Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 41-year-old man was doing well until July 1989, when he noted numbness over soles, followed 4 months later by difficulty in walking. These symptoms were progressively getting worse, and he was admitted to our department on June 12, 1990. General physical examination was unremarkable. Neurologically cranial nerves were intact except old right, traumatic strabismus. Muscle tone and deep tendon reflexes were normal throughout, but bilateral Babinski and Chaddock reflexes were present. Mild weakness of lower extremities were found on muscle testing (4/5). In sensory system, superficial sensory disturbance below T10 was seen, and markedly diminished vibration and position senses of lower extremities were noted. Cerebellar test was intact, although unsteadiness was found on heel-shin test. Romberg sign was definitely positive. His gait was wide-based and ataxic. Laboratory data showed no abnormalities in CBC, chemistry, urinalysis, serological tests and endocrinological examinations. Spinal MRI (Siemens 1.5 Tesla) showed abnormal deposition of epidural fatty tissues compressing spinal cord with flattening of cord from T4 to T8. Spinal ataxia as compressive myelopathy due to epidural lipomatosis was considered and he underwent laminectomy from T4 to T8 with improvement in walking. Epidural lipomatosis is an unusual cause of spinal cord compression, presenting compressive myelopathy, radiculopathy, cauda equina syndrome, intermittent claudication, or back pain. Most of cases were associated with long-term administration of adrenocortical steroid hormone, or underlying diseases, except only 3 cases including ours. This is the first case of spinal epidural lipomatosis presenting progressive gait disturbance due to spinal ataxia.
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PMID:[A case of epidural lipomatosis presenting spinal ataxia]. 206 Feb 46

A 27-year-old man was admitted to our hospital for his legs' numbness of subacute onset and discomfort while standing. No specific previous history was found and his family history was non-contributory. On admission, his general status was unremarkable except for arterial hypertension and mild tachycardia. Moderate impairment of superficial sensations and dysesthesia were noted in the distal extremities, tongue, oral cavity, and lips. Deep sensation was moderately impaired in the lower legs. Romberg sign was positive. He had mild weakness in the proximal muscles of the lower extremities. Hyporeflexia was noted in all extremities, but Achilles reflexes were absent. Pathologic reflexes were not noted. He fainted after two minute standing. On laboratory examination, serum IgM, C3, and C4 were mildly elevated. CSF protein level was prominently high without CSF pleocytosis. MCV was mildly decreased, and F wave conduction velocity was prominently decreased in the posterior tibial nerve, SCV was also mildly decreased in the right sural nerve. Needle electromyography showed mild neuropathic changes. Left sural nerve biopsy showed no abnormal finding in the myelinated and unmyelinated fibers. A 60 degree head-up tilting test caused a hypotensive attack, and Valsalva ratio was decreased. However, hand grip test and cold pressor test were normal. The response to noradrenaline infusion test and CVR-R were also normal. Muscle sympathetic activity (MSA) was recorded from the tibial nerve using a tungsten microelectrode (Iwase, et al.). His basic activity was higher and responsiveness was lower than age-matched normal controls. The regression line existed above the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of chronic inflammatory demyelinating polyradiculoneuropathy with orthostatic hypotension]. 227 59

A 74-year-old man developed progressive deafness and unsteady gait two years after gastrectomy for a gastric cancer. Neurological examination revealed an alert and intelligent Japanese male in no acute distress. The optic fundi were normal. The pupils and the extraocular muscles were normal, however, horizontal nystagmus was noted in right and left gaze. He showed marked bilateral deafness, and loss of caloric response bilaterally. No muscle atrophy nor weakness was noted. His gait was wide-based and ataxic. Tandem gait was impossible. Romberg sign was present. No cerebellar ataxia was noted in the finger-to-nose or the heel-to-knee test. No adiadochokinesis was noted. Hyperextensibility was noted in the lower extremities. Deep reflexes were normal in the upper limbs, and diminished in the lower extremities. Sensation was intact. He showed the jumbling phenomenon, and the disturbance of the righting reflex in the tilt-table examination. Neuroradiological as well as laboratory studies were unremarkable except for the high titer of CEA in the CSF. Four months after his admission, malignant tumor cells were found in the CSF. It seemed likely that he had completely lost bilateral vestibular and auditory functions caused by meningeal carcinomatosis. His disturbance of gait and station was apparently similar to cerebellar ataxic gait, however, he did not have limb ataxia. The cranial CT scans failed to show cerebellar atrophy. It was our impression that his motor disturbance was in all likelihood caused by the bilateral loss of vestibular functions, i.e., vestibular ataxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Vestibular ataxia caused by meningeal carcinomatosis]. 236 34

A seventy-year-old woman was admitted to the hospital because of paresthesias and progressive weakness of the extremities. Ten months previously, tightness in the thighs and numbness in the fingers developed, with subsequent tingling sensations of the hands and feet. Three months before entry, she had difficulty in walking because of severe paresthesias in the extremities. She was found to have an abnormal mass in a X-ray film of the chest, and transferred to our hospital. Neurological examination showed generalized hyporeflexia, marked loss of deep and discriminative sensations in the distal portion of the limbs, positive Romberg sign and severely ataxic gait. Cerebellar sign was negative. Cytologic examination of a transbronchial lung biopsy disclosed small cell carcinoma of the lung. A sural nerve biopsy showed severe loss of myelinated fibers accompanied by axonal degeneration of residual fibers. Immunohistochemically antineuronal antibody was found in the serum but not in the CSF, which reacted to nuclei and cytoplasm of the dorsal root ganglion neurons as well as Purkinje cells. Titers of this autoantibody in the serum were markedly reduced after chemotherapy and irradiation. Western blot analysis demonstrated that autoantibody in the serum recognized neuronal antigen with single band at 38 kd. Pathogenesis of carcinomatous neuropathy is still unexplained, but the findings here presented have given rise to the speculation that antineuronal antibody may be a contributory factor in carcinomatous neuropathy.
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PMID:[Antineuronal antibody in carcinomatous neuropathy]. 256 Apr 16

Both miners exposed to high temperature and excess heat and miners working under permissible temperature conditions (a control group) had similar nonspecific signs, i. e., complaints of heartache and headache, erethism, flaccidity, hydrosis, degradation of appetite and sleep, vertigo, dimness, the sense of air shortage, palpitation in rest, uncertain gait, muscle spasm. There were also presented the following objective data: tremor of close eyelids, asymmetry of tendon reflex, convergence weakness, emotional lability, changes in orthostatic test results, higher Kerdau index, instability of sensitizing Romberg's test. The above signs were more pronounced in miners exposed to high temperature, thus it was possible to regard them as indicators of miners' chronic overheating.
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PMID:[Signs of chronic overheating in miners of deep coal mines]. 276 95

We presented a rare care who had right frontal lobe infarction, with left side pseudoataxia, and the mechanism, causing pseudoataxia, was considered. The patient, a 51 year-old, righ-handed male, was admitted on August 9, 1980, complaining of left-side pseudoataxia. About p.m. 7:00, July 29, 1980, he suddenly noticed numbness of the left foot, and he found himself difficulty in standing in the next morning. He had a mild paresis and tactile-tactile of the left side including the face, which was rapidly improved. However, there was pseudoataxia of the left extremities, which had not been improved. On physical examination, dysarthria, aphasia, finger agnosia, difficulty in right left orientation or muscle weakness was not recognized, and there was no sensory disturbance except for slight impairment of stereognosis, two point discrimination and vibratory sense. Demonstrable impairment of tactiletactile from was observed in the left hand. Notable dysmetria, terminal tremor and dysdiadochokinesia were seen in the left limbs, which were remarkably worsened with eyes closed. However, tapping and line-drawing tests were normal. Babinski-Weil's test disclosed typical compass gait. There was marked swaying in Romberg position. Tandem gait was impossible with a tendency to decline the left. Deep reflexies were normal except for mildly hyperactive radial reflex in the left. Carotid and vertebral angiographies revealed neither evidence of vascular occlusion nor displacement of vessels CT scan demonstrated a low density area, which included the right inferior and middle frontal gyri, the head of the right caudate nucleus and a part of anterior crus of right internal capsule. There was enlargement of anterior horn of the right lateral ventricle. Caloric test, electronystagmography, eye tracking test or optokinetic nystagmus test disclosed no abnormalities. Vibration induced falling, which is the postural reaction to muscle vibration during standing (Ekuland, G., 1972), was not recognized when the left Achiles' tendon was stimulated. Pseudoataxia of this patient differed from the typical cerebellar or vestibular ataxia. From a review of the literatures concerning frontal pseudoataxia, almost all cases had no distinct cerebellar signs, and showed positive Romberg's sign. The impairment of tactile-tactile form and postural reaction to vibratory stimulation to the left leg, appeared in this case, could be hardly explained by the lesion of parietal lobe or deconnection syndrome. Sensory perception of parietal lobe and pyramidal motor system were thought to be almost normal in this case. Therefore, these findings should be due to impairment of integration center between sensory and motor systems. The pseudoataxia in frontal lesion seems to occur as the results of involvement of this center, in which caudate nucleus maybe has important role, but not as the results of disturbances in the front-ponto-cerebellar or front vestibular pathway.
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PMID:[Frontal pseudoataxia, discussion on its mechanism (author's transl)]. 732 87

We report a 65-year-old woman with progressive dysarthria, dysphagia, weakness, and gait disturbance. The patient was well until 59 years of age (January of 1986) when she noted bilateral ptosis. One year later, she noted a gradual onset of difficulty in speech (articulation). Her speech slowly deteriorated and she noted weakness in chewing power and difficulty in swallowing in addition. In October 1987, she developed emotional incontinence. In January of 1988, she started to drag her left foot. She was admitted to our hospital on June 13 of 1988. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed no dementia; her higher cerebral functions appeared intact. Ptosis was present bilaterally more on the right. She showed difficulty in opening her eyes on command; no contraction of the frontal muscles was seen upon attempted eye opening. There was a moderate limitation in the vertical gaze. Forced laughing and crying were seen. Facial muscles were moderately weak without apparent atrophy. The movement of the soft palate was very weak, and swallowing disturbance was more prominent for liquid staff. The tongue appeared somewhat small, however, no fasciculation was noted. Her step was small and the posture was stooped. Retropulsion was present, however, Romberg's sign was absent. No muscle atrophy was apparent, however, diffuse mile to moderate muscle weakness was noted in all four limbs. Cerebellar sign was absent. Deep tendon reflexes were exaggerated bilaterally, and Babinski sign was present on the left side. Sensation was intact. Routine blood tests were unremarkable as was a cranial CT scan. Her ptosis did not improve after 10 mg of edrophonium injection. CSF was also normal. She was transferred to another hospital but her neurological disabilities further progressed. In 1989, she was totally unable to move her limbs; she could only move her eyes; still consciousness was clear without dementia. She developed respiratory difficulty and expired on July 25, 1992. She was discussed in a neurological CPC, and the opinions were divided into ALS and primary lateral sclerosis (PLS). The chief discussant arrived at the conclusion that the patient might have had the pyramidal form of ALS. Postmorten examination revealed marked myelin pallor in the anterior as well as lateral corticospinal tracts. Pyramidal tract degeneration was prominent starting at the level of the cerebral peduncle and was continued to be seen until the level of lumbar cord. The number of anterior horn cells showed only slight decrease in the cervical level, however, it was normal in the lumbar cord.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 65-year-old woman with dysarthria, dysphagia, weakness, and gait disturbance]. 777 10

The natural course of polyneuropathy associated with monoclonal gammopathy of undetermined significance (MGUS) is not well known. We therefore studied 32 untreated patients for a period of 5 years. Fifteen patients had an IgM M-protein, 15 an IgG and two an IgA. There was a male predominance, a mean age of onset at the end of the sixth decade and sensory signs were more pronounced than motor deficits. On entry into the study and during the 5 years of follow-up, we quantified the neuropathy in a standard way: totals of motor and sensory scores; vibration perception threshold; tapping tests; quantified Romberg test; electrophysiological parameters. A significant difference in the natural history between the polyneuropathy associated with IgM-MGUS and IgG/IgA-MGUS was found for the motor and sensory sum scores, the vibration perception threshold and the tapping tests. The polyneuropathy in IgM-MGUS is more progressive, with significantly more weakness and sensory signs, indicating that the neuropathies associated with IgM-MGUS and IgG/A-MGUS may be two different entities. A rapid progression of the neuropathy was found in five patients. We found no predictive factors for this severe progression of the neuropathy of these five patients. Of these five, three (two IgM, one IgG) developed a non-Hodgkin lymphoma.
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PMID:Polyneuropathy associated with monoclonal gammopathy of undetermined significance. A prospective study of the prognostic value of clinical and laboratory abnormalities. 782 May 74

A 32-year-old man developed a rash on his body and extremities following acute fever of a few days duration, and also noticed pain and spontaneous tingling sensations in his lower extremities. Because severe pneumonia with dyspnea and low arterial blood oxygen concentration were found on examination, he was admitted and treated. After recovering from pneumonia in two months, he complained of abdominal symptoms, such as constipation, nausea and vomiting, spontaneous tingling sensations in the lower extremities, and orthostatic dizziness and fainting. On neurological examination, a mild to moderate muscle weakness was found in the distal muscles of both extremities. The ankle jerk was absent. Both superficial and deep sensations were moderately to severely decreased in the feet with positive Romberg's sign. Constipation and vomiting with nausea were noted. Clinical and laboratory examinations revealed marked orthostatic hypotension and hypohidrosis. Motor and sensory conduction studies indicated the presence of axonal degeneration and segmental demyelination and remyelination in the limbs nerves. CSF examination indicated that protein was 150 mg/dl and the cell count to be 18/mm3. Titer of antibody to rubella virus was significantly elevated. There were no other abnormalities to indicate the cause of motor, sensory and autonomic neuropathies. Therefore, the diagnosis of acute polyradiculoneuropathy with autonomic disturbances after rubella infection, which is rare in the literature, was made.
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PMID:[A case of acute polyradiculoneuropathy with autonomic disturbances following rubella infection]. 826 90

The patient was a 55-year-old man. He was well until eleven months earlier, when he noticed the onset of numbness in his right fingers. Over the next three months, the numbness spread up the right arm and involved the right leg, left arm and left leg in succession. Six months before admission, sensory impairment of the trunk appeared progressively. Mild diffuse muscle weakness occurred gradually. Swelling of the right lateral cervical lymph node was found just before admission. On neurological examination, sensory disturbance involving all modalities of sensation was recognized in the extremities and trunk. The sensory findings were asymmetric and predominant at the lower extremities and distal parts. A positive Romberg's sign and poor coordination was recognized. All the deep tendon reflexes were absent without pathological reflexes. Motor weakness, which was less severe than sensory findings, was present. There was no sphincter disturbance nor orthostatic hypotension. Routine laboratory findings were within normal limits. The protein level of cerebrospinal fluid was slightly increased. The electrophysiological studies and histological evaluation of the biopsied peroneal muscle and sural nerve showed degeneration and reduction of large myelinated fibers of sensory nerves with minimal motor nerve changes. Histological study also revealed the increase of regenerating fibers. Squamous cell carcinoma of epipharynx with metastasis of neck lymph nodes was found. Radiotherapy without chemotherapy resulted in a complete tumor remission and probably suppressed the progression of neurological disturbances. After two years from the onset, diffuse high intensity area was noted in the posterior spinal column on T2 weighted MRI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of carcinomatous neuropathy with degeneration of posterior spinal column on MRI]. 839 18


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