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PubMed2001

[A patient with vitamin E deficient, myopathy presenting with amyotrophy].

We report a 61-year-old man with vitamin E deficiency, presenting with, myopathy as an only clinical symptom. In 1997, at 59 years of age, he noted mild proxymal-muscle weakness and atrophy in the four extremities, nine years after he received a Billroth II partial gastrectomy for a gastric ulcer. His muscle weakness slowly exacerbated, and he was admitted to our hospital in 1999. On admission, neurological examination confirmed mild proximal-muscle weakness and atrophy in the four extremities. Intelligence, cranial nerves, coordination, sensation and tendon reflexes were all normal. Laboratory examination showed normochromic anemia (Hb 9.9 g/dl, Ht 30.9%, MCV 97.5 fl, MCHC 31.2 pg), hypoproteinemia (5.0 g/dl), and hypocholesterolemia (107 mg/dl). The levels of serum CK, lactate and pyruvate were normal. The serum vitamin E level was markedly reduced (0.17 mg/dl; normal 0.75-1.41). Cerebrospinal fluid was normal. Nerve conduction, sensory evoked potentials (SEP), electromyography (EMG), head CT and electroencephalography (EEG) were all normal. Muscle biopsy from the right deltoid muscle showed both mild myogenic and neurogenic changes. Remarkably, type 1 muscle fiber predominance and granular accumulation of autofluorescent lipofuscin granules in the muscle fibers were found. These pathological findings were compatible with those of vitamin E-deficient myopathy. Thus, he was diagnosed as having vitamin E-deficient myopathy, which was confirmed by apparent effective supplementation of vitamin E. Interestingly, our present case did not show any other neurological manifestations such as deep sensory disturbance, sensory ataxia or polyneuropathy. A long-term workload due to hard physical labor and smoking in our patient may have accelerated oxidative muscle damage, resulting in amyotrophy mainly due to vitamin E deficient myopathy.

Gastrectomy↗
PubMed2001

[A patient with restless legs syndrome/periodic limb movement successfully treated by wearing a lumbar corset].

We report a 77-year-old woman with restless legs syndrome(RLS) and periodic limb movement(PLM). From 62 years of age, she was awakened by tingling and involuntary movement in her legs during sleep. There symptoms disappeared when she stood up and walked. She was treated with clonazepam (2.5 mg/day) and valproate (400 mg/day) at 77 years of age, and the symptoms clearly ameliorated. However, she developed mild truncal ataxia and was referred to our hospital. On admission, neurological examination revealed Babinski and Chaddock signs bilaterally with depressed tendon reflexes in the lower limbs, mild truncal ataxia and horizontal gaze nystagmus. She did not present with involuntary movement of the legs while taking the anti-epileptic drugs. Cessation of these drugs alleviated the truncal ataxia and nystagmus, but reexacerbated abnormal sensation with involuntary movement in her legs during sleep. The involuntary movements in her legs were slower than myoclonus and resembled a Babinski reflex (duration about 1 second), and they appeared periodically (around every 30 seconds) in I-II sleep stages. Neither brain MRI nor EEG detected any abnormality. Cervical MRI revealed focal compression of the spinal cord by osteophytes at C5-C6 (more severe on the left side). Motor evoked potentials with transcranial magnetic stimulation revealed a mild delay in the central conduction time (CCT), which was more prolonged on the left side. She was thus diagnosed as having RLS/PLM with involvement of the bilateral pyramidal tracts. Although nerve conduction studies did not detect any abnormality in the peripheral nerves, RLS/PLM of the left leg was induced by electric stimulation of the left tibial nerve. Because she did not want medication any more, we treated her with a lumbar corset, hoping that wearing a lumbar corset might induce contraction of the truncal muscles that would mimic standing and walking or might produce additional sensory input that would induce a 'sensory trick'. Consequently, her abnormal sensation and involuntary movement during sleep as well as the stimulation of the tibial nerve disappeared. Wearing a lumbar corset may inhibit the excitability of the spinal cord that generates RLS/PLM, though the level of sensory input by the corset was higher than the input level of abnormal sensation in her legs. A lumbar corset may be a useful alternative choice for patients with RLS/PLM, who cannot tolerate either anti-epileptic or dopaminergic drugs.

Aged↗
PubMed2001

Superior mesenteric artery syndrome associated with hereditary motor and sensory neuropathy type II--a case report.

A 14-year-old girl with superior mesenteric artery (SMA) syndrome associated with hereditary motor and sensory neuropathy (HMSN) type II is reported. The initial presentations of HMSN type II were developmental delay and gait disturbance at 2 years of age. All deep tendon reflexes were absent. Nerve conduction velocities and left sural nerve biopsy all revealed axonal changes. Recently, she suffered from intermittent bilious vomiting and epigastralgia for 6 months. That caused body weight loss from 40 kg to 28 kg. Abdominal echography showed narrowed superior mesenteric artery angle. Upper gastrointestinal series revealed obstruction of third portion of duodenum. Accordingly, SMA syndrome was diagnosed. To the best of our knowledge, this case is the first report of SMA with HMSN type II in the world. When a child with chronic neurological disease presents with intermittent vomiting, SMA should be considered as a disease entity of differential diagnosis.

Adolescent↗
PubMed2002

[A 68-year-old woman with dementia and parkinsonism].

We report a 68-year-old woman who developed progressive dementia and parkinsonism. She was well until 1990 when she was 58 years of age. She started to show memory loss. Four years later, she developed difficulty in dressing and behavioral problems such as eating rice with her hands, going out of her house without purposes, and difficulty in finding the rest room in her house. She was admitted to the neurology service of Hatsuishi Hospital on January 19, 1996, when she was 64 years of the age. On admission, she was alert but markedly demented. The score of Hansegawa Dementia Scale was 0/30. She was unable to make any coherent conversation. She appeared to have dressing apraxia but did not appear to have aphasia. Cranial nerves were intact. She walked in small steps with stooped posture. She did not have motor weakness but she showed plastic rigidity in all four limbs. No tremor or ataxia was noted. Deep tendon reflexes were within normal limits but the plantar response was extensor bilaterally. She continued to deteriorate after admission. In May of 1998, she started to fall. In June of 1998, she had a generalized convulsion. In January of 1999, she became unable to take foods orally and a gastrostomy was placed. She expired on May 29, 1990. She was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had Alzheimer's disease. The question was whether her parkinsonism was a part of her Alzheimer's disease or she had an additional disease to explain her parkinsonism. Post-mortem examination revealed moderate to marked atrophy of the frontal and the temporal lobes as well as in the limbic areas with dilatation of the lateral ventricles. Marked neuronal loss was noted in the CA 1 to the subiculum region with gliosis. Neurofibrillary tangles were seen in the remaining neurons. Neuropil threads were seen by Gallyas-Braak staining. Similar changes were seen in the parahippocampal gyrus and in the entorhinal cortex. Senile plaques were seen in the insular cortex and in other cortical areas. Cortical type Lewy bodies were seen in the cingulate cortex. The Meynert nucleus showed marked neuronal loss and gliosis. The substantia nigra and the locus coeruleus showed moderate loss of pigmented neurons. Lewy bodies were seen in these regions. The dorsal motor nucleus of the vagal nerve was retained, however, one Lewy body was observed. Pathologic diagnosis was Alzheimer's disease plus Parkinson's disease. It is an interesting question whether or not her parkinsonism was due to nigral lesion or frontal lesions. It is known that parkinsonism may complicate in advanced Alzheimer's disease not necessarily due to nigral lesion. On the other hand, in incidental Lewy body disease, the substantia nigra shows mild Parkinson's disease-like change without clinical parkinsonism. This patient appeared to have been a true complication of Alzheimer's disease and Parkinson's disease.

Aged↗
PubMed2001

[A case of Machado-Joseph disease presenting pure cerebellar ataxia].

We report a 61-year-old woman with Machado-Joseph disease (MJD) presenting with pure cerebellar ataxia. The patient exhibited an unsteady gait at the age of 51 years. She was admitted to our hospital at the age of 61 years. Her older brother had been diagnosed as having spinocerebellar degeneration (SCD). Our patient showed gaze-evoked nystagmus, wide-based gait, slight lack of coordination of the four extremities, mildly ataxic speech and slight decrease in the bilateral Achilles tendon reflexes. Babinski's sign was absent. Sensory impairments were not present and muscle tone and muscle strength were normal. There was no autonomic dysfunctions. MRI revealed moderate atrophy of the cerebellum and pons. We performed gene analysis of SCD using white blood cells from the patient, and the analysis showed 70 CAG repeats in the MJD1 gene, which is an abnormally high number of repeats. Compared with three reported cases of MJD presenting pure cerebellar ataxia, only our patient showed a nasal voice. The number of CAG repeats in the MJD1 gene of our patients was the most prolonged of the four cases. MJD should be considered in patients with familial SCD even if their neurological signs and symptoms outside the cerebellum are not obvious.

Ataxin-3↗
PubMed2002

[Dopa-responsive dystonia--a hereditary dystonia easy to treat].

BACKGROUND: Dopa-responsive dystonia is a genetically determined disorder with early onset. The dystonia usually manifests as a disturbance of gait with fatigue and may be confused with spasticity. The diagnosis is based on clinical recognition and response to l-dopa, which is usually complete and long lasting. The most common genetic defect involves the gene for GTP cyclohydroxylase I. MATERIAL AND METHODS: We describe a Norwegian family in which three generations are affected. RESULTS: All those affected had gait disturbance from childhood; the disturbance became worse during the day and after exercise. Clinical examination revealed reduced fine motor skills and brisk tendon reflexes. Dystonic posturing of one or both legs could be seen during walking. All patients were treated with l-dopa with excellent effect. INTERPRETATION: Though uncommon, this disorder is an important differential diagnosis in children with gait disturbance, particularly in those suspected as having spastic paraparesis.

Adolescent↗
PubMed2001

[A case of atopic myelitis in the area other than Kyushu Island].

A case of acute myelitis associated with atopic dermatitis, hyperIgEemia and mite antigen specific IgE was reported. A 22-year old woman with a history of atopic dermatitis since her childhood began to have numbness in her legs, which extended upward to her upper part of chest in four days. Neurological examination revealed Lhermitte's sign, moderate disturbance of superficial and deep sensation below the Th4 level, and sensory ataxia. She also showed exaggerated deep tendon reflexes in the upper extremities and urinary difficulty. MRI studies revealed an intramedullary T1-low, T2-high lesions without Gd-DTPA contrast enhancement in the posterior part of the cervical spinal cord at C3 level. The laboratory examination revealed normal CSF, and the elevated level of serum IgE and mite-antigen-specific IgE in sera. We conclude that this case is thought to be atopic myelitis, which was reported as acute myelitis associated with hyperIgEemia and atopic dermatitis proposed by Kira et al. This is the first report of a case outside of Kyushu area in Japan.

Adult↗
PubMed2001

[A patient with neuroborreliosis presenting gadolinium-enhanced MRI lesions in bilateral facial nerves].

We report a 33-year-old man with bilateral facial paralysis due to neuroborreliosis. About three weeks after rhinorrhea and fever lasting four days, he noticed fatigue in the legs and paresthesia in all four extremities. Another week later, he developed paresthesia in his tongue and bilateral facial muscle weakness, and was admitted to our hospital. On admission, neurological examination revealed moderate bilateral facial muscle weakness, mild paresthesia in the tongue and four extremities, and decreased Achilles tendon reflex bilaterally. Mild pleocytosis and increased protein were found in the cerebrospinal fluid (CSF). IgM antibodies that reacted with the antigens of Borrelia garinii and Borrelia afzelii were found in his serum. Clinically and serologically, he was thus diagnosed as having neuroborreliosis. Brain MRI revealed gadolinium-enhanced lesions of the bilateral facial nerves in the facial nerve canal portion. After three weeks of treatment with 100 mg/day doxycycline and 2 g/day ceftriaxone sodium, his symptoms and CSF abnormalities were rapidly improved. Although facial nerve paralysis is a major symptom of neuroborreliosis, the present report is the first to detect the inflammatory lesions of the facial nerves in the facial nerve canal portion by MRI.

Adult↗
PubMed2001

[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.

Endothelial Growth Factors↗
PubMed2001

[A case with upper limb dominant Guillain-Barré syndrome and serum IgG anti-GT1a antibodies: sparing oropharyngeal palsy].

We report a 78-year-old man with Guillain-Barré syndrome (GBS) who showed upper limb dominant muscle weakness following an upper respiratory infection. He had no weakness in extraocular, oropharyngeal and neck muscles. Tendon reflexes were absent in his upper limbs. Electrophysiological studies suggested demyelination of motor nerves in his upper and lower extremities. He had serum IgG antibodies to GM1 and GT1a but not to GQ1b. Anti-GT1a antibodies did not cross-react to GM1 by means of the absorption test. Titers of the antibodies decreased after recovering from muscle weakness of upper limbs. Since the presence of serum antibodies to GT1a but not to GQ1b were reported in patients with pharyngeal-cervical-brachial weakness of Guillain-Barré syndrome, it has been suggested that anti-GT1a antibodies play a role in acute oropharyngeal neuropathy. This is the first report of a patient with GBS lacking oropharyngeal palsy who had serum IgG antibodies to GT1a but not to GQ1b. Our case suggests that anti-GT1a antibodies are related not only with acute oropharyngeal neuropathy but also with upper limb dominant motor neuropathy.

Aged↗
PubMed2002

[Syringomyelobulbia associated with cervical spondylosis. Pathophysiology and therapeutic implications].

Spinal spondylosis is rarely implicated in syringomyelia. We report the case of a 70-year-old patient with a 10-year history of gait disturbance; constrictive pain of lower limbs and urinary incontinance. Physical examination disclosed spastic tetraparesis. In the upper limbs, deep tendon reflexes were abolished, with hyposthesia and hands amyotrophy. Brain and cervical MRI showed syringomyelobulbia with cervical spondylotic myelopathy. Extensive cervical laminectomy induced a mild clinical improvement. A second MRI performed 6 months after surgery depicted a complete disappearance of the bulbo-medullar cavitation with secondary atrophy. Extradural spondylotic compression of the spinal cord should be firmly considered as an etiology of syringomyelia. A purely extradural decompression could be sufficient to induce regression of the medullary cavitation.

Aged↗
PubMed2001

[A case of recurrent aseptic meningitis caused by high-dose intravenous gammaglobulin therapy for chronic inflammatory demyelinating polyneuropathy].

We experienced a patient of CIDP who was twice complicated with aseptic meningitis following high-dose intravenous gammaglobulin therapy. The patient was a 29-year-old woman who first developed gait disturbance in September 1998. Neurological examination revealed muscle weakness and sensory disturbance in the distal parts of four extremities and decrease of deep tendon reflexes. Cerebrospinal fluid analysis revealed an elevated protein content and a normal cell count. Steroid therapy was effective in early stage, however, this effectiveness had been reduced gradually. She received high-dose intravenous gammaglobulin administrations in September 1999. On the fourth day after start of this therapy, she developed severe headache, nausea and nuchal rigidity without fever. Cerebrospinal fluid analysis revealed an increased cell count of mononuclear predominance and an elevated protein content. As bacterial culture remained negative and viral titers were not elevated, aseptic meningitis was diagnosed. The therapy was stopped, and thereafter her headache continued for 7 days. The muscle weakness and sensory disturbance were remarkably improved, but 9 months later, her symptoms became worse again. She received high-dose gammaglobulin administrations for 2 days in June 2000 and developed aseptic meningitis again. Over again, 9 months later, she received the same medication for only 1 day in March 2001 and she developed mild headache but not meningitis. Aseptic meningitis with CIDP following high-dose gammaglobulin therapy was rare, however, we should pay attention to this therapy in patients with CIDP and may prevent the occurrence of aseptic meningitis by reducing the total dose and shortening the administration periods of gammaglobulin.

Adult↗
PubMed2001

[Sequential magnetic resonance imaging and neurophysiological studies in a patient with inferior spinal cord infarction].

A 66-year-old woman suddenly developed anterior spinal artery syndrome with complete flaccid paraplegia, superficial sensory disturbance caudally to the L5 dermatome level with preservation of deep sensation, incontinence, and absent deep tendon reflexes in both legs. An MRI of the whole spine and an analysis of the CSF 4 hours after onset were normal. The electrophysiological study showed an absence of F wave on the posterior tibial nerve stimulation on admission, while the peripheral nerve conduction velocities and amplitudes of upper and lower limbs were normal. T2-weighted MRI 4 days after onset demonstrated an area of high signal intensity in the gray and white matters of the epiconus and conus medullaris, and T1-weighted MRI showed the swelling. Three weeks later, F wave became evoked nd the high signal areas on axial T2-weighted MRI were localized in the bilateral anterior horns of the gray matter. T1-weighted MRIs after an administration of Gd-DTPA 3 and 7 weeks after onset demonstrated an enhancement of the ventral roots of the lumbar nerves and cauda equina, while the enhancements disappeared 8 months after onset. The patient was finally able to walk independently over 10 meter. An absent F wave was an only positive finding at the hyperacute (hours after onset) stage of the spinal cord infarction.

Aged↗
PubMedDate not supplied

[Roussy-Levy's syndrome: clinical aspects (author's transl)].

A case of non familial Roussy-Lévy syndrome is presented: optic atrophy, gait ataxia, bilateral hypotrophy of thenar and hypothenar muscles, weak deep tendon reflexes of the upper limbs, weak knee jerks, absent ankle jerks, bilateral Babinski, anapallaesthesia from the bisiliac spine distally, bilateral pes cavus. The literature on Roussy-Lévy syndrome is discussed and whether this syndrome should be considered as a precise entity among heredo-degenerative diseases. The overlapping of differing clinical features may suggest an intermediate form between Friedreich's and Charcot-Marie-Tooth's diseases.

Adult↗
PubMedDate not supplied

The silent period in patients with chronic renal failure undergoing hemodialysis.

Silent period was evaluated in 20 adult male patients with chronic renal failure undergoing hemodialysis. Readings were obtained by supramaximal stimulus to the median nerve, during maximum isometric effort of the abductor pollicis brevis muscle against resistance. Two types of abnormalities were observed, motor neuron hypoexcitability with elongated silent period, and motor neuron hyperexcitability with reduction or absence of silent period. Some abnormalities are probably linked with dialysis duration, but show no correlation to presence or absence of peripheral neuropathy. The silent period alterations described in this study could possibly correlate with some other clinical feature frequently seen in patients with chronic renal failure such as hypereflexia of the deep tendon reflexes.

Adult↗
PubMed2002

[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.

Diabetic Neuropathies↗
PubMed2002

Temporal arteritis and Guillain-Barré syndrome.

The association of temporal arteritis and Guillain-Barré syndrome has rarely been reported. We describe a patient who sequentially suffered from both disorders. An 81-year-old woman presented with headache and loss of appetite. Analysis showed anemia and an erythrocyte sedimentation rate of 94 mm/hr. Temporal artery biopsy disclosed giant cell arteritis. Upon treatment with prednisone, all symptoms improved. A few weeks later, the patient began having low back pain, paresthesias, ascending weakness, and unexplained intermittent hypotension. Examination showed absent tendon reflexes in the knees. Cerebrospinal fluid contained one mononuclear cell/dL, and a protein level of 81 mg/dL. An electrophysiologic study revealed reduced nerve conduction velocities. Intravenous immunoglobulin therapy was instituted, and all symptoms slowly disappeared. This is the third reported case of Guillain-Barré syndrome in association with temporal arteritis. The other two patients recovered. Although the association of Guillain-Barré syndrome and temporal arteritis in these three patients could be coincidental, a common immunologic mechanism is also a possibility.

Aged↗
PubMed2002

Neurophysiological changes in Japanese encephalitis.

Japanese encephalitis (JE) is an encephalomyelitis involving cortex, subcortex, brainstem and spinal cord. There is paucity of studies on the neurophysiological evaluation in JE. This study aims at comprehensive evaluation of EEG, sensory and motor evoked potentials, nerve conduction and electromyography; and correlate these with clinical findings. Sixty five patients with JE diagnosed on the basis of clinical, radiological and virological criteria were subjected to a detailed clinical evaluation during the acute stage of illness. Cranial CT scan or MRI was carried out in all the patients. All the patients underwent 10 or 18 channel EEG, motor and sensory evoked potentials to both upper and lower limbs bilaterally as well as peroneal and sural nerve conductions and concentric needle EMG. Outcome, was defined at the end of 3 months into poor, partial and complete recovery. The patient's age ranged between 2-65 years. There were 40 males and 25 female patients. Fifteen patients were less than 12 years of age. History of seizure was present in 31 patients. Quadriplegia was seen in 39 and hemiplegia in 8 patients. Muscle wasting was present in 16 patients and tendon reflexes were reduced in 12 and of mixed pattern in 14 patients. Cranial MRI revealed thalamic lesion in 38, basal ganglia in 21, substantia nigra in 30, pons in 5, cerebellum in 3 and cerebral cortex in 7 patients out of 57 patients. EEG revealed nonspecific theta to delta slowing in 45, alpha pattern coma in 5 and epileptiform discharges in 8 patients. EMG revealed fibrillations in 23 patients. Motor evoked potentials were abnormal in 34 out of 46 patients and revealed patchy and focal abnormalities comprising of unrecordable, prolonged and normal pattern. Somatosensory evoked potentials were abnormal in 8 patients only. At 3 month, 26 patients had complete, 13 partial and 15 had poor outcome. Eight patients died in acute stage and 3 were lost to followup. MEP correlated with weakness and 3 month outcome whereas EEG, SEP and EMG did not have any correlation. MEP changes were more frequent in JE and had prognostic significance.

Adolescent↗