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Year : 2020  |  Volume : 4  |  Issue : 1  |  Page : 100-101

Role of add on rTMS in management of insomnia

Department of Psychiatry, King George's Medical University, Lucknow, Uttar Pradesh, India

Date of Submission01-Aug-2019
Date of Decision22-Aug-2019
Date of Acceptance04-Sep-2019
Date of Web Publication30-May-2020

Correspondence Address:
Dr. Sujita Kumar Kar
Department of Psychiatry, King George's Medical University, Lucknow, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aip.aip_47_19

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How to cite this article:
Kar SK, Kumar A, Upadhyay A. Role of add on rTMS in management of insomnia. Ann Indian Psychiatry 2020;4:100-1

How to cite this URL:
Kar SK, Kumar A, Upadhyay A. Role of add on rTMS in management of insomnia. Ann Indian Psychiatry [serial online] 2020 [cited 2020 Dec 6];4:100-1. Available from: https://www.anip.co.in/text.asp?2020/4/1/100/285502


Insomnia is a major health concern. The interhemispheric connectivity is disrupted in specific brain areas (middle occipital, posterior middle temporal gyrus) without alterations in structural and local morphological changes in patients with chronic insomnia.[1] Studies have found cortical alterations as well as intracortical excitability in patients with insomnia and also among healthy controls with sleep deprivation, using single and paired pulse repetitive transcranial magnetic stimulation (rTMS).[2],[3] These neurophysiological changes are amenable to be altered by neuromodulation techniques such as rTMS. We describe here a case of an adult male with predominant insomnia who improved with rTMS.

A 49-years-old nondiabetic and nonhypertensive male sought psychiatric consultation for multiple, nonspecific pain symptoms (body ache and burning pain in the eyes) and gastric discomfort (fullness of the abdomen, acid reflux, and epigastric pain). These complaints were associated with anxiety. Premorbidly, he used to have 6–8 h of sleep, but during the course of his illness, the sleep duration had been reduced to <1 h/day. There was no past or family history of psychiatric illness. The patient had never used any psychoactive substance. The patient consulted several physicians and was investigated extensively with no noticeable abnormalities. He had been treated with various antidepressants and benzodiazepines in combination, in the past without much benefit. Due to little improvement in sleep, the patient had overmedicated himself several times in the past. He adopted several lifestyle modifications (regular aerobic exercise, dietary modifications, and practice of yoga), without any noticeable benefit. He was always preoccupied with the thought of having some major physical illness.

He was hospitalized for his complaints of persistent sleep disturbance. His general physical examination and systemic examination did not reveal any abnormality. On mental status examination, his mood was anxious and he had illness preoccupation. He was diagnosed with somatoform disorder with chronic tension-type headache with chronic primary insomnia. At the time of hospitalization, the patient was on desvenlafaxine 100 mg/day, trazodone 100 mg/day, zolpidem 10 mg/day, and clonazepam 1 mg/day, with a sleep duration of 2–3 h/day. Due to inadequate response to pharmacotherapy, he was considered for rTMS. After informed consent, he was started with low-frequency rTMS (1 Hz) over the left dorsolateral prefrontal cortex at 80% of resting motor threshold. We adopted the protocol used in a previous study.[4] At baseline evaluation, his Pittsburgh Sleep Quality Index (PSQI) score was 16 (poor sleep quality) and Insomnia Severity Index (ISI) score was 19 (clinical insomnia of moderate severity). He was given a total of 15 sessions of rTMS with 1800 pulses per se ssion along with ongoing pharmacotherapy. After 15 days of daily rTMS, he showed a significant improvement in his sleep. His sleep increased to 4–5 h per night and his PSQI and ISI scores became 11 and 10, respectively. His somatic complaints were also resolved completely. He was discharged on desvenlafaxine 100 mg/day, trazodone 100 mg/day, and zolpidem (sustained-release preparation) 12.5 mg/day. In 3-week follow-up, he was well-maintained.

There was no medical cause that attributed to the symptoms in our case. The patient's insomnia was refractory to pharmacotherapy, psychological interventions, and lifestyle modification measures. As insomnia was of longer duration (>30 days), unrelated to the course of psychiatric illness and causing significant distress to the individual, the possibility of primary insomnia was more likely. Symptoms of somatoform disorder did not improve completely with conventional pharmacotherapy, which might be due to persisting insomnia. Behavioral interventions focusing on sleep hygiene are the mainstay treatment of chronic insomnia.[5] Pharmacological and psychological interventions are commonly recommended for the treatment of insomnia.[6]

Jiang et al. had evaluated the therapeutic efficacy of rTMS in chronic primary insomnia and found that patients receiving rTMS had a significant improvement in Stage III and rapid eye movement sleep and sleep architecture as well as had fewer relapses and recurrence rates.[4] Considering the refractoriness of insomnia, we considered rTMS for our patient. The patient had shown noticeable benefits to add on rTMS, which remained stable over the next 3 months (till last follow-up). Recent evidence suggests that bilateral sequential low-frequency rTMS was useful in the management of primary insomnia. The therapeutic effect of bilateral sequential low-frequency rTMS is mediated through elevation of levels of neurotransmitter gamma-aminobutyric acid and brain-derived neurotrophic factor.[7]

The uniqueness in our case was that the patient's somatic symptoms had also improved substantially after 15 sessions of rTMS. This shows the effect of rTMS as an augmenting therapy in nonorganic insomnia patients. Further research is needed to understand the efficacy of rTMS in insomnia management as a stand-alone treatment.

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.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Zhou F, Zhao Y, Huang M, Zeng X, Wang B, Gong H. Disrupted interhemispheric functional connectivity in chronic insomnia disorder: A resting-state fMRI study. Neuropsychiatr Dis Treat 2018;14:1229-40.  Back to cited text no. 1
Lanza G, Cantone M, Lanuzza B, Pennisi M, Bella R, Pennisi G, et al. Distinctive patterns of cortical excitability to transcranial magnetic stimulation in obstructive sleep apnea syndrome, restless legs syndrome, insomnia, and sleep deprivation. Sleep Med Rev 2015;19:39-50.  Back to cited text no. 2
van der Werf YD, Altena E, van Dijk KD, Strijers RL, De Rijke W, Stam CJ, et al. Is disturbed intracortical excitability a stable trait of chronic insomnia? A study using transcranial magnetic stimulation before and after multimodal sleep therapy. Biol Psychiatry 2010;68:950-5.  Back to cited text no. 3
Jiang CG, Zhang T, Yue FG, Yi ML, Gao D. Efficacy of repetitive transcranial magnetic stimulation in the treatment of patients with chronic primary insomnia. Cell Biochem Biophys 2013;67:169-73.  Back to cited text no. 4
Kay-Stacey M, Attarian H. Advances in the management of chronic insomnia. BMJ 2016;354:i2123.  Back to cited text no. 5
Riemann D, Baglioni C, Bassetti C, Bjorvatn B, Dolenc Groselj L, Ellis JG, et al. European guideline for the diagnosis and treatment of insomnia. J Sleep Res 2017;26:675-700.  Back to cited text no. 6
Feng J, Zhang Q, Zhang C, Wen Z, Zhou X. The effect of sequential bilateral low-frequency rTMS over dorsolateral prefrontal cortex on serum level of BDNF and GABA in patients with primary insomnia. Brain Behav 2019;9:e01206.  Back to cited text no. 7


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