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Evidence for the relation between neurological dysfunction and chronic neuropathic pain associated with self-mutilation comes from experimental laboratory studies with animals and clinical reports from humans experiencing pain disorders. Rats typically engage in self-mutilation of a paw that has been enervated following transection of the sciatic and saphenous nerves (Coderre & Melzack, 1986). In nonhuman primates, experimental injury of the peripheral or central nervous system (CNS) leads to targeted SIB, producing various degrees of tissue damage from excoriations to mutilation and self-cannibalism of the enervated limb (autonomy; Mailis, 1996). Temporal-lobe and spinal cord lesions in macaques (bilateral dorsal rhizotomy) result in self-injury (Busbaur, 1974; Sweet, 1981), as do sectioning of the sciatic nerve and the lateral funiculus (Harris, 1995; Jones & Barraclough, 1978). In humans, self-injury has been reported in association with brachial plexus avulsions (Procacci & Maresca, 1990), alcohol injection into the gasserian ganglion (Schorstein, 1943), and following complete spinal cord injury (Dahlin, Van Buskirk, Novotny, Hollis, & George, 1985). Furthermore, there are clinical examples of intellectually normal individuals engaging in SIB related to neuropathic pain, targeting body sites characterized by thermoalgesia, allodynia, or hyperalgesia (Mailis, 1996).
Although various models accounting for self-injury associated with neurological dysfunction have been proposed, the specific mechanism related to SIB and pain transmission and regulation are less clear and not universally accepted. In some cases with congenital or acquired sensory disturbances, self-injury is considered a pain response to relieve the dysesthesia (i.e., abnormal sensations) commonly accompanying the disorder. In some people, dysesthesia is associated with pain. In this model, intense rubbing, biting, scratching, or otherwise targeting the affected area reduces the discomfort associated with the underlying peripheral nerve dysfunction. This model is consistent with reports of SIB that is localized and patient reports of burning and itching of the extremities toward which they direct their self-injury. In other people, self-injury is considered a "side effect" of injury in a system that is characterized by diminished pain perception or complete anesthesia; therefore, the individual has no biological reason to avoid noxious stimuli.
is unclear whether self-mutilation related to nerve damage or dysfunction is regulated by dysesthesia associated with pain or regulated by anesthesia associated
with the absence of sensation. Coderre and Meizack (1986) showed that procedures
that increase pain sensitivity also increase self-injury in rats, suggesting that
self-injury in such cases was primarily a sensory phenomenon related to painful
dysesthesia. The underlying mechanisms regulating this effect are not certain,
but controlled studies suggest that the enhancement of self-mutilation in rats
is not related to stress or a general increase in excitability. Rather, the self-mutilation
is associated with an initial injury related to an increase in neural activity
resulting in peripheral and central sensitization sustained for prolonged periods
(Coderre & Meizack, 1986). In the human model, although the mechanism regulating
self-injury related to chronic pain is unknown, Mailis (1996) concluded that the
painful dysesthesia arising from peripheral or central somatosensory system lesions
in the presence of idiosyncratic personality, neural, humoral, and environmental
factors seem to release or facilitate the expression of SIB targeted to the painful
body part. Because most of the evidence is based on collections of case reports,
no studies have examined systematically the way unique intraindividual and contextual
variables set the occasion for the expression of SIB. To date, the limited treatment
data suggest that reducing pain leads to corresponding decreases of painful dysesthesia
and termination of SIB in individuals with identified neurological disorders.
Reflection Exercise #6
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