A case of polyneuropathy associated with increased levels of vascular endotherial growth factor (VEGF) insera]

A 54-year-old woman began to notice numbness and motor weakness in the lower extremities in July 1999. These symptoms rapidly progressed and she could not walk any more. When she admitted to our hospital, she showed peripherally dominant, moderate motor weakness, drop foot and loss of superficial and deep sensation in the lower extremities, but only slight weakness in the hands. Cranial nerves were intact. Deep tendon reflexes were all absent. Nerve conduction velocities were reduced and cerebrospinal fluid protein was elevated. VEGF was greatly increased in serum (1,850 pg/ml), which has been found to be increased exclusively in patients with Crow-Fukase syndrome. Many characteristic manifestations of the syndrome except polyneuropathy are well explained to be resulted from the abnormal production of VEGF. She did not, however, exhibit any constellation of Crow-Fukase syndrome such as edema, skin change, organomegaly, bone lesions or M-proteinemia. Steroid therapy improved her symptoms and lessened the levels of serum VEGF and cerebrospinal fluid protein. This case indicated that overproduction of VEGF could induce polyneuropathy rather than the other symptoms of Crow-Fukase syndrome, and that a polyneuropathy associated with increased VEGF might exist.     

A case of sarcoid polyradiculopathy with nerve roots swelling demonstrated by myelography]

A 62-year-old woman was admitted to our hospital because of tingling numbness in the trunk and upper extremities. She was well until 18 days earlier, when she began to feel tingling numbness on the ulnar side of the left arm. During the next two weeks it spread gradually over the trunk and ulnar side of the bilateral arms. She had also progressive difficulty in taking hold of objects. On neurological examination she was alert and cooperative with normal articulation. The neck was supple. The cranial nerves were intact. Superficial sensation was bilaterally hypesthetic in the distribution from the 7th cervical through 12th thoracic segments. Mild weakness was distally noted in the upper extremities. Deep tendon reflexes were reduced or absent without laterality. Plantar responses were bilaterally flexor. Coordination and gait were normal. Routine laboratory examinations including blood counts, blood chemistries and urinalysis were unremarkable. Serum angiotensin converting enzyme (ACE) was slightly elevated. A lumbar puncture yielded clear, colorless cerebrospinal fluid (CSF) containing 22 white cells/mm3 and protein of 106 mg/dl. Conventional nerve conduction studies were normal. F-wave conduction studies revealed elevated F-ratios for the upper and lower extremities. Studies of short-latency somatosensory evoked potential showed mild prolongation of N13 recorded after stimulation of the right median nerve. An X-ray film of the spine was unremarkable except for mild narrowing of the C5-6 intervertebral disk space. Postcontrast magnetic resonance imaging of the spine with gadolinium-DTPA was unrevealing as well as a precontrast study. A myelogram disclosed enlarged lateral filling defects corresponding to cervical nerve roots from C6 through C8 bilaterally.(ABSTRACT TRUNCATED AT 250 WORDS)     

A case of Guillain-Barré syndrome with bulbar palsy showing the elevations of the anti-GD1a and GT1b antibodies]

We reported a 44-year-old woman with Guillain-Barré syndrome (GBS) showing elevations of serum anti-GD1a and anti-GT1b antibody levels. A few days after an upper respiratory infection, she felt numbness in her hands and feet, dysphagia and dysarthria, and weakness in her limbs. On admission, examination showed the paralysis of pharynx and neck, moderate weakness of face and upper limbs, and mild weakness of lower limbs. Sensory deficits were minimal on the distal side of extremities. Deep reflexes were decreased or absent. Laboratory examinations revealed the albumino-cytological dissociation in cerebrospinal fluid and the increase of anti-GD1a and anti-GT1b antibodies in serum. Nerve conduction studies demonstrated axonal damage to the motor nerves. With immunoadsorption therapy, she gradually recovered and the anti-GD1a and anti-GT1b antibodies were normalized. It was reported that the anti-GT1a antibody may be associated with a pharyngeal-cervical-brachial (PCB) variant of GBS (Ropper) and the similar cases including the present case. However, in the present case, the serum anti-GT1a antibody level was not increased, whereas those of anti-GD1a and anti-GT1b antibodies did. Therefore, these antibodies may also play a role in the development of PCB signs in GBS.     

Multifocal acquired demyelinating sensory and motor neuropathy: report of a case and review of the literature

Multifocal acquired demyelinating sensory and motor (MADSAM) neuropathy is characterized by an asymmetric multifocal pattern of motor and sensory loss, and conduction block and other features of demyelination in nerve conduction studies. MADSAM neuropathy needs to be differentiated from chronic inflammatory demyelinating polyneuropathy (CIDP) and multifocal motor neuropathy (MMN). In classic CIDP, there are symmetric proximal and distal weakness, sensory deficit in both upper and lower extremities and reduced deep tendon reflex. In MMN, limb weakness without sensory loss is asymmetric in the distribution of individual peripheral nerves and the weakness typically begins in the distal upper extremities. We report one patient with chronic progression of asymmetric numbness and weakness in four extremities. MADSAM neuropathy was diagnosed after extensive clinical and laboratory evaluations. It is very important to distinguish between CIDP, MADSAM neuropathy, and MMN by clinical, laboratory, and histological features because of different effective therapeutic strategies.     

A case of multiple sclerosis with polyradiculitis and spinal subarachnoid block

A case of 53-year-old female with multiple sclerosis was reported. In August 1987, she suffered from weakness in her legs and urinary retention. These signs had progressed with incomplete remissions and exacerbations. In March 1988, she developed sensory loss of all modalities below C2 level, spastic paralysis of upper extremities and flaccid paraplegia of lower extremities. Electromyography showed evidence of denervation in affected muscles of all extremities and paraspinal muscles. On lumber puncture, spinal fluid pressure fell to 0 mmH2O after removal of the spinal fluid of 12 ml, and the CSF protein was 740 mg/dl, indicating subarachnoid space block. The oligoclonal band was positive. MRI showed swelling in the cervical and upper thoracic cord, and multiple lesions in the periventricular white matter in the cerebrum. We diagnosed this case as multiple sclerosis in combination with acute polyradiculitis. The spinal subarachnoid block was considered to be caused by the swelling of the spinal cord.     

A case of brachial amyotrophic diplegia accompanied with Sj?gren's syndrome presenting good response to immunotherapies in the early course of the disease]

A 74-year-old woman suffered from progressive muscle atrophy and weakness of her arms since she was seventy two years old. Before referral to our department, she was diagnosed as having cervical spondylotic myeloradiculopathy and received spinal fusion. Though spinal decompression was successful, muscle weakness of her upper limbs were progressive even after the surgery. On admission, neurological examinations revealed marked atrophy and weakness of her bilateral upper limbs with absent deep tendon reflexes showing man-in-the-barrel syndrome. Her lower extremities had normal muscle strength, but fasciculations were seen in her all four limbs. Electrophysiologically, motor nerve conduction velocity was almost normal but the amplitude was remarkably decreased, conduction block was not detected, and electromyography showed neurogenic patterns on her all extremities. Spinal progressive musclar atrophy (SPMA) accompanied with Sj?gren's syndrome was the likely diagnosis. Because 50 kDa anti-neuronal antibodies were found in her serum, we assumed that anterior horn cells were impaired by an autoimmune mechanism. Thus we treated her with corticosteroid pulse therapy, plasma exchange (PE) and intravenous immunoglobulin infusion therapy (IVIG). Although steroid pulse therapy only had a minimal effect, PE and IVIG promoted a remarkable improvement on her weakness, and the effect lasted for about three months. This is the first case of SPMA with Sj?gren's syndrome which showed good response to PE and IVIG in the early course of the disease. We considered that some SPMA-like motor neuron syndrome accompanied with autoimmune features may require immunomodulating therapies.     

A patient of sensorimotor neuropathy with small cell lung carcinoma and anti-GM1 antibody]

We reported a 62-year-old woman had sensorimotor neuropathy with small cell lung carcinoma (SCLC) and anti-GM1 antibody. She was admitted with several months history of progressive numbness, walking disturbance and anorexia. Neurologic examination revealed severe numbness and deep sensory disturbance of extremities and body, and mild weakness of distal extremities. Deep tendon reflexes were absent. Her limbs were ataxic. Nerve conduction studies showed no sensory evoked responses. CSF protein was elevated. Sural nerve biopsy revealed severe loss of myelinated fibers and perivascular mononuclear cells surrounding the perineurial vessel. Vasculitic neuropathy was diagnosed, and prednisolone was started, with no benefit. In the clinical course, she developed cough attacks and was found the lymphnode swelling in the mediastinum and supraclavicular fossa, which was diagnosed SCLC. Although anti-Hu antibody were not detected, anti-GM1 antibody was positive. She was treated with intravenous immunoglobulin, with transient improvement. The rare case of the paraneoplastic peripheral neuropathy with SCLC and anti-GM1 antibody was reported.     

Sensori-motor neuropathy associated with congenital bilateral club feet: histological and ultrastructural study of the sural nerve

A 53-year-old female with sensori-motor neuropathy associated with bilateral club feet was reported. She was admitted because of numbness in the bilateral feet and gait disturbance. Her parents were not related. There was no family history of any neurological diseases. She had bilateral club feet which were present at birth to developed in early childhood. She could walk, but could not run. Since 5 years prior to the admission she noted gradually increasing disturbance of gait. Neurological examination revealed muscular weakness and wasting in the distal parts of the lower extremities and decreased deep tendon reflexes. There were hypesthesia, hypalgesia and dysesthesia in the lateral portions of the bilateral feet. Deep sensation was normal. There was no weakness or wasting in the upper extremities. Motor nerve conduction velocities were normal and sensory nerve conduction velocities were reduced in the median nerve. No action potentials could not be elicited in the bilateral tibial and peroneal nerves. A sural nerve biopsy showed a markedly hypertrophic perineurium, 28-150 micron thick, a large Renaut body measured 140 micron by 200 micron in diameters and a markedly reduced number of the myelinated fibers. Fiber size histogram showed many unmyelinated fibers larger than 1 micron, despite loss of fibers of the usual size. Therefore, a part of the unmyelinated fibers might be demyelinated. There were no axonal degeneration and onion-bulb formation. Segmental demyelination was found in approximately 30% of the myelinated fibers.(ABSTRACT TRUNCATED AT 250 WORDS)     

A case of CIDP with diabetes mellitus who had good response to intravenous immune globulin]

A 64 year-old man began to feel numbness on his bilateral feet in 1990. He was diagnosed as diabetes mellitus with a high fasting glucose level of 580 mg/dl in 1993 and he received oral hypoglycemic agents. Since then, his blood glucose levels had been in good control under diet therapy and medication. However, his numbness worsened and progressive weakness of bilateral lower legs occurred in 1997. Bilateral anterior tibial muscles were atrophic and deep tendon reflexes were decreased on bilateral upper and lower limbs. Protein level of his cerebrospinal fluid was 63 mg/dl. Nerve conduction study fulfilled the electrophysiological diagnostic criteria of CIDP. Superficial peroneal nerve biopsy showed loss of myelinated fibers, small amount of onion bulbs and thickening of the basement membrane of arterioles. Demyelination was predominant in teased fiber study. These findings were compatible with CIDP combined with diabetes mellitus (DM-CIDP). His numbness and leg weakness improved after intravenous high dose immune globulin therapy. DM-CIDP must be distinguished from diabetic peripheral polyneuropathy because immunological therapy may be effective in DM-CIDP patients.     

A case of acute autonomic, sensory and motor neuropathy (AASMN)--less favorable response of the autonomic dysfunctions to IVIg treatment]

We report a rare case of acute autonomic, sensory and motor neuropathy (AASMN). The patient, a 26-year-old woman, developed fever and common cold around January 20, 2001 and was admitted because of abdominal pain due to ileus on January 30. After admission, the patient complained of muscle weakness and numbness in the extremities, difficulty in seeing with the right eye, and dysuria. Neurologically, marked orthostatic hypotension, right tonic pupil, distal dominant moderate muscle weakness in extremities, areflexia in both lower limbs, glove and stocking type of paresthesia, and neurogenic atonic bladder were noted. Sensation to pin prick, light touch, temperature, and vibration were markedly impaired in upper limbs and below the level of the 5th thoracic cord. Cerebrospinal fluid examination revealed albumino-cytologic dissociation. Peripheral nerve conduction study revealed lower limb dominant axonal type impairment of sensory conduction and slight impairment of motor conduction velocity. Clinical autonomic testings revealed dysfunction of both sympathetic and parasympathetic systems. As having AASMN, she was given the intravenous high-dose immunoglobulin (IVIg) therapy twice. After IVIg, the sensory and motor symptoms improved remarkably, but pandysautonomia did not. To our knowledge, this is the first report of AASMN treated by IVIg, and the notable clinical feature in this case was the favorable motor and sensory recovery to IVIg, as opposed to poor autonomic outcome.     

Guillain-Barré syndrome after a jellyfish sting

This is the case of a jellyfish sting associated with the rare development of Guillain-Barré syndrome. The patient, a 66-year-old woman, was stung by a jellyfish on the right thigh while swimming in the Atlantic Ocean, off Charleston, SC. Ten days later, she developed low back and right thigh pain followed by progressive numbness and weakness in all extremities. These symptoms reached their peak in 30 days and slowly began to improve. Initial neurologic examination showed areflexia, weakness, absent vibration and position sense, and hyperesthesia to pin and light touch in the mid to distal region of all four extremities. Serial electromyography and nerve conductions were consistent with an improving predominantly demyelinating polyneuropathy. Spinal fluid analysis showed no cells, elevated protein (108), gammaglobulin 6 (normal less than 5.4), and immunoglobulin G 8.2 (normal less than 6). The only treatment was gabapentin for neuropathy pain. The patient made an excellent recovery in less than 1 year with minimal residual numbness in both thumbs, index fingers, and middle toes.     

Familial amyotrophic lateral sclerosis with rapid progression]

We report a family with autosomal dominant (AD) motor neuron disease. A 41-year-old man developed muscle weakness and fasciculation of the lower extremities. The weakness progressed to the upper extremities and bulbar muscles. The cerebrospinal fluid (CSF) protein level was slightly elevated. A nerve conduction study revealed reduced compound muscle action potentials, but conduction block was not observed. Electromyogram showed acute and chronic neurogenic changes. He was treated with intravenous immunoglobulin (IVIg) and methylprednisolone pulse therapy, but his condition rapidly deteriorated. He developed respiratory failure necessitating artificial ventilation within three months after the onset of the disease. His father developed muscle weakness and atrophy of the upper extremities at age 70, and his cousin developed muscle weakness of the legs at age 41. Their conditions rapidly progressed to quadriplegia. CSF and electrophysiological findings were similar to those of the proband. Treatments by steroid pulse therapy, IVIg, and plasmapheresis were not effective. The father and cousin also required artificial ventilation within 3-4 months from the onset of symptoms, and became locked-in state. Autosomal dominant amyotrophic lateral sclerosis (AD-ALS) was considered, but SOD1 gene mutation was not detected. The present pedigree may have familial ALS caused by a gene mutation other than SOD1.     

An adult case of transverse myelitis with erythema infectiosum]

We reported an adult case of transverse myelitis with erythema infectiosum. A 33-year-old female was admitted to Kyoto University Hospital because of a weakness in the lower extremities and "cloth-wearing" sensation of the trunk and legs. One month before admission, she became febrile and developed a symmetrical erythema on the extremities. At the same time she noticed a slight weakness of the legs and numbness in her fingers and toes, which disappeared next few days. A week later, she again developed a fever, severe weakness of the legs and "cloth-wearing" sensation on the trunk, and erythema appeared on the cheek. Physical examination on admission revealed a weakness and hyperreflexia in the extremities, in particular, knee and ankle jerk, and hypesthesia of the trunk and legs below the level of Th6. Cerebrospinal fluid (CSF) examination revealed 181/mm3 cells (mononuclear cell dominant) and 30 mg/dl protein. Magnetic resonance imaging, CT and electrophysiological studies indicated no abnormalities. IgM antibody against human parvovirus (B19) was detected in the serum and CSF. She was diagnosed as transverse myelitis with parvovirus infection and was medicated with prednisolone 40-60 mg/day, and improved gradually with the residua of a mild weakness of the legs and hypesthesia on the trunk between the level of Th6 and Th10.     

A case of mitochondrial myopathy with mononeuritis multiplex

A case of mitochondrial myopathy with mononeuritis multiplex was described. A 55-year-old man was hospitalized because of blepharoptosis and muscle weakness. His mother also showed blepharoptosis in her elderly stage of life. He had been healthy until 46 years of age, when he first noticed difficulty of speech, followed by bilateral blepharoptosis, weakness of upper limbs, and sensory disturbance in the left occipital, and left upper and lower extremities. These symptoms progressed slowly. On admission, bilateral blepharoptosis was recognized. Slightly to moderate muscle wasting and weakness were observed in the face, neck, trunk, and extremities. Areflexia was observed in the upper extremities. Paresthesia was observed in the left occipital and left hip, and superficial sensation was impaired in the left upper and lower extremities. Electromyographic examination of extremities showed neurogenic changes in the distal muscles and myogenic changes in the proximal muscles. Motor conduction velocities were normal, but sensory conduction velocities decreased in amplitude on the left upper extremity and were not evoked on the left lower extremity. Muscle biopsy specimen revealed numerous "ragged-red" fibers. Cytochrome c oxidase stain showed a decrease in intensity of staining. A sural nerve biopsy showed slight axonal degeneration and slight loss of nerve fibers. Biochemical analysis on biopsy muscle showed partial deficiency of cytochrome c oxidase activity.     

A case of chronic demyelinating polyneuropathy with benign IgM anti-myelin-associated glycoprotein paraproteinenia--transient improvement with weekly plasmapheresis]

We report a case of chronic demyelinating polyneuropathy accompanying benign IgM monoclonal gammopathy treated with plasmapheresis, which brought the improvement of the neurological signs and conduction velocities of peripheral nerves. A 60-year-old man developed numbness in the hands and legs and unstable gait. These symptoms became worse slowly. Three years after the onset, he was admitted to Matsuyama Red Cross Hospital because mild clumsiness in the hands was added. The neurological examinations revealed marked loss of both superficial and deep sensations of the glove-stocking type, mild weakness of distal muscles and hyporeflexia in the upper and lower extremities, and mild sensory ataxia. On the laboratory examinations, the serum showed a marked increase of IgM with a monoclonal IgM of lambda light chain. The cytological examination of the bone marrow showed no evidence of malignancy. Marked decrease of nerve conduction velocities was noted in the electrophysiological examinations of the peripheral nerves. Segmental demyelination and widely spaced major dense lines of myelin were observed in the histological examinations of the sural nerve. The immunological examination revealed the antibody activity of IgM against myelin-associated glycoprotein in the patient's serum. He was treated with double-filtration plasmapheresis of 2 liters once a week for 3 months as inpatient. During this treatment, the concentration of IgM in the serum was kept to be much lower than before the treatment, and the sensory disturbances, grasping powers and nerve conduction velocities were mildly improved at the end of the treatment. After discharge, he was treated with monthly plasmapheresis of 2 liters for 3 months.(ABSTRACT TRUNCATED AT 250 WORDS)     

A case of distal lower motor neuron syndrome associated with IgM anti-GM1 antibodies

A 34-year-old man had noted progressive weakness in his right hand. On admission at age 39, cranial nerves were not involved. Fasciculations were observed in his upper limb girdles. Neurological examination revealed severe wasting and weakness of arms and the right hand, whereas mild in the left hand. The deep tendon reflexes were absent in the upper extremities, but normal in the lower extremities. No sensory disturbances were observed. Motor and sensory nerve conduction velocities were normal, and multifocal conduction block was not observed. EMG showed neuropathic changes in all 4 limbs and sternocleidomastoideus muscles. Serum immunoelectrophoresis failed to detect an M protein. High-performance thin-layer chromatography with immunostaining revealed that his serum IgM reacted with GM1, but not reacted with GM2, GD1a, GD1b, and asialo-GM1.     

Nontraumatic spinal intramedullary hemorrhage in an infant

After an uncomplicated pregnancy and delivery, this female child suddenly became quadriplegic on the fifth day of life. She gradually regained movement in her upper extremities. At 2 months of age, she exhibited paraplegia with exaggerated deep tendon reflexes in the lower extremities. Babinski reflex was present bilaterally and sensory disturbances below the trunk were suspected. Somatosensory evoked potentials after median and ulnar nerve stimulation revealed preserved conduction from the upper extremities through the cervical spinal cord to the cortex. Somatosensory evoked potentials after posterior tibial nerve stimulation suggested disturbed conduction in the upper thoracic spinal cord. Magnetic resonance imaging disclosed a hypodense area in the thoracic cord between T1 and T4 on both the T1-weighted and gradient echo images consonant with an old hematoma cavity. Digital subtraction angiography failed to demonstrate any vascular malformation.     

A case of multiple sclerosis associated with myelin associated glycoprotein neuropathy]

A 28-year-old woman had developed chronic, recurrent, visual disturbance (bilateral), and girdle sensation at Th 5-6. She was admitted to our hospital because of left visual disturbance, distal limb weakness on right side, and numbness of four extremities. The neurological examination revealed decreased visual acuity of the left eye with abnormality of the optic disk, moderate muscle weakness of the right upper and lower extremities, absent tendon reflexes and paresthesia on distal portions of the four limbs. Laboratory examinations disclosed the titration of anti-myelin associated glycoprotein (MAG) antibody (IgM) and CSF protein was elevated (104 mg/dl). Motor nerve conduction studies revealed conduction block in more than one nerve. The conduction velocities in the upper and lower extremities were all diminished. P100 latency was prolonged by flash visual evoked potential (VEP) studies. N13-N20 interpeak latency of somatosensory evoked potential (SEP) of median nerve was also prolonged. She was treated with steroid pulse therapy, followed by an oral dose of 30 mg/day of prednisolone. Her symptoms resolved completely three months later, and multifocal conduction block subsided on electrophysiological study. There are some cases of multiple sclerosis with multifocal conduction block, but such a case is very rare in Japan. We discussed the pathogenic mechanisms of these conditions, and we conclude that we must take notice of demyelinating neuropathy in multiple sclerosis and that nerve conduction studies are useful for detecting them.     

A case of acute sensory neuropathy associated with cytomegalovirus infection]

We report a non-compromised patient with acute sensory neuropathy (ASN) developed following cytomegalovirus (CMV) hepatitis. A 67-year-old man admitted to a hospital because of acute hepatic dysfunction accompanying fever and skin eruption. One month later, when hepatic function normalized, numbness and clumsiness started acutely first in the right upper limb next to all the extremities. He found difficulty in walking in a couple of weeks. One month after the commencement of neurological illness, he was referred to us. On examination, he had sensory limb ataxia. His gait was wide-based, and Romberg sign was positive. Position sense was severely diminished in the extremities. Skin sensation was also attenuated distally, while no motor weakness was noted. Tendon reflexes were almost absent. Nerve conduction studies revealed absent sensory potentials in all but the left median nerve, in which amplitude was 5.5 microV with sensory conduction velocity of 40.7 m/s. Motor conduction studies, on the other hand, appeared normal except for a slight focal delay in the right ulnar nerve across the elbow. Mild increase in F-wave latencies was noted. A sural nerve specimen taken two months after the neurological onset showed a marked decrease in myelinated fiber density and active fiber degenerations accompanying axonal sproutings. Sj?gren syndrome and paraneoplastic neuropathy were excluded serologically and by comprehensive imaging techniques. Although IgM anti-CMV antibody was not detected, serum IgG anti-CMV antibody was positive and significantly increased during the neurological illness. The intrathecal antibody synthesis of IgG anti-CMV antibody was suggested by a low serum/cerebrospinal fluid (CSF) antibody ratio and a high CSF IgG index. From these observations, it was strongly suggested that acute hepatitis and subsequent ASN were associated with CMV infection in this patient. Although some cases with post-infectious ASN have been previously reported, this is the first report of ASN preceded by CMV infection.     

Case of herpes zoster associated Guillain-Barré syndrome with a relapse of eruptions after intravenous immunoglobulin therapy]

A 77-year-old woman developed progressive dysesthesia, hypesthesia and weakness in four extremities immediately after improvement of herpes zoster in the left Th10 dermatome area. Examination of the cerebrospinal fluid (CSF) showed an increase in protein concentrations. Evidence of demyelinating polyneuropathy was demonstrated by nerve conduction studies. Her hypesthesia and weakness in the extremities were gradually improved following intravenous immunoglobulin therapy (IVIg). Varicella zoster virus (VZV) titer levels in CSF well correlated both with neurological symptoms and CSF protein concentrations. VZV DNA in the CSF was not detectable. These findings suggested autoimmune Guillain-Barré syndrome (GBS) associated with herpes zoster. An interesting finding in the present patient is that one day after the completion of IVIg, when the neurological symptoms in the extremities were apparently ameliorating, the herpes zoster eruptions again emerged in the left L3 dermatome area. By treatment with intravenous acyclovir, the vesicular eruptions were improved. We assume that IVIg might suppress the immune response against VZV and promote the recurrence of eruptions.