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Biomedical subjects

K Negoro

Publications and source records attributed to K Negoro.

At least 37 records · Page 2Linked to original sources
PubMed1997

[A case of rapidly progressive T cell type malignant lymphoma which started with multiple cranial neuropathy].

A 35-year-old man had suffered from recurrent right trigeminal nerve palsy and flaccid paraparesis for about five months. Cerebrospinal fluid (CSF) showed a marked increase of protein (400 mg/dl) and mononuclear cells (146/mm3), but there were no malignant cells. Antibiotic therapy remitted his inguinal and mediastinal lymph nodes swelling, and trigeminal nerve palsy had recovered spontaneously. Then he developed left trigeminal and facial nerve palsy, mononeuropathy multiplex, and cauda equina syndrome. Nerve conduction studies revealed delayed velocity and reduction of amplitude. Enhanced magnetic resonance imaging showed increased signal intensity in bilateral trigeminal nerves, left internal auditory meatus, and meninges of the basal cistern. Also, there were two mass lesions in cauda equina. They were operated by orthopedist, and were not malignant. After that, CSF cells of malignant lymphoma were elevated and revealed T cell type (large cell). Then the patient exacerbated in bulbar palsy and died. When there is lymph node swelling with multiple neurological deficits, despite remission of lesions and signs, biopsies should be positively pursued early in the patient's clinical course.

Adult↗
PubMed1996

[A case of diffuse idiopathic skeletal hyperostosis (DISH) with various neurological complications].

A 71-year-old female presented with a 10-year history of slowly progressive gait disturbance and dorsolumbar pain. Motion of he neck and trunk was severely restricted. She showed decreased sensation of vibration and position in the upper and lower limbs and had Romberg's sign. Hyperesthesia of touch sensation was distributed in a stocking pattern. She showed hyporeflexia and pathological reflexes in lower limbs. Her gait was ataxic and spastic. Laboratory examination of blood and urine revealed no remarkable findings. Radiographic examination revealed ligamentous calcification and ossification along the anterolateral aspect of the vertebral column at several levels, and there was ossification of hte ligament and tendon attachment to the bone at extraspinal sites. The radiographic features were characteristic of diffuse idiopathic skeletal hyperostosis (DISH). Computed tomography at lower thoracic and lumbar vertebral portions showed compression of the spinal cord by ossification of the flavatum ligament. The conduction velocity of tibial nerves and sural nerves were delayed, and the mechanism of the occurrence of peripheral nerve lesions in this patient could be explained by extrinsic compression by heterotopic calcification or some metabolic factor due to DISH.

Aged↗
PubMed1996

[Polymyositis followed by myasthenia gravis].

A 63-year-old woman was admitted to the hospital because of swelling of both forearms and muscle weakness in the limbs. Laboratory examination revealed abnormally high levels of serum creatine kinase, glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, and lactate dehydrogenase. Polymyositis was diagnosed, and prednisolone was administered. Her condition had been well controlled on prednisolone until several months before admission, when bilateral blepharoptosis and diplopia developed. An edrophonium test was positive: muscle weakness was transiently alleviated. High titers of anti-acetylcholine receptor antibodies were found. A chest CT scan showed a mass in the anterior part of the mediastinum. We diagnosed myasthenia gravis associated with thymoma. After an extended thymectomy, the patient's condition improved. When muscle weakness recurs after remission of polymyositis, myasthenia gravis should be considered.

Anti-Inflammatory Agents↗
PubMed1996

[Progressive ataxic hemiparesis with asymmetric cortical and cerebral peduncular atrophy--report of two cases].

We report two patients, 73- and 70-year-old men, characterized by progressive hemiparesis and homolateral limb ataxia as the main clinical symptoms; magnetic resonance (MR) imaging of the brain revealed asymmetric cerebral cortical and peduncular atrophy; 99mTc-ECD single photon emission computed tomography (SPECT) of brain showed decreased RI uptake in the cerebral hemisphere correlated with clinical deficits. Brain SPECT of case 1 showed decreased RI uptake in the cortex of the right hemisphere and the left cerebellar hemisphere ("crossed cerebellar diaschisis; CCD"). These findings indicate that ataxia of our patients may depend on the lesions of the corticopontocerebellar tracts, although it is possible that ataxia may be related to lack of spatial orientation associated with parietal lobe lesion. The mechanism of the occurrence of asymmetric cerebral peduncular atrophy would be explained by wallerian degeneration of the pyramidal tract and other cortically originated fibers associated with the cortical degeneration. From these clinical and radiologic features, it seems likely that our two patients are categorized in the "asymmetric cortical degeneration syndromes", and we propose the term "progressive ataxic hemiparesis" for our patients.

Aged↗
PubMed1996

[A case of psittacosis with psychiatric symptoms, abnormal EEG, and abnormal SPECT].

A 40-year-old woman was admitted to our hospital with disorientation, delusional idea, and sensory disturbance of lower face after having a fever and cough for 5 days. A chest X-ray examination revealed an infiltration in the left lower lobe field. Psittacosis was diagnosed because the serum antibody titer against chlamydia psittaci was elevated. Electroencephalogram showed right temporal lobe spikes. SPECT showed decreased accumulation of 99mTc-HMPAO in the right frontal and temporal lobe. Computed tomography scan of the brain was normal. This patient was diagnosed as ornithsis Encephalitis.

Adult↗
PubMed1996

[Two siblings with sarcoidosis diagnosed by younger sister's central nervous symptoms].

We report two siblings with sarcoidosis; the younger sister had symptoms of central nervous system, and both sisters had subcutaneous mass lesions in the gluteal region. Case 1. A 30-year-old woman presented with two episodes of right leg paresis. On admission, neurological examination revealed right leg weakness, spasticity of both legs, increased deep tendon reflexes in all extremities, urinary disturbance and hearing loss of the right ear, but she had no meningeal signs. Serological studies were normal including angiotensin converting enzyme. Cerebrospinal fluid revealed elevated protein to 340 mg/dl, mild pleocytosis, decreased glucose. CSF culture was negative, and cytology showed no malignant cells. Enhanced MR imaging showed diffuse leptomeningeal enhancement in both the brain around basal meninges and the whole spinal cord. Case 2. A 34-year-old woman (the elder sister of Case 1) presented with visual disturbance. She had been diagnosed to have bilateral iritis at Hiroshima Red Cross Hospital before visiting our hospital. Neurological examination and serological studies were normal. In both cases, left gluteal subcutaneous mass was detected and its biopsy revealed characteristic sarcoid nodules and confirmed the diagnosis of sarcoidosis. A tendency of familial occurrence and positive associations of the specific HLA antigens in sarcoidosis have been reported. Though the diagnosis of neurosarcoidosis has been difficult without extraneurological signs, sarcoidosis should be considered as a differential diagnosis in all the patients with myelopathy, and enhanced MRI and measure of CSF angiotensin converting enzyme seem to be useful for diagnosis and evaluation of drug effect during the course of steroid therapy.

Adult↗
PubMed1995

[A case of myotonic dystrophy with morning headache following sleep apnea syndrome].

We reported a 39-year-old man with myotonic dystrophy. He suffered from morning headache. Respiratory function tests showed restrictive pattern and arterial gas analysis showed hypoxia and hypercapnia with respiratory acidosis (PaCO2 50.8 mmHg, PaO2 63.8mmHg, pH 7.317, SaO2 89.8%). Polysomnograph showed central apneas exclusively in light sleep (stage 1 and 2). O2 saturation fell at most to as low as 50% during the apneas. We conclude that sleep apnea should be consider in patients with myotonic dystrophy associated with morning headache.

Adult↗
PubMed1995

[A case of secondary carnitine deficiency due to anorexia nervosa and severe liver damage].

We reported an 18-year-old woman with anorexia nervosa and liver damage who showed carnitine deficiency. Her unbalanced diet had little carnitine, and severely damaged liver could not synthesize carnitine. Since total parenteral nutrition (TPN) and tube-feed formulas contain little or no carnitine, the patient had progressive weakness and muscle atrophy. Muscle biopsy revealed variability of fiber diameter, type 1 fiber atrophy and copious amount of lipid granules. Carnitine deficiency must be diagnosed in the early stage by muscle biopsy or muscle carnitine levels, and treated with oral intake of L-carnitine.

Adolescent↗
PubMed1995

[Guillain-Barré syndrome associated with anti-GalNAc-GD1a antibody subsequent to Campylobacter jejuni enteritis].

We report a 15-year-old man with Guillain-Barré syndrome (GBS) following Campylobacter jejuni enteritis. Neurologic examination revealed distal muscle weakness and mild disturbance of superficial sense on right plantar area. Serial electrophysiologic studies indicated that the predominant process was axonal degeneration of motor nerves. Thin-layer chromatography with immunostaining revealed that serum IgG strongly reacted with GalNAc-GD1a and weakly with GM2, but did not react with GM1. This is the first report of GBS subsequent to C. jejuni enteritis associated with anti-GalNAc-GD1a antibody.

Adolescent↗
PubMed1995

[Corticobasal degeneration: symptomatological, brain-imaging and electrophysiological studies].

Eight cases of clinically diagnosed corticobasal degeneration (CBD) were studied with reference to their symptomatology, brain-imagings and electrophysiological findings. The diagnosis was based on the combination of limb-kinetic apraxia (cortical sign), akinetic-rigid sign (extrapyramidal) and their unilateral predominance. Magnetic resonance imaging (MRI) and 123I-IMP or 99mTc-HMPAO SPECT findings were used to reinforce the diagnosis. The age at onset of 8 cases (4 males, 4 females) was 61 to 80 years (mean 66). Other common symptoms on admission consisted of dysequilibrium (8 cases), dysarthria (8), grasp reflex (6), supranuclear gaze palsy (6), tremor (6), limb dystonia (6) and alien limbs (5). MRI revealed parietal (3 cases) or frontoparietal (3) atrophy. SPECT showed decrease in cerebral blood flow in frontoparietal (3 cases) or frontoparietotemporal lobes (5). SPECT surpassed MRI to detect unilateral predominance of the lesions. With magnetic stimulation of the head and neck central motor conduction time (CMCT) was normal, while motor inhibitory periods (IPs) were significantly shorter in CBD patients compared with those in normal controls and the patients with Parkinson's disease. In 3 patients with reflex myoclonus, giant SEPs were not evoked, though with positive C-reflex, suggesting an elevated excitability of cerebral cortex unrelated to the production of giant SEPs.

Basal Ganglia↗
PubMed1994

[Clinical analysis of benign transient shuddering-like involuntary movement in elderly people].

We described 9 patients who developed acute onset benign transient shuddering-like involuntary movement in elderly people. There was no consciousness disturbance or sensorimotor dysfunction. There were finger tremor, dysarthria, or gait disturbance in some patients. Asterixis was observed in the upper extremities in 2 patients. Duration of an involuntary movement was less than 1 second, and the series of the involuntary movements continued for several days. This state appeared acutely and disappeared within 0.5 -4 days in the natural course without any sequelae. Oral administration of clonazepam was very effective to suppress this tremulousness. Seven of 9 patients developed recurrence. Although the cause of this syndrome remains unknown, we believe that this condition is clinically important for differential diagnosis of acute onset involuntary movements in elderly people.

Aged↗
PubMed1994

[A case of painful involuntary contraction of the left latissimus dorsi muscle, successfully treated with left thoracodorsal nerve resection].

A 66-year-old Japanese man underwent the resection of the upper lobe of the left lung for primary lung cancer. One year later, his back muscles neighboring the operation scar gradually began to twitch upwards intermittently. The involuntary muscle twitch was accompanied with severe local pain, and intensity of the pain and contraction slowly increased. The abnormal muscle contractions were confined to the left latissimus dorsi muscle on needle EMG. The pain and movement ceased by blocking of either thoracodorsal nerve or brachial plexus, and disappeared finally by resection of the nerve. The impulses causing involuntary, painful contractions were thought to originate in the damaged thoracodorsal nerve, transmitted to CNS and re-transmitted to the thoracodorsal nerve.

Aged↗
PubMed1994

[18p-syndrome with bilateral pyramidal tract signs, dystonia of the lower extremities and concentric visual field defect].

A case, diagnosed as 18p-syndrome by typical clinical appearance and by chromosomal analysis, presented with multiple nervous system defects consisting of bilateral pyramidal tract signs, weakness and focal dystonia of the lower extremities, and concentric visual field defect. Chromosomal analysis revealed karyotype 46, X, dic (Y;18) (p11;p11), inv(9) (p11q13), and the points of chromosomal breakages were thought to be in the short arm of chromosome 18 and in the short arm of Y chromosome. 18p-syndrome is caused by a chromosomal deletion, and presents with a wide variety of clinical appearances. Many cases have been reported since the original descriptions by de Grouchy in 1963, though with few mentions of neurological deficits other than mental retardation. Furthermore, there have been no reports of pyramidal tract signs, weakness and focal dystonia of the lower extremities, or visual field defect, without recognizable anatomical abnormalities. Our case of 18p-syndrome is quite rare because of multiple nervous system abnormalities mentioned above, not accompanied by malformations of the central nervous system.

Adult↗