Hiroaki Iguchi

Bupivacaine Hydrochloride Induces Muscle Fiber Necrosis and Hydroxyl Radical Formation-Dimethyl Sulphoxide Reduces Hydroxyl Radical Formation

We induced acute skeletal muscle necrosis in rats using bupivacaine hydrochloride and found that both 2,5- and 2,3-dihydroxybenzoic acid significantly increased in skeletal muscle. A single administration of dimethyl sulphoxide, a free radical scavenger, significantly lowered concentrations of 2,5- and 2,3-dihydroxybenzoic acid. These results suggest that dimethyl sulphoxide is an effective hydroxyl radical scavenger and may be useful in the treatment of myopathy.

Ulcerative colitis presenting as sensorineural deafness, brainstem encephalopathy, and white matter lesions.

Background:Several rare neurologic complications of ulcerative colitis have been reported. Review Summary:We report a 69-year-old Japanese woman who developed bilateral sensorineural deafness, 2 attacks of bilateral ophthalmoplegia, and bilateral facial nerve palsy in association with ulcerative colitis. Laboratory data showed elevated cerebrospinal fluid (CSF) protein without pleocytosis, abnormal auditory brainstem evoked potentials, and multiple high signal lesions on magnetic resonance imaging of the brainstem and cerebral deep white matter. Her symptoms improved with corticosteroid therapy except for sensorineural deafness and an exacerbation of cerebral deep white matter lesions without any new clinical signs. Conclusion:Immunologic mechanisms may have led to her central and peripheral nervous system findings in addition to her colon disorder.

A case of Vernet syndrome with varicella zoster virus infection.

A 40-year-old man was admitted to our department, because of sudden onset of dysphagia, hoarseness, left neck pain and headache. There were no skin lesions. On neurological examination, there were paralysis of the left soft palate and constrictor muscles of the pharynx, weakness of the left sternocleidomastoid and left upper trapezius. In cerebrospinal fluid (CSF) examination, cell count and protein concentration were elevated. Antibody titer to varicella zoster virus (VZV) was elevated in both the serum and CSF. And VZV-DNA was detected by PCR from CSF. Gd enhanced MRI showed the nodular lesion at the left jugular foramen. The diagnosis of Vernets syndrome (VS) associated with VZV infection was made. The patients symptoms were immediately improved with 30 mg of prednisone and 3 g of varaciclovir daily for 14 days. Only a few cases of VS due to VZV have been reported previously. Our case is the first case that detected VZV-DNA in CSF by PCR.

A case of voluntary palatal myoclonus with ear click: relationship between palatal myoclonus and click.

Introduction Anatomy and pathology of palatal myoclonus are well established and commonly involve hypertrophic degeneration of the inferior olivary nucleus including the Guillain-Mollaret triangle (dentate nucleus, red nucleus, and inferior olivary nucleus and central tegmental tract). Deuschl et al. [1], after a survey of the literature, reported that cerebrovascular disease was present in 55% of the patients having symptomatic palatal myoclonus. Other conditions present included multiple sclerosis, meningoencephalitis, infectious diseases, head trauma, vertebral artery aneurysms, neoplasms, psychosis, and heredofamilial tremor. We encountered a patient with essential palatal myoclonus who was able to voluntarily induce the disturbance. His condition was associated with clicking, and to clarify the mechanism responsible for this, we conducted an otorhinolaryngological study.

Relapse of ocular symptoms after remission of myasthenia gravis—a comparison of relapsed and complete remission cases

Extended thymectomy and high-dose alternate-day prednisolone administration may increase the chance of remission in myasthenia gravis (MG) patients. In cases of remission, ocular symptoms sometimes reappear after a gradual decrease or discontinuation of prednisolone administration. We compared relapsed patients with those who experienced complete remission. We found that the period from onset of MG to thymectomy and initiation of prednisolone administration was longer in the relapsed cases, which suggests that early thymectomy and administration of prednisolone can lead to a superior outcome in MG patients.

A case of myasthenia gravis accompanied by erythema elevatum diutinum and rheumatoid arthritis

Sirs: Myasthenia gravis can occasionally be accompanied by many autoimmune diseases, such as rheumatoid arthritis [9, 12], systemic lupus erythematosus [9, 12], Sjogrens syndrome [2, 3], ulcerative colitis [10], Hashi toxicosis [9, 12], alopecia areata [10, 11], lichen planus [10], vitiligo [10] and lympoma [6]. We have never experienced a case of myasthenia gravis associated with erythema elevatum diutinum (EED). The aetiology of EED is still unknown; however, immunological causes have been postulated. A 56-year-old woman first experienced a nasal voice in December 1993, a symptom which worsened in the afternoon, though she could speak comfortably after resting. In May 1994, she experienced dysphagia and subsequently visited an otolaryngologist, where weak palatal movement was discovered. In June, she visited a neurologist. She was diagnosed with myasthenia gravis because of facial weakness, dysarthria and weakness of palatal movement, though her symptoms disappeared with an edrohoneum chloride test. Subsequently, she was treated with 180 mg/day pyridostigumine bromide. In June, she was admitted to an university hospital. Serum antiACh-receptor antibody was 65 nmol/ml. Median nerve repetitive stimulation test revealed waning (50~60 % decrease). She was administered prednisolone (PSL) on alternate days, and the dose was gradually increased to 100 mg on alternate days. Her symptoms gradually improved. Thymectomy was performed on August 8, and pathology of thymus revealed hyperplasia. The dose of PSL was gradually decreased and finally discontinued on 15 March, 1997. In May 1997, she suffered polyarthralgia, and an orthopaedist diagnosed rheumatoid arthritis. In January 1999, multiple skin lesions appeared in the limbs. On May 5, 1999 she visited our hospital, and her myasthenic symptoms were almost recovered except for slight weakness of the upper limbs. Rheumatoid factor was 107 IU/ml. Symmetrical multiple red-purple erythematous, nodular lesions were observed on the extensor surface of the hands, especially the extensor surface of joints (Fig. 1-a,b,c). Dermatologists diagnosed this condiLETTER TO THE EDITORS

CNS INVOLVEMENT IN HEREDITARY NEUROPATHY WITH PRESSURE PALSIES (HNPP)

We read the excellent article by Tackenberg et al., who reported that prolonged latency of blink reflex (BR) and T2-weighted hyperintensities were seen in their patients with HNPP.1 Physical examination did not show any evidence of …

T-588 Protects Motor Neuron Death Following Axotomy

R(—)-1-(benzo [b] thiophen-5-yl)-2-[2-(N,N-diethylamino)ethoxy] ethanol hydrochloride) (T-588) enhances acetylcholine release. This compound slows the motor deterioration of wobbler mouse motor neuron disease and enhances neurite outgrowth and choline acetyltransferase activity in cultured rat spinal motor neurons. We examined the ability of T-588 on axotomized spinal motor neuron death in the rat spinal cord. After the postnatal unilateral section of sciatic nerve, there was approximately a 50% survival of motor neurons in the fourth lumbar segment. In comparison with vehicle, intraperitoneal injection of T-588 for 14 consecutive days rescued spinal motor neuron death. Our results showing in vivo neurotrophic activity of T-588 for motor neurons support the applicability of T-588 for the treatment of motor neuron diseases, such as amyotrophic lateral sclerosis and motor neuropathies.

Cheiro-oral-pedal syndrome due to brainstem hemorrhage

Cheiro-oral-pedal syndrome is characterized by specific sensory disturbance around the corner of the mouth, in the hand and in the foot on the same side. Lesions responsible for causing this syndrome vary. We report two cases of cheiro-oral-pedal syndrome due to midbrain and pontine hemorrhage, respectively. Pontine hemorrhage producing cheiro-oral-pedal syndrome has been reported in three cases, but this is the first case that midbrain hematoma exhibits this syndrome. Damage in the sensory pathway can cause cheiro-oral-pedal syndrome. Difference in the threshold may explain the specific sensory pattern in this syndrome. Cheiro-oral-pedal syndrome is caused by lacunar infarction in majority of the cases. However, it should be kept in mind that hematomas can cause cheiro-oral-pedal syndrome.

Cheiro-pedal syndrome following pontine infarction

Abstract We report the case of a 64-year-old man with sudden onset of numbness in the right hand and foot. Neurological examinations were normal except for hypersthesia, and hyperalgesia of the right hand and foot. Brain MRI demonstrated a high signal intensity on T2-weighted image and a low signal intensity on T1-weighted image in the left tegmetum of the pons. He was diagnosed with pontine infarction presenting with cheiro-pedal syndrome (CPS). Damage in the sensory pathways can cause CPS. Difference in the threshold may explain the specific sensory pattern in this syndrome. Further examination of the relationship between sensory symptoms and localization on MRI is needed to clarify this syndrome.