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• W1989743819 abstract "Herpes zoster is a viral disease characterized by skin rashes and persistent pain. Antiviral drugs, analgesics, and neural blockade have been used as treatment. Epidural analgesia is very effective in the acute stage of herpes zoster [1]. Herpes zoster features various complications [2] including myelitis which is characterized by neurologic deficits such as motor neuropathy and sensory disorders [3,4]. Since similar neurologic deficits may be induced accidentally by epidural analgesia, the differential diagnosis is very important when neurologic deficits develop after initiation of epidural analgesia in patients with herpes zoster. We report a case of herpes zoster myelitis which manifested after epidural analgesia. Case Report A 61-yr-old male developed left-sided herpes zoster in a T5-6 dermatomal distribution. He complained of continuous burning pain and cutaneous eruptions typical of herpes zoster. He had no significant past or family medical history. He had been treated with acyclovir 1 g intravenously daily for 6 days and loxoprofen 120 mg orally daily for 3 wk. Five weeks after the onset of pain, he was referred to our department for treatment of persistent pain. Complete blood count, urinalysis, blood chemistry, electrocardiogram, and chest and spine radiographs were all normal. Bleeding, coagulation, and prothrombin times were within normal ranges. The serum complement fixation titer of varicella-zoster virus was 1:256 (normal range, less than 1:4). On admission, the patient was completely free of neurologic deficits. Continuous epidural analgesia was planned for treatment of the herpes-zoster-induced pain. An 18-gauge epidural catheter was inserted 3 cm cephalad through a 17-gauge Tuohy needle at the T5-6 interspace. The epidural space was detected by loss of resistance to air. Catheterization of the epidural space was performed easily, and no blood or cerebrospinal fluid was aspirated through the catheter. The patient was without complaint of paresthesia or sensory impairment during the procedure. A single dose of 0.25% plain bupivacaine, 5 mL, produced complete pain relief and bilateral sensory block of the T5-8 dermatomes as determined by the pinprick method. Continuous epidural infusion of 0.25% plain bupivacaine was begun at a rate of 2 mL/h with a portable disposable pump, and his pain was completely relieved thereafter. On the day after catheterization, body temperature increased abruptly to 38.5 degrees C. The patient complained of urinary retention, and catheterization of the bladder was required. He was given cefazolin and indomethacin. On the third hospital day, his temperature was 38.0 degrees C. He noticed the sudden onset of muscular weakness in his left leg and was unable to stand unaided. The epidural catheter was removed immediately after the onset of muscular weakness. No bacterial growth was detected on the catheter. Emergency neurologic examination revealed severe weakness of the left anterior tibialis, iliopsoas, quadriceps, and triceps muscles, and slight weakness of the left gastrocnemius muscle. Muscular strength was normal in the right leg. The patellar reflex was increased on the left side. Babinski's and Chaddock's reflexes were negative in both legs. Examination of sensation disclosed hyperesthesia below the T10 level bilaterally. No disorder in disposable pump function was noted, and approximately 80 mL of the local anesthetic in the cylinder had been infused at an unchanging rate during the 40 h preceding catheter removal. Neurologic deficits were rapidly progressive, evolving within 2 days to total loss of sensation at the T5 level on the left side, and to reduced sensation in all modalities bilaterally below T6. Computed tomography and magnetic resonance imaging (MRI) studies performed on the fourth hospital day revealed no abnormalities. Laboratory findings were unremarkable except for a white blood cell count of 12,300/mm3 in the blood, with 80% neutrophils, 14% lymphocytes, and 6% monocytes. The cerebrospinal fluid obtained on lumbar puncture was clear, colorless, and contained 688 white blood cells (50% monocytes and 50% granulocytes)/mm3 (normal range, <5/mm3), with a protein concentration of 1.11 g/L (normal range, <0.5 g/L) and a glucose level of 5.3 mmol/L (normal range, 2.8-4.2 mmol/L). Cultures of the cerebrospinal fluid yielded no bacterial growth, but the complement fixation titer of varicella-zoster virus in the cerebrospinal fluid was 1:2. Antibodies to other viruses including influenza, cytomegalovirus, and measles were not detected. During the course of this episode, the patient's consciousness remained clear. A diagnosis of herpes zoster myelitis was made based on the skin lesions, the acute onset of the neurologic deficits, unilateral paralysis of the leg, and detection of varicella-zoster virus antibody in the cerebrospinal fluid. From the fifth hospital day, the patient was treated with acyclovir 1.5 g daily for 1 wk and betamethasone 10 mg daily for 10 days. His temperature returned to normal after initiation of administration of acyclovir and betamethasone. On the 10th hospital day, the white blood cell count decreased to 120/mm3 (97% monocytes and 3% granulocytes), and the cerebrospinal fluid complement fixation titer of varicella-zoster virus became negative. Urinary bladder function returned to normal. He was able to raise the left leg against gravity 1 mo after the onset of muscular weakness. Although the number of white blood cells in the blood remained increased for 3 wk, there were no other abnormal laboratory findings. He was able to walk with a cane after 2 mo of exercise and was discharged from the hospital. When he was seen 12 mo after primary admission, he still needed a cane to walk and impaired sensation remained unchanged. Discussion Myelitis is a rare complication of herpes zoster [3]. Although the etiology of herpes zoster myelitis has not yet been fully determined, direct viral invasion and/or immune-mediated destruction of the spinal cord have been postulated [4,5]. The onset is usually subacute, with a delay of 1-4 wk after the initial herpes zoster rash [4-6]. Various neurologic complications, including encephalitis, cranial nerve palsies, muscular weakness, and sensory disorders, have occurred with herpes zoster [2,3]. Although there are no established criteria for the diagnosis of herpes zoster myelitis, the presence of skin lesions, spinal cord dysfunction, and absent or only mild supraspinal central nervous system signs have been suggested. Pleocytosis in the cerebrospinal fluid is reported in patients with herpes zoster myelitis [4], and it is commonly observed in patients with other neurologic disorders. Increase of varicella-zoster antibody in the serum is specific for varicella-zoster infections. The typical eruptions, neurologic deficits without disturbance of consciousness, and increase of varicella-zoster antibody in the serum observed in our patient meet these criteria. Asymmetrical neurologic symptoms and signs with principal involvement of motor and posterior column functions ipsilateral to the rash, which were noted in the present case, have also been reported as characteristic clinical features of herpes zoster myelitis [4]. Although epidural analgesia has been used successfully to treat herpes zoster, the effect of epidural analgesia on the neurologic outcome of herpes zoster myelitis has never been reported. In the present case, muscular weakness and sensory disorders due to herpes zoster myelitis developed after the initiation of continuous epidural analgesia. Since these neurologic complications have also been reported after epidural anesthesia [7], neurologic examinations must be performed as soon as possible to elucidate the cause of neurologic deficits. Serious complications, such as epidural abscess [8], hematoma [9,10], arachnoiditis [11], and anterior spinal artery syndrome [12] can be induced by epidural anesthesia. However, most of these complications are associated with bilateral neurologic deficits, and the incidence of unilateral muscular weakness is very rare [7-11]. Epidural abscess and hematoma are easily detected with MRI [13,14], and neurologic disorders caused by arachnoiditis are characterized by delayed onset and very slow progress [11]. In contrast to the neurologic complications secondary to epidural anesthesia described above, the muscular weakness observed in the present case was unilateral, and no abnormalities were detected on computed tomography or MRI examination, even though muscular weakness and sensory impairment were rapidly progressive. In the present case, neurologic deficits might have been induced by hypotension during epidural analgesia [15]. Insertion of an epidural needle or catheter can result in direct trauma to the spinal cord and nerve roots, usually followed by severe lancinating pain in dermatomes adjacent to or below the site of puncture [16]. However, there were no episodes of hypotension or abnormal sensation during the procedure. These findings suggest that the patient's neurologic deficits were due to varicella-zoster virus infection of the spinal cord, rather than epidural anesthesia, although the possibility that epidural analgesia might be involved in precipitating the herpes zoster myelitis cannot be completely eliminated. In the present case, varicella-zoster viral antibody was detected in the cerebrospinal fluid, indicating the presence of direct viral effects on the spinal cord. This finding strongly suggests this was a case of herpes zoster myelitis. Confirmation of increased titer of varicella-zoster virus antibody in the cerebrospinal fluid is important for diagnosis of herpes zoster myelitis [6], and the increased white blood cell count in the cerebrospinal fluid also occurs in patients with herpes zoster myelitis [4,17,18]. Although herpes zoster myelitis is sometimes detected as a focal region of hypersensitivity in the spinal cord on MRI [19], it is not always detectable with MRI [18]. Early therapeutic intervention with antiviral drugs, particularly acyclovir, is beneficial in the treatment of herpes zoster myelitis [20]. Corticosteroids have also been postulated to be beneficial by some authors [17,18], although there is controversy concerning with the effectiveness of corticosteroids because of the immunosuppressive effect [4]. We administered a corticosteroid, betamethasone, as well as acyclovir in the present case, and partial recovery of neurologic deficits was obtained. No complications of betamethasone administration were detected. Recovery usually commences within 2 wk of maximum neurologic deficit after the onset of herpes zoster myelitis, and the greatest improvement occurs during the subsequent 2 mo [4]. Although recovery of muscular strength is generally good, only partial recovery of sensory deficits is reported in most cases [6,7,18]. In summary, we treated a patient with herpes zoster myelitis who developed muscular weakness during continuous epidural analgesia. Unilateral muscle weakness was characteristic and distinguishable of herpes zoster myelitis in this patient from neurologic complications associated with epidural analgesia. Although the etiologic relationship between herpes zoster myelitis and epidural analgesia is unknown, the possibility of myelitis should be considered when a patient with herpes zoster complains of muscular weakness during epidural analgesia, and in this case viral studies of the cerebrospinal fluid are strongly recommended." @default.
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• W1989743819 title "A Case of Herpes Zoster Myelitis Occurring During Epidural Analgesia" @default.
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