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Mov Disord Clin Pract. Author manuscript; available in PMC 2017 September 01. Published in final edited form as: Mov Disord Clin Pract. 2016 ; 3(5): 510–512. doi:10.1002/mdc3.12310.

Leg Movements During General Anesthesia Nora Vanegas, MD1,2, Kareem Zaghloul, MD, PhD3, Mark Hallett, MD2, and Codrin Lungu, MD1 1Office

of the Clinical Director, National Institute of Neurologic Disorders and Stroke, Bethesda, MD, USA

2Human

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Motor Control Section, National Institute of Neurologic Disorders and Stroke, Bethesda, MD, USA

3Surgical

Neurology Branch, National Institute of Neurologic Disorders and Stroke, Bethesda, MD,

USA

Keywords Leg Movements; Parkinson Disease; general anesthesia

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We report a case of atypical leg movements in a 56 year-old man during general anesthesia. The patient had a history of tremor-predominant Parkinson Disease (PD) since age 43. He underwent deep brain stimulation (DBS) surgery at the National Institutes of Health (NIH) after an overnight dopaminergic medication withdrawal. During anesthetic induction he received 2mg of Midazolam IV and 100mcg of Fentanyl and Propofol at an infusion rate of 125 mcg/kg/min. Shortly thereafter, he developed periodic involuntary movements of his legs (Video 1). The movements were stereotyped, bilateral and synchronous, characterized by partial flexion of the ankle, knee, and hip for 3–4 seconds, at intervals of 5 to 10 seconds. After cessation of Propofol infusion, his movements promptly subsided. The total duration of the event was approximately 2 minutes. There were no residual motor or sensory deficits on neurological examination.

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His past medical history included a similar episode during cholecystecomy surgery approximately 13 years prior, but details of this remote event were not available. The patient denied a history of restless legs and his wife denied observing the presence of leg movements during his sleep. The patient described difficulty initiating and maintaining sleep. A polysomnograpic study performed one month after surgery revealed the presence of severe obstructive sleep apnea with mild desaturations. Most events of sleep disordered

Corresponding Author: Nora Vanegas, Building 10, Room 7D42 10 Center Drive. Bethesda, MD 20892, Phone number: 301 402 2383. Fax: 301 480 2286, [email protected]. Author roles: Concept and execution: Dr. Vanegas, Dr. Hallett and Dr. Lungu. Review and critique: Dr. Vanegas, Dr. Zaghloul Dr. Hallett and Dr. Lungu. Drafting/revising the manuscript: Dr. Vanegas, Dr. Zaghloul, Dr. Hallett and Dr. Lungu. Conflict of Interests: The authors declare that there are no conflicts of interest relevant to this work.

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breathing were respiratory-effort related arousals and it was difficult to distinguish between mild episodes of sleep disordered breathing and periodic leg movement (PLM) related arousals. There were 18 leg movements per hour.

Discussion

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We describe a case of atypical leg movements during general anesthesia. The differential diagnosis of this presentation includes rhythmic movement phenomena such as leg myoclonus, alternating leg muscle activation and periodic leg movements of sleep (PLMS). Alternating leg muscle activation is characterized by sequences of alternating leg movements with less than 2 seconds between activations and a frequency of 1–2 Hz [1]. PLMS are involuntary, predominantly leg movements, lasting 0.5 to 10 seconds [2]. PLMS typically occur every 20 to 40 seconds but the inter-movement intervals may vary between 5 and 90 seconds [2]. In this case, the movement duration is similar to the duration of leg movements in PLMS, however the inter-movement intervals are variable and unusually short (5 to 10 seconds). In addition, the leg movements described in our patient were characterized by quick, jerk-like movements with hip, knee and plantar flexion. This observation is also atypical when compared to PLMS, as the latter are characterized by dorsiflexion of the foot and toes, followed by partial flexion of the knee and sometimes the hip. Therefore, although myoclonus can not be excluded, the periodicity and duration of the observed movements has partial similarity to periodic leg movements of sleep (PLMS).

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PLMS are known to increase with age and are more frequent in patients with restless legs syndrome, PD and several sleep disorders. The pathophysiology of PLMS is unknown; however, the beneficial effects of dopaminergic medications have suggested that dopamine receptors play an important role in the development of this phenomenon [3]. In addition, the contribution of the spinal cord in the pathophysiology of PLMS has been supported by the presence of PLMS in patients receiving spinal anesthesia and after spinal cord lesions [4] [5]. The reported cases of anesthesia-related periodic leg movements (AR-PLM) demonstrate, however, longer inter-movement intervals than the ones observed in our case. It is believed that spinal AR-PLM are due to the disruption of supraspinal influences on the spinal cord. The inhibition of inhibitory interneurons in the spinal cord with local anesthesia results in uncontrolled excitation of spinal interneurons and releases involuntary motor responses resembling the mechanism of a Babinski reflex [4].

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Conversely, our patient developed involuntary leg movements after the concomitant administration of three intravenous anesthetics. Propofol and Midazolam facilitate GABAA receptors. GABA receptors are widely distributed in the human brain and are highly concentrated in cortical, hippocampal, thalamic, basal ganglia and cerebellar structures [6]. Similar to GABA receptors, opioid receptors are widely expressed in the central nervous system (CNS). Fentanyl, the third agent administered to our patient, is a type of opioid receptor agonist, known to suppress PLMS [3]. Thus, in the present case, despite the administration of an opioid medication, there was facilitation of involuntary leg movements in the context of predisposing factors including age, PD, mild PLMS and the overnight withdrawal of dopaminergic medications.

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Dopamine neurons have GABA receptors and the inhibition of striatal dopamine release by GABA has been documented [7]. Hence, the administration of two GABA agonists would cause dopamine suppression in a situation where dopamine synthesis is already low and exogenous dopamine supplementation has been suspended. Although opioids are known to cause inhibition of GABAergic transmission and GABA release [8], the presence of two exogenous GABAergic medications could have overcome these inhibitory effects, allowing further dopamine reduction. In addition, exposure to benzodiazepines has been shown to up regulate glutamate receptors and potentiate hyperlocomotor behavior induced by opioids in animal models [9]. While the exact mechanism responsible for the described observation requires further investigation, this phenomenology should be known, as its occurrence under intravenous anesthetics could be confused for other, pathophysiologically different phenomena.

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Supplementary Material Refer to Web version on PubMed Central for supplementary material.

Acknowledgments Funding: NIH/NINDS Intramural Program for all authors Financial Disclosures for the previous 12 months:

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Dr. Vanegas received a Medtronic Deep Brain Stimulation Therapy Fellowship Grant 2014–2015. Dr. Zaghloul has no disclosures. Dr. Hallett serves as Chair of the Medical Advisory Board for and receives honoraria and funding for travel from the Neurotoxin Institute. He may accrue revenue on US Patent #6,780,413 B2 (Issued: August 24, 2004): Immunotoxin (MAB-Ricin) for the treatment of focal movement disorders, and US Patent #7,407,478 (Issued: August 5, 2008): Coil for Magnetic Stimulation and methods for using the same (H-coil); in relation to the latter, he has received license fee payments from the NIH (from Brainsway) for licensing of this patent. He is on the Editorial Board of 20 journals, and received royalties and/or honoraria from publishing from Cambridge University Press, Oxford University Press, John Wiley & Sons, Wolters Kluwer, Springer, and Elsevier. He has received honoraria for lecturing from Columbia University. Dr. Hallett’s research at the NIH is largely supported by the NIH Intramural Program. Supplemental research funds have been granted by the Kinetics Foundation for studies of instrumental methods to monitor Parkinson’s disease, BCN Peptides, S.A. for treatment studies of blepharospasm, Medtronics, Inc., for studies of deep brain stimulation, Parkinson Alliance for studies of eye movements in Parkinson’s disease, Merz for treatment studies of focal hand dystonia, and Allergan for studies of methods to inject botulinum toxins. Dr. Lungu has no disclosures.

Bibliography

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1. Chervin RD, Consens FB, Kutluay E. Alternating leg muscle activation during sleep and arousals: a new sleep-related motor phenomenon? Mov Disord. 2003; 18:551–9. DOI: 10.1002/mds.10397 [PubMed: 12722169] 2. Iber C, Ancoli-Islrael S, Chesson A Jr, et al. American Academy of Sleep Medicine. The AASM manual for the scoring of sleep and associatedevents: rules, terminology and technical specifications. American Academy of Sleep Medicine. 2007 3. Karatas M. Restless Legs Syndrome and Periodic Limb Movements During Sleep: Diagnosis and Treatment. The Neurologist. 2007; 13:294–301. DOI: 10.1097/NRL.0b013e3181422589 [PubMed: 17848868] 4. Watanabe S, Ono A, Naito H. Periodic leg movements during either epidural or spinal anesthesia in an elderly man without sleep-related (nocturnal) myoclonus. Sleep. 1990; 13:262–6. [PubMed: 2356397]

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5. Dickel, Renfrow, Moore, et al. Rapid eye movement sleep periodic leg movements in patients with spinal cord injury. Sleep. 1994; 17:733–8. [PubMed: 7701185] 6. Taylor C. GABA receptors and GABAergic synapses as targets for drug development. Drug Development Research. 1990; 21:151–60. DOI: 10.1002/ddr.430210302 7. Dewey S. GABAergic Inhibition of Endogenous Dopamine Release Measured in viva with llCRaclopride and Positron Emission Tomography. The Journal of Neuroscience. 1992; 12:3773. [PubMed: 1357114] 8. Vaughan, Christie. Presynaptic inhibitory action of opioids on synaptic transmission in the rat periaqueductal grey in vitro. The Journal of Physiology. 1997; 498:463–72. DOI: 10.1113/jphysiol. 1997.sp021872 [PubMed: 9032693] 9. Shibasaki M, Ishii K, Masukawa D, et al. Implication of mGlu5 receptor in the enhancement of morphine-induced hyperlocomotion under chronic treatment with zolpidem. European Journal of Pharmacology. 2014; 738:360–7. DOI: 10.1016/j.ejphar.2014.06.001 [PubMed: 24930812]

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