Literature DB >> 12589923

Pain and rehabilitation after spinal cord injury: the case of sensory spasticity?

Bengt H Sjölund1.   

Abstract

Sixty percent of patients with posttraumatic para- or tetraplegia suffer from severe, continuous burning and/or lancinating pain. Multiple sclerosis produces pain in more than 30%. This pain can be as important as the absent mobility or sexual function as a cause of lowered quality of life. Two unique types of longstanding neuropathic pain can be recognized in persons with spinal cord injury: (1). segmentally distributed pain at the lesion; and (2). pain in the body below the lesion, often with late onset. The first type could be produced by nerve root entrapment or by direct segmental deafferentation. The second type probably contains several forms of central pain, evoked either by the original spinal lesion, by an expanding syrinx in the spinal cord or by secondary changes at higher levels of the somatosensory systems. Patients with central pain almost always have stimulus-independent pain. Its intensity may vary independently, be related to the presence of visceral activity/inflammation or be constant. In addition, stimulus-dependent pain is sometimes present, usually because skin areas or viscera below the lesion are allodynic. Partial spinal lesions, especially centrally in the cervical spinal cord, may be more prone to produce pain than are complete lesions. There is limited analgesic effectiveness in controlled studies of serotonin reuptake inhibitors, of sodium channel blockers (lidocaine, tetracaine), of the GABA receptor agonist baclofen (one study) and of the NMDA-receptor antagonist ketamine (one study). There are anecdotal reports on oral carbamazepine, on gabapentin, on intrathecal opiates and also on the alpha(2)-agonist clonidine, being effective in central neuropathic pain. Neurostimulation is effective only if it evokes paraesthesia in the painful area; hence TENS may give relief of segmental pain. Neurodestructive procedures and central neurostimulation have been largely unsuccessful. As in other longstanding pain, improved coping through cognitive-behavioural rehabilitation may be helpful for the clinical outcome.

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Mesh:

Year:  2002        PMID: 12589923     DOI: 10.1016/s0165-0173(02)00207-2

Source DB:  PubMed          Journal:  Brain Res Brain Res Rev


  20 in total

Review 1.  Spinal Cord Stimulation for Pain Treatment After Spinal Cord Injury.

Authors:  Qian Huang; Wanru Duan; Eellan Sivanesan; Shuguang Liu; Fei Yang; Zhiyong Chen; Neil C Ford; Xueming Chen; Yun Guan
Journal:  Neurosci Bull       Date:  2018-12-17       Impact factor: 5.203

2.  Efficacy and safety of higher doses of botulinum toxin type A NT 201 free from complexing proteins in the upper and lower limb spasticity after stroke.

Authors:  Andrea Santamato; Francesco Panza; Maurizio Ranieri; Vincenza Frisardi; Maria Francesca Micello; Serena Filoni; Francesca Fortunato; Domenico Intiso; Mario Basciani; Giancarlo Logroscino; Pietro Fiore
Journal:  J Neural Transm (Vienna)       Date:  2012-09-07       Impact factor: 3.575

Review 3.  Review of Treatment for Central Spinal Neuropathic Pain and Its Effect on Quality of Life: Implications for Neuromyelitis Optica Spectrum Disorder.

Authors:  Maureen A Mealy; Sharon L Kozachik; Michael Levy
Journal:  Pain Manag Nurs       Date:  2019-05-15       Impact factor: 1.929

Review 4.  Neuropathic pain and spasticity: intricate consequences of spinal cord injury.

Authors:  N B Finnerup
Journal:  Spinal Cord       Date:  2017-07-11       Impact factor: 2.772

5.  Extensor spasms triggered by imposed knee extension in chronic human spinal cord injury.

Authors:  Ming Wu; T George Hornby; Jennifer Hilb; Brian D Schmit
Journal:  Exp Brain Res       Date:  2004-12-07       Impact factor: 1.972

6.  Hip proprioceptors preferentially modulate reflexes of the leg in human spinal cord injury.

Authors:  Tanya Onushko; Allison Hyngstrom; Brian D Schmit
Journal:  J Neurophysiol       Date:  2013-04-24       Impact factor: 2.714

7.  Flexor reflex decreases during sympathetic stimulation in chronic human spinal cord injury.

Authors:  M Kevin Garrison; Brian D Schmit
Journal:  Exp Neurol       Date:  2009-07-15       Impact factor: 5.330

8.  Gliopathy ensures persistent inflammation and chronic pain after spinal cord injury.

Authors:  Claire E Hulsebosch
Journal:  Exp Neurol       Date:  2008-07-29       Impact factor: 5.330

Review 9.  Current management of pain associated with multiple sclerosis.

Authors:  Walter Pöllmann; Wolfgang Feneberg
Journal:  CNS Drugs       Date:  2008       Impact factor: 5.749

10.  Peripheral and central sensitization in remote spinal cord regions contribute to central neuropathic pain after spinal cord injury.

Authors:  Susan M Carlton; Junhui Du; Huai Yu Tan; Olivera Nesic; Gregory L Hargett; Anne C Bopp; Ammar Yamani; Qing Lin; William D Willis; Claire E Hulsebosch
Journal:  Pain       Date:  2009-10-22       Impact factor: 6.961

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