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 Table of Contents    
Year : 2020  |  Volume : 62  |  Issue : 6  |  Page : 743-745
A rare association of lithium carbonate with blepharospasm: A case report

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

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Date of Submission14-Jul-2019
Date of Decision17-Oct-2019
Date of Acceptance02-Apr-2020
Date of Web Publication12-Dec-2020

How to cite this article:
Kumar A, Grover S. A rare association of lithium carbonate with blepharospasm: A case report. Indian J Psychiatry 2020;62:743-5

How to cite this URL:
Kumar A, Grover S. A rare association of lithium carbonate with blepharospasm: A case report. Indian J Psychiatry [serial online] 2020 [cited 2022 Dec 7];62:743-5. Available from:

Blepharospasm is characterized by repetitive, sustained, involuntary contractions of the orbicularis oculi which if severe can cause functional blindness.[1] It is a type of dystonia, which is known to be associated with lesions in basal ganglia[2] and diencephalon[3] or upper brain stem,[4] besides its association with use of various medications.[5] Blepharospasm is understood as an extrapyramidal side effect of antipsychotic medications, and when it is associated with dystonia of the lower face, jaw, and neck, it is referred as Meige's syndrome. Rarely, blepharospasm is seen as the only manifestation of neuroleptic-induced tardive dyskinesia, and when seen, it is known as tardive blepharospasm (TB).[6] Although there is literature on neuroleptic-induced blepharospasm,[1],[5],[6],[7],[8] there is no information on lithium-associated blepharospasm. In this case report, we present a case who developed blepharospasm while receiving lithium alone.

   Case Description Top

A 41-year-married male, diagnosed with bipolar affective disorder, presented with a history of 12-year duration, with three episodes of depression and one hypomanic episode in the lifetime. He has also been consuming alcohol 60–90 ml/day for 20 years. He was initially treated with antidepressants in the form of selective serotonin reuptake inhibitors (i.e., escitalopram and fluoxetine), with which he would achieve clinician remission and then stop medications. In his second depressive episode, i.e., about 8 years prior to presentation, he also received lithium, at a dose of 600 mg/day for 1 year, after which he discontinued the medications. Later, following the hypomanic episode, he was restarted on lithium carbonate 600 mg/day, 7 years prior to the presentation. His serum lithium levels were 0.45 mmol/L, and he remained compliant on the same. After about 1 year of being on lithium carbonate, he developed hypothyroidism and resultantly was started on thyroxine 50 mcg/day in consultation with the endocrinologist. However, in subsequent follow-ups, his serum lithium was found to be 0.4 mmol/L, and in view of the relapse of depressive symptoms, the dose of lithium was further increased to 750 mg/day. Within 2–3 weeks of increasing the dose of lithium carbonate, he developed sudden spasmodic opening and closing movements of the eyes, which were usually precipitated by blow of air, leading to dysfunction in his work performance. In addition, the blepharospasm would increase with work pressure, anxiety, and exposure to bright light and would subside while sleeping. At this time, his serum lithium level was found to be 0.49 mmol/L. There was no history of use of any other medications, increase in the use of alcohol, any other movements of the body, fever, head injury, comorbid physical diseases, and evidence of any nutritional deficiency. There was no family history of any movement disorders.

His routine investigations, electroencephalogram, and magnetic resonance imaging of the brain did not reveal any abnormality. His repeat thyroid profile during this period also did not reveal any abnormality while receiving thyroxine.

He was evaluated by an ophthalmologist, was diagnosed with blepharospasm, and was started on tablet trihexyphenidyl 10 mg/day, with which he did not show any improvement over the next 6 weeks. Following this, he was managed with injection botulinum (56/80 unit; 4-8-16 regime) in bilateral orbicularis oculi muscle, with which there was a significant improvement in blepharospasm, but the symptoms reappeared after 1 month. During this time, he had continued to receive lithium 750 mg/day.

At this moment, a possibility of lithium-associated blepharospasm was considered. On evaluation, he did not have any other extrapyramidal symptoms (EPS). In view of the possibility of association with lithium, the dose of lithium was reduced to 450 mg/day, with which there was a significant improvement in blepharospasm within 4 weeks. Following this, lithium was stopped, and his mood symptoms were managed with valproate. Over the next 2 years of follow-up, there was no recurrence of blepharospasm.

   Discussion Top

Tardive syndromes are well-known side effect of neuroleptics,[6] which occur in approximately 1%–2% of patients on long-term neuroleptics.[7],[9] TB, is a special category of tardive dystonias which is characterized by isolated repetitive, persistent, and marked contraction of orbicularis oculi muscle.[6],[10]

Besides the use of neuroleptics, blepharospasm has also been reported to occur with the use of antihistaminic, dopaminomimetics,[11] and sympathomimetic medications.[12] However, in the index case, there was no history of use of such medications. In terms of the etiology of blepharospasm, in a large series of 264 patients, 14 (5.3%) cases of blepharospasm were attributed to the use of neuroleptic medications.[13] There are occasional reports of lamotrigine-induced frequent blinking.[14]

There are reports of increased risk of acute extrapyramidal side effects,[15],[16] neuroleptic malignant syndrome,[17] and tardive syndromes[18] with the use of lithium alone or while receiving lithium in combination with typical and atypical antipsychotics.[19] Occasional case reports have also reported an association of TB with a combination of atypical antipsychotics with lithium. However, we could not find any published literature on the association of TB with the use of lithium alone.

In our case, the patient was on lithium carbonate (600 mg/day; serum lithium level 0.45 mmol/L) for around 1 year, without any movements, and when lithium carbonate was increased to 750 mg/day (serum lithium level 0.49 mmol/L), he developed blepharospasm, which subsided on decreasing the dose of lithium carbonate to 450 mg/day. In fact, initially, the possibility of lithium-associated blepharospasm was not considered at all. Only when he did not respond to trihexyphenidyl and relapsed after receiving botulinum toxin, a possibility of lithium carbonate-associated TB was considered. When one evaluates the existing literature on association of TB with the use of neuroleptics, it has also been reported to be dose related, as was seen in the index case with the dose of lithium. In terms of Naranjo's score, the patient scored 8, suggesting a probable association between the side effect and the medication in the index case.

The exact mechanism of action of lithium in the development of blepharospasm is not known. The existing literature suggests the association of lithium with extrapyramidal side effects, such as rigidity. The EPS due to lithium is hypothesized to be an outcome of chronic use of lithium, leading to a reduction in dopamine receptors in the striatum or limbic system.[20] The same mechanism may also be responsible for blepharospasm.

The index case highlights the association of lithium with TB and suggests that, whenever, a patient develops TB, while receiving lithium alone or in combination with other medications, lithium-associated blepharospasm should also be considered as a differential diagnosis.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

Weiner WJ, Nausieda PA, Glantz RH. Meige syndrome (blepharospasm-oromandibular dystonia) after long-term neuroleptic therapy. Neurology 1981;31:1555-6.  Back to cited text no. 1
Keane JR, Young JA. Blepharospasm with bilateral basal ganglia infarction. Arch Neurol 1985;42:1206-8.  Back to cited text no. 2
Powers JM. Blepharospasm due to unilateral diencephalon infarction. Neurology 1985;35:283-4.3.  Back to cited text no. 3
Jankovic J, Patel SC. Blepharospasm associated with brainstem lesions. Neurology 1983;33:1237-40.  Back to cited text no. 4
Sachdev P. Tardive blepharospasm. Mov Disord 1998;13:947-51.  Back to cited text no. 5
Burke RE, Fahn S, Jankovic J, Marsden CD, Lang AE, Gollomp S, et al. Tardive dystonia: Late-onset and persistent dystonia caused by antipsychotic drugs. Neurology 1982;32:1335-46.  Back to cited text no. 6
Friedman JH, Kucharski LT, Wagner RL. Tardive dystonia in a psychiatric hospital. J Neurol Neurosurg Psychiatry 1987;50:801-3.  Back to cited text no. 7
Micheli F, Cersósimo G, Scorticati MC, Ledesma D, Molinos J. Blepharospasm and apraxia of eyelid opening in lithium intoxication. Clin Neuropharmacol 1999;22:176-9.  Back to cited text no. 8
Yassa R, Nair V, Dimitry R. Prevalence of tardive dystonia. Acta Psychiatr Scand 1986;73:629-33.  Back to cited text no. 9
Kiliç A, Erten E, Özdemir A. Tardive Blepharospasm and Meige Syndrome during Treatment with Quetiapine and Olanzapine. Noro Psikiyatr Ars 2015;52:207-9.  Back to cited text no. 10
Weiner WJ, Nausieda PA. Meige's syndrome during long-term dopaminergic therapy in Parkinson's disease. Arch Neurol 1982;39:451-2.  Back to cited text no. 11
Powers JM. Decongestant-induced blepharospasm and orofacial dystonia. JAMA 1982;247:3244-5.  Back to cited text no. 12
Grandas F, Elston J, Quinn N, Marsden CD. Blepharospasm: A review of 264 patients. J Neurol Neurosurg Psychiatry 1988;51:767-72.  Back to cited text no. 13
Kim DG, Oh SH, Kim OJ. A case of lamotrigine-induced excessive involuntary eye blinking. J Clin Neurol 2007;3:93-5.  Back to cited text no. 14
Ghadirian AM, Annable L, Bélanger MC, Chouinard G. A cross-sectional study of parkinsonism and tardive dyskinesia in lithium-treated affective disordered patients. J Clin Psychiatry 1996;57:22-8.  Back to cited text no. 15
Kane J, Rifkin A, Quitkin F, Klein DF. Extrapyramidal side effects with lithium treatment. Am J Psychiatry 1978;135:851-3.  Back to cited text no. 16
Patil V, Gupta R, Verma R, Balhara YP. Neuroleptic malignant syndrome associated with lithium toxicity. Oman Med J 2016;31:309-11.  Back to cited text no. 17
Chakrabarti S, Chand PK. Lithium-induced tardive dystonia. Neurol India 2002;50:473-5.  Back to cited text no. 18
[PUBMED]  [Full text]  
Unaldi M, Sayhan MB, Sogüt O, Demirhan R, Güzel B. Neuroleptic malignant syndrome after the addition of lithium to risperidone treatment: A case report and review of the literature. Hong Kong J Emerg Med 2010;17:289-92.  Back to cited text no. 19
Addonizio G. Rapid induction of extrapyramidal side effects with combined use of lithium and neuroleptics. J Clin Psychopharmacol 1985;5:296-8.  Back to cited text no. 20

Correspondence Address:
Sandeep Grover
Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/psychiatry.IndianJPsychiatry_413_19

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