Pascal Vanelderen

Cervical radicular pain presents itself as pain radiating from the neck to the arm. If conservative treatment fails, a cervical epidural steroid injection can be considered. A rare but possible complication resulting from the interlaminar approach is unintentional cervical dural puncture that may result in post-dural puncture headache (PDPH). Dural puncture from an interlaminar cervical epidural injection reportedly range from 0.25% to 2.65%. An epidural blood patch is a possible treatment option when conservative treatment fails. Relief could be secondary to 'sealing' of the dural tear from the clotted blood and reestablishment of physiological intracranial pressure. Another theory is an increase in the subarachnoid pressure from the injected blood. The increased pressure may restore normal intracranial pressure. We describe 2 cases of cervical PDPH treated with lumbar epidural blood patch. In 1 case, there was complete resolution of the symptoms and in the other case, there was great improvement of symptoms and a high thoracic blood patch was performed to resolve the remaining headache.

Background In animal models of neuropathic pain (NP), promising results have been reported with the administration of minocycline, possibly through inhibition of spinal brain-derived neurotrophic factor (BDNF) expression. No data are available on the effect of amitriptyline and gabapentin on spinal BDNF expression. If the mechanism of action of the latter drugs does not involve brain-derived NP inhibition, further clinical research in BDNF is warranted. Methods In this placebo-controlled study, we investigated the effects of amitriptyline (5 mg/kg), gabapentin (50 mg/kg), and minocycline (25 mg/kg) twice a day on NP behavior in a sciatic chronic constriction injury (CCI) rat model. Drug treatment started 7 days after CCI and lasted 14 days. At postoperative day 21, spinal BDNF expression in laminae I and II was quantified using immunocytochemistry. Results Sciatic CCI resulted in NP behavior throughout the duration of the experiment in the placebo group. When administered for 2 weeks, minocycline (P ⩽ 0.001) and amitriptyline (P ⩽ 0.05), but not gabapentin, reduced thermal hyperalgesia. None of these drugs reduced mechanical allodynia. As opposed to amitriptyline and gabapentin, 2 weeks of treatment with minocycline reduced brain-derived, neurotrophic factor immunoreactivity (P ⩽ 0.05) in the ipsilateral dorsal horn. Conclusions Minocycline and amitriptyline both reduce NP behavior in a sciatic CCI rat model, but only minocycline reduces spinal BDNF, indicating different modes of action of these 2 drugs. The observed actions of minocycline closely fit the clinical needs for the treatment of NP.

The sacroiliac joint accounts for approximately 16% to 30% of cases of chronic mechanical low back pain. Pain originating in the sacroiliac joint is predominantly perceived in the gluteal region, although pain is often referred into the lower and upper lumbar region, groin, abdomen, and/ or lower limb(s). Because sacroiliac joint pain is difficult to distinguish from other forms of low back pain based on history, different provocative maneuvers have been advocated. Individually, they have weak predictive value, but combined batteries of tests can help ascertain a diagnosis. Radiological imaging is important to exclude “red flags” but contributes little in the diagnosis. Diagnostic blocks are the diagnostic gold standard but must be interpreted with caution, because false‐positive as well as false‐negative results occur frequently. Treatment of sacroiliac joint pain is best performed in the context of a multidisciplinary approach. Conservative treatments address the underlying causes (posture and gait disturbances) and consist of exercise therapy and manipulation. Intra‐articular sacroiliac joint infiltrations with local anesthetic and corticosteroids hold the highest evidence rating (1 B+). If the latter fail or produce only short‐term effects, cooled radiofrequency treatment of the lateral branches of S1 to S3 (S4) is recommended (2 B+) if available. When this procedure cannot be used, (pulsed) radiofrequency procedures targeted at L5 dorsal ramus and lateral branches of S1 to S3 may be considered (2 C+).

Even in present day pain therapy, neuropathic pain remains a challenge for clinicians to treat and a challenge for researchers to investigate. Different animal models have been developed to mimic neuropathic pain. Neurotrophins such as nerve growth factor, brain‐derived neurotrophic factor and neurotrophin 3 have been studied extensively in these models, yet few review articles concerning brain‐derived neurotrophic factor have been published. This article reassesses the literature concerning brain‐derived neurotrophic factor expression in the sciatic nerve chronic constriction injury model, the sciatic nerve transection model, the spinal nerve ligation model and the spinal nerve transection model and discusses differences in regulation of brain‐derived neurotrophic factor between these models and their causality with neuropathic pain.