Pain is an unpleasant sensation that is subjective as well as emotional. Newly developed neuroimaging technologies such as functional magnetic resonance imaging (fMRI) and magnetoencephalography (MEG) have extensively revealed the neural circuitry of the human brain and the cerebral mechanism of pain. In this review, we describe our recent studies of the emotional component of pain and its effect on pain perception in humans. In the first study, to testify the hypothesis that psychological pain was reflected in the pain-related neural network, we recorded cerebral hemodynamic responses using fMRI during imagination of pain (to imagine pain while viewing photographs showing painful events). The results showed that the imagination of pain was associated with increased activities in several brain regions involved in the pain-related neural network, especially in the anterior cingulate cortex, insula, and secondary somatosensory cortex. In another study, we recorded MEG and fMRI following noxious laser stimulation in a Yoga Master who claimed not to feel pain during meditation. The results showed that pain-related cortical activities recorded from the primary and secondary somatosensory cortices by MEG were absent during meditation. fMRI recording showed weaker activities in the thalamus, secondary somatosensory cortex, insula, and anterior cingulate cortex during meditation in contrast to those during non-meditation. Thus our recent neuroimaging studies indicate that the imagination of pain even without physical injury engages cortical representations of the pain-related neural network, and have clarified that our subjective emotional component of pain influences pain perception.

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We report the effect of second cervical ganglion block (C2 ganglion block) on ophthalmic zoster-associated pain. Eleven patients with ophthalmic zoster-associated pain received C2 ganglion block. The results were compared with those of 94 patients who received spinal root blocks for spinal zoster-associated pain. Included were patients aged ≥ 50 years who received nerve blocks for zoster-associated pain ‹ 60 days after the onset of symphtoms of herpes zoster infection. The intensity of ophthalmic zoster-associated pain decreased after C2 ganglion block in 64 % of the patients. In 27 % of the patients, the decrease in pain was › 50 %. These results were not statistically different from those after spinal root blocks for spinal zoster-associated pain. There were no statistically significant differences in the rates of pain disappearance among ophthalmic, cervical, thoracic, or lumbosacral zoster-associated pain after C2 ganglion block or spinal root block. We conclude that C2 ganglion block decreases ophthalmic zoster-associated pain as does spinal root block for spinal zoster-associated pain.

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We report a patient who developed drug-induced hypersensitivity syndrome on phenytoin. A woman aged in her sixties with trigeminal neuralgia who had had drug-induced hypersensitivity syndrome while taking carbamazepine developed generalized skin rash 23 days after taking phenytoin. She also had fever > 38 °C, elevated transaminases, and atypical lymphocytosis. The antibody titer to human herpes virus-6 immunoglobulin G was not markedly elevated. Although the patient did not take steroid, the symptoms and signs of drug-induced hypersensitivity syndrome spontaneously subsided after cessation of phenytoin.

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We report two patients with post-spinal cord injury pain who were treated with gabapentin. The pain had not been relieved by various conventional treatments in either patient. Although gabapentin did not relieve the pain, it improved psychological status and activity of daily life in both patients. We conclude that gabapentin may be useful to improve psychological status and activity of daily life in some selected patients.

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We report a patient who developed pyogenic spondylitis during repeated neural blockade without inserting an epidural catheter for the treatment of pain in the back and lower limbs. A 78-year-old woman, who had had lumbar laminectomy to treat lumbar spinal canal stenosis, had persistent pain in the back and lower limbs. As the pain worsened, the patient was admitted and treated with repeated trigger point injections. Spinal root block (L5) and bilateral facet joint blocks (L4/5, L5/6 ; the patient had six lumbar vertebrae) were performed 10 and 16 days after admission, respectively. The body temperature rose to 38.1 °C. The leucocyte count and level of CRP were also elevated. Magnetic resonance imaging and computed tomography of the lumbar area suggested the presence of pyogenic spondylitis. Blood culture yielded MRSA. Conservative treatment with sensitive antibiotics to the MRSA resolved the spondylitis 1 year after the onset, when the MRI did not show any evidence of inflammation.

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We report a patient with spontaneous intracranial hypotension who developed repeated subdural hematoma despite removal of the hematoma. Epidural blood patch with 30 ml of autologous blood under fluoroscopic guidance resolved the headache. There was no recurrence of subdural hematoma or headache after applying the epidural blood patch. A 51-year-old man had postural headache after awakening in the morning. Since the headache gradually worsened, he was admitted to our hospital, 6 days after the onset. Nausea and tinnitus accompanied the headache. Computed tomography (CT) of the head showed bilateral subdural hygroma, and magnetic resonance imaging (MRI) demonstrated enhanced images of the pachymeninges. His course was complicated with repeated bilateral subdural hematoma with deterioration of the consciousness. He received evacuation of the hematoma; however, severe postural headache persisted after the surgery. Radionuclide cisternogram showed early accumulation of radioactivity in the urinary bladder. MRI of the spine and CT myelogram revealed the presence of extradural effusion ranging from T2 to T8. Autologous blood 12 ml was injected through T4/5 and 18 ml through T6/8, under fluoroscopic guidance. The headache promptly resolved after the autologous epidural blood patch. There was no recurrence of subdural hematoma or complication related to epidural blood patch.

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We report four patients who had lumbago resistant to conventional treatment. The initial X-ray examinations and MIR findings suggested that the lumbago seemed to be caused by benign vertebral compression fracture; however, later bone marrow examination revealed that the lumbago was caused by multiple myeloma. Among the four patients, three were aged > 70 years older. Laboratory examinations revealed anemia, thrombocytopenia, and hyperproteinemia. Multiple myeloma should be borne in mind when conventional treatments do not relieve lumbago in older patients.

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Neo Vitacain INJECTION^® (Neo Vitacain) is an analgesic preparation containing dibucaine hydrochloride (0.1 %), sodium salicylate (0.3 %) and calcium bromide (0.2 %). We report prolonged paralysis in two patients after accidental intrathecal injection of Neo Vitacain. Case 1: A 65-year-old man with lumbar disc herniation had low back pain. Trigger point injection with Neo Vitacain (5 ml) and betamethasone (2 mg) was performed into the tender point around the right L4/5 facet joint. Caudal block with 1 % mepivacaine was performed 2 minutes after the trigger point injection. Aspiration for cerebrospinal fluid (CSF) was negative for both procedures. The patient reported warm sensation in both legs during caudal block. Complete paralysis of the lower limbs occurred in 10 minutes. Neo Vitacain was suspected to be injected intrathecally. The paralysis resolved 16 hours after the blocks. Case 2: A 25-year-old woman with complex regional pain syndrome of the left leg received injection of 5 ml of Neo Vitacain into the presumable epidural space through the L3/4 intervertebral space. Complete paralysis of the lower limbs occurred in a few minutes. The paralysis resolved in 11 hours after the block. We should be careful when we inject Neo Vitacain around the paravertebral region and into the epidural space, since accidental intrathecal injection of Neo Vitacain can cause prolonged paralysis.

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