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

We report a 77-year-old Japanese man with progressive gait disturbance. He was well until his 71 years of the age (1992), when he noted an onset of disturbance in his speech, which was followed by difficulty in using his left hand. He did not attempt to use his left hand afterwards. He started to fall down in the spring of 1994. He was admitted to our service on October 6, 1994. Neurologic examination revealed an alert and oriented man. He showed limb-kinetic apraxia in his left hand with anosognosia for his apraxia. Vertical gaze was impaired. He walked in small steps. He had moderate axial and limb rigidity. He had no weakness, ataxia, or tremor. Deep tendon reflexes were normal. Plantar response was flexor. Sensation was intact. His gait had progressively become worse and he was admitted to another hospital in April of 1996. At that time he was disoriented to time. He was only able to walk a few steps with support. He continued to show limb-kinetic apraxia in his left hand. He developed dementia and dysphagia and he expired on October 27, 1998. He was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had corticobasal degeneration. Most of the participants agreed with this diagnosis, but a few of them thought that progressive supranuclear palsy would be more likely. Post-mortem examination revealed no gross cortical atrophy. The right hemisphere was kept frozen for future biochemical analysis. The left precentral gyrus showed spongy changes, neuronal loss and gliosis. The pallidum, putamen, and the subthalamic nucleus were unremarkable, however, neurofibrillary tangles were seen in the subthalamic nucleus. The substantia nigra showed only slight neuronal loss; neuronal pigments were well retained. A few neurofibrillary tangles were seen in the remaining neurons. The cerebellar dentate nucleus showed grumose degeneration. Gallyas-Braak staining revealed many tuft-shaped astrocytes in the precentral gyrus. Pathologic diagnosis was progressive supranuclear palsy. Some participants thought that this diagnosis was unacceptable, because the pathologic changes in the substantia nigra, globus pallidus, and the subthalamic nucleus, which were usually severely involved in PSP, did not show typical changes of PSP. In addition, the predominant clinical feature was limb-kinetic apraxia, although he showed vertical gaze paresis and parkinsonian gait, which could also be seen in corticobasal degeneration. There was a big discussion among participants with regard to the diagnosis.
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PMID:[A 77-year-old man with gait and gaze disturbance]. 1076 50

We report a case of a unique eye sign following right hemispheric infarction. This patient was a 78 year old right-handed woman. There was a history of a left hemispheric stroke 1 year previously. On admission, she showed left hemianopia, dysarthria, mild left central facial paresis, bilateral sensory deficit and quadriparesis which were marked on the left side. Babinski sign was elicited on the left. She did not have anosognosia or visual neglect. She had mild orofacial apraxia, but ideomotor and ideational apraxia was absent. There was no motor impersistence. Magnetic resonance imaging of the brain revealed a recent infarction in the territory of the right middle cerebral artery and an old infarction in the left tempro-parietal lobe. The patient could not open her eyelids to verbal command or voluntarily until about two weeks later, when she became able to open her eyes but showed difficulty keeping her left eye closed. She was aware of this problem and could repeat the command and comprehend what was requested to her. On verbal command to close the eyes, her right eye would be closed continuously and excessively and the left eye would only blink. When requested to blink, however, she could blink correctly without excessive eye closure. Spontaneous, reflex and voluntary blinking were normal. Her eyes were closed normally during sleep. Blepharospasm was not seen. The patient showed a striking dissociation between a failure to close her eyes continuously and a preserved ability to blink voluntarily. We suggest that her ability to contract palpebral portion of her left orbicularis oculi muscle is preserved. Regarding the mechanism of the voluntary eye closure system, separate control mechanisms should exist on closing eyes continuously and blinking.
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PMID:[Dissociation of voluntary eye closure--to keep the eyes closed and to blink--following right hemisphere stroke]. 1087 26

Normally, we are aware that our arms and legs belong to us and not to someone else. However, some stroke patients with hemiparesis/-plegia after right-sided stroke show a disturbed sensation of limb ownership and a disturbed self-awareness of actions and such patients with anosognosia for hemiparesis/plegia typically deny their paresis/-plegia and are convinced that their limbs function normally. They may experience their limb(s) as not belonging to them and may even attribute them to other persons. Modern lesion analyses techniques in such patients and recent neuroimaging results in healthy subjects suggest a prominent role of the right insula for our sense of limb ownership as well as for our feeling of being involved in a movement-our sense of agency. We thus hypothesize that the right insular cortex constitutes a central node of a network involved in human body scheme representation.
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PMID:Right insula for our sense of limb ownership and self-awareness of actions. 2051 80