|LETTER TO THE EDITOR
|Year : 2020 | Volume
| Issue : 2 | Page : 118-120
Movement disorders associated with hypoglycemia and hyperglycemia
Jamir Pitton Rissardo, Ana L Fornari Caprara
Medicine Department, Federal University of Santa Maria, Santa Maria, Brazil
|Date of Submission||05-Apr-2020|
|Date of Acceptance||27-Apr-2020|
|Date of Web Publication||28-Jul-2020|
Dr. Jamir Pitton Rissardo
Medicine Department, Federal University of Santa Maria, Rua Roraima, Santa Maria, Rio Grande do Sul.
Source of Support: None, Conflict of Interest: None
|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 2022 Sep 27];3:118-20. Available from: https://www.aomd.in/text.asp?2020/3/2/118/291078
We read the article entitled “Sudden jerky head movement in hypoglycemia” on the esteemed Annals of Movement Disorders with great interest. Shah and Sardana 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. 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.
|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. 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. Moreover, the pathological explanation of hypoglycemia and hypoglycemia causing brain damage may have a similar pathway [Figure 1]., 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. 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.
|Figure 2: Model proposed by Sutherland et al. 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. 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
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[Figure 1], [Figure 2]