Postherpetic neuralgia (PHN) is a common and often severely painful peripheral neuropathy. Several recent studies in patients with PHN have been performed using quantitative sensory testing of primary afferent function, skin biopsies, and controlled treatment trials. Moreover, our knowledge of the pain generating mechanisms in PHN has been increased by the comparison of PHN with experimental models of neuropathic pain. Studies on PHN patients suggest several pathophysiological mechanisms in both the peripheral and central nervous system: (1) Pathological active or sensitized nociceptors (irritable nociceptors) can induce secondary changes in central processing, leading to spinal cord hyperexcitability that causes input from mechanoreceptive Aβ-fibers (light touching) to be perceived as pain. These patients characteristically have minimal sensory loss and severe allodynia. (2) Nociceptor function may be selectively impaired within the allodynic skin. In such patients pain and temperature sensation are profoundly impaired but light moving mechanical stimuli can often produce severe pain (allodynia). Anatomical reorganization in the dorsal horn resulting from C-fiber degeneration may lead to Aβ-fiber mediated allodynia. (3) Other patients have severe spontaneous pain, profound sensory loss but no hyperalgesia or allodynia. These patients presumably have lost both large and small diameter fibers. The pain is likely due to increased spontaneous activity in deafferented central neurons and/or reorganization of central connections. In one clinical entity with a single etiology several distinct peripheral and central pathophysiological mechanisms can contribute to pain generation. The three types of mechanisms may even coexist in individual patients. The treatment of PHN is currently unsatisfactory. Improved therapeutic outcomes require that mechanism-based interventions for each of the different mechanisms be developed. In recent years several possible predictors for the development of PHN have been evaluated. Besides age, the acute zoster pain intensity and a preexisting polyneuropathy may be important. Based on the pathophysiological mechanisms several therapeutical interventions may be effective in preventing PHN. Until now, an adaquate analgesia in the acute phase and an early therapy with antiviral drugs might be the most successful options.

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In summary, the low systemic toxicity of ropivacaine allows it's clinical use in relatively high concentrations and doses for reliable surgical anaesthesia. The separation between sensory and motor block at low concentrations makes ropivacaine an effective and opioid-saving epidural analgesic for the relief of pain after surgery and during labour.

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We investigated the fluctuations of short latency of SEP, serum β-endorphin and ACTH, in order to evaluate the inhibitory effects of either the intravenous (i.v.) or the epidural (Epi) administration of fentanyl and the epidural administration of lidocaine on the nociceptive stimulation of mastectomy. Breast cancer patients were divided into the four groups as follows; 1) control group, 2) lidocaine Epi group (L2: 20mg, L4: 40mg, L6: 60mg), 3) fentanyl i.v. group (FI50: 50μg, FI100: 100μg, FI200: 200μg), 4) fentanyl Epi group (F50: 50μg, F100: 100μg, F200: 200μg). In the control group, no significant changes were detected in the latency of P13 and N19 and the amplitude of SEP during the recording. In the group of lidocaine (L4 and L6), significant prolongation of the latency of P13 and N19, and a decrease of short latency SEP amplitude were detected. In the groups of fentanyl i.v. and Epi, FI50 and F200 caused an increase in the amplitude of the short latency SEP, although FI100 and FI200 decreased its SEP. In addition, prolongation of P13 and N19 were not observed in all fentanyl groups. During the operation, a marked increase of β-endorphin and ACTH levels were observed in the control group, although these increases were in the normal ranges. In the groups of lidocaine and fentanyl, however, no changes of these stress hormones were detected during operation. In this study, the synchronization between the fluctuation of short latency SEP and stress hormons was confirmed in the lidocaine group, but an increase in the short latency SEP was seen in the fentanyl group. These results indicated that the evaluation of changes in the short latency SEP can be the marker of nociception, particularly in case of the local anesthesia treatment, and this evaluation might implicate the excitation of central nervous system induced by the opioid analgesics.

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We examined the effects of bupivacaine added to epidural fentanyl and a difference in the volume of fentanyl solution alone on postoperative pain relief in patients who had undergone upper abdominal surgery.
Methods: Fifty-eight patients received O₂, nitrous oxide, sevoflurane and epidural local anesthetics during surgery, and epidural injection of fentanyl 50μg with saline 4ml at the end of surgery. The patients were allocated to three groups and fentanyl 20μg/h was given together with the following: Group B, 0.2% bupivacaine 2ml/h; Group S2, saline 2ml/h; Group S0.5, saline 0.5ml/h. We recorded the analgesic scores and side effects 0, 2, 6, 12, 18, 24 and 48h after surgery. Results: There was no significant difference in the analgesic score or the frequency of requests for supplemental analgesics between group B and group S2. The analgesic score in group S 0.5 was significantly lower than that in the group B and group S2 (p<0.05). Neither severe hypotension nor severe respiratory depression was observed in any patient.
Conclusion: Addition of 0.2% bupivacaine to epidural fentanyl 20μg/h had no advantageous effect on postoperative analgesia. Analgesic effect of epidural fentanyl in 2ml/h was significantly stronger than that of fentanyl in 0.5ml/h.

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We examined the effects of bupivacaine added to epidural fentanyl and a difference in the volume of fentanyl solution alone on postoperative pain relief in patients who had undergone lower abdominal surgery, and a difference in the volume of solution in the case of fentanyl alone.
Method: Sixty-eight patients received O₂, nitrous oxide, sevoflurane and epidural local anesthetics during surgery, and epidural injection of fentanyl 50μg with saline 4ml at the end of surgery. The patients were allocated to three groups and fentanyl 20μg/h was given together with the following: Group B, 0.2% bupivacaine 2ml/h; Group S2, saline 2ml/h; Group S0.5, saline 0.5ml/h. We recorded the analgesic scores and side effects 0, 2, 6, 12, 18, 24 and 48h after surgery.
Results: There were no significant differences in the analgesic score or the frequency of requests for supplemental analgesics between group B and group S2. The analgesic score in the group S0.5 was significantly lower than that in the group B and group S2 (p<0.05). Two patients (9%) in the group B complained of lower limb numbness after 6hour operation. Neither severe hypotension nor severe respiratory depression was observed in any patient, but somnolence was revealed in about 20% patients.
Conclusion: Addition of 0.2% bupivacaine to epidural fentanyl 20μg/h had no advantageous effect on postoperative analgesia. Analgesic effect of epidural fentanyl in 2ml/h was significantly stronger than that of fentanyl in 0.5ml/h.

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In our previous report, diurnal variations of pain sensitivity were abolished by exposure to constant light or constant dark for only one day, and pain threshold was decreased significantly for some period. In this study, we investigated the effects of exposure to constant light or constant dark for 7 days on the pain threshold. Experiments were conducted on 5-week-old male inbred mice (C3H/He, CBA/N, BALB/c, DBA/2 and C57BL/6 strains) using three photoperiods: light-dark cycle of 12:12h (lights on 0630-1830h), constant light and constant dark. The pain threshold was measured by the hot plate test (55.0±0.2°C) at 1100-1400h. In the C3H/He, CBA/N and BALB/c strains, the pain thresholds under both of the constant conditions were significantly lower than those under the light-dark cycle (p<0.01). The pain threshold of DBA/2 mice decreased significantly in constant light (p<0.01). whereas that of C57BL/6 mice increased significantly under the same condition (p<0.01). A strain difference on the pain threshold was observed under the light-dark cycle. Part of the mechanism responsible for the strain difference may involve endogenous opioids, because a difference sensitivity to naloxone was observed among the strains. Intraperitoneal injection of melatonin (0.1μg/kg) for 7 days (single dose/day) produced time-dependent effects on the pain threshold under constant light: a decrease at 2330h (p<0.01), no significant difference at 0300h and an increase at 0900h (p<0.05). These results suggest that melatonin may play a role in pain sensitivity.

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Intravenous regional sympathetic block (IRSB) under continuous prostaglandin E₁ (PGE₁) intravenous infusion was effective for refractory ulcerative pain in the toe of a patient with progressive systemic sclerosis (PSS). In a 55-year-old female patient with PSS, after thrombectomy of the right common iliac artery were performed, intense refractory ulcerative pain of the right big toe continued. Lumbar epidural block and lumbar sympathetic ganglion block were performed to decrease the pain and improve hypopurfusion of the right big toe. Due to the side effects of long-term administration of anticoagulant drug and platelet aggregation inhibitor which induce easy bleeding, IRSB under continuous PGE₁ intravenous infusion was selected and performed. The pain decreased and the ulcer was reduced successfully. IRSB which decreases the pain and increases peripheral blood flow with continuous PGE₁ intravenous infusion which increases blood flow seems effective for refractory ulcerative pain in extremities of a patient with PSS.

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A 70-year-old male developed complex regional pain syndrome-like painful state of the upper extremity after an attack of varicella zoster involving C4, C5, C6, C7, and C8, on the left. He was successfully treated with oral mexiletine and laser early in the course, but symptoms recurred. A series of left stellate ganglion blocks was helpful in relief of discomfort in the fingers, but wrist pain and edema continued. He needed aggressive physical therapy daily for improvement of his wrist symptoms. Physical therapy seemed to be absolutely necessary in his treatment.

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We describe a patient with trigeminal neuropathy, involving the maxillary and mandibular divisions, caused by an arachnoid cyst in the cerebellopontine angle. A 47-year-old woman had abnormal sensation and numbness in the left upper lip and hypogeusis on the left after a common cold. She visited us because the symptoms did not disappear three months after the onset. Neurological examination revealed hypoesthesia limited to the maxillary and mandibular divisions of the left trigeminal nerve. Other abnormal neurological signs were not noted. The trigeminal neuropathy did not improve one year and five months after onset. MRI showed the presence of a space-occupying lesion in the left cerebellopontine angle. An arachnoid cyst compressing the left trigeminal nerve was found at surgery, and fenestration of the cyst was performed. The numbness of the lip and hypogeusis improved rapidly after the operation.

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We report two cases of extrapyramidal reactions apparently caused by epidural droperidol. Two patients (18-yr-old man and 20-yr-old woman) were given continuous epidural droperidol with a dose of 2.5mg/day or below to provide a prophylactic antiemetic effect during administration of epidural morphine. Both patients experienced prolonged somnolence acute dystonia and Parkinsonism. The first patient showed the extrapyramidal reactions 51 hours after the inset of epidural droperidol with a total dose of 3.9mg, and the second patient showed the same reactions at 33 hours of administration, with a total 2.9mg. We consider that because they were both young and particularly sensitive to droperidol, even low doses were excessive to them and caused extrapyramidal reactions. We must be careful about prolonged somnolence in the patients receiving droperidol as antiemetic agent because somnolence can be a symptom of overdose and a premonitory sign of severe adverse side effects, such as extrapyramidal reactions.

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Pain having relief was successfully achieved in two patients with severe back pain. These patients were finally diagnosed as pyogenic spondylitis.
Case 1: A 54-yr-old man visited our clinic complaining of NSAIDs-resistant low back pain that had developed after mowing. Physical examination revealed no neurologic deficit and negative SLR test. The X-ray films of lumbar spine showed no significant abnormality. Several epidural blocks relieved the pain. A moderate systemic inflammation was implied by ESR 73mm/h and CRP 6.1mg/ dl. Magnetic resonance imaging (MRI) showing osteolysis in L4 vertebral body suggested pyogenic spondylitis. Case 2: A 66-yr-old woman with a six-month history of increasing pain of the chest and back was admitted to our hospital because of unsatisfactory results from several prior analgesics. Physical examination on admission disclosed kyphosis with tenderness and no neurologic dysfunction except for bilateral hyperactivity of the patellar tendon reflex. Metastatic tumor of the thoracic spine was suspected because of osteolytic lesions in TV 5-6 on MRI scan performed prior to admission. A slight systemic inflammation was implied by ESR 82mm/h and CRP 0.1mg/dl. A bone scintigraphy showing slightly increased activity in TV 5-6 did not support the previous diagnosis. Osteolysis with a spotty pattern demonstrated by tomogram of the thoracic spine gave the diagnosis of pyogenic spondylitis. The chest and back pain were successfully controlled by continuous epidural block and bed rest. Both patients recovered without neurologic sequelae. Antibiotics were given in case 1, but not in case 2. In conclusion, epidural block might be a therapeutic option for severe pain from pyogenic spondylitis in which neuraxial block is considered to be a contraindication.

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