|Year : 2022 | Volume
| Issue : 2 | Page : 139-141
Lithium-induced bilateral flapping tremors (asterixis) in geriatric mania
Ranganath R Kulkarni1, Swapna A Pandurangi2, Raghavendra C Patil3, NS Divyashree4
1 Associate Professor, Department of Psychiatry, Dharwad Institute of Mental Health and Neurosciences, Dharwad, Karnataka, India
2 Assistant Professor, Department of Psychiatry, Dharwad Institute of Mental Health and Neurosciences, Dharwad, Karnataka, India
3 Senior Resident, Department of Psychiatry, Dharwad Institute of Mental Health and Neurosciences, Dharwad, Karnataka, India
4 Junior Resident, Department of Psychiatry, Dharwad Institute of Mental Health and Neurosciences, Dharwad, Karnataka, India
|Date of Submission||30-Dec-2021|
|Date of Acceptance||15-Mar-2022|
|Date of Web Publication||15-Apr-2022|
Dr. Ranganath R Kulkarni
Department of Psychiatry, Dharwad Institute of Mental Health and Neurosciences, Dharwad - 580 008, Karnataka
Source of Support: None, Conflict of Interest: None
Asterixis (flapping tremors) is a movement disorder due to cortical or subcortical pathology that usually indicates serious underlying disease processes such as encephalopathy secondary to severe hepatic dysfunction, metabolic derangements, toxic agents, or serious adverse drug events. Mood stabilizers such as valproate and carbamazepine with or without concomitant administration of antipsychotics such as clozapine and risperidone have been implicated to induce asterixis. Lithium, a first-line mood stabilizer drug for geriatric mania, with its unique profile of side-effects due to narrow therapeutic window, is very rarely implicated to induce asterixis, especially when used as a monotherapy. We report a case of lithium-induced asterixis, ataxia, acute cognitive impairment, and altered sensorium in an elderly male with first-episode of mania, both during toxic and therapeutic serum levels of lithium. This case highlights the association between asterixis, ataxia, delirium, and lithium, substantiating the dictum “start low and go slow” in geriatric psychopharmacology.
Keywords: Asterixis, ataxia, bipolar disorder, delirium, flapping tremors, lithium
|How to cite this article:|
Kulkarni RR, Pandurangi SA, Patil RC, Divyashree N S. Lithium-induced bilateral flapping tremors (asterixis) in geriatric mania. Arch Ment Health 2022;23:139-41
|How to cite this URL:|
Kulkarni RR, Pandurangi SA, Patil RC, Divyashree N S. Lithium-induced bilateral flapping tremors (asterixis) in geriatric mania. Arch Ment Health [serial online] 2022 [cited 2023 Jan 29];23:139-41. Available from: https://www.amhonline.org/text.asp?2022/23/2/139/343321
| Introduction|| |
Asterixis (flapping tremors), initially described by Raymond Adams and James Foley in hepatic encephalopathy in 1949 as a movement disorder due to pathophysiology in cortical or subcortical areas. It usually manifests as a bilateral flapping tremor at the wrist, metacarpophalangeal, and hip joints, but rarely can also be seen in the tongue, foot, and any skeletal muscle due to an inability to maintain sustained posture with subsequent brief, shock-like, involuntary movements.
Mood stabilizers such as valproate and carbamazepine are known to induce asterixis. Lithium-induced asterixis is a very rare adverse drug event (ADE), with only four such case report/s (total of 10 cases) published in the English literature since 1978,,,, to our knowledge. We report a case of lithium-induced asterixis, ataxia, acute cognitive impairment, and altered sensorium in first-episode, acute onset geriatric mania.
| Case Report|| |
A 70-year-old normotensive male presented to the emergency department with first-episode, acute onset psychiatric illness of 2 weeks duration, characterized by increased talk, increased goal-directed activity, reduced need for sleep, irritability, overfamiliarity, verbal abusiveness, increased religiosity, and grandiose delusion. He had no significant preexisting psychiatric or medical illness, including tremors, ataxia, or cognitive decline. He received diagnoses of bipolar-I disorder-manic episode with mood-congruent psychotic features and tobacco use disorder currently in active use, as per DSM-5 diagnostic criteria. His general physical and systemic examination showed no abnormalities.
Baseline Hindi Mental Status Examination (HMSE) score was 29/31 screening out cognitive impairment, Brief Psychiatric Rating Scale (BPRS) score was 32/126, and Young Mania Rating Scale (YMRS) was 31/60 suggestive of moderate severity. His blood investigations such as complete hemogram, serum electrolytes, and liver and renal profiles were within normal limits, with retroviral infection being nonreactive. His computed tomography of the brain was normal, but magnetic resonance imaging (MRI) of the brain revealed the coincidental finding of mild diffuse cerebral atrophy and old lacunar infarcts in bilateral basal ganglia with discrete areas of hyperintensities in bilateral centrum semiovale.
Considering elderly patient, initial lower daily dose of risperidone 2 mg, trihexyphenidyl 2 mg, and diazepam 5 mg was planned. A week later, due to risperidone-induced extrapyramidal ADE (abnormal involuntary movement scale suggestive of moderate severity), it was substituted with olanzapine 5 mg/day initially and gradually increased to 10 mg/day. During week-3, due to poor-responsive mania, lithium was slowly titrated to 600 mg/day, which gradually led to dysarthria, parkinsonian-like features, and ataxia at serum lithium of 1.1 mmol/L on day-7 of lithium therapy. Hence, lithium dose was reduced to 450 mg/day with resultant serum lithium of 0.84 mmol/L on day-14 of lithium therapy. Subsequently, he developed anorexia, bilateral coarse flapping tremors of hands with exacerbation on dorsiflexion at wrist joints, altered sensorium, and mild cognitive dulling (HMSE = 23/31), despite therapeutic dose of lithium. However, due to persistent serious lithium-related ADE, its discontinuation led to drastic clinical improvement in sensorium with reduced frequency of asterixis over the next 72 h, with complete recovery from signs of delirium, asterixis, anorexia, and ataxia at the end of 1 week after discontinuation of lithium. He was discharged with olanzapine 10 mg, trihexyphenidyl 2 mg, and diazepam 5 mg showed clinical improvement in 4 weeks (BPRS = 18/126 and YMRS = 2/60), with good compliance and without any ADE.
| Discussion|| |
Asterixis is generally indicative of serious underlying pathology such as encephalopathy occurring secondary to severe hepatic dysfunction, metabolic derangements, toxic agents, or medications [Table 1]. Lithium is an established, first-line mood stabilizer for treating mania, with narrow therapeutic window and unique profile of common side-effects such as fine tremors, weight gain, sedation, gastritis, anorexia, and some rare ADE such as dysphoria, lack of spontaneity, memory difficulties, hypothyroidism, T-wave changes on electrocardiograph, interstitial nephritis, and nephrogenic diabetes insipidus.
|Table 1: Causes of bilateral and unilateral asterixis,,,,,,,,|
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Lithium-induced ADE is pronounced in geriatric patients that include fine tremors, myoclonus, parkinsonian-like symptoms or worsening of cognitive functions, or preexisting Parkinson's disease and delirium. However, lithium is a very rare cause of asterixis with only four case report/s published to date, with the first case reported in 1978, in a 48-year-old female with mania and primary hyperparathyroidism, treated with lithium, thioridazine, and electroconvulsive therapy. Asterixis was reported in a 22-year-old woman in 1979, with relatively high serum lithium levels (1.27 mEq/L) and an unusually high red blood cell lithium level.
In 1996, a case series (n = 10) observed asterixis related to various combinations of psychotropic medications, of which 70% received lithium in combination with carbamazepine and/or clozapine, but none were on lithium monotherapy. In 2000, an another geriatric case with vascular dementia and possible bipolar disorder-mania on lithium monotherapy (300 mg qhs) developed asterixis even with therapeutic serum lithium levels of 0.7 meq/L, that resolved completely within 2 weeks of its discontinuation.
Generally, unilateral asterixis can be caused by discrete brain lesions, such as lacunar infarcts, whereas bilateral asterixis is caused by metabolic or toxic agents. Unilateral acute lacunar infarcts may produce asterixis on contralateral side, while rarely bilateral acute lacunar infarcts cause asymmetric, sudden-onset asterixis which is also associated with other localizing sensorimotor deficits.,, In contrary, our normotensive geriatric case with preexisting nicotine dependence, lacked either history of prior neurological deficit or medical/medicinal causes for asterixis, rising possibility of preexisting, asymptomatic, coincidental finding of “silent” old bilateral lacunar infarct on MRI brain, without any neurological deficits.
In our case, asterixis, ataxia, and delirium occurred during both toxic and therapeutic serum levels of lithium despite prescribing lower therapeutic dosage of lithium, similar to finding by Bahroo and Shamim. Complete resolution of ADE happened only upon discontinuation of lithium, while olanzapine was continued without any ADE. Although there are reports of asterixis due to concomitant administration of mood stabilizers (valproate, carbamazepine, or lithium) and antipsychotics (clozapine, risperidone, thioridazine, or zuclopenthixol);,, except clozapine, antipsychotics have not been independently linked to cause asterixis. The ADE probability score using algorithm laid by Naranjo et al. was 9/13, indicating “definite” role of lithium-induced asterixis, ataxia, anorexia, and delirium in our case.
| Conclusion|| |
Asterixis is a very rare and possible serious ADE of lithium. High-index of suspicion is warranted during lithium therapy, in addition to monitoring of adequate hydration and urine output, especially in the geriatric population, to prevent signs of lithium toxicity even at lower therapeutic doses. The dictum of “start low– go slow” to mitigate ADE appears prudent in extreme ages to ensure better compliance and treatment outcomes.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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