Self-injurious behavior in neurodevelopmental disorders: Relevance of nociceptive and immune mechanisms

Frank J. Symons

doi:10.1016/j.neubiorev.2011.01.002

Self-injurious behavior in neurodevelopmental disorders: Relevance of nociceptive and immune mechanisms

Frank J. Symons

Administration (CEHD)

Research output: Contribution to journal › Review article › peer-review

41 Scopus citations

Abstract

Self-injurious behavior (SIB) among individuals with intellectual and related neurodevelopmental disorders (IDD) is a clinical challenge and scientific puzzle. The physiological mechanisms regulating the sensory components of SIB remain a mystery with no clear understanding of the underlying pathophysiology. The central dogma regarding sensory processing in general and pain in particular among individuals with IDD and chronic SIB is that sensory processing is reduced and pain is absent or blunted. In this paper, recent findings challenging some of the conventional wisdom regarding pain and sensory function among individuals with IDD and SIB are reviewed. It seems that at least a subgroup of individuals with IDD and chronic SIB may be in a physiological state similar to neuropathic pain in which hyperalgesia is mediated by plasticity mechanisms regulating inflammatory, immune, and nociceptive systems. In response to repeated tissue damage associated with chronic self-injury, innate immune cells may be producing pro-inflammatory and pro-nociceptive cytokines that act on the brain to cause sickness-like behavior and sensitize primary sensory nerve afferents contributing to pain hypersensitivity (i.e., hyperalgesia).

Original language	English (US)
Pages (from-to)	1266-1274
Number of pages	9
Journal	Neuroscience and Biobehavioral Reviews
Volume	35
Issue number	5
DOIs	https://doi.org/10.1016/j.neubiorev.2011.01.002
State	Published - Apr 2011

Bibliographical note

Funding Information:
Funding for this work was provided, in part, by the University of Minnesota in the form of a McKnight Land-Grant Professorship and Minnesota Futures award as well as NICHD Grant Nos. 44763 and 47201; the NICHD had no further role in the work; in the collection, analysis and interpretation of data appearing herein; in the writing of the report; and in the decision to submit the paper for publication. Thanks to Kirstin Koppen for her diligance and patience with figure preparation. I am grateful to the insightful comments tirelessly provided by Jim Bodfish on this line of thinking, the constructive critiques of Jennifer McComas and John Hoch, as well as more recent conversations with Lois Kehl, Alice Larson, Gwen Wendelschafer-Crabb, Bill Kennedy, and George Wilcox.

Keywords

Developmental disorder
Immune
Pain
Self-injury

Publisher link

10.1016/j.neubiorev.2011.01.002

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title = "Self-injurious behavior in neurodevelopmental disorders: Relevance of nociceptive and immune mechanisms",

abstract = "Self-injurious behavior (SIB) among individuals with intellectual and related neurodevelopmental disorders (IDD) is a clinical challenge and scientific puzzle. The physiological mechanisms regulating the sensory components of SIB remain a mystery with no clear understanding of the underlying pathophysiology. The central dogma regarding sensory processing in general and pain in particular among individuals with IDD and chronic SIB is that sensory processing is reduced and pain is absent or blunted. In this paper, recent findings challenging some of the conventional wisdom regarding pain and sensory function among individuals with IDD and SIB are reviewed. It seems that at least a subgroup of individuals with IDD and chronic SIB may be in a physiological state similar to neuropathic pain in which hyperalgesia is mediated by plasticity mechanisms regulating inflammatory, immune, and nociceptive systems. In response to repeated tissue damage associated with chronic self-injury, innate immune cells may be producing pro-inflammatory and pro-nociceptive cytokines that act on the brain to cause sickness-like behavior and sensitize primary sensory nerve afferents contributing to pain hypersensitivity (i.e., hyperalgesia).",

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note = "Funding Information: Funding for this work was provided, in part, by the University of Minnesota in the form of a McKnight Land-Grant Professorship and Minnesota Futures award as well as NICHD Grant Nos. 44763 and 47201; the NICHD had no further role in the work; in the collection, analysis and interpretation of data appearing herein; in the writing of the report; and in the decision to submit the paper for publication. Thanks to Kirstin Koppen for her diligance and patience with figure preparation. I am grateful to the insightful comments tirelessly provided by Jim Bodfish on this line of thinking, the constructive critiques of Jennifer McComas and John Hoch, as well as more recent conversations with Lois Kehl, Alice Larson, Gwen Wendelschafer-Crabb, Bill Kennedy, and George Wilcox.",

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AB - Self-injurious behavior (SIB) among individuals with intellectual and related neurodevelopmental disorders (IDD) is a clinical challenge and scientific puzzle. The physiological mechanisms regulating the sensory components of SIB remain a mystery with no clear understanding of the underlying pathophysiology. The central dogma regarding sensory processing in general and pain in particular among individuals with IDD and chronic SIB is that sensory processing is reduced and pain is absent or blunted. In this paper, recent findings challenging some of the conventional wisdom regarding pain and sensory function among individuals with IDD and SIB are reviewed. It seems that at least a subgroup of individuals with IDD and chronic SIB may be in a physiological state similar to neuropathic pain in which hyperalgesia is mediated by plasticity mechanisms regulating inflammatory, immune, and nociceptive systems. In response to repeated tissue damage associated with chronic self-injury, innate immune cells may be producing pro-inflammatory and pro-nociceptive cytokines that act on the brain to cause sickness-like behavior and sensitize primary sensory nerve afferents contributing to pain hypersensitivity (i.e., hyperalgesia).

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Self-injurious behavior in neurodevelopmental disorders: Relevance of nociceptive and immune mechanisms

Abstract

Bibliographical note

Keywords

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