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Treatment of Nonsuicidal Self-Injury in Adolescents
10 CEUs Physical Pain Stops my Pain - Treating Teen Self Mutilation

Section 20
Neurological Disorders that Increase Self-Injurious Behavior

Question 20 | Test | Table of Contents | Self-Mutilation CEU Courses
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It has been known for some time that self-injury occurs in association with congenital sensory neuropathies and insensitivity to pain (Critchley, 1934; Kirman & Bicknell, 1968; Pinsky & Digeorge, 1966), and more recently it is recognized in acquired sensory neuropathies (Roach, Abramson, & Lawless, 1985; Swoboda, Engle, Scheindlin, Anthony, & Jones, 1998) and Tourette's syndrome (Robertson, Trimble, & Lees, 1989), Self-injury among people with neurological disorders tends to be directed toward the distal extremities (Swoboda et al., 1998), but reports also include head-directed and oral or facial SIB, as well as mutilation of the tongue and mouth (Rasmussen, 1996). Overall, the forms of self-injury seem best characterized by localized biting, scratching, and rubbing rather than nonspecific banging, hitting, or slapping (Zammarchi, Savelli, Donati, & Pasquini, 1994). Swoboda et al. reported a case of a typically developing 7-year-old boy self-mutilating the digits of his hand. Electromyogram evidence showed severe median nerve entrapment, and clinical evaluation suggested pain insensitivity in the hand region. In cases of SIB associated with acquired neuropathies, the onset is usually rapid with no prior history of self-injury or related repetitive movement disorder. Roach, Abramson, and Lawless (1985) documented the onset of SIB within days following acute trauma for two typically developing children with acquired peripheral neuropathies. Most clinical reports characterize the SIB associated with neurological dysfunction as intense and almost always associated with significant tissue damage (Mailis, 1996). Prevalence estimates of SIB associated with neurological disorders are unknown. Cases of self-injury co-occurring with documented neurological impairment in typically developing children and intellectually normal adults suggest that self-injury may be regulated by pathological pain mechanisms associated with neurological dysfunction of either central or peripheral origin.

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.

It 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.
- Schroeder, Stephen, Oster-Granite, Mary, & Travis Thompson, Self-Injurious Behavior, American Psychological Association: Washington DC, 2002.

Personal Reflection Exercise #6
The preceding section contained information about neurological disorders that increase self-injurious behavior. Write three case study examples regarding how you might use the content of this section in your practice.

According to Coderre and Meizack, what did procedures that increased pain sensitivity in rats also increase? Record the letter of the correct answer the Test.

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