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PubMed2002

Epidural cooling for the prevention of ischemic injury to the spinal cord during aortic occlusion in a rabbit model: determination of the optimal temperature.

PURPOSE: This experiment was designed for the determination of the optimal epidural cooling temperature for the allowance of spinal cord protection with minimal side effects during an aortic occlusion-induced spinal cord ischemia model in rabbits. METHODS: Spinal cord ischemia was induced in rabbits with infrarenal aortic occlusion for 40 minutes. Spinal cord cooling was effected with epidural infusion of normal saline solution at the following different temperatures: group 1, 17 degrees C (n = 6); group 2, 24 degrees C (n = 6); group 3, 32 degrees C (n = 6); and group 4, 39 degrees C (n = 3). Sham-operated rabbits without aortic occlusion were used as controls with epidural infusion at healthy body temperature (39 degrees C; n = 3). Motor function was assessed at 48 hours with Tarlov's criteria, and the animals were killed. The spinal cord was sectioned into multiple segments, and semiquantitative histologic scoring (0 to 5) was used to grade ischemic injury. RESULTS: Cooling solution and spinal cord temperatures showed linear correlation (r = 0.95). All the rabbits in groups 1 (except one with mild weakness), 2, and 3 were neurologically intact, and all in group 4 had paraplegia develop (P < .001). One rabbit in group 1 died from increased intracranial pressure (ICP). Mean blood pressure, ICP, and body temperature were similar among the groups. Histology correlated with the clinical findings. In groups 1 and 2, minimal histologic changes were noted. Low-grade ischemic changes were present in group 3 in the low-lumbar and mid-lumbar segments. Severe ischemic injury occurred at the same segments in group 4 (P < .05). CONCLUSION: These study results suggest that in rabbits satisfactory spinal cord protection during aortic occlusion can be achieved at moderate regional hypothermia (24 degrees C). Large volume infusion for the achievement of profound hypothermia may cause deleterious effects of increased ICP and is not warranted.

Animals↗
PubMed1995

Quinolinic acid accumulation and functional deficits following experimental spinal cord injury.

Quinolinic acid (QUIN) is an excitotoxic tryptophan metabolite that is produced by activated macrophages. Accumulations of QUIN are implicated in the aetiology of a broad spectrum of human neurological diseases, particularly inflammatory conditions. To determine whether QUIN is an endogenous neurotoxin requires agents that reduce QUIN synthesis, and animal models where QUIN levels increase in association with neurological disease. Compression injury of the spinal cord of guinea pigs results in secondary neurological deficits, related to inflammation and macrophage activation. We evaluated whether 4-chloro-3-hydroxyanthranilate (4Cl-3HAA), an inhibitor of 3-hydroxyanthranilate-3,4-dioxygenase, reduces QUIN accumulations in this model and influences the progression of neurological deficits. Intraperitoneal injections of 4Cl-3HAA (100 mg/kg every 12 h) attenuated QUIN accumulations in spinal cord following injury, and reduced the severity of delayed functional deficits. Intraperitoneal injections of the macrophage toxin, silica, also reduced QUIN levels and attenuated neurological deficits. A direct subdural infusion of Cl-3HAA into the injured spinal cord (50 microM, 1 microliter/h) promptly exacerbated functional impairments, which suggests that the infusate had direct toxic effects. These studies demonstrate that guinea pigs with spinal cord injury constitute a useful model to study the mechanisms that increase central nervous system (CNS) QUIN levels in conditions of CNS inflammation, and to evaluate the neurochemical and neurological effects of agents designed to reduce the accumulations of QUIN and other potential pathogenic mediators within the CNS. The results are consistent with a contributory role for QUIN in the pathogenesis of secondary functional impairments following spinal cord injury, although the possibility that 4Cl-3HAA had additional effects independent of QUIN cannot be excluded. Further studies are required to determine whether the beneficial effects of 4Cl-3HAA are sustained. While it is unknown whether secondary inflammatory processes contribute significantly to neurological deficits in human spinal cord injury, strategies that reduce the accumulation of QUIN are worthy of consideration and evaluation as a therapeutic target.

3-Hydroxyanthranilate 3,4-Dioxygenase↗
PubMed1993

Capsaicin inhibits whereas rhizotomy potentiates substance P-induced release of excitatory amino acids in the rat spinal cord in vivo.

The origin of the excitatory amino acids (EAA) aspartate (Asp) and glutamate (Glu) released into the dorsal spinal cord extracellular fluid of rats following intradialysate infusion of substance P (SP) was studied using neonatal capsaicin, dorsal rhizotomy and proximal spinal cord transection. Neonatal capsaicin (50 mg/kg i.p.) had no effect on basal EAA release, but significantly inhibited SP-induced release of both Asp (86%) and Glu (70%). Bilateral dorsal rhizotomy enhanced SP-induced release of Asp (152%) and had no effect on Glu release compared to sham-operated controls. Proximal spinal transection (T8-9) had no effect on basal or SP-induced release of EAAs compared to sham-operated controls. The ability of neonatal capsaicin to inhibit, and dorsal rhizotomy to potentiate Asp release correlates well with their distinct effects on hyperalgesia and suggests that these manipulations do not produce identical lesions. Neonatal capsaicin likely interferes with the normal development of EAA interneurons innervated by SP primary afferent C-fibers. Rhizotomy may result in a compensatory up-regulation of SP receptors on EAA interneurons.

Animals↗
PubMedDate not supplied

Cerebrospinal and plasma amino acid concentrations after administration of i.v. glycyl-glutamine and glycyl-tyrosine containing amino acid solutions in humans.

BACKGROUND: Glycyl-glutamine and glycyl-tyrosine may supply adequate glutamine and tyrosine in amino acid solutions for parenteral nutrition. However, plasma peptides may be transported into the cerebrospinal fluid, exerting effects on the neuronal tissue. Cerebrospinal fluid (CSF) and plasma amino acid concentrations after administration of a glycyl-glutamine/glycyltyrosine supplemented amino acid solution were therefore evaluated in a randomized controlled comparison with a conventional amino acid infusion. METHODS: Dipeptide/amino acid solutions (0.60 mL/h/kg; 82.2 mg total dipeptides/amino acids/h/kg) or conventional amino acid solutions (0.73 mL/h/kg; 83.2 mg total amino acids/h/kg) were infused in 15 patients per group scheduled to undergo spinal anesthesia for urologic surgery over a 12-hour period preoperatively. Plasma amino acids were measured before the infusion was started. CSF and venous concentrations were analyzed simultaneously before the infusion was stopped. CSF samples were drawn through the spinal needle for anesthesia. RESULTS: The dipeptide-containing solution did not increase either dipeptide to detectable levels in the CSF (detection limit < 5.0 nmol/mL). Venous glycyl-glutamine increased from below detection limits up to 308 +/- 111 nmol/mL (p < .05), whereas glycyl-tyrosine could not be found. In the dipeptide group, venous glutamine and tyrosine were higher (p < .05) but only tyrosine appeared in small amounts (p < .05) in the cerebrospinal fluid. CONCLUSIONS: This study provides no evidence to support a CSF entry of IV glycyl-tyrosine and glycyl-glutamine under conditions of a normal blood-brain barrier in the adult (detection limit 5 nmol/mL). The data suggest that amino acid solutions containing these dipeptides may be used in parenteral solutions for nutrition support.

Aged↗
PubMed1994

Modulation of substance P-ergic system in the rat spinal cord by an opioid antagonist.

Substance P- and opioid peptide-immunoreactive nerve terminals functionally interact in the spinal cord as two opposing systems in the regulation of the nociceptive pathway. In order to determine how SP-ergic system adapts to chronic opioid receptor blockade, the effects of naltrexone on SP level, SP receptor and the second messenger system coupled to the SP receptor were examined in the rat spinal cord. Male Sprague-Dawley rats were treated with naltrexone or vehicle for seven days by constant minipump infusion. Animals were sacrificed on day 8, spinal cords rapidly removed, segmentally sectioned and used to determine SP and inositol 1,4,5-trisphosphate [ins(1,4,5)P3] tissue contents, and to examine the regulation of their respective receptors in in vitro receptor binding assays. Following chronic naltrexone treatment, SP content in the lumbosacral segment of the spinal cord was increased by 53% over matched control values. The binding capacity (Bmax) of SP receptors, determined using [125I]BHSP, in lumbosacral synaptosomal membranes was significantly increased by 92%, but the binding affinity (Kd) remained unchanged. In addition, the concentration of [Sar9, Met(O2)11]SP, an NK-1 receptor-specific agonist, required to inhibit half of [125I]BHSP binding (IC50) in lumbosacral synaptosomal membranes was significantly decreased, but the IC50s for SP, the endogenous ligand for the SP receptor, and [Pro7]NK B, an NK-3 receptor-specific agonist, were unaltered by chronic blockade of opioid receptors. The data suggest that although naltrexone does not directly interact with tachykinin receptors, it acts indirectly on SP-ergic neurons to cause a change in the apparent affinity of NK-1 receptor (as reflected by a change in IC50 value). Formation of cellular ins(1,4,5)P3 in the lumbosacral cord, quantified by a highly sensitive and selective radioreceptor assay, was significantly increased by 34% relative to matched controls. A time course study indicated that increases in ins(1,4,5)P3 contents over the time studied corresponded qualitatively with increases in SP level in the lumbosacral cord. With [3H]ins(1,4,5)P3 as a ligand, Scatchard analyses of the concentration dependent saturation curves showed that the density of intracellular ins(1,4,5)P3 receptors was also increased by 119%, with no change in binding affinity. The data suggest that ins(1,4,5)P3 formation, possibly coupled to functional SP receptor activation, and ins(1,4,5)P3 receptors, which mediate ins(1,4,5)P3-induced alterations in intracellular Ca2+ flux, are increased in the lumbosacral cord by chronic blockade of opioid receptors. Taken together, the data support the concept of a role for endogenous opioids in the regulation of SP receptor activity in the spinal cord.

Animals↗
PubMed2006

Can selective CT angiography reduce the incidence of severe complications during transcatheter arterial embolization or infusion chemotherapy for thoracic diseases?

PURPOSE: To evaluate the usefulness of selective computed tomography (CT) angiography in preventing severe complications, such as spinal cord injury and broncho- esophageal fistula, during the transcatheter arterial embolization or infusion chemotherapy for thoracic diseases. MATERIALS AND METHODS: Data from 28 patients with thoracic diseases were retrospectively analyzed in terms of selective CT angiography procedures carried out before transcatheter arterial embolization or transcatheter arterial infusion chemotherapy. RESULTS: There were no spinal cord injuries (0/13 and 0/15) or broncho-esophageal fistula developments (0/13 and 0/15) during transcatheter arterial embolization and transcatheter arterial infusion chemotherapy, respectively. CONCLUSION: We conclude that selective CT angiography is potentially useful for reducing the incidence of severe complications during transcatheter arterial embolization or infusion chemotherapy for thoracic diseases.

Adult↗
PubMed1994

Nerve growth factor in CNS repair.

The hypothesis that neurotrophic factors play important roles in the adult central nervous system (CNS) has been successfully investigated in the past decade with regard to experimental and pathologic situations. Trophic roles in adult CNS axonal regeneration, on the other hand, have received much less attention. We review three groups of recent studies that demonstrate the relevance of nerve growth factor (NGF) for the regeneration of selected axons into adult central nervous tissue. The first group concerns a septohippocampal model where transected septal cholinergic axons are allowed to regrow into the hippocampal formation through a peripheral nerve bridge implanted into the transection lesion gap. NGF is required in the bridge, enhances penetration of the hippocampal tissue when infused there, and both attracts and promotes sprouting within the septum when infused in the lateral ventricle or the septal tissue itself. The second group of studies concerns the development of a spinal cord sensory regeneration model, where dorsal root ganglionic axons regrow into a nerve bridge placed within the dorsal spinal cord. Preliminary data indicate that NGF infusion rostral to the bridge once again promotes substantial penetration of the adult cord tissue by the regenerating NGF-sensitive fibers. In the third group of studies, attention has been shifted to the location of endogenous NGF in the adult rat hippocampal formation and the normal or lesion-induced occurrence of extrasomal NGF immunoreactivity. These regions of anchored NGF have the ability to attract NGF-sensitive growing axons and may provide opportunities to investigate local cues for final definition of terminal fields.

Animals↗
PubMed1998

Involvement of spinal dopamine receptors in mediation of the hypotensive and bradycardic effects of systemic quinpirole in anaesthetised rats.

This study examined the involvement of spinal dopamine D2 receptors in the cardiovascular effects induced by intravenous administration of the selective dopamine D2 receptor agonist quinpirole, as has been previously reported for the hypotensive action of systemic bromocriptine. In normotensive pentobartitone-anaesthetised rats, intravenous injection of quinpirole (25 to 1000 microg/kg) decreased mean aortic pressure and heart rate in a dose-related manner. The intravenous (0.5 mg/kg) or intrathecal (40 microg/rat at T9-T10) pretreatment with domperidone, a dopamine D2 receptor antagonist that does not cross the blood-brain barrier, significantly reduced the maximal hypotensive and bradycardic responses to intravenous quinpirole (1000 microg/kg). In contrast, the latter effects were fully abolished either by intravenous metoclopramide (5 mg/kg) or combined pretreatment with intravenous and intrathecal domperidone. In addition, when injected intrathecally at the T9-T10 level of the spinal cord, quinpirole (7.7 to 61.4 microg/rat) also produced dose-dependent depressor and bradycardic effects which could be blocked by intrathecal, but not intravenous, domperidone pretreatment. This suggests that, in anaesthetised normotensive rats, the hypotensive and bradycardic responses to intravenous quinpirole are fully mediated by dopamine D2 receptors, some of which are located in the peripheral circulation and some of which are located within the spinal cord. The latter finding is novel, suggesting that partial spinal mediation may not be peculiar to bromocriptine, as was previously thought. Rather, partial spinal mediation may be common to most dopamine D2 receptor agonists.

Animals↗
PubMed2004

Comparison of intrathecal levobupivacaine with and without fentanyl in combined spinal epidural for labor analgesia.

BACKGROUND: The initiation of epidural infusion immediately after intrathecal (IT) injection to prolong labor analgesia has gained increasing popularity. The effect of additional intrathecal fentanyl on levobupivacaine for labor analgesia has not been fully investigated. We wished to determine if addition of IT fentanyl to IT levobupivacaine in combined spinal epidural (CSE) could prolong obstetric analgesia when epidural infusion is initiated promptly. MATERIAL/METHODS: In this randomized controlled trial, 40 nulliparous parturients in labor were recruited to receive either IT 2.5 mg levobupivacaine (L) or IT 2.5 mg levobupivacaine + 25 microg fentanyl (LF). A 10 ml/h epidural infusion of 0.125% levobupivacaine and 2 microg/ml fentanyl was immediately started. The proportion of parturients who delivered without breakthrough pain and the duration of analgesia were analyzed with the x2 test and Kaplan-Meier technique (using a log-rank test), respectively. Sensory block, motor block, pain scores, and post-block side effects were also evaluated. RESULTS: The percentage of parturients with "successful" blocks, i.e. parturients not requiring further analgesic supplementation, was significantly higher in LF (87.5% vs. 44%, p<0.05). The duration of analgesia was also significantly longer in group LF (mean 530 min +/- SE65 vs. 361 +/- 66, p<0.05). CONCLUSIONS: The addition of 25 microg intrathecal fentanyl to 2.5 mg levobupivacaine as part of CSE for labor analgesia decreased the incidence of labor breakthrough pain and resulted in a longer duration of labor pain relief. This may decrease the need for supplemental labor pain relief and the anesthetists' workload in the delivery suite.

Adult↗
PubMed2003

Clinical application of drug pump for spasticity, pain, and restorative neurosurgery: other clinical applications of intrathecal baclofen.

Intrathecal baclofen has been successfully used for control of severe spasticity. Baclofen, an agonist of GABA-B receptor, has other potential effects on pain and recovery from coma. Sporadic episodes of dramatic recovery from persistent vegetative state are reported after intrathecal administration of baclofen. There are also reports on the use of baclofen for neuropathic pain including post-stroke central pain syndrome. Baclofen is also used for control of dystonia due to cerebral palsy or reflex sympathetic dystrophy. On the other hand, epidural spinal cord stimulation has been used for pain, spasticity, dystonia, or attempt to improve deteriorated consciousness, though the effects seem variable and modest. Similarity between baclofen and spinal cord stimulation is interesting in that both involves in spinal GABAergic system. The GABAergic system in the spinal cord plays a pivotal role in various clinical effects of these procedures.

Baclofen↗
PubMed1999

The neurotrophins NGF and NT-3 reduce sensory neuronal loss in adult rat after peripheral nerve lesion.

The effect of three different neurotrophins on axotomy-induced death of adult rat sensory neurons was examined. The ventral branch of the 13th spinal nerve was transected and the corresponding neurons in the 13th thoracic (T13) dorsal root ganglion (DRG) were pre-labelled with Fast Blue (FB). For a period of 4 weeks, animals received either no treatment, continuous intrathecal infusion of phosphate buffer, nerve growth factor (NGF), neurotrophin-3 (NT-3), or brain-derived neurotrophic factor (BDNF). Labelled neurons remaining after this period were counted. Inert, or no treatment, resulted in extensive loss of the DRG neurons. BDNF application was virtually non-effective, while NGF or NT-3 resulted in a greater number of FB-labelled neurons compared to normal controls. This suggests that NGF and NT-3 are survival factors for adult sensory neurons with a therapeutic potential in peripheral nerve injuries.

Animals↗
PubMed2002

Neuronal apoptosis associated with morphine tolerance: evidence for an opioid-induced neurotoxic mechanism.

Tolerance to the analgesic effect of an opioid is a pharmacological phenomenon that occurs after its prolonged administration. Activation of the NMDA receptor (NMDAR) has been implicated in the cellular mechanisms of opioid tolerance. However, activation of NMDARs can lead to neurotoxicity under many circumstances. Here we demonstrate that spinal neuronal apoptosis was induced in rats made tolerant to morphine administered through intrathecal boluses or continuous infusion. The apoptotic cells were predominantly located in the superficial spinal cord dorsal horn, and most apoptotic cells also expressed glutamic acid decarboxylase, a key enzyme for the synthesis of the inhibitory neurotransmitter GABA. Consistently, increased nociceptive sensitivity to heat stimulation was observed in these same rats. Mechanistically, the spinal glutamatergic activity modulated morphine-induced neuronal apoptosis, because pharmacological perturbation of the spinal glutamate transporter activity or coadministration of morphine with the NMDAR antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine maleate affected both morphine tolerance and neuronal apoptosis. At the intracellular level, prolonged morphine administration resulted in an upregulation of the proapoptotic caspase-3 and Bax proteins but a downregulation of the antiapoptotic Bcl-2 protein in the spinal cord dorsal horn. Furthermore, coadministration with morphine of N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (a pan-caspase inhibitor) or acetyl-aspartyl-glutamyl-valyl-aspart-1-aldehyde (a relatively selective caspase-3 inhibitor) blocked morphine-induced neuronal apoptosis. Blockade of the spinal caspase-like activity also partially prevented morphine tolerance and the associated increase in nociceptive sensitivity. These results indicate an opioid-induced neurotoxic consequence regulated by the NMDAR-caspase pathway, a mechanism that may have clinical implications in opioid therapy and substance abuse.

Amino Acid Transport System X-AG↗
PubMed2006

A randomised trial comparing 5 mL/kg and 10 mL/kg of pentastarch as a volume preload before spinal anaesthesia for elective caesarean section.

BACKGROUND: Colloid solutions are more effective at preventing hypotension than crystalloids when used as a volume preload before caesarean delivery under spinal anaesthesia. The ideal volume to infuse has not been established. METHOD: In a randomised double-blind trial 70 women presenting for elective caesarean section received either 5 mL/kg of pentastarch (group A) or 10 mL/kg of pentastarch (group B) as a volume preload before spinal anaesthesia. Hypotension was defined as a systolic pressure below 90 mmHg or a decrease of 30% from a baseline value. Treatment was with 6-mg increments of ephedrine until resolution. RESULTS: In group B, 7/35 patients (20%) developed hypotension, significantly fewer than the 15/35 (42.8%) in group A (P<0.05). The patients in group B also required less ephedrine (total in group, 114 mg) than those in group A (total in group, 198 mg) CONCLUSIONS: Pentastarch, 10 mL/kg is more effective than 5 mL/kg at preventing hypotension following spinal anaesthesia for caesarean delivery.

Adult↗
PubMed1985

Continuous extradural infusion of 0.0625% or 0.125% bupivacaine for pain relief in primigravid labour.

The efficacy of an extradural infusion of 0.0625% or 0.125% bupivacaine was studied in 98 primigravid mothers in active labour. No special measures were taken to posture the mother (except to avoid aorto-caval compression). The study regimen included a control group (no infusion) receiving intermittent top-ups (0.25%. bupivacaine 8-10 ml), two groups receiving bupivacaine 6.25 mg h-1 infusion in different concentrations (0.0625% and 0.125%), a fourth group receiving 0.125% bupivacaine 12.5 mg h-1 infusion, and a fifth group receiving 0.125% bupivacaine 18.75 mg h-1 infusion. The optimum infusion rate was 0.125% bupivacaine 10 ml h-1, at which 69% of primigravid mothers required none or only one "top-up" of 0.25% bupivacaine 8-10 ml during a mean duration of 7.1 h labour. In the group who had no extradural infusion, only 32% of mothers managed with one or no top-up. The median interval between top-ups was increased from 145 min in the no infusion group to 245 min in those mothers receiving 0.125% bupivacaine 10 ml h-1 by infusion. Increasing the rate of infusion to 15 ml h-1 did not improve the results. Spread of local anaesthetic to higher levels was limited (less than T5) so that testing sensory loss at the T5-6 level at 2-hourly intervals should detect accidental spinal blockade resulting from inadvertent intrathecal infusion.

Adult↗
PubMed1992

Continuous intrathecal opioid treatment abolishes the regulatory effects of magnesium and guanine nucleotides on mu opioid receptor binding in rat spinal membranes.

The regulatory effects of cations and guanine nucleotides on mu receptor binding after opioid drug and pertussis toxin treatment were studied in the rat spinal cord model. Continuous intrathecal (i.t.) infusion with PL017 for 5 days induced tolerance in a dose-dependent manner. Maximal tolerance was observed at day 2. A single i.t. dose (1 microgram) of pertussis toxin also induced tolerance to opioid. When mu receptor binding of the high-affinity sites was determined by 125I-FK33824, spinal membrane preparations from morphine- and pertussis toxin-induced tolerant animals demonstrated approximately 30% less binding than control membranes. Analysis of equilibrium competition binding of FK33824 against [3H]naloxone under a variety of experimental conditions (i.e., cations and guanine nucleotides) revealed differences among control and treated membranes. With Na+ (100 mM) + GDP (100 microM) pretreated membranes and binding assays conducted in the presence of Mg++, all mu receptors were observed to be in a high-affinity state in control membranes, whereas about 30% of receptors were in the low-affinity state in membranes from opioid- and pertussis toxin-treated animals. The increase in the proportion of low-affinity sites was dependent upon the infusion dose of PL017, and the increase correlated well with the degree of opioid tolerance developed. The regulatory effect of 5'-guanylylimidodiphosphate on opioid agonist binding was reduced in membranes from pertussis toxin- or opioid-treated animals. In binding assays conducted in the presence of Na+ (100 mM) + Mg++ (5 mM) + 5'-guanylylimidodiphosphate (30 microM) or Na+ (100 mM) + GDP (100 microM), all mu receptors in control membranes were in a low affinity-state, while those from opioid- or pertussis toxin-treated animals existed in both the high- and the low-affinity states. Continuous i.t. infusion with PL017 at the high dose of 1 microgram/hr for 5 days also decreased significantly (about 40%) the total number of receptors. These studies indicate that continuous opioid infusion and pertussis toxin treatment results in impairment in the receptor-G-protein coupling. This is reflected by the decreased regulatory effects of Mg++ and guanine nucleotides. Thus, in addition to receptor down-regulation, which is induced by PL017 at high doses, receptor-G-protein uncoupling may play a role in opioid tolerance induced by continuous infusion with morphine and PL017.

Animals↗
PubMedDate not supplied

Pharmacological treatment of cancer pain: alternative routes of opioid administration.

Cancer-related pain is present in 51% of patients at various stages of the disease, and the incidence increases up to 74% in advanced and terminal stages. The World Health Organization proposed and issued very simple guidelines for the pharmacologic treatment of cancer-related pain. According to the guidelines, opioid analgesics are the mainstay of analgesic therapy, and the first choice for drug administration is considered to be the oral route. However, in some clinical situations, the oral route is not feasible, and analgesic drugs consequently have to be administered via an alternative route. For example, this is the case when the patient presents vomiting, bowel obstruction, severe dysphagia, mental confusion and when the opioid dose has to be increased drastically in order to achieve adequate pain control. This review of the literature is aimed at describing the indications, the limits and the main aspects of the pharmacokinetics and pharmacodynamics relative to the alternative routes of administration of opioids most commonly used in clinical practice. Sublingual, rectal, subcutaneous, intravenous, transdermal and spinal administration routes are examined.

Administration, Cutaneous↗