title: Sympathetic neuropathy in diabetes mellitus patients does not elicit Charcot osteoarthropathy.
abstract: OBJECTIVE
  The aim of the study was to determine the degree of neuropathy (autonomic and somatic) in patients with diabetes mellitus with or without Charcot osteoarthropathy (CA).
  
  
  METHODS
  Forty-nine patients with diabetes mellitus type 1 or 2 were investigated. The patient population of interest was the patients with acute Charcot foot (n=17) or chronic Charcot foot (n=7). The inclusion criterion for an acute Charcot foot was a temperature difference of more than 2° between the two feet, oedema of the affected foot, typical hotspots in a bone scintigram and a typical clinical course. In addition, patients with first toe amputation (n=5), a high-risk group for development of CA, and two control groups consisting of diabetes patients with (n=9) or without somatic neuropathy (n=11) were investigated. Regional blood flow in the feet was measured by venous occlusion plethysmography. Quantitation of somatic neuropathy was done by the Neuropathy Disability Score and modified Neuropathy Symptom Score. Quantitation of autonomic neuropathy was done by measurements of local venoarteriolar sympathetic axon reflex in the feet and of heart rate variability during deep breathing and orthostatic challenge.
  
  
  RESULTS
  The patients with acute Charcot foot and first toe amputation had an increased blood flow in the affected foot and weakened but not absent venoarteriolar sympathetic axon reflex. In the other patient groups, a normal venoarteriolar sympathetic axon reflex in the feet was found.
  
  
  CONCLUSIONS
  Peripheral sympathetic neuropathy is not likely to be the pathophysiologic mechanism behind the hyperemia in the foot during an acute attack of CA. The hyperemia is more likely secondary to local inflammatory events.
authors.affiliation: Department Endocrinology and Gastroenterology I, Bispebjerg University Hospital, Denmark. tomas@dadlnet.dk
authors.forename: Tomas M
authors.initials: TM
authors.lastname: Christensen
authors.forename: Lene
authors.initials: L
authors.lastname: Simonsen
authors.forename: Per E
authors.initials: PE
authors.lastname: Holstein
authors.forename: Ole L
authors.initials: OL
authors.lastname: Svendsen
authors.forename: Jens
authors.initials: J
authors.lastname: Bülow
mesh_terms: D000368:Aged; D000671:Amputation, Surgical; D001177:Arthropathy, Neurogenic / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology / Q000601:surgery; D001341:Autonomic Nervous System / Q000276:immunology / Q000503:physiopathology; D017719:Diabetic Foot / Q000209:etiology; D003929:Diabetic Neuropathies / Q000276:immunology / Q000503:physiopathology*; D004487:Edema / Q000209:etiology; D005260:Female; D005528:Foot / Q000098:blood supply / Q000601:surgery; D006339:Heart Rate; D006801:Humans; D006940:Hyperemia / Q000209:etiology; D008297:Male; D008875:Middle Aged; D010991:Plethysmography; D012021:Reflex, Abnormal; D012039:Regional Blood Flow; D012720:Severity of Illness Index; D013564:Sympathetic Nervous System / Q000276:immunology / Q000503:physiopathology*; D014034:Toes / Q000601:surgery