A method of investigating the effects of close arterial injections on spinal cord activity.
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Peripheral osmo - and bradykinin-sensitive receptors which have been previously localised within the hepatic portal vein area, activate the hypothalamo-neuro-hypophysial system through a neural pathway projecting to the lower thoracic spinal cord. In this paper we attempted to identify the spinal transmitter(s) involved and to answer the question whether osmoreceptors are in fact chemosensitive nociceptors. The portal vein of anesthetised rats was superfused with 0.2 ml of 4% NaCl or 1 microM bradykinin, and hypothalamo-neurohypophysial responses were measured either electrophysiologically or by radioimmunoassay of arginine vasopressin. Responses to bradykinin, but not to hypertonic saline, were abolished in rats pretreated 2 wks previously with capsaicin s.c., and immunocytochemistry for substance P in these animals showed that substance P was strongly depleted both in the dorsal thoracic spinal cord and in the portal vein. The spinal injection of 8 microliter 0.1 mM capsaicin at T8-T9 elicited a pronounced hypothalamo-neurohypophysial response, and diminished reversibly the response to bradykinin superfusion of the portal vein. Spinal capsaicin had no effect on responses to hypertonic saline. Similarly, the spinal (T8-T9) injection of 8 micrograms substance P antagonist, the [D-Pro4, D- Trp7 ,9,10, Val8 ]substance P (4-11), reduced reversibly the responses to bradykinin by about 50% without affecting those to hypertonic saline. The spinal injection of 8 micrograms substance P, at the same site where substance P antagonist was applied, elicited within 4 s a prolonged response (several min). A slightly longer delay between stimulus and neurophysiological response was observed for spinal capsaicin and for bradykinin superfusion. Responses to hypertonic saline superfusion of the portal vein, however, occurred within 1-2 s. The results show that portal vein osmoreceptors are distinct from chemo-sensitive nociceptors, and suggest that substance P may be a spinal mediator for chemo-sensitive portal vein nociceptors. The spinal transmitter for osmosensitive afferents, and the physiological importance of the portal vein area in chemosensation remain to be established.
UNLABELLED: Decreases in blood pressure after the spinal injection of opioids suggest that intrathecal (IT) opioids may have a sympatholytic effect similar to that of local anesthetic drugs. We compared two groups of patients aged 10-16 yr (n = 10 in each group). Group One (IT group) received IT opioids. Group Two (Epidural group) received 0.5% bupivacaine epidurally. The sympathetic effects of IT opioids and epidural bupivacaine were monitored by the changes in toe relative to calf temperature and by the changes in pulse wave gradients with digital plethysmography. Changes in temperature gradients comparing calf to toe and increases in pulse amplitude indicate vasodilatation caused by sympathetic blockade in this model. Calf to toe temperature gradients (Deltacalf-Deltatoe) were evaluated by subtracting the two measurements. Pulse wave plethysmography was recorded before and after spinal and epidural injection at intervals of 10 min for 40 min. All patients demonstrated changes in their calf to toe gradients after IT and epidural injections (-3.2 +/- 1.6). Systolic blood pressure decreased from a mean of 70 +/- 15 mm Hg to 55 +/- 10 mm Hg. Pulse wave plethysmography amplitude increased after the intrathecal opioid and epidural bupivacaine injection similarly. We conclude that the increases in pulse wave amplitude and decreases in calf-toe gradients indicate a sympatholytic effect after IT opioids similar to that of local anesthetics. IMPLICATIONS: The sympatholytic effects of neuraxial opioids were compared with those of local anesthetics. Two groups of patients were assigned to receive a neuraxial opioid or bupivacaine. Our results demonstrate that opioids cause hypotension and peripheral vasodilatation similar to bupivacaine. This finding suggests that neuraxial opioids have a sympatholytic effect comparable to that of local anesthetic drugs.
We have previously demonstrated that the antinociception induced by either endomorphin-1 or endomorphin-2 given supraspinally is mediated by the stimulation of mu-opioid receptors. However, the antinociception induced by endomorphin-2 given supraspinally contains additional components, which are mediated by the spinal release of dynorphin A (1-17) acting on kappa-opioid receptors and the spinal release of [Met5]enkephalin acting on delta2-opioid receptors in the spinal cord. The present studies were performed to determine whether there are any differential effects on the tail-flick inhibition induced by endomorphin-1 and endomorphin-2 given intrathecally (i.t.) in mice. Endomorphin-1 or endomorphin-2 given i.t. inhibited the tail-flick response in a dose-dependent manner. The tail-flick inhibition induced by endomorphin-1 was blocked by i.t. pretreatment with mu-opioid receptor antagonist D-Phe-Cys-Tyr-D-Try-Orn-Thr-Pen-Thr-NH2 (CTOP), but not kappa-opioid receptor antagonist nor-binaltorphimine (nor-BNI), delta1-opioid receptor antagonist 7-benzylidene naltrexamine (BNTX), or delta2-opioid receptor antagonist naltriben (NTB). In contrast, the tail-flick inhibition induced by endomorphin-2 given i.t. was blocked by i.t. pretreatment with CTOP or nor-BNI, but not BNTX or NTB. Intrathecal pretreatment with antiserum against dynorphin A (1-17), but not antiserum against [Met5]enkephalin, [Leu5]enkephalin, or beta-endorphin, blocked the tail-flick inhibition induced by i.t.-administered endomorphin-2. None of these antisera attenuated the i.t.-administered endomorphin-1-induced tail-flick inhibition. It is concluded that the tail-flick inhibition induced by endomorphin-1 and endomorphin-2 given spinally is mediated by the stimulation of mu-opioid receptors. However, the tail-flick inhibition induced by spinally injected endomorphin-2 contains an additional component, which is mediated by the spinal release of dynorphin A (1-17) acting on kappa-opioid receptors in the spinal cord. We propose that there are at least two different subtypes of micro-opioid receptors for endomorphin-1 and endomorphin-2 to produce antinociception in the spinal cord.
Nerve root blocks and epidural perineural injections are main part in the conservative treatment of degenerative spine diseases. These injections should be done without imaging because degenerative spine diseases - discogenic oder spinal stenotic - tend to recurrence and danger arises from too many imaging with cumulative ionizing radiation over the years, especially in younger people. After certain training it is possible to perform spinal injections without imaging only considering topographic anatomical landmarks like in any other local anesthesia for surgical reasons. Repetitive periradicular injections desensitize the nerve root by local anesthetics and reduce its inflammatory swelling by steroids. The decompensated symptomatic deformity turns back into an asymptomatic compensated status.
In this case report, we present a 42-year-old man with history of chronic low back pain after a work-related injury. The patient failed multiple therapeutic modalities both conservative and interventional, including numerous spinal injections and placement of a spinal cord stimulator. Finally, an intrathecal morphine pump was placed to control his pain in addition to oral pain medications. The course of the treatment included adding a muscle relaxant, tizanidine (Zanaflex), to control spasms in the lower extremities. Six weeks after starting tizanidine, a large pleural effusion was noted incidentally on a computerized tomography scan of the thoracic and lumbar spine. The patient underwent work-up for the pleural effusion; all tests came back negative. Finally, a drug reaction to tizanidine was suspected. The drug was discontinued, and 4 weeks later the pleural effusion resolved.
A 33-yr-old man undergoing anorectal surgery developed cauda equina syndrome and bilateral profound hearing loss after single-injection spinal anesthesia with isobaric bupivacaine. There was no pain on needle placement. Neurologic assessment found impaired sensation to pinprick in the perineal region, lower extremity paralysis, and bowel and bladder incontinence. In addition, he developed a bilateral profound hearing loss involving the low frequencies, with the left side more affected than the right side. Although hearing impairment can occur with cerebrospinal fluid leakage, the etiology of cauda equina syndrome is uncertain. The simultaneous occurrence of these events has not been previously reported.
UNLABELLED: We sought to determine whether spinal clonidine 50 microg prolongs the analgesia from the spinal administration of sufentanil 7.5 microg and bupivacaine 2.5 mg early in the first stage of labor. Thirty patients were randomized to receive a 2-mL spinal injection of sufentanil 7.5 microg + bupivacaine 2.5 mg with or without clonidine 50 microg using a combined spinal-epidural (CSE) technique. Pain, nausea, pruritus, sedation, motor block, blood pressure, and heart rate were assessed until the patient requested additional analgesia. Analgesia was significantly prolonged in patients who received spinal sufentanil + bupivacaine + clonidine (197 +/- 70 vs 132 +/- 39 min; P = 0.004). Pain scores and side effects, including motor block, sedation, and hypotension, were similar between groups. Spinal clonidine significantly prolongs labor analgesia from spinal sufentanil and bupivacaine without producing serious adverse side effects. IMPLICATIONS: We studied the effects of spinal clonidine administered with spinal sufentanil and bupivacaine on labor analgesia using a combined spinal-epidural technique and conclude that spinal clonidine significantly prolongs labor analgesia from spinal sufentanil and bupivacaine without producing serious adverse effects.
Nine patients undergoing cardiopulmonary bypass surgery were given either 2 mg diamorphine or 2.5 mg morphine by intrathecal injection. Spinal fluid (sf) samples were collected over 25 min and drug concentrations measured by HPLC. Concentrations in sf were about 4000 times as great as after 1 mg/kg IV morphine. The kinetic properties of morphine and heroin in sf differed; diamorphine was removed from sf much more rapidly than morphine. Lipophilic opiates may be safer for intrathecal use because of the shorter life of substantial drug concentrations in the mobile sf phase.
BACKGROUND: We tested the hypothesis that selective spinal anesthesia for ambulatory knee arthroscopy can be accomplished with a small dose of bupivacaine at the L3/4 interspace with or without a head-down tilt of 5 degrees when the patients were in the lateral decubitus position. METHODS: In this double-blind study, 123 patients were randomly allocated to receive spinal anesthesia with 4 mg of hyperbaric bupivacaine inserted at either the L2/3 interspace, while the vertebral column was kept horizontal (L2/3 group), or the L3/4 level, with the vertebral column horizontal (L3/4H) or tilted 5 degrees head-down (L3/4T). At 7 min, an additional head down tilt was used in all groups if the sensory block was inadequate. RESULTS: In the L3/4T group the sensory block (Th8) reached a significantly higher level 30 min after spinal injection, compared with both the L2/3 (Th10) and L3/4H (Th11) groups. In the L3/4H group, 39% of the patients needed an additional tilt for 3 min at 7 min, compared with 10% (P=0.004) in the L3/4T group. Sacral block developed later and recovered faster (P<0.05) in the L3/4T group compared to the L3/4H group. Home-readiness was achieved equally fast in all groups. CONCLUSION: When producing selective spinal anesthesia, the posture of the vertebral column is a major determinant of both sensory and motor segments to be blocked. A 4-mg dose of hyperbaric bupivacaine at the L3/4 interspace with a 5 degrees head-down tilt of the vertebral column for 6 min is recommended for knee arthroscopy.
A C-fiber reflex elicited by electrical stimulation within the territory of the ipsilateral sural nerve, was recorded from the biceps femoris muscle in anesthetized rats. The temporal evolution of the reflex was studied using a constant level of stimulus intensity (3 x threshold) and recruitment curves were built by varying stimulus intensity from 0 to 7 x threshold. Intrathecal doses of buprenorphine in the 0.2 to 10 micrograms range, elicited a facilitation of the C-fiber reflex in a dose-dependent manner. A large dose (100 micrograms) depressed but did not block the reflex. Intracerebroventricular doses of buprenorphine in the 0.1 to 10 micrograms range, facilitated the C-fiber reflex. A higher dose (100 micrograms) elicited a biphasic effect: depressive when the stimulus intensity was weak and facilitatory when the stimulus intensity was strong. It is concluded that the antinociceptive properties of buprenorphine cannot be related to a direct or indirect depressive spinal effect. In terms of spinal and supraspinal effects of buprenorphine, it is likely that buprenorphine facilitates the C-fiber reflex via a supraspinal mechanism that acts on sensory and/or motor components of the reflex arc although the depression of the reflex involves a spinal mechanism. The lipophilic properties of buprenorphine could explain a substantial diffusion from its spinal injection site to the brain. From a clinical standpoint, this study confirms that intrathecal administration of buprenorphine is an inadequate way of accessing spinal opioid receptors.
The combined spinal-epidural technique is a modification of epidural analgesia which combines the rapid onset of spinal analgesia with the flexibility of an epidural catheter. We sought to evaluate the effectiveness of an intrathecal opioid--low-dose local anaesthetic combination for parturients in advanced labour, a setting where satisfactory epidural analgesia is often difficult to achieve. The technique was evaluated in an open-label, non-randomized trial using parturients in advanced, active labour for the provision of pain relief during the late first stage and second stage of labour. Thirty-eight term parturients in active, advanced labour received a spinal injection of bupivacaine 2.5 mg and sufentanil, 10 micrograms, via a 25- or 27-gauge Whitacre needle placed into the subarachnoid space through a 17- or 18-gauge Weiss epidural needle which had been placed into the epidural space. This was followed by placement of an epidural catheter for supplemental analgesia if required. Onset of analgesia was noted by asking patients if their contractions were comfortable. Motor blockade was assessed using the Bromage criteria. Patients were asked if they experienced either pruritus or nausea on a four-point scale (none, mild, moderate, severe). The mean cervical dilatation at placement of the spinal medication was 6.1 +/- 2.2 cm. Thirty-two patients had spontaneous vaginal delivery, two were delivered by outlet forceps, and four by Caesarean section. Onset of analgesia was rapid (< five minutes) in all cases. Twenty-three patients (60%) delivered vaginally with no additional anaesthetic. The remaining 15 had supplemental local anaesthetic given via the epidural catheter, a mean of 123 +/- 33 min after the original spinal dose.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: The effects of volume and baricity of spinal bupivacaine on block onset, height, duration, and hemodynamics were studied. METHODS: Ninety patients undergoing endoscopic urologic procedures were randomized to receive 10 mg of intrathecal bupivacaine at L2-L3 level in sitting position. In the operating room, commercial products were diluted as needed with NaCl 0.9% to obtain isobaric solutions (density, 1.005-1.008) or with NaC 10.9% and glucose 30% to obtain hyperbaric solutions (density, 1.031-1.037) of 2, 5, or 10 ml (six groups of 15 patients each). Three minutes after spinal injection the patients were placed in lithotomy position. Sensory blockade was assessed using pinprick and cold sensation tests, and motor blockade was assessed using a four-point scale. RESULTS: Onset times to maximal cephalad spread of spinal blockade were similar with isobaric and hyperbaric solutions. A greater maximal cephalad spread of anesthesia was obtained with diluted isobaric bupivacaine but was not associated with more hypotension. Volume had no effect on cephalad extent of anesthesia with hyperbaric bupivacaine. Times for regression of anesthesia to L2 and offset of motor block were longer with isobaric than with hyperbaric solutions of bupivacaine. The intensity of motor blockade was decreased with diluted hyperbaric bupivacaine. No patient reported back pain. CONCLUSION: In this study, volume had no significant influence on either cephalad spread or duration of sensory blockade for either isobaric or hyperbaric bupivacaine. Time for offset of anesthesia was shorter with hyperbaric bupivacaine compared with isobaric solutions.
INTRODUCTION: Spinal nitric oxide (NO) is thought in many circumstances to play a pronociceptive role, because spinal injection of NO synthase inhibitors block hypersensitivity after nerve injury and enhance antinociception from spinal opioids. Conversely, intravenous injection of morphine has been demonstrated to activate descending noradrenergic pathways and to increase spinal synthesis of NO. This study examined the role of spinal NO in antinociception produced by intravenously administered morphine. METHODS: Polyethylene catheters were inserted with tips in the lumbar intrathecal space and in a jugular vein in male rats. Antinociception in response to intravenous injection of morphine was determined by latency to withdrawal of the hind paw from a heat source. Animals received an intrathecal injection of saline, an alpha2-adrenergic antagonist (idazoxan), a muscarinic antagonist (atropine), two NO synthase inhibitors, or an NO scavenger after intravenously administered morphine. RESULTS: Intravenously administered morphine produced dose-dependent antinociception, which was stable for 45 min and unaffected by intrathecally administered saline or atropine injection. In contrast, idazoxan, each of the NO synthase inhibitors, and the NO scavenger produced dose-dependent attenuation of intravenously administered morphine-induced antinociception. DISCUSSION: These results confirm a spinal alpha2-adrenergic mechanism of antinociception from intravenously administered morphine, consistent with morphine's activation of descending noradrenergic pathways. Further, these data suggest that spinal NO mediates antinociception produced by intravenous morphine.
In the past decade, there has been a substantial increase in interest in minimally invasive procedures in all areas of medicine, particularly for spinal disorders. Some of these techniques represent notable advances in spinal care and have major roles in the care of patients with back-related symptoms. Other techniques appear to offer no benefit and in some cases may be less effective than conventional treatments. Percutaneous lumbar diskectomy techniques hold considerable promise; however, lumbar microdiskectomy is the gold standard for surgical treatment of lumbar disk protrusion with radiculopathy. Intradiskal electrothermal therapy is emerging as a useful option for selected patients with intractable mechanical back pain whose only other option historically has been a spinal fusion. Percutaneous fusion techniques are in their infancy and may prove to be beneficial for these patients as well. Percutaneous vertebral augmentation, including vertebroplasty and kyphoplasty, has become the treatment of choice for many patients with intractable back pain secondary to vertebral insufficiency fractures. Spinal injections are important for evaluating and managing spinal pain and can be extremely useful diagnostically and therapeutically. This multidisciplinary review outlines the status of these procedures and offers suggestions for their use in patient care.
Chronic axial neck pain and cervicogenic headache are common problems, and there have been significant advances in the understanding of the etiology and treatment of each. The severity and duration of pain drives the process. For patients who have had slight to moderate pain that has been present for less than 6 months and have no significant motor loss, strength training of anterior, posterior, and interscapular muscle groups coupled with body mechanics training is prescribed. After 8 weeks, if the patient is better, exercises are continued at home or in a gym. If the patient is not better, physical therapy is continued for up to 8 more weeks. In patients with motor loss or severe pain, radiographs and magnetic resonance imaging (MRI) should be ordered at the initial visit. In patients with slight to moderate pain who are not better by 4 to 6 months, plain radiographs of the neck and MRI should be ordered. Based on the results, a spinal injection is usually prescribed. If MRI reveals spinal stenosis of the central or lateral canal, or a disc herniation, an epidural corticosteroid injection should be ordered. If the epidural provides good relief, the patient can be referred for more aggressive physical therapy and repeat the epidural as needed up to a maximum of three times. If there is no pathology within the canal, medial branch blocks and intra-articular steroid injections can be ordered based on the joints that are most tender or where disc space narrowing is greatest, or MRI or radiographs are recommended. If there is excellent relief from the medial branch block and joint injections, repeat when the steroids wear off. If there is good relief again, but pain recurs, medial branch radiofrequency neurotomy is recommended. For patients with one or two level disc degeneration that has not responded, a psychologic evaluation and discography is recommended. If there are no significant psychologic abnormalities, and one or two (rarely three) painful discs, surgical consultation is recommended. Adjunctive low-dose opioid analgesics, nonsteroidal anti-inflammatory drugs, and perhaps tricyclic antidepressants are used to supplement the program at mid- and late stages.
Rarely we are faced with accidental spinal injection of potentially toxic substances. We present 2 cases in which amidetrizoate, water-soluble ionic contrast medium, was accidentally injected intrathecally. Our treatment consisted of vigorous hydration and barbiturate coma. This report suggests that for water-soluble ionic contrast media increasing cerebrospinal fluid circulation by vigorous hydration may be as effective as spinal lavage in diminishing toxicity.