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Neuropathic pain is usually managed pharmacologically, rather than with botulinum toxin type A (BTX-A). However, medications commonly fail to relieve pain effectively or have intolerable side effects. We present the case of a 62-year-old man diagnosed with an intracranial chondrosarcoma, which was removed surgically and treated with radiation therapy. He suffered from neuropathic pain despite combined pharmacological therapy with gabapentin, amitriptyline, tramadol, diazepam, and duloxetine because of adverse effects. BTX-A (100 units) was injected subcutaneously in the most painful area in the posterior left thigh. Immediately after the injection, his pain decreased significantly from 6/10 to 2/10 on a visual analogue scale. Pain relief lasted for 12 weeks. This case report describes intractable neuropathic pain caused by a brain tumor that was treated with subcutaneous BTX-A, which is a useful addition for the management of neuropathic pain related to a brain tumor.
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Ocular Neuropathic Pain: An Overview Focusing on Ocular Surface Pains
Being located in the hypogastric area, the ilioinguinal nerve, together with iliohypogastric nerve, can be damaged during lower abdominal surgeries. Conventionally, the diagnosis of ilioinguinal neuropathy relies on clinical assessments, and standardized diagnostic methods have not been established as of yet. We hereby report the case of young man who presented ilioinguinal neuralgia with symptoms of burning pain in the right groin and scrotum shortly after receiving inguinal herniorrhaphy. To raise the diagnostic certainty, we used a real-time ultrasonography (US) to guide a monopolar electromyography needle to the ilioinguinal nerve, and then performed a motor conduction study. A subsequent US-guided ilioinguinal nerve block resulted in complete resolution of the patient's neuralgic symptoms.
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To determine whether providing education about the disease pathophysiology and drug mechanisms and side effects, would be effective for reducing the use of pain medication while appropriately managing neurogenic pain in spinal cord injury (SCI) patients.
In this prospective study, 109 patients with an SCI and neuropathic pain, participated in an educational pain management program. This comprehensive program was specifically created, for patients with an SCI and neuropathic pain. It consisted of 6 sessions, including educational training, over a 6-week period.
Of 109 patients, 79 (72.5%) initially took more than two types of pain medication, and this decreased to 36 (33.0%) after the educational pain management program was completed. The mean pain scale score and the number of pain medications decreased, compared to the baseline values. Compared to the non-response group, the response group had a shorter duration of pain onset (p=0.004), and a higher initial number of different medications (p<0.001) and certain types of medications.
This study results imply that an educational pain management program, can be a valuable complement to the treatment of spinal cord injured patients with neuropathic pain. Early intervention is important, to prevent patients from developing chronic SCI-related pain.
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Pudendal nerve entrapment syndrome is an unusual cause of chronic pelvic pain. We experienced a case of pudendal neuralgia associated with a ganglion cyst. A 60-year-old male patient with a tingling sensation and burning pain in the right buttock and perineal area visited our outpatient rehabilitation center. Pelvis magnetic resonance imaging showed the presence of multiple ganglion cysts around the right ischial spine and sacrospinous ligament, and the pudendal nerve and vessel bundle were located between the ischial spine and ganglion cyst at the entrance of Alcock's canal. We aspirated the lesions under ultrasound guidance, and consequently his symptoms subsided during a 6-month follow-up. This is the first report of pudendal neuralgia caused by compression from a ganglion cyst around the sacrospinous ligament.
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To investigate the effect of pulsed radiofrequency (PRF) applied proximal to the injured peripheral nerve on the expression of tumor necrosis factor-α (TNF-α) in a neuropathic pain rat model.
Nineteen male Sprague-Dawley rats were used in the study. All rats underwent chronic constriction injury (CCI) procedure. After 7 days of CCI, withdrawal frequency of affected hind paw to mechanical stimuli and withdrawal latency of affected hind paw to heat stimulus were measured. They were randomly divided into two groups: group A, CCI group (n=9) and group B, CCI treated with PRF group (n=10). Rats of group B underwent PRF procedure on the sciatic nerve. Withdrawal frequency and withdrawal latency were measured at 12 hours, and 7 days after PRF. Immunohistochemistry and Western blot analysis were performed using a TNF-α antibody.
Before PRF, withdrawal frequency and withdrawal latency were not different in both groups. After PRF, withdrawal frequency decreased and withdrawal latency prolonged over time in group B. There was significant interaction between time and group for each withdrawal frequency and withdrawal latency. Group B showed decreased TNF-α immunoreactivity of the spinal cord and sciatic nerve at 7 days.
PRF applied proximal to the peripheral nerve injury is potentially helpful for the reduction of neuropathic pain by neuromodulation of inflammatory markers.
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To investigate the effects of aerobic exercise on neuropathic pain and verify whether regular treadmill exercise alters opioid receptor expression in the rostral ventral medulla (RVM) in a neuropathic pain rat model.
Thirty-two male Sprague-Dawley rats were used in the study. All rats were divided into 3 groups, i.e., group A, sham group (n=10); group B, chronic constriction injury (CCI) group (n=11); and group C, CCI+exercise group (n=11). Regular treadmill exercise was performed for 30 minutes a day, 5 days a week, for 4 weeks at the speed of 8 m/min for 5 minutes, 11 m/min for 5 minutes, and 22 m/min for 20 minutes. Withdrawal threshold and withdrawal latency were measured before and after the regular exercise program. Immunohistochemistry and Western blots analyses were performed using antibodies against µ-opioid receptor (MOR).
Body weight of group C was the lowest among all groups. Withdrawal thresholds and withdrawal latencies were increased with time in groups B and C. There were significant differences of withdrawal thresholds between group B and group C at 1st, 2nd, 3rd, and 4th weeks after exercise. There were significant differences of withdrawal latencies between group B and group C at 3rd and 4th weeks after exercise. MOR expression of group C was significantly decreased, as compared to that of group B in the RVM and spinal cord.
In neuropathic pain, exercise induced analgesia could be mediated by desensitization of central MOR by endogenous opioids, leading to the shift of RVM circuitry balance to pain inhibition.
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To characterize neuropathic pain in patients with spinal cord injury (SCI) according to classification used in the study by Baron et al. (Baron classification), a classification of neuropathic pain based on the mechanism. To also compare the patterns of neuropathic pain in SCI patients with those in patients with other etiologies and to determine the differences in patterns of neuropathic pain between the etiologies.
This was a descriptive cross-sectional study. We used the Baron classification to investigate the characteristics of neuropathic pain in SCI. Sixty-one SCI patients with neuropathic pain (The Leeds assessment of neuropathic symptoms and signs score ≥12) were enrolled in this study between November 2012 and August 2013, after excluding patients <20 of age, patients with visual analog scale (VAS) score <3, pregnant patients, and patients with systemic disease or pain other than neuropathic pain.
The most common pain characteristic was pricking pain followed by electrical pain and numbness. The mean VAS score of at-level neuropathic pain was 7.51 and that of below-level neuropathic pain was 6.83. All of the patients suffered from rest pain, but 18 (54.6%) patients with at-level neuropathic pain and 20 (50.0%) patients with below-level neuropathic pain suffered from evoked pain. There was no significant difference in between at-level and below-level neuropathic pains.
The result was quite different from the characteristics of post-herpetic neuralgia, but it was similar to the characteristics of diabetic neuropathy as shown in the study by Baron et al., which means that sensory nerve deafferentation may be the most common pathophysiologic mechanism of neuropathic pain after SCI. Since in our study, we included short and discrete symptoms and signs based on diverse mechanisms, our results could be helpful for determining further evaluation and treatment.
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Objective: To assess the clinical manifestation of acute herpes zoster associated pain (AHP) and postherpetic neuralgia (PHN) and nerve block effect in AHP and PHN.
Method: We assessed twenty eight patients by physical examination and pain questionairre, and nerve block effect in thirty one patients. We injected local anesthetics and triamcinolone into nerve root or trunk in study group, and saline in control group. The effect was assessed by visual analogue scale.
Result: 1. Clinical manifestation: There was high incidence in thoracic dermatome. AHP and PHN patients expressed "sharp" pain. Pain rating index of AHP and PHN were 32.9, 33.0. 2. Nerve block effect: There was no nerve block effect in AHP (p＞0.05) and PHN (p＞0.05), but four patients of PHN patients in study group had significant pain relief, who suffered from pain during 2 month, 10 month, 6 years, 8 years.
Conclusion: AHP and PHN had variable clinical manifestation but no difference between them. There was no nerve block effect in AHP and PHN but we can consider nerve block as a additive method for pain relief of PHN because some patients responded to nerve block and there was no significant complication in nerve block.
Postherpetic neuralgia(PHN) is a common complication of herpes zoster and one of most common intractable conditions in pain clinics. The PHN is defined solely by the persistence of pain after the herpes zoster. There has been no known pathophysiology for the PHN and the role of scars, local muscles, tendons and ligaments has not been addressed.
The characteristics, duration, and location of the referred pain were evaluated along with the electromyographic(EMG) examination of involved muscles. Then treatment was given under the concept of a myofascial pain syndrome till the pain was completely resolved. Most of the patients with acute or chronic pain were relieved from the pain.
This study revealed a practical and important new concept on herpes zoster related pains. In some cases of herpes zoster, acute herpes zoster seems to be an initiating factor to form an acute trigger point in the muscles of the related area. And uncomplicated trigger points neglected in an acute stage become chronic intractable problems, when they were neglected.
In conclusion, myofascial pain syndrome should be taken into account when a postherpetic neuralgia is diagnosed. The recognition of this possible relationship between PHN and myofascial pain syndrome and an early proper care can greatly reduce the suffering of patents from chronic pain.
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