The refined NeuroDigm GEL™ Model of persistent neuropathic pain ... a
soft tissue matrix model
Gradually, through biogenesis, a change in the matrix microenviornment of a nerve at the site causes the pain behaviors of neural persistent pain. The ONLY persistent neural pain model without nerve damage lasting over 6 months and longer. This model demonstrates that tissue repair may induce changes resulting in pain behavior.
▪ a model representing the "pain generator" or "ectopic focus" theory of perisitent neural pain etiology
▪ uses biocompatible
collagen gel or hydrogels percutaneously; can be performed on any peripheral
nerve, autonomic nerve or spinal nerve root: data on L4-L5 Spinal nerves,
Sciatic Nerve; Saphenous, Peroneal and Posterior Tibial
▪ uses no irritant or trauma for initiation of "neuritis"
▪ no cutting of skin, bones, nerves or ligation of nerves
▪ able to walk normally after procedure - no limping
▪ no acute pain behaviors after injection of gel
▪ gradual onset of pain behavior over 7 - 21 days
▪ in young rats (250-300 grams) Has cold allodynia, static and dynamic mechanical allodynia; and mechanical hyperalgesia; no heat allodynia (human patients use heating pads frequently)
▪ prolonged pain behaviors more than 6 months
▪ No autotomy of paws
▪ microscopy shows immune cells at site tisuue and nerve remodeling with Wallerian degeneration and Regeneration... similar to human nerve biopsies
Compared to other neuropathic
▪ more sensitive to gabapentin (25 mg/kg) (over 90 days)
▪ less sensitive to morphine; no analgesic repsonse at 3 mg/kg (over 60 days)
▪ easily created in MICE
▪ easy to learn percutaneous procedure
▪ high reliability of procedure > 95% or more
▪ less numbers of animals needed (n=6 in mice by power analysis)
▪ greater validity of drug testing; months of comparative research on the same subjects possible
▪ Creates a "window" over time to enable the defining of the initiation and maintenance of neural pain ... or neurogenic inflammation
The model demonstrates the sequelae of tissue repair that naturally happens after an injury, which can cause an ectopic neural focus, neuritis, persistent pain or Complex Regional Pain Syndrome I. This model demonstrates the initiation of neurogenic pain behavior without direct trauma or an acute immune activation. A small change in the perineural matrix can cause sequelae resulting in pressures that alter axonal flow resulting in a localized ”lesion” or dysfunction of the somatosensory tissues, known as neuropathic pain.
Histology shows at 5 months a localized lesion with neural edema, neural remodeling with Wallerian degeneration and evidence of neural regeneration, with an increase in smaller axons.
Extensive nerve axonal damage is found in the Spinal Nerve Injury L5-L6 ligation model and the Chronic Constriction Injury (CCI) ligation model ... such damage is not present in the NeuroDigm GEL Model and also not in CRPS I, and not in the majority of patients with neuropathic pain. This refined nonsurgical GEL Model is representative of neural regeneration rather than cell death.
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