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PubMed1990

[Neurogenic bladder in patients with lumbar vertebral disorders].

Bladder and urethral functions were evaluated urodynamically in 114 patients with lumbar disorders including prolapsed lumbar intervertebral disc (66 patients), lumbar canal stenosis (19 patients), lumbar spondylolysis and/or spondylolisthesis (21 patients), lumbar spondylosis deformans (5 patients) and ossification of the yellow ligament of the lumbar spine (3 patients). The patients consisted of 88 males and 26 females with an average age of 47 years (range 17 to 73 years). Symptomatic organic infravesical obstruction was excluded by physical and radiographic examination. Cystometry revealed preoperative neurogenic bladder in 23 patients (20%); normal detrusor with overactive sphincter in 2 (9%), underactive in 8 (36%), overactive in 5 (23%) and equivocal in 7 (32%). One patient not receiving cystometry revealed abnormal uroflowmetry with 140 ml residual urine. Twenty of them underwent electromyographic examination of the external sphincter and 15 (75%) had an overactive sphincter. Nine (39%) of them complained no urological symptoms. Neurogenic bladder seemed to highly associate in those having abnormal tendon reflex in the lower extremities, decreased bulbocavernosus reflex and sensory disturbance in the perineal area, but there was no statistical significance. Of twenty-three neurogenic bladder patients, eighteen underwent a lumbar vertebral operation and fifteen received postoperative urodynamic evaluation. Uroflowmetry was improved in more than half of the patients within 3 months after the operation and cystometry was normalized in 4 of 7 patients who underwent cystometry over 6 months after the operation. Preoperative overactive detrusor remained unchanged in two of three patients who underwent cystometry over 6 months after the operation.

Adolescent↗
PubMed1975

Neuromuscular disease in secondary hyperparathyroidism.

Neuromuscular function was evaluated in six patients with osteomalacia or secondary hyperparathyroidism, or both, as demonstrated by bone biopsy showing osteomalacia or increased immunoreactive parathyroid hormone, or both. Each patient had weakness, atrophy, and fatigability of proximal muscles, especially of the lower extremities. Most also showed involuntary fine movements of the tongue, hyperactive tendon reflexes with abnormal spread, and decreased vibration sensation, abnormalities similar to those observed in primary hyperparathyroidism. Every patient studies had evidence of neuropathic muscle disease, either on electromyography or muscle biopsy studies histochemically or both. Muscle biopsies showed no definite myopathic features. Treatment of the osteomalacia improved muscle strength. Patients with osteomalacia therefore have a treatable neuromuscular disease that is neuropathic in nature and resembles closely that found in primary hyperparathyroidism.

Adolescent↗
PubMed1999

Type 1 GM1 gangliosidosis with basal ganglia calcification: a case report.

This report concerns a 10-month-old boy, admitted to the Veterans General Hospital-Kaohsiung with generalized tonic convulsion and aspiration pneumonia. He was found to have had developmental regression, progressive hypotonia and hepatosplenomegaly since four months of age. Physical examination revealed a large head circumference (97th percentile), frontal bossing, depressed nasal bridge, hepatosplenomegaly, broad hands and short fingers. Neurologic examination showed poor control of eye movement, profound hypotonia, muscle weakness, brisk deep tendon reflexes and Babinski's sign. Hypoplasia of the vertebral bodies with anterior beaking, wedge-shaped metacarpals, spatulated ribs and a J-shaped sella turcica were displayed on bone radiographs. Cranial computerized tomography scans showed diffuse brain atrophy, dilated ventricles and calcification of the bilateral basal ganglia. Vacuolated lymphocytes were noted in a peripheral blood smear. Type 1 GM1 gangliosidosis was diagnosed based on a deficiency of beta-galactosidase activity. To our knowledge, basal ganglia calcification in type 1 GM1 gangliosidosis has never been reported in the literature. We suggest that type 1 GM1 gangliosidosis be considered in the differential diagnosis of patients with an early onset of neurologic decline, organomegaly and basal ganglia calcification.

Basal Ganglia Diseases↗
PubMed1998

[A case of atypical Guillain-Barré syndrome exclusively showing multiple cranial nerve palsy with an elevation of anti-GQ1b and anti-GT1a IgG antibodies].

This is a case report of atypical Guillain-Barré syndrome (GBS). A 42-year-old woman displayed pharyngeal paralysis after a mild upper respiratory infection, subsequently having developed ophthalmoplegia, facial diplegia and accessory nerve palsy within about ten days. She had neither weakness nor abnormal tendon reflexes in the extremities. During the acute phase of the disease we found significant elevation of anti-GQ1b and anti-GT1a IgG antibodies in the serum, and immunoadsorption therapy had a remarkable effect on the symptoms. Although our case was extremely atypical of GBS in terms of exclusively showing multiple cranial nerve palsy and lacking areflexia, the elevation of anti-glycolipid antibodies during the acute phase suggests that this case shares pathogenesis with GBS.

Adult↗
PubMed1999

[A 40-year-old woman with progressive dementia and abnormal behavior].

We report a 40-year-old Japanese woman who died after 12 years history of progressive dementia and abnormal behaviors. She was well until 1985 at her age of 28 years old, when she had an onset of behavioral change in which she drank much, neglected house-keeping works, and her life style became sloppy. At age 30, she became unable to understand written sentences, and paced up- and down in and out of her house. She was admitted to other hospital where marked dementia with disorientation and memory loss were noted. Slight increase in CSF protein and decrease in the peripheral nerve conduction velocity were also noted at that time. In the next year, she started to have convulsions. These symptoms had progressively become worse and was admitted to Tokyo Metropolital Matsuzawa Hospital in June of 1991 when she was 34 years of age. Despite marked dementia, she was able to walk normally, no motor paralysis, cerebellar ataxia, nor dyskinesia were noted. Deep tendon reflexes were diminished. MRI revealed T-2 high signal intensity lesions involving the white matter of the cerebrum predominantly in the frontal region. In about one year, she started to show difficulty in gait, and she became bed-ridden in July of 1994. She was discharged to home for a while, but required admission again. She expired on February 5, 1998. Her younger brother had an essentially similar dementing disease and he expired at the age of 35 years. The parents were of first cousins. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had adult form of metachromatic leukodystrophy, because of white matter change in the frontal lobe, decrease in nerve conduction velocity, convulsion, marked dementia, and consanguineous marriage with a similarly affected brother. Most of the audience agreed with this conclusion, but the differential diagnosis from globoid cell leukodystrophy was felt difficult from the clinical findings alone. Post-mortem examination revealed marked atrophy in the frontal lobe. Cerebellum appeared to be smaller than normal. In the coronal sections, marked atrophy of the white matter with brown discoloration was noted. The lateral ventricles were dilated. Klüver-Barrera staining revealed marked demyelination with relative preservation of the U-fibers. PAS-positive materials were deposited in some astrocytes as well as neurons. Metachromatic deposits were noted not only in the cerebrum but also cerebllum after staining with acid cresyl violet. Pathologic diagnosis was consistent with adult type of metachromatic leukodystrophy.

Adult↗
PubMed1999

[Progressive muscular weakness due to subacute postinfectious polyradiculitis and myelitis].

In a 67-year-old patient, generalised stable muscular weakness preexisting for several years became rapidly progressive within a few weeks prior to hospitalisation. He died one month after admission from acute cardiocirculatory failure. There was no history of muscular pain, clinical examination showed weak or absent tendon reflexes, hyposensibility of the dorsa of his feet, fasciculations and myocloni of the muscles of the lower limbs as well as a generalised muscular atrophy. Polyneuropathy due to diabetes mellitus and monoclonal IGG-kappa-type gammopathy were preexisting. CSF examination showed inflammatory cerebral fluid changes and further investigations revealed inflammatory polyradiculopathy affecting mainly motor nerve fibres. There was evidence of a reactivated varicella-zoster infection in serum and in the cerebrospinal fluid samples. The search for a tumour, vasculitis or a drug-related cause for this syndrome remained negative. Neuropathological examination at autopsy showed subacute polyradiculitis accompanied by myelitis. The most probable cause of this disorder is immune-mediated polyradiculitis after varicella-zoster infection.

Aged↗
PubMedDate not supplied

[A case of McLeod syndrome].

A 52-year-old man was admitted to our hospital in 1997 because of high serum creatine kinase (CK) level. Neurologic findings revealed chorea on the trunk and extremities, mild weakness of proximal muscles, and absence of deep tendon reflexes in four extremities. Serum CK was elevated to 3,494 U/l (normal, below 235). A peripheral blood smear showed acanthocytes in approximately 1% of the red blood cells (RBCs). Very weak expression of the Kell antigens (K2, K4, K5, and K7) on his RBCs led us to make a final diagnosis of McLeod syndrome. Muscle biopsy from the left biceps showed increased variability in fiber diameter, a few regenerating fibers, scattered fibers with internal nuclei, and mild fiber type grouping. Immunohistochemical analyses of dystrophin. merosin, and adhalin were normal. Although McLeod syndrome is a rare X-linked recessive disorder, it is clinically important for differential diagnosis of chorea acanthocytosis and hyperCKemia.

Acanthocytes↗
PubMedDate not supplied

[A case of mononeuropathy multiplex associated with anti-GM1 and -SGLPG antibodies in a patient with ongoing Hashimoto disease].

We reported a case of mononeuropathy multiplex associated with anti-GM1 and -SGLPG antibodies in a patient with ongoing Hashimoto disease. A 56-year-old woman was admitted with asymmetrical patchy sensory and motor disturbance in the extremities. Muscle atrophy and weakness in the left palm and bilateral tibialis anterior muscles were also noted. Deep tendon reflexes were normal in all the extremities. Superficial and deep sensations were reduced in the hands and feet bilaterally, and the distribution of sensory loss was irregular. Her serum was positive for antinuclear antibody, rheumatoid factor, anti-RNP antibody, and anti-SS-A antibody. Serial electrophysiological studies suggested that the predominant process was axonal degeneration of the sensorimotor nerves. On sural nerve biopsy, there were no findings of vasculitis but severe axonal degeneration was observed. Thin-layer chromatography with immunostaining revealed anti-GM1 and -SGLPG antibodies. Treatment with corticosteroids was successful. In this case, the anti-GM1 antibody may have played a role in the pathogenesis of mononeuropathy multiplex associated with autoimmune disease.

Autoantibodies↗
PubMedDate not supplied

[A case of subacute necrotizing lymphadenitis complicated with brachial plexus neuritis].

A 22-year-old female noted a low grade fever and swelling of the cervical lymph nodes in May 1997, and later developed a dry cough. She was diagnosed to have interstitial pneumonitis, and then administration of corticosteroids alleviated her symptoms. On February 6, 1998, however, a high fever recurred and her swollen cervical lymph node on the right side was biopsied on February 9, 1998. A histological examination revealed an increased number of histiocytes and karyorrhexis of the lymphocytes in the paracortical areas, and she was therefore diagnosed to have histiocytic necrotizing lymphadenitis. She could not fully elevate her arm on February 16, 1998. On admission, her cervical lymph node was swollen on the left side. A neurological examination revealed a marked weakness of the right deltoid muscle, moderate weakness of the right latissimus dorsi, triceps and brachioradialis muscles and also a mild weakness of the serratus anterior, supra- and infra-spinatus, and biceps brachii muscles. The muscle power of the other muscles were normal and no muscle atrophy was evident. Winging of the right scapula was observed. The deep tendon reflexes were normal in all four limbs, and her sensation was also normal. No cerebellar sign was found. The Jackson, Spurling, Allen, Morley and Adson tests were all negative. ESR was mildly elevated to 18 mm/hr, but CRP was negative. RF, ANA and anti-SS-A and SS-B antibodies were positive, whereas LE-test, direct and indirect Coombs tests and other autoantibodies were negative. Needle EMG disclosed fasciculation potentials in the right triceps muscle and polyphasic waves in the right deltoid muscle. MRI showed gadolinium-enhancement of the right brachial plexus. Although an abnormal accumulation of gallium was detected in the right parotid and bilateral submandibular glands, no sicca symptoms were found and the Schirmer test findings were normal. Oral prednisolone (50 mg/day with gradual tapering) alleviated both her symptoms and the gadolinium-enhancement of the right brachial plexus. As a result, her right upper limb paresis was thus considered to have been caused by right brachial plexus neuritis, which was probably associated with histocytic necrotizing lymphadentis. Although acute cerebellar ataxia and meningitis have previously been reported to be complicated with histiocytic necrotizing lymphadenitis, this is the first report to describe the complication of peripheral neuritis with this condition.

Adult↗
PubMed1999

Reversible neurotoxicity induced by a combination of clozapine and lithium: a case report.

A combination of clozapine and lithium can be used in the treatment of refractory schizophrenia, schizoaffective disorder and bipolar disorder with rapid cycling. We report a patient with refractory bipolar disorder who developed side-effects after combination therapy with clozapine and lithium at usual therapeutic dosages. Reversible neurotoxicity developed twice during the therapeutic course, once with the restarting of lithium, the other with increasing the dose of lithium, despite the lithium concentrations being less than 0.5 mEq/l. Neurotoxicity manifested as ataxia, coarse tremor, myoclonus, facial spasm and increased deep tendon reflex. While the mechanism causing toxicity is not clear, interaction between the serotonergic effect of clozapine and lithium may be the cause. This report is evidence that a combination of clozapine and lithium may increase the risk of neurotoxicity. We suggest the need to keep clozapine and lithium at lower dosages and closely monitor their side-effects as necessary when these drugs are used concomitantly.

Adult↗
PubMed1999

[Molecular and clinical features in spinocerebellar ataxia type 6 (SCA6) in Japanese].

Spinocerebellar ataxia type 6 (SCA6, MIM 183086) is an autosomal dominant spinocerebellar degeneration. Mild expansion of a CAG repeat in voltage-dependent Ca2+ channel alpha 1A subunit (CACNL1A) gene, which was predicted to encode a polyglutamine tract, has been identified as a causative mutation for SCA6. SCA6 is one of the common subtypes of spinocerebellar degeneration, accounting for approximately 12% in the dominantly inherited ataxias in Japan. Mean age at onset in the SCA6 patients is 52 years, which is much later than those reported for other autosomal dominant ataxias including SCA1, SCA2, Machado-Joseph disease, and dentatorubral-pallidoluysian atrophy. Anticipation in SCA6 is quite mild. The size of expanded CAG repeats ranged 21 to 26 repeats and was found to be correlated inversely with age at onset in patients with SCA6. Ataxia is most common and cardinal clinical features in SCA6. Patients with a prolonged clinical course, however, show other accompanying clinical features including dystonic postures, involuntary movements, and abnormalities in tendon reflexes. Investigations of the mechanisms of neuronal death in the cerebellum, in particular relation to the impaired function of the voltage-dependent Ca2+ channel and the toxic effects of expanded polyglutamine tracts, will be indispensable for the development of therapeutic measures for SCA6.

Adult↗
PubMed1999

[An autopsy case of multiple system atrophy presenting with rapid progression of autonomic disturbance].

We report an autopsy case of multiple system atrophy (MSA) presenting with rapid progression of autonomic disturbance. He was admitted to our hospital because of gait disturbance and dysarthria. The patient was a Japanese man, who first noticed gait disturbance and dysarthria at age 58, followed by syncope 3 months later. He developed urinary incontinence and frequency of urination 8 months after the disease onset. His gait disturbance, dysarthria, syncope, and urinary symptoms progressed, and he was admitted to the department of neurology 1 year after the onset of the disease. He was clinically diagnosed as having MSA and was followed in the outpatient office. He deteriorated rapidly and was readmitted to the department of neurology 19 months after the onset of the disease. Physical examination showed orthostatic hypotension. Neurological examination revealed nystagmus, dysarthria of cerebellar type, increased deep tendon reflexes, bilateral positive Babinski signs, ataxic and spastic gait, mild right hypesthesia and hypalgesia, impotence, constipation, and urinary incontinence. Routine blood examination showed slight anemia, elevated BUN, GOT, and blood sugar. Electrocardiography revealed sinus tachycardia and chest rentogenogram showed cardiac enlargement. Brain MRI showed atrophy of cerebellum and pons, and lacunae in basal ganglia. Autonomic function tests revealed abnormal in head-up tilt test, and CVR-R in May and November 1995. However 123I-MIBG myocardial scintigraphy showed normal uptake of MIBG in May 1995 and decreased uptake in November 1995. He deteriorated rapidly and died in May 1996. Autopsy findings revealed not only prominent olivopontocerebellar and slight striatonigral lesions, but also autonomic lesions with massive appearance of glial cytoplasmic inclusions. He was pathologically verified as having MSA. In the present patient, autonomic nervous system, especially cardiac sympathetic nerve, deteriorated rapidly, which might result in short duration of the illness.

3-Iodobenzylguanidine↗
PubMed1976

[A case of the anterior choroidal artery aneurysm combined with the abnormal intracranial vascular network (author's transl)].

A case of the anterior choroidal artery aneurysm combined with the abnormal intracranial vascular net-work was reported. The patient was 43-year-old male who was attacked by subarachnoid hemorrhage in February 25th 1975. When he was admitted to our clinic 30 days after the ictus, his general status was good and the neurological examination showed no particular findings except only slightly accelerated deep tendon reflexes on the left side. Cerebrospinal fluid still remained xanthochromic although no nuchal rigidity was denoted. Based on the angiographic four vessel studies, the circulatory condition of the patient's brain was summarized as follows; the internal carotid arteries were stenosed or occluded between the C1 and C2 segment on both sides, and abundant collateral circulation was developed mainly around the circle of Willis making an angiographically peculiar vascular net-work in tha base of the brain. Another angiographic finding to be noticed was a berry aneurysm which originated from the distal part of the left anterior choirdal artery. No special treatment was performed on him. He was discharged without any neurological residuals. It would be difficult to find out any hemodynamic relationship between the occlusion of the internal carotid arteries and occurence of the aneurysm. But the abnormally dilated anterior choroidal artery might suggest that the vessel wall of this artery would be burdened in the abnormal distension stress due to the increased transaxial pressure in this artery. Unqder such a hemodynamically stressed state, it would be possible the aneurysm like outpouching of the vessel wall being developed in some fragile portion of the artery functioning as a prominent collateral circulation.

Adult↗
PubMed1998

[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.

Adult↗
PubMed1999

[What is your diagnosis? Aneurysm of the abdominal aorta destroying the lumbar spine].

A 58 year old woman suffering from lumbalgia over 3 years is admitted for bilateral cruralgia. Ten years before, she was treated for cervix carcinoma by hysterectomy, pelvic and lumbo-aortic radiotherapy and chemotherapy. On admission, physical examination reveals L2 level hypoesthesia and abolition of deep tendon reflexes. Plain films and CT scan show a lysis of L3, L4 and L5 vertebral bodies and a cuneiform appearance of vertebral body of L2 due to a large abdominal aortic aneurysm.

Aortic Aneurysm, Abdominal↗
PubMed1999

The Smith-Magenis syndrome: a new case with infant spasms.

The Smith-Magenis syndrome (SMS) is characterized by congenital anomalies, mental retardation and the interstitial deletion of the 17p. 11.2 chromosome. The subjects affected by this syndrome show cranio-facial dysmorphias, brachycephalia, skeletal, ocular, cardiac, genitourinary and otolaryngological anomalies. The central nervous system is affected and this may be shown by psychomotor retardation, intellective deficit, electroencephalographic alterations (reduced/missing REM phase); the neuroradiological tests detect megacisterna magna, cerebellar hypoplasia, cortical dysplasia, ventricular asymmetry. Behavioural troubles are frequent and, among them, self-aggressive conducts (tearing out the nails). The syndrome is associated with the interstitial deletion of the 17p. 11.2 chromosome. The diagnosis can be made in the pre-natal period and a mosaic situation is possible. Even though the cases of SMS reported in the literature allow defining a characteristic phenotype, studies have been carried out to quantify the deletion of the chromosome 17 in order to identify the chromosomic tract which is responsible for the phenotypical induction. The deletion can either appear de novo or come from one of the parents. In addition, these subjects can show peripheral neuropathy, missing or reduced deep tendon reflexes and (rarely) epileptic crises. However, by reviewing the literature, no descriptions of patients affected by infant spasms are pointed out. This report refers to a new case of Smith-Magenis syndrome in a nine-month-old girl with spasms in extension.

Brain↗
PubMedDate not supplied

[A case of bilateral brachial plexopathy after median sternotomy].

A 53-year-old man with bilateral brachial plexopathy after median sternotomy for cardiac surgery was described. When he was awakened six days after cardiac surgery, he experienced weakness and paresthesia of both upper limbs. Neurological examination revealed moderate to severe atrophy and weakness of right biceps, brachioradialis, left triceps, and distal muscles of both upper limbs, and paresthesia around the right thumb and the left hypothenar. Deep tendon reflex of the right biceps, triceps, brachioradialis and left triceps was absent. In addition, he showed Horner's syndrome at the left side. The results of needle EMG and nerve conduction study indicated the damage of the right upper trunk and left middle and lower trunks of the brachial plexus. Although brachial plexopathy following median sternotomy has previously been reported in Western literatures, there is only a single report of unilateral brachial plexopathy in Japan. This is the first report in Japan of the bilateral brachial plexopathy following median sternotomy, and suggests that brachial plexopathy should be recognized as a complication of median sternotomy.

Brachial Plexus↗
PubMed1999

[A case of atypical Miller Fisher syndrome associated with antiphospholipid antibodies].

We report a 56-year-old man with external ophthalmoplegia and ataxic gait following a diarrhea, being diagnosed atypical Miller Fisher syndrome (FS). On admission, he had severe diplopia and bilateral external ophthalmoplegia were observed. The deep tendon reflexes were decreased on the right upper extremity. He could not walk straight and his tandem gait was impaired. Serum IgG anticardiolipin antibody (aCL) and APTT-lupus anticoagulant (LA) were found to be increased. The serum of the patient had low titer of anti-GQ 1 b and anti-GM 1 antibodies. After the first immunoadsorption therapy, his ophthalmoplegia was improved moderately, but peripheral facial palsy appeared. He was treated with immunoadsorption again, then all neurologic symptoms improved and a follow-up study revealed normalized aCL and LA titers. There have been no previous reports of FS associated with antiphospholipid antibody. The low titer of serum anti-GQ1b and anti-GM 1 antibodies in this patient suggests that the antiphospholipid antibodies, such as aCL and LA, may be linked to the pathogenesis of FS.

Antibodies, Antiphospholipid↗