Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acupuncture has been practiced in the treatment of many diseases in Japan. "Okibari" is one of the procedures in acupuncture treatment: a fine stainless steel or silver needle is inserted into the subcutaneous tissue through the skin, to remain in the subcutaneous tissue. A 57-year-old pharmacist was knocked down by a motorcycle in 1971, since then moderate weakness of left extremities and stiffness of muscles have remained as sequelae. She was consequently treated with acupuncture. Many small needles were inserted permanently in the nuchal, occipital and other areas of the body ten to twelve years before she developed gradual clumsiness and dysesthesia in her right hand in 1984. When she was admitted for the first time in 1985, neurological examination revealed left Horner's syndrome and diminished deep sensation in her right extremities with pseudo-athetosis of her right hand, along with spastic paresis of left extremities and right carpal tunnel syndrome. An old needle which had strayed into left dorsal medulla was considered to be responsible for these symptoms. In 1988 loss of pain and temperature sensation in the right side of her body below the shoulder, and diminished deep sensation of left extremities were appended, and weakness of her left extremities became aggravated. Pseudo-athetosis of her right hand was seen less prominently. In plain X-ray films many needle shadows were visualized. On CT scan needle shadows could be seen also in the left dorsal medulla, right cerebellum and in the subarachnoid space of left dorsal C1-C2 level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acupuncture needles, straying in the central nervous system and presenting neurological signs and symptoms]. 227 62

Nine cases of progressive supranuclear palsy are reported in this paper. There are 6 males and 3 females in this series. The average age at admission was 62 years. The clinical features of those cases are: (1) onset at the presenile with gradual progression, (2) supranuclear vertical ophthalmoplegia, especially downgaze paresis, (3) disarthria, (4) gait disturbances, (5) dystonia and rigidity of the limbs, (6) clumsiness and ataxia, (7) masked face, (8) bilateral pyramidal signs and (9) mental disturbances. The CT scan in this series showed dilatation of the ventricular system, enlargement of the Sylvius fissure and cortical sulci. There was also enlargement of quadrigeminal and cisterns in the CT scan. The CT diagnosis were cerebral atrophy in 9 cases and brainstem atrophy in 8 cases in this series.
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PMID:[Progressive supranuclear palsy]. 263 3

Calcification of ligamenta flava in the cervical spine is rarely seen. Only few cases in the literature have been available. Recently we have had experience with two cases on that lesion who had progressive radiculomyelopathy. The purpose of this report is not only case presentation but also an analysis of 11 cases from the literature in clinical, radiological and histological aspects. Case 1 was a 60-year-old woman who had numbness in both hands, mild weakness of the right foot on walking and clumsiness of the right hand. Ten years before she had suffered tbc. meningitis, but no history of neck injury. Neurological examination revealed spastic paresis in right extremities, muscle atrophy in both forearms, hypesthesia and hypalgesia in both hands and feet. Vibration sense was disturbed below the knee joint and both feet. Sphincter function was normal. Radiological examination of cervical spine revealed oval calcified nodules in the posterior spinal canal at the level of C34, C45, C56 and C67. These were all situated in the paramedian portion and symmetrically situated at C56. Air myelogram demonstrated that the spinal cord was displaced forward and choked by the posterior situated calcification. Cervical laminectomy was carried out from C2 through Th1 and calcified nodules in the hypertrophied ligamenta flava were successfully removed. Case 2 was also 66-year-old woman who had been suffering from cerebral thrombosis with left hemiparesis. In addition with left hemiparesis she started to complain with paresthesia in right hand, deteriorated numbness in left extremities and gait disturbance developed a year later.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Radiculomyelopathy due to calcification of the cervical ligamenta flava--report of 2 cases and a review of literature]. 665 77

We report a 57-year-old woman with progressive gait disturbance, headache, character change, convulsion and coma. She was well until 55 years of age, when she noted an onset of unsteady gait. At times she experienced transient weakness in her right hand, which was followed some difficulty in articulation. She was admitted to our service for the work up on April 6, 1992. Neurologic examination at that time revealed an alert Japanese lady in no acute distress. She was oriented to all spheres, however, she was somewhat bradyphrenic and had some disturbance in recent memory. Higher cerebral functions appeared intact. The visual acuity and visual fields were normal as were the optic fundi. Pupils were round and isocoric reacting promptly to light. Ocular movement was full, however, horizontal nystagmus was noted upon right lateral gaze. The sensation of the face was intact. She showed right facial paresis of the central type. Hearing was intact. She showed slurred speech and some difficulty in swallowing. The tongue was deviated to the right. Her gait was wide based and unsteady; tandem gait was difficult, however, walking on toes and on heels were performed well. No cerebellar ataxia was noted, but she showed some clumsiness in her right hand. Deep reflexes were symmetric and normally reactive; plantar response was extensor bilaterally. Sensation was intact; no meningeal sign was elicited. Routine laboratory work up was unremarkable; the CSF was under a borderline pressure (180 mmH2O) and contained 39 mg/dl of protein and 59 mg/dl of sugar. Cranial CT scan revealed diffuse low density areas involving bilateral cerebral white matter as well as the brain stem; MRI revealed high signal intensity lesions in those areas; gadolinium enhancement was negative; cortical sulci were effaced and the anterior part of the left lateral ventricle was compressed without deviation of the midline structure. The patient was treated with steroid pulse therapy without effect. She was discharged for out patient follow up, however, she developed a convulsion which was followed by loss of consciousness, and was admitted again to our service. She had never gained consciousness after this episode, and remained in the state of akinetic mutism. Follow-up CT and MRI did not show much change, although the area of high signal density lesions slightly enlarged on June 1, 1993. Her clinical course was complicated by drug induced bone marrow suppression and nephrotic syndrome. She expired on September 8, 1993 after developing sudden drop of blood pressure and bradycardia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 57-year-old woman with gait disturbance, headache, character change, convulsion, and coma]. 761 89

A 26-year-old housewife, born of consanguineous parentage, began to have gait and speech disturbance. Her brother had died from suffocation because of dysphagia. At thirty-two, she developed difficulty in swallowing, clumsiness and incontinence. When she was thirty-six she had pseudobulbar palsy, vertical gaze paresis, hyperreflexia and muscular atrophy of the upper half of the body. CT scan showed cerebral atrophy. Her mental function progressively deteriorated and amyotrophic lateral sclerosis associated with dementia was suspected. She died at the age of thirty-seven. Diagnosis was made only by autopsy. There was no particular general pathologic finding excepting aspiration pneumonia. Microscopical examination revealed numerous distended neurons with accumulation of light brown pigments by Luxol fast blue/H & E stains, especially in hypothalamus, substantia nigra and nuclei of oculomotor nerves. To a lesser extent such neurons were noted ubiquitously. The stored material was mainly composed of lipofuscin and ceroid. Ultrastructurally they presented the various structures which have previously been reported, except for finger print profiles. The pigmentary deposits were shown to be immunoreactive with polyclonal antibody directed against amyloid beta-protein.
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PMID:[Dementia and amyotrophy in Kufs disease. The adult type of neuronal ceroid lipofuscinosis]. 774 8

Five cases are reported of patients with so-called primary progressive apraxia, defined as a slowly worsening disturbance of gestural abilities, without other major cognitive changes during a long period, in relation to degenerative cortical atrophy. All five cases, as other cases in the literature, share the following common features: 1) asymmetrical onset of upper limb clumsiness, more often involving the left side, later involving the contralateral side and lower limbs; 2) after a variable delay, the occurrence of symptoms suggesting subcortical involvement (akinesia, limb stiffness, various kinds of movement disorders, dystonia, paresis of vertical gaze); 3) diffuse cortical atrophy typically more pronounced in the superior parietal cortex opposite to the first side affected. The unusual nature of apraxia in all these cases is pointed out and referred to as Luria's "kinesthaesic apraxia", ascribed to a loss of "selectivity" of distal elementary movements. This pattern of symptoms and their specific outcome could represent a distinct entity.
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PMID:[Characterization of gestural disorders in primary progressive apraxia: diagnostic and nosographic contribution]. 859 46

Clinical symptoms and patho-anatomic changes in cervical myelopathy due to spondylotic changes are described. The leading symptoms are numbness and clumsiness of upper and lower extremity, mostly combined with gait disturbances. Muscle wasting primarily on the upper extremity leads to the myelopathic hand. Cervical myelopathy can be classified into five main groups: 1. Spastic tetraparesis with numbness and hyperreflexivity of upper and lower extremity. The majority of patients present with the myelopathic hand. 2. Spastic paraparesis with lesion below C6. 3. Spastic tetraparesis, mild or moderate, with deltoid muscle paresis. 4. Amyotrophic myelopathic hand with mild long tract signs. 5. Central cord syndrome due to cervical spondylosis combined with trauma. From the therapeutic aspect, conservative treatment is often unsuccessful. It is important to relieve pressure on the spinal cord, and decompressive procedures, especially posterior laminoplasty techniques, are required. Earlier surgery provides better results.
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PMID:[Symptoms and pathological anatomy of the degenerative cervical spine]. 899 3

We report a case of transient left lateral gaze paresis due to a hemorrhagic lesion restricted in the right precentral gyrus. A 74-year-old female experienced a sudden clumsiness of the left upper extremity. A neurological examination revealed a left central facial paresis, distal dominant muscle weakness in the left upper limb and left lateral gaze paresis. There were no other focal neurological signs. Laboratory data were all normal. Brain CTs and MRIs demonstrated a subcortical hematoma in the right precentral gyrus. The neurological symptoms and signs disappeared over seven days. A recent physiological study suggested that the human frontal eye field (FEF) is located in the posterior part of the middle frontal gyrus (Brodmann's area 8) and the precentral gyrus around the precentral sulcus. More recent studies stressed the role of the precentral sulcus and the precentral gyrus. Our case supports those physiological findings. The hematoma affected both the FEF and its underlying white matter in our case. We assume the lateral gaze paresis is attributable to the disruption of the fibers from the FEF. It is likely that fibers for motor control of the face, upper extremity, and lateral gaze lie adjacently in the subcortical area.
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PMID:[Left lateral gaze paresis due to subcortical hematoma in the right precentral gyrus]. 971 Nov 28

This paper reports a surgically treated case of Sturge-Weber syndrome (SWS) in which the epileptic foci and haemangiomatosis were successfully resected under monitoring of intraoperative electrocorticography. The patient was a 19-month-old female infant who was referred to our hospital because of frequent hemi-tonic-clonic convulsions that were resistant to anticonvulsant therapy. Serial MRI showed progressive atrophy in the left fronto-parieto-temporal lobe, and gyral enhancement by gadolinium corresponded to venous haemangiomatosis of SWS. Three-dimensional reconstruction of the MR images was performed using the Viewing Wand System. Conventional EEG taken before the operation showed slow activity in the left frontal lobe. Intraoperative ECoG revealed spike focus at the posterior temporal cortex to the margin of the haemangiomatosis. Lesionectomy with lobar corticectomy of the total frontal and parietal lobe and part of the temporal lobe was performed. The epileptogenic focus detected by ECoG in the posterior temporal lobe was also resected. In post-excisional ECoG, epileptogenic activities had disappeared. The patient had hemiparesis and hemihypesthesia just after the surgery, but gradually recovered from the paresis and almost has normal motor function except for right-hand clumsiness up to 1 year after Surgery. The present study demonstrated that lobar corticectomy of the haemangiomatosis-affected cortex with resection of the neighbouring epileptogenic focus is a good surgical alternative even if a haemangiomatosis of the SWS affected multilobar corti of the hemisphere.
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PMID:Intraoperative electrocorticography and successful focus resection in a case of Sturge-Weber syndrome. 988 97

A 69-year-old, right-handed, Japanese male patient presented with pure agraphia with topographical disorientation after hemorrhage in the right parietal lobe. Upon developing cerebral hemorrhage, he was referred to our hospital for close examination of agraphia. There was no paresis or clumsiness in his extremities. His speech was fluent and well-articulated. Neither aphasia nor reading impairments was found, although there was a clear writing impairment with effort and hesitation. His writing of both kanji and kana letters contained additional, absent or deformed strokes or parts. No hemianopia, prosopagnosia, constructional disturbances and dressing apraxia were found. He could recognize familiar buildings or landscapes, but often lost his way around well-known areas. MR images revealed subcortical lesions of precuneus, superior and inferior parietal lobules in the right hemisphere, around the posterior horn of the lateral ventricle. He revealed pure agraphia and topographical disorientation after the right brain haemorrhage, without dementia or personality change. These findings indicate that the right parietal lobe participates in the kinesthetic movements of writing. Some authers have been documented cases of aphasic agraphia or alexia with agraphia caused by right hemisphere damage in dextrals, but pure agraphia caused by the lesion in the right hemisphere is very rare.
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PMID:[Pure agraphia with topographical disorientation caused by right hemisphere lesion]. 1871 86


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