title: Chronic ischemic monomelic neuropathy from critical limb ischemia.
abstract: OBJECTIVE
  To describe the peripheral neuropathy resulting from chronic and critical arterial leg ischemia.
  
  
  METHODS
  The authors evaluated 19 patients on entry to a gene therapy treatment trial for chronic and critical leg ischemia. Measurements included medical history, examination, neurologic symptom (NSS) and neurologic examination (NES) scores, motor and sensory nerve conduction studies, and quantitative sensory testing. The critically ischemic leg was compared with the less affected contralateral limb.
  
  
  RESULTS
  All patients experienced pain from skin ulceration or vascular claudication, but many also had rest pain (58%), numbness (58%), burning (42%), and paresthesias (37%) in the ischemic foot that were consistent with peripheral nerve ischemia. Only three patients (16%) were free of neuropathic symptoms. The most common asymmetric neurologic signs included hypalgesia (74%), toe weakness (64%), hyperesthesia (63%), and pallanesthesia (53%) in the distal leg. NSS and NES were more abnormal in the critically ischemic leg, as were distal motor, total motor, and sensory examination subscores (p < 0.01 for each). Sural sensory potentials were reduced or absent, frequently on both sides. The symptomatic limb had reduced tibial motor amplitudes and increased thermal (cold) sensory thresholds (p < 0.01 for both) whereas the distal latencies, conduction velocities, and vibration thresholds were similar in the two legs.
  
  
  CONCLUSIONS
  There is a predominantly sensory neuropathy associated with chronic and critical limb ischemia. Neuropathic symptoms are often obscured by the effects of ischemia on other tissues. The neurophysiologic changes suggest that the underlying pathophysiology is a distal axonopathy affecting nerve fibers of all sizes. Measures of blood flow in the leg correlate with neurologic symptom scores, examination scores, and electrophysiologic testing.
authors.affiliation: Department of Neurology, Tufts University School of Medicine, St. Elizabeth's Medical Center, Boston, MA 02135, USA. David.Weinberg.MD@cchcs.org
authors.forename: D H
authors.initials: DH
authors.lastname: Weinberg
authors.forename: D
authors.initials: D
authors.lastname: Simovic
authors.forename: J
authors.initials: J
authors.lastname: Isner
authors.forename: A H
authors.initials: AH
authors.lastname: Ropper
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002908:Chronic Disease; D004568:Electrodiagnosis; D005260:Female; D007839:Functional Laterality / Q000502:physiology*; D015316:Genetic Therapy; D006801:Humans; D007383:Intermittent Claudication / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D007511:Ischemia / Q000175:diagnosis / Q000503:physiopathology* / Q000628:therapy; D007866:Leg / Q000098:blood supply*; D008297:Male; D008875:Middle Aged; D009460:Neurologic Examination; D010523:Peripheral Nervous System Diseases / Q000175:diagnosis / Q000503:physiopathology* / Q000628:therapy; D012684:Sensory Thresholds / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology