Pain
-
Clinical Trial
Neurophysiological assessment of spinal cord stimulation in failed back surgery syndrome.
Despite good clinical results, the mechanisms of action of spinal cord stimulation (SCS) for the treatment of chronic refractory neuropathic pain have not yet been elucidated. In the present study, the effects of SCS were assessed on various neurophysiological parameters in a series of 20 patients, successfully treated by SCS for mostly unilateral, drug-resistant lower limb pain due to failed back surgery syndrome. Plantar sympathetic skin response (SSR), F-wave and somatosensory-evoked potentials (P40-SEP) to tibial nerve stimulation, H-reflex of soleus muscle, and nociceptive flexion (RIII) reflex to sural nerve stimulation were recorded at the painful lower limb. ⋯ Analgesia induced by SCS mainly correlated with RIII attenuation, supporting a real analgesic efficacy of the procedure. This study showed that SCS is able to inhibit both nociceptive (RIII-reflex) and non-nociceptive (P40-SEP, H-reflex) myelinated sensory afferents at segmental spinal or supraspinal level, and to increase cholinergic sympathetic skin activities (SSR facilitation). Complex modulating effects can be produced by SCS on various neural circuits, including a broad inhibition of both noxious and innocuous sensory information processing.
-
Neuropathic pain is accompanied by both positive and negative sensory signs. To explore the spectrum of sensory abnormalities, 1236 patients with a clinical diagnosis of neuropathic pain were assessed by quantitative sensory testing (QST) following the protocol of DFNS (German Research Network on Neuropathic Pain), using both thermal and mechanical nociceptive as well as non-nociceptive stimuli. Data distributions showed a systematic shift to hyperalgesia for nociceptive, and to hypoesthesia for non-nociceptive parameters. ⋯ The most frequent combinations of gain and loss were mixed thermal/mechanical loss without hyperalgesia (central pain and polyneuropathy), mixed loss with mechanical hyperalgesia in peripheral neuropathies, mechanical hyperalgesia without any loss in trigeminal neuralgia. Thus, somatosensory profiles with different combinations of loss and gain are shared across the major neuropathic pain syndromes. The characterization of underlying mechanisms will be needed to make a mechanism-based classification feasible.
-
We aimed to study the quality of communication between health care providers and patients with low back pain with emphasis on information giving in a back pain clinic, including if characteristics of patients could be associated with communication quality. We videotaped 79 encounters in which 21 providers informed patients about the results of magnetic resonance imaging of the back. Background information about the patients was collected by questionnaires and interview after the encounter. ⋯ The results were significant for all professional subgroups (doctors, physiotherapists, chiropractors). Communication quality in encounters with back pain patients is worse, the longer the patient has suffered pain. Poor communication quality also seems to be associated with patients being older.
-
Widespread sensory hypersensitivity is present in acute whiplash and is associated with poor recovery. Decreased nociceptive flexion reflex (NFR) thresholds (spinal cord hyperexcitability) are a feature of chronic whiplash but have not been investigated in the acute to chronic injury stage. This study compared the temporal development of sensory hypersensitivity and NFR responses from soon after injury to either recovery or to transition to chronicity. ⋯ In contrast generalized sensory hypersensitivity (pressure and cold) was only ever present in those with persistent moderate/severe symptoms and remained unchanged throughout the study period. This suggests different mechanisms underlie sensory hypersensitivity and NFR responses. In multivariate analyses only initial NDI scores (p=0.003) were a unique predictor of persistent spinal cord hyperexcitability indicating possible ongoing peripheral nociception following whiplash injury.