was noticed to make alternate dorsi-/plantar-flexion of feet with heels fixed on ground. She referred to these particular movements as a habit and displayed a voluntary control over them. In the lying down position, she would frequently rub her soles together and make alternate dorsi-/plantar-flexion of her feet. She failed to provide any explanation for these movements. It was also noticed that all movements decreased in frequency when she was engaged in conversation or any activity. Moreover, no movements or intense desire to move about occurred when she was prevented from making these movements by "pinning her to ground" by applying mild to moderate pressure on her shoulders. For these reasons, a possibility of some voluntary component to these movements was considered.

Since the patient did not respond to anti-akathisia medication, behavioral intervention using distraction as the main behavioral technique was planned. The movements in sitting and standing positions were tackled one after another. First, the patient was given various tasks involving reading and copying of medical texts and listening to music while in a sitting position. The duration and frequency of these sessions was increased from 15 minutes once a day to 30 minutes four times a day, over a period of 3 weeks. In about 70 sessions of this type a gradual reduction of about 70-80% in movements in the sitting position was noted, as measured by Abnormal Involuntary Movement Scale (AIMS).5 There was a spontaneous decrease of 30-40% in the movements in the standing position that extended further to the extent of 80-90% once these tasks were carried out in a standing position. The whole behavioral treatment lasted for about 6 weeks. All through, the patient was maintained on olanzapine 10 mg per day.

At the end of about 2 months of stay in the hospital the patient was discharged with 80-90% improvement. She continued to perform these behavioral techniques at her home in the prescribed fashion under the supervision of her family members. Four months after discharge from the hospital she stopped performing these tasks on her own with no worsening of symptoms. At 6 months follow-up she was maintaining the improvement at the same level.


Antipsychotic-induced akathisia got recognized by the clinicians after they noticed restless, rhythmic or jittery movements, often involving the feet, in patients taking antipsychotics.3 By current definitions, acute akathisia refers to a strong unpleasant subjective feeling of a desire to move about, without much relief despite making the movements.2 It typically appears 5-60 days after the initiation of antipsychotics.1 Characteristic movements of akathisia are rocking from foot to foot and walking in place. Others movements include shuffling movements while being seated, inability to stand without walking and fidgety leg movements on lying down.6

Later, 2 variants of akathisia_pseudoakathisia and chronic akathisia—were described.7 Pseudoakathisia is the motoric manifestation of akathisia without the subjective experience of restlessness. It is seen in older patients with long duration of antipsychotic treatment and is associated with a high incidence of dyskinesia.6 Chronic akathisia develops with no temporal correlation with initiation or increase in doses of antipsychotics and may appear during withdrawal of the drugs. It has been suggested that acute akathisia, chronic akathisia and pseudoakathisia are stages in clinical progression, in that order.8

In the index patient the initial presentation of a subjective restlessness (a desire to move about) resulting in motoric activity mimicked acute akathisia. Similarly, later, the emergence of the movements of walking at a place, tapping of feet and rubbing of soles, within 2 months of the initiation of risperidone point towards a diagnosis of akathisia. However, the patient denied any subjective restlessness being associated with these movements ever since their emergence. She regarded walking-at-a-place movements as a `habit'. These features point towards a diagnosis of pseudoakathisia. However, it may be argued that the patient's movements were due to akathisia. This argument is based on the observation of some authors that schizophrenic patients may have difficulty in describing their inner restlessness and ascribe the movements to other reasons.9

The patient's description of her movements as `involuntary' or `a habit' also open up the possibility of these movements being due to tardive dyskinesia. Attempts to distinguish akathisia from tardive dyskinesia have been made in terms of the primary/secondary role of distress and movements i.e. in akathisia the movements are secondary to subjective distress and in tardive dyskinesia the distress is secondary to the movements. Thus, the movements in akathisia are voluntary to relieve distressing internal stimuli, while those of tardive dyskinesia are involuntary. In mild or less severe akathisia this voluntary need can be suppressed but in severe cases the need may be sufficiently strong to call it involuntary.10 There is an overlap between the various sites involved in both types of movements. Rapid walking and swinging of a crossed leg is described to be more common in akathisia while rubbing movements of arms and legs are more common in dyskinesia.6

In the index case, purposeless movements of peripheral parts of the body that are considered as involuntary by the patient and the distress being the result of movements rather than their cause, point towards the possible presence of tardive dyskinesia. This conclusion is further reinforced by the fact that a proposal has been made by some researchers about the possible progression of akathisia to tardive dyskinesia with typical involvement of involuntary leg movements without subjective restlessness. However this `progression hypothesis' remains to be proven.3

Another aspect of the movements in the index patient—observable decrease of movements on distraction and on pinning down by pressing the shoulders—pointed towards a voluntary component. Distraction used as the principle technique in the behavioral approach to treat this patient was able to reduce the movements by 80-90%. It was assumed and proved correct that with increasingly difficult assignments, the patient got more distracted from the movements, resulting in their decrease. Generalization of this reduction of movements outside the therapy sessions and continued benefit even after total cessation of practice sessions points towards the possibilities of the movements having been learnt and their subsequent unlearning during behavioral treatment. Though akathisia movements have been described to reduce by distraction,7 behavioral treatment of these movements has not been described. Thus the behavioral treatment approach assumes importance given the complexity of the diagnosis and management of akathisia.


1. Marder SR. Schizophrenia: somatic treatment. In: Sadock BJ, Sadock VA, editors. Kaplan & Sadock's Comprehensive Textbook of Psychiatry. 7th Edn. Lippincott: Williams & Wilkins, Baltimore; 2000. Vol 1. pp. 1205-6.
2. Bakheit A. The syndrome of motor restlessness _ a treatable but under-recognized disorder. Postgrad Med J 1997;73:529-30.
3. Stahl S. Akathisia and tardive dyskinesia: changing concepts. Arch Gen Psychiatry 1985;42:915-7.
4. Barnes TRE, Braude WM. Akathisia variants and tardive dyskinesia. Arch Gen Psychiatry 1985;42:874-8.
5. Psychopharmacology Research Branch, National Institute of Mental Health. Abnormal Involuntary Movement Scale (AIMS). In: Guy W, editor. ECDEU Assessment Manual for Psychopharmacology. Revised. National Institute of Mental Health. US: Department of Health, Education and Welfare publication 1976; pp. 76-338.
6. Tarsy D. Akathisia. In: Joseph AB, Young RR, eds. Movement Disorders in Neurology and Neuropsychiatry. Massachusetts: Blackwell Scientific; 1992. pp. 88-100.
7. Sachdev P, Kruk J. Clinical characteristics and predisposing factors in acute drug induced akathisia. Arch Gen Psychiatry 1994;51:963-74.
8. Kidger T, Barnes TRE, Trauer T, Taylor PJ. Sub-syndromes of tardive dyskinmesia. Psychol Med 1980;10:513-20.
9. Van Putten T, May PRA, Marder SR. Akathisia with haloperidol and thiothixine. Arch Gen Psychiatry 1984;41:1036-9.
10. Munetz MR, Cornes CL. Distinguishing akathisia and tardive dyskinesia: a review of the literature. J Clin Psychopharmacol 1983;3:343-9.

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