The aim of this study was to investigate the postnatal development of mu-(MOR) and delta-opioid receptor (DOR) immunoreactivity in rat dorsal root ganglia. Lumbar dorsal root ganglia (DRG) from postnatal day (P) 0, 3, 7 and 21 rat pups were immunostained for MOR and DOR. Proportions of MOR +ve and DOR +ve cells were calculated from profile counts. Diameters of MOR +ve and DOR +ve cells were measured and compared to -ve cells. The coexpression of MOR and neurofilament (NF200) in DRG over this postnatal period was also investigated. A greater proportion of cells were immunoreactive for MOR and DOR in neonatal rat DRG at P0, P3 and P7 compared to P21. At P3, 39.5+/-1.7% of cells were MOR +ve and 30.3+/-1.5% were DOR +ve, whereas at P21, the values were 30.1+/-1.7% and 21.8+/-1.6% (mean+/-SEM), respectively. During the first postnatal week both opioid receptors were expressed in cells across the whole diameter range but by 3 weeks of age, expression was restricted to small and medium diameter cells. Furthermore, a significantly higher proportion of NF200 +ve cells expressed MOR in new-born compared to P21 rats. The results show that MOR and DOR expression is downregulated in the largest diameter, NF200 +ve primary sensory neurons postnatally. Since these neurons are mainly non-nociceptive, this may explain previous reports of opioid agonists affecting reflex responses to both innocuous and noxious stimuli in rat pups. The results highlight an important difference between opioid function in the immature and adult nervous system.

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Bacteraemia and septicaemia are generally thought to be relative or absolute contraindications for central neural axis (CNA) blocks. Postulated mechanisms for haematogenous infection of the central nervous system (CNS) caused by subarachnoid or epidural puncture might be an accidental vessel puncture, a change of pressure in the subarachnoid space, and the induction of a "locus minoris resistentiae." Infectious complications of diagnostic lumbar puncture, spinal or epidural anaesthesia are very rare. Although in animals meningitis can be induced by subarachnoid puncture during bactaeremia, there is no study that proves an increased risk for bacteraemic patients. Transient bacteraemia is common, especially in urological and obstetrical-gynecological procedures that are often done in regional anaesthesia, but the incidence of infectious complications is low. This review investigates the few published cases in which a haematogenous infection of the CNS may have been caused by regional anaesthesia. Based on current knowledge, bacteraemia cannot be an absolute, but only a relative contraindication for CNA blocks. Antibiotic chemoprophylaxis should be given before the puncture and the patients must be closely followed after the anaesthesia, particularly for the development of spinal epidural abscess. Because of the possibly increased risk of infectious complications, informed consent should be obtained from the patient.

Serious neurological complications caused by spinal hematoma or abscess following central neuraxial block have been reported more often during the last years. In contrast, severe complications are extremely rare associated with peripheral nerve blocks. Concerned about the safety of spinal and epidural anesthesia, we encourage the use of peripheral regional techniques for procedures on the lower extremity and especially for postoperative regional analgesia. Motor block due to lumbar epidural anaesthesia using high concentrations of local anesthetic makes spinal hematoma or abscess difficult to recognize. Therefore, low concentrations of local anesthetic should be used for postoperative epidural analgesia. Any increase in motor block following neuraxial blockade should raise the suspicion of a spinal compression (e.g. hematoma or abscess). Other symptoms are back pain, radicular pain or paresthesia and incontinence. Disastrous neurological injuries can only be prevented by immediate diagnosis (MR, CT or myelography) and therapy (surgical decompression).