Whiplash remains a challenging condition because the pathology is undefined. The purpose of this study was to evaluate the response of chronic neck, shoulder and arm pain to decompression of the median nerve at the wrist and pronator teres level. In a prospective study of 150 cases following whiplash injury (108 carpal tunnel and 42 pronator teres syndrome) clinical symptoms were assessed by clinical, neurological, radiological and visual analogue scale. The pathophysiology of pain and effects of surgery have also been assessed by neuropeptide studies. Clinical and neurological examination revealed signs and symptoms of carpal tunnel and pronator teres syndrome along with severe neck, shoulder and arm pain. Local anesthetic infiltration around the median nerve at the wrist and forearm abolished the chronic neck and shoulder pain within 10mins of injection. This demonstrated the site of pathology and temporarily relieved upper limb symptoms and trapezius muscle spasm as well. Neurophysiological studies were always normal. Surgical intervention in successful cases cured chronic neck shoulder and arm pain with sensory and motor recovery. Also activities of daily life normalised permanently. The main neurotransmitter peptides Substance P and Calcitonin gene related peptide levels returned to control levels six weeks after surgery in successful cases (p<
0. 005 and p<
0. 05 respectively). This is the biochemical evidence of effect of surgery in relieving pain and neuroinflammatory process. Our study suggests that neck shoulder and arm pain following whiplash injury is caused by entrapment of the median nerve due to stretching. Surgical decompression of the carpal tunnel and pronator teres muscle yielded 93% and 80% good results respectively with the disappearance of chronic neck shoulder and arm pain. Consequently normalisation of daily activities were observed. Although mild hand symptoms caused by carpal tunnel syndrome have also been cured the primary aim of surgical intervention is to cure chronic neck shoulder and arm pain.
To determine the effect of normal human ageing on neutrophil function and to assess the contribution that any decline may play in the increased susceptibility of elderly patients to bacterial infections following minor trauma. Furthermore, to determine any contribution, of trauma, to further neutrophil decline in these elderly patients. Phagocytic index, CD16 (FcγRIIIB) and CD11b (CR3) expression were determined in neutrophils isolated from the peripheral blood of 15 healthy young (average age 26. 5 yrs, range 23–35 yrs; 8 male, 7 female) and elderly (average age 72. 9 yrs, range 65–71 yrs; 8 male, 7 female) volunteers. CD11b levels were unaltered, but phagocytic index and CD16 expression were both significantly reduced (p<
0. 05 and p<
0. 001 respectively) in the elderly group. CD16 levels were monitored in a large volunteer group and were found to correlate with phagocytic index. To determine whether trauma produces additional compromise to neutrophil function in the elderly, peripheral blood neutrophils from individuals (average age 82. 5 yrs, range 65–96 yrs; 7 male, 21 female) during neutrophilia, post-trauma, due to fracture of the femur, were analysed as described above. Patients with chronic inflammatory disease, diabetes or kidney disease, or who were receiving steroid medication, were excluded. The data showed that neutrophil CD16 expression was significantly reduced in the elderly group (p<
0. 05), furthermore following fracture of the neck of femur superoxide generation is significantly reduced. Patient follow up revealed that 17 (60. 8 %) of these patients subsequently acquired bacterial infections (including wound), within 4 weeks of trauma. Normal human ageing was accompanied by a decline in neutrophil phagocytic ability and this may be in part due to reduced levels of the Fcγ receptor CD16. The reduced neutrophil CD16 expression accompanied by reduced superoxide generation in the elderly trauma patients may significantly undermine their ability to combat bacterial infections and contribute to increased incidence of post-traumatic infections in the elderly.
We investigated the response of chronic neck and shoulder pain to decompression of the carpal tunnel in 38 patients with whiplash injury. We also determined the plasma levels of substance P (SP) and calcitonin gene-related peptide (CGRP), which are inflammatory peptides that sensitise nociceptors. Compared with normal control subjects, the mean concentrations of SP (220 In spite of having neuropathic pain arising from the median nerve, all these patients had normal electromyographic and nerve-conduction studies. Chronic pain in whiplash injury may be caused by ‘atypical’ carpal tunnel syndrome and responds favourably to surgery which is indicated in patients with neck, shoulder and arm pain but not in those with mild symptoms in the hand. Previously, the presence of persistent neurological symptoms has been accepted as a sign of a poor outcome after a whiplash injury, but our study suggests that it may be possible to treat chronic pain by carpal tunnel decompression.