[Writing by James Parkinson and epidemiology].
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England↗
Biomedical subjects
H Kowa
Publications and source records attributed to H Kowa.
Platelet superoxide dismutase in migraine and tension-type headache.
Superoxide dismutase (SOD) is a radical-scavenging enzyme. We determined Cu, Zn-SOD concentrations and activities in platelets from subjects with migraine and tension-type headaches. Thirty migraine without aura (MWoA) patients, 9 migraine with aura (MWA) patients, and 53 tension-type headache patients were selected for study. Thirty healthy volunteers composed the control group. Concentrations of platelet SOD were determined using enzyme-linked immunosorbent assay techniques. The activity of platelet SOD was determined by measuring reductivity of nitroblue tetrazolium. Low concentrations of platelet SOD were found in patients with MWA and MWoA. Platelet SOD activity decreased in MWA patients but not in patients with MWoA or tension-type headaches. These findings suggest vulnerability to oxidative stress in patients with migraine. It is suggested that low platelet SOD levels may play an important role in the etiology of migraine.
Adult↗
Seven-year follow-up study of bromocriptine therapy for Parkinson's disease.
A 7-year nationwide study of bromocriptine monotherapy and combination therapy with bromocriptine and levodopa in Parkinson's disease is reported. Of 22 patients who had been on bromocriptine monotherapy for 7 years (group B), 16 remained improved or remained in the same stages of Hoehn and Yahr, and no wearing-off phenomenon or dyskinesia was observed. In another 56 patients who were started on bromocriptine alone, but in whom combination therapy with levodopa was instituted at some time in the 7 years (group BL), disease progressed faster than in group B. A wearing-off phenomenon and dyskinesia occurred in 34% and 5.4% of the patients, respectively. These manifestations appeared only after initiation of levodopa. The favorable course of group B suggests possible neuroprotective effects of bromocriptine or may be due to the inevitable selection of patients who had a favorable course originally.
Adult↗
Antineuronal antibodies in acute cerebellar ataxia following Epstein-Barr virus infection.
A 29-year-old man developed acute cerebellar ataxia following Epstein-Barr virus infection. Serum IgG and IgM antibodies reacted with both nuclear and cytoplasmic elements of neurons. Western blot revealed IgG binding to the 34- and 29-kd bands and IgM binding to the 44-, 37-, and 29-kd bands. The IgM reactivity gradually reduced. There was no identifiable neoplasm and the ataxia gradually improved. These findings suggest a role for autoimmune mechanisms in the pathogenesis of acute cerebellar ataxia.
Adult↗
[Clinical factors relating to the presence of serum anti-GM1 and GD1b antibodies in demyelinating neuropathy--study using a multivariate analysis].
We studied clinical factors relating to the presence of serum anti-GM1 and GD1b antibodies in patients with demyelinating neuropathy using a multivariate analysis. Sera were obtained from 46 patients with chronic inflammatory demyelinating polyneuropathy (CIDP) and 33 with Guillain-Barré syndrome (GBS) and kept frozen at -20 degrees C until use. Anti-GM1 and GD1b IgM and IgG antibodies were measured by ELISA at serum dilution of 1:100 and considered to be positive when those values were more than the cut off values determined by means and standard deviations in 35 normal controls. Age, sex, duration, prodromal disease, neurological findings, concentration of CSF protein, nerve conduction, treatment, and outcome were investigated in all patients retrospectively. Multivariate logistic models using all those characteristics were used to clarify the clinical factors relating to the presence of anti-GM1 and GD1b antibodies. In CIDP, anti-GM1 antibodies associated with or without anti-GD1b antibodies were frequently seen in patients with motor dominant neuropathy than those with sensory dominant neuropathy (P = 0.007, odds ratio = 11.6). There was significant difference in anti-GM1 IgM antibodies (P = 0.003, odds ratio = 22.2), but no difference in IgG antibodies. Anti-GM1 antibodies were observed 5 (IgM, 5; IgG, 2) of 7 patients with pure motor neuropathy, 9 (IgM, 8; IgG, 4) of 17 with motor dominant neuropathy, 5 (IgM, 2; IgG, 3) of 16 with sensori-motor neuropathy, and none of 6 with sensory dominant neuropathy.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[A case of chronic inflammatory demyelinating polyneuropathy with recurrent ophthalmoplegia, persistent conduction block, antibody activity against gangliosides GM1].
We report a 19-year-old female with chronic inflammatory demyelinating polyneuropathy (CIDP) with recurrent ophthalmoplegia. The patient had chronic, recurrent, asymmetrical, predominantly, distal limb weakness, and numbness of extremities with recurrent external ophthalmoplegia. Ophthalmoplegia developed in each attack of distal limb weakness, and also rapidly subsided with recovery of limb weakness. Motor nerve conduction studies revealed conduction block in more than one nerve and conduction velocities were generally normal in those segments of the nerve where conduction block was not detected. Serum anti-gangliosides GM1 IgM antibody investigated by ELISA was elevated. Thin-layer chromatography immunostaining also confirmed this result. Sural nerve biopsy showed normal findings. In spite of improvement of her signs and symptoms after prednisolone therapy, multifocal conduction block was persistent. Muscle power improved in association with decreased in anti-GM1 antibody activity. There were many reports of CIDP with cranial nerve involvements, but recurrent ophthalmoplegia in CIDP is rare. It is widely accepted that serum anti-GQ1b IgG antibody is associated with ophthalmoplegia in Miller Fisher syndrome and Guillain-Barré syndrome. However, serum anti-GQ1b IgG antibody was not detected in this case. It is unclear whether anti-GM1 antibody may play a role to pathogenesis of ophthalmoplegia or not in this case.
Adult↗
[Epidemiology of headache].
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Adolescent↗
A clinico-pathological study of adult histiocytosis X involving the brain.
Adult histiocytosis X involving the CNS caused progressive spastic paraparesis. The diagnosis was made by immunoreactive anti-S100 protein antibody staining and from the presence of Birbeck granules in biopsy specimens of skin lesions. Neuropathological examination showed massive proliferation and infiltration of S-100 containing histiocyte-like cells and reactive astrocytes throughout the CNS.
Brain Diseases↗
[A case of flaccid paraplegia associated with HTLV-I infection].
A 63-year-old female began to have progressive gait disturbance at the age of 50. Neurologic examination revealed weakness and hypotonus of bilateral leg muscles. Deep tendon reflexes were hypoactive with positive Babinski sign and vibration sense was diminished in the legs. HTLV-I antibody titers were elevated both in serum (x 131,072) and in CSF (x 512). The result of nerve conduction velocities and short latency somatosensory evoked potentials suggested mild peripheral nerve lesion. Needle EMG studies showed myogenic changes in the upper limbs and also, neurogenic changes in the lower limbs. Histological examination verified mild myogenic changes in biopsied deltoid muscle and neurogenic and myogenic changes in the quadriceps femoris muscle, with ragged-red fibers. We consider that this patient has myelopathy, myopathy, peripheral neuropathy and anterior horn cell involvement associated HTLV-I infection. The relationship between HTLV-I infection and mitochondrial abnormalities of the biopsied muscles remains unclear.
Female↗
[A case of X-linked recessive bulbospinal muscular atrophy with demyelinating neuropathy and hypertrophy of the calves].
We report a 53-year-old man of X-BSMA with neuropathy. The patient developed slowly progressive muscular weakness and wasting over a 2-year period with an accompanying numbness in the finger tip. He can run normally but not so fast. When he was aged 52-year old, difficulty in running progressed. General physical examination revealed nothing particular except for hypertension and gynecomastia. He showed muscular weakness and atrophy in the tongue, shoulder girdle, and upper and lower limbs. Calf muscle hypertrophies were prominent on both sides. The tendon reflexes were absent. Slight sensory impairment for vibration and pin-prick was present distally in all limbs. Autonomic nerve dysfunction was not observed. Hyperglycemia, elevated HbA1c and elevated serum CK (1,242 IU/l) were seen. The computed tomographic analyses on skeletal muscle showed hypertrophic changes in the calf muscles with a few fatty infiltrations. Electromyography showed a systemic neurogenic pattern. Motor nerve conduction velocities were slightly delayed in the lower limits. Sensory nerve action potentials were not elicited in all nerves tested. Sural nerve biopsy disclosed marked reduction of myelinated fibres for that of large diameter with thin myelin. Teased fibre studies showed a definite increase in the incidence of fibres with segmental demyelination and remyelination. In electron microscopic examination, typical or atypical onion bulb formation was observed on individual fibres. Axonal changes were minimum. We believe that segmental demyelination observed in this patient is not secondary to axonal damage. We, also, investigated AR gene abnormality by polymerase chain reaction (PCR) in this patient.(ABSTRACT TRUNCATED AT 250 WORDS)
Demyelinating Diseases↗
[A case of hereditary motor and sensory neuropathy type I with optic atrophy, neural deafness and pyramidal tract signs].
A case of hereditary motor and sensory neuropathy (HMSN) type I with optic atrophy, neural deafness and pyramidal tract signs was described. The patient was a 53-year-old man who had suffered from difficulty in walking, decreased visual acuity since age 16 years. These symptoms were slowly progressive. At the age of 37, he was pointed out optic atrophy, positive pyramidal tract signs. Distal muscle weakness with atrophy of four limbs was prominent at the age of 50. Since then, he noticed progressive hearing loss with blindness. His elder sister was diagnosed Charcot-Marie-Tooth disease. On neurological examination, he showed to have optic atrophy without retinitis pigmentosa and neural deafness. Also he showed mild degree of muscle weakness and atrophy in four limbs, severe in the distal part of lower limbs. Deep tendon reflexes were absent in all limbs with right Babinski sign. Superficial sensation was decreased slightly in the distal parts of four limbs. Deep sensation was markedly decreased in the leg. There were no cerebellar signs. Audiometric examination revealed bilateral neural hearing loss. There were no findings of spinal cord compression on spinal MRI. On the nerve conduction studies, sensory nerve action potential was not elicited in all nerves tested. Motor nerve conduction velocity of the right median was 41.1 M/sec, also ulnar nerve 44.7 M/sec, but M-wave was not elicited with the electrical stimulation of other tested nerves. On sural nerve biopsy, the density of myelinated fibers was severely decreased. Well-myelinated axon surrounded by onion bulb formation was observed in electron microscopic examination.(ABSTRACT TRUNCATED AT 250 WORDS)
Charcot-Marie-Tooth Disease↗
Extrapyramidal system involvement in motor neuron disease.
Three cases of motor neuron disease (MND), in which neuropathological findings were atypical, are reported. The first case manifested widespread and severe degeneration of the spinal cord, as in spinal fibrosis. Case 2 revealed severe degeneration of the pyramidal tract with many spheroids, which made it difficult to differentiate from primary amyotrophic lateral sclerosis. The last case revealed degeneration of the nigro-pallido-luysian system, even though no clinical manifestation of extrapyramidal and/or cerebellar symptoms had been noted throughout the clinical course. In MND, degeneration might occur in various locations other than the motor system.
Aged↗
Immunoglobulin kappa/lambda ratios in migraine and tension-type headache.
The possibility of immunological mechanisms causing headaches has been proposed in the past. To investigate the immunological system activation in patients with chronic headaches, we evaluated the kappa/lambda ratios of immunoglobulins in 40 patients with migraine and 49 patients with tension-type headache. Nineteen healthy volunteers composed the control group. The serum kappa and lambda levels of immunoglobulins were determined by using the enzyme-linked immunosorbent assay (ELISA) techniques. The kappa/lambda ratios of IgG in the patients with tension-type headache were significantly higher than those in the controls. The kappa/lambda ratios of IgA and IgM in the patients with headaches were higher than those in the controls, but they were not statistically significant. The total concentrations of IgG, IgA and IgM were significantly higher in the patients with migraine. In the patients with tension-type headache, the total concentrations of IgG and IgA were significantly higher than those in the controls. The high levels of kappa/lambda ratios of IgG in the patients with tension-type headache and the increase in the total concentrations of immunoglobulins in the patients with migraine and tension-type headache, observed in this study, suggest that the humoral immunological system activation might exist, and it might be related to the etiology of tension-type headache and migraine.
Adult↗
Platelet gamma-aminobutyric acid levels in migraine and tension-type headache.
Gamma-aminobutyric acid (GABA) levels in platelets were measured in 19 patients with migraine (7 males and 12 females, average age: 36.5 years) and 27 patients with chronic tension-type headache (TH; 9 males and 18 females, average age: 48.9 years). Twenty-one normal healthy volunteers composed the control group (11 males and 10 females, average age 34.9 years). The GABA levels in platelets were determined using high performance liquid chromatography with fluorescent detection (HPLC-FC). The GABA levels in platelets were 30.8 +/- 11.7 pmol/10(9) platelets (mean +/- S.D.) in the patients with migraine, 43.1 +/- 11.8 pmol/10(9) platelets in the patients with TH and 34.7 +/- 8.1 pmol/10(9) platelets in the healthy controls. The platelet GABA levels in the patients with TH were significantly higher than in the migraine patients and the healthy controls (p less than 0.05). The possible role of GABA in headache is discussed. We consider that TH may be a state of neuronal hyperexcitability similar to migraine and that GABA in the platelets of patients during TH attacks may be elevated to counterbalance it. Alternatively, we suggest that the rise of GABA levels in platelets is related to emotional factors, such as depression, in the TH patients. Further studies must be undertaken concerning the relationship between platelet GABA levels and headache.
Adult↗
Nation-wide collaborative study on the long-term effects of bromocriptine in the treatment of parkinsonian patients. Final report.
Final results of the 5-year multicentric collaborative study on the long-term effects of bromocriptine in the patients with Parkinson's disease are reported. This prospective study started in May 1985 in order to see whether the early combination therapy with bromocriptine and levodopa is really superior to the levodopa monotherapy with regard to the late side effects of levodopa in the treatment of parkinsonian patients. Another project of the study was to see the therapeutic efficacy of bromocriptine monotherapy without concomitant use of levodopa. For these purposes, a total of 702 patients with Parkinson's disease were enrolled into three groups: Group 1 (n = 286) with bromocriptine monotherapy, Group 2A (n = 216) with early combination of bromocriptine and levodopa, and Group 2B (n = 200) with levodopa alone. At the end of the 5-year study, 48 patients in Group 1 (16.8%) were still continuing bromocriptine monotherapy with satisfactorily good therapeutic effects. About half (49.1%) of the Group 2A patients remained on the combined therapy, and the comparable number of the Group 2B patients (46.0%) were also kept on the initial mode of therapy, while 13.5% of the latter group with levodopa monotherapy needed bromocriptine to be added in order to assure the good therapeutic effects. Moreover, significant differences were seen between group 2A and Group 2B with regard to the incidence of wearing-off phenomenon and dyskinesias. Disappearance rate of dyskinesias which were present at the time of enrollment was significantly higher in Group 2A than in Group 2B. No significant difference was noted as to the incidence of untoward symptoms and the death rate among all three therapeutic groups. These results support the view that the early combination of bromocriptine with levodopa is superior to levodopa alone in the treatment of Parkinson's disease.
Activities of Daily Living↗
Nation-wide collaborative study on the long-term effects of bromocriptine in the treatment of parkinsonian patients: analysis on the maintenance and the change of the original mode of treatment.
A nation-wide collaborative study to evaluate the long-term effects of bromocriptine in patients with Parkinson's disease was completed as described in the accompanying paper. The present study analysed the same data by paying attention to a group of patients who maintained the original mode of therapy and to a group of patients who changed the mode of treatment by adding levodopa or bromocriptine to the original drug. Surprisingly, 48 among 286 patients in a group of bromocriptine monotherapy maintained the original mode of therapy. This group has particular features of a short duration of illness and a low grade of Hoehn-Yahr's scale. It is noteworthy that this group of patients did not show wearing-off phenomenon. The effects of additional bromocriptine to levodopa for a 5-year period were analysed by comparing two groups of combination therapy and levodopa alone therapy maintained for 5 years, with 106 and 92 patients, respectively. Results were essentially the same as those obtained from the accompanying paper, i.e., in general, treatment by combination with bromocriptine may be more suitable than treatment by levodopa alone. In order to find the best timing of the combination of levodopa and bromocriptine, results of 3 groups were compared, i.e. a group of patients who started with bromocriptine alone and later added with levodopa (82 patients), a group of patients who maintained the combination for 5 years (106 patients) and a group of patients who started with levodopa alone and later added bromocriptine (27 patients). The best results were obtained in the group of 5-year combination.(ABSTRACT TRUNCATED AT 250 WORDS)
Activities of Daily Living↗
[Antibodies to GM1 ganglioside in motor neuron disease--in comparison with demyelinating neuropathy].
We studied serum antibodies to GM1 ganglioside by enzyme linked immunosorbent assay (ELISA) in 55 patients with motor neuron disease (MND) composed of 36 ALS and 19 lower motor neuron disease (LMND), 44 patients with demyelinating neuropathy (DN) composed of 29 Guillain-Barré syndrome (GBS) and 15 chronic inflammatory demyelinating polyneuropathy (CIDP), and 21 healthy controls. High levels of serum antibodies against GM1 were confirmed by thin-layer chromatography overlay procedure. In MND group, the mean level of anti-GM1 IgM antibodies was not significantly elevated in comparison with controls. There was no significant difference in anti-GM1 antibodies between ALS group and LMND group, while anti-GM1 IgM antibodies in DN group, especially in GBS group, were significantly elevated (p < 0.001). High levels of anti-GM1 IgM antibodies (greater than the mean level plus 3 standard deviations of controls) were detected in 9 patients (6 with ALS and 3 with LMND) with MND (16.4%) and 16 patients (11 with GBS and 5 with CIDP) with DN (36.4%). Serum antibodies to GM1 reacted with GD1b ganglioside in only one patient with MND and 10 patients (8 with GBS and 2 with CIDP) with DN. Anti-GM1 IgG antibodies were elevated significantly in DN group. There was no correlation among anti-GM1 IgM antibodies and both duration and severity of illness in MND. In some patients with MND, levels of anti-GM1 IgM antibodies became high in the advanced stage. It is unclear whether these antibodies are primary manifestation or consequence of motor neuron disease.(ABSTRACT TRUNCATED AT 250 WORDS)
Autoantibodies↗
[Paraproteinemia and motor neuron disease].
In some patients, motor neuron disease (MND) is associated with a paraprotein, raising the question that there may be a relationship between MND and monoclonal gammopathy. We analysed the presence of monoclonal immunoglobulin in the serum from 53 patients with MND using immunofixation in cellulose acetate membrane. The incidence of paraproteins in 6 cases (11.3%) of patients with MND exceeds values found with cellulose acetate membrane supports in reported populations (below 1%), even when age was also considered. Monoclonal components were IgG (33%), IgM (33%) and IgA (33%). In six cases, four showed typical changes of amyotrophic lateral sclerosis and other two patients were spinal progressive muscular atrophy (SPMA) in autopsy. No malignancy was detected in all cases. These results corroborate the concept of a probable association between MND and benign monoclonal gammopathy (plasma cell dyscrasia). A patient with SPMA had transient elevation of IgG-GM1 antibodies. Other five patients with M-proteinemia did not show elevated serum anti GM1 antibodies.
Female↗