Abstract
Background:Insulin resistance (hyperinsulinemia) is said to be the signal event and causal in the development of type 2 diabetes mellitus. Pulsatile arterial compression of the right anterolateral medulla oblongata is associated with autonomic dysfunction, including “driving” the pancreas, which increases insulin resistance causing type 2 diabetes mellitus. In this prospective study, we hypothesize that decompressing the right cranial nerve X and medulla will result in better glycemic control in patients with type 2 diabetes mellitus.Methods:Ten patients underwent retromastoid craniectomy with microvascular decompression for type 2 diabetes mellitus. Patients were followed for 12 months postoperatively by blood glucose monitoring and studies of glycemic control, pancreatic function and insulin metabolism. No changes in diet, weight or activity level were permitted during the course of the project.Results:Seven of the 10 patients who received microvascular decompression for type 2 diabetes mellitus showed significant improvement in their glucose control. This was noted by measurement of diabetes markers and decrease of diabetes medication dosages. One patient was completely off diabetes medication, while attaining euglucemia. The other 3 patients did not improve in their glucose control. The body mass index of these 3 patients was higher (mean, 34.4) than those with better outcomes (mean, 27.9).Conclusion:Arterial compression of the right anterolateral medulla appears to be a factor in the etiology of type 2 diabetes mellitus. Microvascular decompression may be an effective treatment for non-obese type 2 diabetes mellitus patients.
Highlights
Over the past 43 years, we have studied pulsatile vascular compression of the cranial nerves
We demonstrated that a number of hyperactive dysfunction syndromes were caused by vascular compression but that they could be relieved without loss of function by mobilizing the offending blood vessel or vessels away from the Surgical Neurology International 2010, 1:31 nerve.[1,2]
We studied the right anterolateral medulla oblongata for the presence of arterial compression in 15 consecutive patients operated upon for right-sided cranial nerve vascular compression syndromes
Summary
Over the past 43 years, we have studied pulsatile vascular compression of the cranial nerves. We demonstrated that a number of hyperactive dysfunction syndromes were caused by vascular compression but that they could be relieved without loss of function by mobilizing the offending blood vessel or vessels away from the Surgical Neurology International 2010, 1:31 nerve (microvascular decompression, MVD).[1,2] It is generally accepted in the international neurosurgical community that vascular cross-compression causes cranial nerve hyperactive syndromes These include, among others, trigeminal neuralgia, hemifacial spasm, vertigo and disequilibrium, Miniere’s disease, glossopharyngeal neuralgia and spasmodic torticollis.[2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18] In 1973 the first observations were made on essential hypertension, which proved to be a vascular compression syndrome of the left anterolateral medulla.[19] The vagus nerve is the only cranial nerve with an asymmetrical distribution. We hypothesize that decompressing the right cranial nerve X and medulla will result in better glycemic control in patients with type 2 diabetes mellitus
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