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Table of Contents
Year : 2020  |  Volume : 3  |  Issue : 2  |  Page : 118-120

Movement disorders associated with hypoglycemia and hyperglycemia

Medicine Department, Federal University of Santa Maria, Santa Maria, Brazil

Date of Submission05-Apr-2020
Date of Acceptance27-Apr-2020
Date of Web Publication28-Jul-2020

Correspondence Address:
Dr. Jamir Pitton Rissardo
Medicine Department, Federal University of Santa Maria, Rua Roraima, Santa Maria, Rio Grande do Sul.
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/AOMD.AOMD_18_20

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How to cite this article:
Pitton Rissardo J, Fornari Caprara AL. Movement disorders associated with hypoglycemia and hyperglycemia. Ann Mov Disord 2020;3:118-20

How to cite this URL:
Pitton Rissardo J, Fornari Caprara AL. Movement disorders associated with hypoglycemia and hyperglycemia. Ann Mov Disord [serial online] 2020 [cited 2023 May 29];3:118-20. Available from: https://www.aomd.in/text.asp?2020/3/2/118/291078

Dear Editor,

We read the article entitled “Sudden jerky head movement in hypoglycemia” on the esteemed Annals of Movement Disorders with great interest. Shah and Sardana[1] reported a case of an elderly female who developed two episodes of hemiparesis and a single episode of jerky head movement. She was diabetic and had a low blood sugar level in both times. It is noteworthy that according to Shah and Sardana their report was the first to describe the occurrence of jerky head movement secondary to hypoglycemia.

Herein, we would like to highlight some important facts about glycemic levels and related movement disorders.

The first point to discuss is that all movement disorders were already reported in association with hypo/hyperglycemia [Table 1]. But not all abnormal movements were already associated. Our literature review shown in the table revealed that the most reported abnormal movements, in decreasing order of frequency, are as follows: tremor, chorea, ballism, ataxia, myoclonus, and  Parkinsonism More Details. By the way, tremor, when compared to the other movements, probably represents >99% of the movement disorders secondary to altered glycemic states.[23] Also, its possibly pathophysiological mechanism is distinct from the other abnormal movements. The tremor noted in these reports is probably related to an exacerbation of physiological tremor, in which the movement is associated with the noradrenergic tone.[24]
Table 1: Abnormal movements associated with hypoglycemia and hyperglycemia

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The explanation for the other movement disorders, except tremors, may be associated with a dysbalanced inhibitory/excitatory effect on the basal ganglia structures. One supporting finding of this theory is the fact that both hypoglycemia and hyperglycemia can lead to restricted diffusion, especially, in these regions.[1] Based on animal models, it was observed that during glycemic abnormalities the cerebral metabolism is adapted, and these adaptations the release of cytokines leads to cerebral ischemia, blood–brain barrier damage, and increased levels of excitatory neurotransmitters.[25] Moreover, the pathological explanation of hypoglycemia and hypoglycemia causing brain damage may have a similar pathway [Figure 1].[23],[25] Thus, both may have similar movement disorders; for example, abnormal movements that have not yet been reported with hypoglycemia but have been reported with hyperglycemia may in the future be reported in a patient with hypoglycemia, and vice versa.
Figure 1: Schematic diagram of the neuroinflammatory mechanisms involved in hypo/hyperglycemic states, showing a similar pathway of both glycemic states leading to the neuronal damage

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The hypothesis for the increased excitatory substances in hypoglycemia was proposed by Sutherland et al.[26] They explained that in the occurrence of hypoglycemia there will be a truncation of the Krebs cycle. In this context, the decreased levels of pyruvate, under severe hypoglycemia, would lead to the metabolism of oxaloacetate directly to α-ketoglutarate with the use of glutamate [Figure 2]. In this way, the decrease of glutamine levels and increased levels of aspartate could cause excitation, inhibition, or disinhibition of the direct/indirect pathways and result in an abnormal movement.[27]
Figure 2: Model proposed by Sutherland et al.[5] describing cerebral metabolism adaption during the hypoglycemic state. OAA = oxaloacetate, α-KG = alpha-ketoglutarate

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Another interesting fact is that the majority of the reports were related to patients affected by diabetes and some hypoglycemic individuals with insulinoma.[23] So, it is worthy of mentioning that when starting or increasing the dose of hypoglycemic agents, the physician should be aware of these side effects and advise the patient to avoid complications such as falls and even fractures.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Shah VS, Sardana V Sudden jerky head movement in hypoglycemia. Ann Mov Disord 2020;3:44-6.  Back to cited text no. 1
Berz JP, Orlander JD Prolonged cerebellar ataxia: An unusual complication of hypoglycemia. J Gen Intern Med 2008;23: 103-5.  Back to cited text no. 2
Indiran V, Maduraimuthu P Rare presentation of unilateral weakness, involuntary movements and ataxia with subcortical t2 hypointensity in a diabetic patient: A case report. Case Rep Radiol 2012;2012:768189.  Back to cited text no. 3
Vittal P, Comella C, Shannon K Acute recurrent, persistent hypoglycemia-induced chorea/ballism in a diabetic patient on hemodialysis. Neurology 2014;82:P4.059.  Back to cited text no. 4
Takahashi S, Ohkawa S [Paroxysmal bilateral ballism induced by hypoglycemia]. Rinsho Shinkeigaku 2006;46:278-80.  Back to cited text no. 5
Jagota P, Bhidayasiri R, Lang AE Movement disorders in patients with diabetes mellitus. J Neurol Sci 2012;314:5-11.  Back to cited text no. 6
Cosentino C, Torres L, Nuñez Y, Suarez R, Velez M, Flores M Hemichorea/hemiballism associated with hyperglycemia: Report of 20 cases. Tremor Other Hyperkinet Mov 2016;6:402.  Back to cited text no. 7
Lai SL, Tseng YL, Hsu MC, Chen SS Magnetic resonance imaging and single-photon emission computed tomography changes in hypoglycemia-induced chorea. Mov Disord 2004;19: 475-8.  Back to cited text no. 8
Wolz M, Reichmann H, Reuner U, Storch A, Gerber J Hypoglycemia-induced choreoathetosis associated with hyperintense basal ganglia lesions in T1-weighted brain MRI. Mov Disord 2010;25:966-8.  Back to cited text no. 9
Newman RP, Kinkel WR Paroxysmal choreoathetosis due to hypoglycemia. Arch Neurol 1984;41:341-2.  Back to cited text no. 10
Ahlskog JE, Nishino H, Evidente VG, Tulloch JW, Forbes GS, Caviness JN, et al. Persistent chorea triggered by hyperglycemic crisis in diabetics. Mov Disord 2001;16:890-8.  Back to cited text no. 11
Kandiah N, Tan K, Lim CT, Venketasubramanian N Hyperglycemic choreoathetosis: Role of the putamen in pathogenesis. Mov Disord 2009;24:915-9.  Back to cited text no. 12
Tan NC, Tan AK, Sitoh YY, Loh KC, Leow MK, Tjia HT Paroxysmal exercise-induced dystonia associated with hypoglycaemia induced by an insulinoma. J Neurol 2002;249:1615-6.  Back to cited text no. 13
Clark JD, Pahwa R, Koller C, Morales D Diabetes mellitus presenting as paroxysmal kinesigenic dystonic choreoathetosis. Mov Disord 1995;10:353-5.  Back to cited text no. 14
Jaladyan V, Darbinyan V Insulinoma misdiagnosed as juvenile myoclonic epilepsy. Eur J Pediatr 2007;166:485-7.  Back to cited text no. 15
Matsumura K, Sonoh M, Tamaoka A, Sakuta M Syndrome of opsoclonus-myoclonus in hyperosmolar nonketotic coma. Ann Neurol 1985;18:623-4.  Back to cited text no. 16
Gil YE, Yoon JH Hypoglycemia-induced parkinsonism with vasogenic basal ganglia lesion. Parkinsonism Relat Disord 2018;49:112-3.  Back to cited text no. 17
Teodoro T, Lobo PP, Ferreira J, Sousa R, Reimão S, Peralta R, et al. Delayed Parkinsonism after acute chorea due to non-ketotic hyperglycemia. J Neurol Sci 2015;354:116-7.  Back to cited text no. 18
Nakajima N, Ueda M, Nagayama H, Katayama Y Hypoglycemiainduced spontaneous unilateral jerking movement in bilateral internal capsule posterior limb abnormalities. J Neurol Sci 2014;338:220-2.  Back to cited text no. 19
Debruyne F, Van Paesschen W, Van Eyken P, Bex M, Vandenberghe W Paroxysmal nonkinesigenic dyskinesias due to recurrent hypoglycemia caused by an insulinoma. Mov Disord 2009;24:460-1.  Back to cited text no. 20
Bandyopadhyay SK, Dutta A Hemifacial spasm complicating diabetic ketoacidosis. J Assoc Physicians India 2005;53:649-50.  Back to cited text no. 21
Tan JH, Chan BP, Wilder-Smith EP, Ong BK A unique case of reversible hyperglycemic Holmes’ tremor. Mov Disord 2006;21:707-9.  Back to cited text no. 22
Jagota P, Bhidayasiri R, Lang AE Movement disorders in patients with diabetes mellitus. J Neurol Sci 2012;314:5-1.  Back to cited text no. 23
Smaga S Tremor. Am Fam Physician 2003;68:1545-52.  Back to cited text no. 24
Shukla V, Shakya AK, Perez-Pinzon MA, Dave KR Cerebral ischemic damage in diabetes: An inflammatory perspective. J Neuroinflammation 2017;14:21.  Back to cited text no. 25
Sutherland GR, Tyson RL, Auer RN Truncation of the Krebs cycle during hypoglycemic coma. Med Chem 2008;4:379-85.  Back to cited text no. 26
Rissardo JP, Caprara ALF Buspirone-associated movement disorder: A literature review. Prague Med Rep 2020;121: 5-24.  Back to cited text no. 27


  [Figure 1], [Figure 2]

  [Table 1]

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