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Department of Pain Management, The Cleveland Clinic Foundation, Cleveland, Ohio
Address correspondence and reprint requests to Leonardo Kapural, MD, PhD, Pain Management Center, The Cleveland Clinic Foundation, 9500 Euclid Ave. Desk C25, Cleveland, OH 44195. Address e-mail to Kapural{at}ccf.org
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Abstract |
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IMPLICATIONS: Spinal cord stimulation when used for control of chronic pain in diabetics may provide additional benefits of improving glycemic control and insulin requirements.
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Introduction |
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Electrical stimulation of the spinal cord has proven beneficial for the treatment of type-2 diabetes mellitus in people with spinal cord injury. In those patients, glucose use and insulin sensitivity improved significantly (2).
Spinal cord stimulation (SCS) through multiple mechanisms produces pain relief. We describe an insulin-dependent diabetic female patient who had a SCS implant to control her chronic pain state secondary to complex regional pain syndrome Type 1. Her insulin requirements halved after initiation of SCS.
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Case Report |
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A review of her medical history revealed mild autonomic neuropathy related to her severe type-2 diabetes mellitus. She had an implanted insulin pump for improved control of her hyperglycemia (MiniMed 508; Medtronic Inc, Minneapolis, MN).
After thermographic imaging of both lower extremities and diagnostic lumbar sympathetic block, the diagnosis of the complex regional pain syndrome Type 1 was confirmed, and therapy was initiated with a series of lumbar sympathetic blocks. We used a 0.375% bupivacaine total of 30 mL after the needle was positioned properly under fluoroscopy at the L3 level. She received several lumbar sympathetic blocks with the minimal prolongation of her pain-free time (approximately 2 wk with prolongation measured in hours to a few days). Her glucose levels ranged from 180 to 260 mg/dL with the average insulin requirements of 124 U/d during that time period, and she had periods of total pain relief during that time. Because of the short-lived effect of the lumbar sympathetic blocks, SCS was proposed as one of the options to control her neuropathic pain. A 1-wk SCS trial was then completed and resulted in significant pain relief (1–2 of 10 visual analog scale). SCS system implant followed. She received an Itrel 3 generator with a Quad lead (Medtronic Inc) whose tip was placed under fluoroscopy over the top of the T9 vertebral body. This resulted in sustained pain relief, better control of her blood glucose levels, and a dramatic decrease in her insulin requirements (Fig. 1). Her glucose levels were consistently decreased with <50% of insulin daily usage via the insulin pump. Her hemoglobin (Hb) A1c decreased from 10.1, 3 mo before the implant, to 6.4, 3 mo after the implant. She maintained similar glucose control after implant.
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Discussion |
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Pain decreases insulin sensitivity, and it seems that the mechanism involves non-oxidative glucose metabolism (3). The same study suggested counter regulatory hormonal response as the reason for improved glucose control after analgesia. Therefore, pain relief is important for reestablishment of normal glucose metabolism. However, this patient had significant periods of pain relief after lumbar sympathetic blocks but no significant decrease in insulin requirements.
Besides pain control, other factors may affect glucose metabolism. Stimulation of the autonomic nerves affects islet hormone secretion. Thus, insulin secretion is stimulated by parasympathetic nerves or their neurotransmitters and inhibited by sympathetic nerves or their neurotransmitters (4). An important mechanism of action of SCS is blockade of supraspinal and spinal sympathetic mechanisms. Those effects persist after transection of the dorsal roots and spinal cord section rostrally to the stimulating electrode (5).
SCS of the upper thoracic segments was shown to decrease sympathetic outflow from the stellate ganglion.1 SCS placement at T8-9 may provide some sympathetic blockade to upper abdominal viscera and pancreas. It may be that additional, likely rostral, modulation of the autonomic system in our case contributed to better control of the patient’s diabetes.
The effects of spinal cord stimulation on peripheral insulin sensitivity are unknown. Those effects of neurostimulation seem to be long-term and not just temporary phenomena caused by a decrease of pain-induced stress because HbA1c showed a significant decrease three months after the SCS implant.
Exercise induces expression of key regulatory proteins involved in glucose uptake and metabolism (6,7). Our patient had improved exercise tolerance after each of the sympathetic blocks as well.
There are some other effects of SCS that could play a role in maintenance of better glucose control in this patient. They are mediated by multiple mediators like calcitonin gene-related peptide (8) and neuronal release of nitric oxide (9). The pancreatic islets are richly innervated by sensory nerves, and calcitonin gene-related peptide is localized in those sensory nerves (4). Nitric oxide was more recently implicated as the important inducer of endogenous insulin production (10).
In summary, we found a dramatic decrease of insulin requirements with better glycemic control when SCS was used for chronic pain control in our patient.
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Footnotes |
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This article has been cited by other articles:
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  Y. Ao, N. Toy, M. K. Song, V. L. W. Go, and H. Yang Altered Glucose and Insulin Responses to Brain Medullary Thyrotropin-Releasing Hormone (TRH)-Induced Autonomic Activation in Type 2 Diabetic Goto-Kakizaki Rats Endocrinology, December 1, 2005; 146(12): 5425 - 5432. [Abstract] [Full Text] [PDF]
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