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)

Consideration is given to how and why categories of ill health are divided into diseases. Aetiology is a fundamental criterion for the delineation of individual diseases. The same clinical and pathological picture may have many different causes; for example meningococcal meningitis and pneumococcal meningitis are distinct diseases that may display the same symptoms and signs. On the other hand, a single aetiology may lead to quite separate clinical and pathological phenomena; for example, neurosyphilis is a disorder that can present with general paresis or tabes dorsalis (or any combination of the two). In attempting to find a nosological placement for Parkinson's disease, we must take into account the extensive overlap with idiopathic dementia (Alzheimer's disease). Present evidence raises the possibility of several causes for Parkinson's disease, some of which may also be responsible for idiopathic dementia. A classification in accord with its position is desirable, and as a first step it would be helpful to replace "Parkinson's disease" with a term that is not saddled with implications of a single causal mechanism. "Idiopathic Parkinsonism" is suitable nomenclature for what is really a syndrome of unknown origin.
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PMID:Is "Parkinson's disease" one disease? 266 75

Analysis of the neurologic symptomatology in 22 patients with Niemann-Pick disease type C revealed 3 phenotypes: (1) an early-onset, rapidly progressive form associated with severe hepatic dysfunction and psychomotor delay during infancy and later with supranuclear vertical gaze paresis, ataxia, marked spasticity, and dementia; (2) a delayed-onset, slowly progressive form heralded by the appearance, usually in early childhood, of mild intellectual impairment, supranuclear vertical gaze paresis, and ataxia, and later associated with dementia and, variably, seizures and extrapyramidal deficits; (3) a late-onset slowly progressive form distinguished from the 2nd pattern by later age of onset (adolescence or adulthood) and a much slower rate of progression. The existence of the 1st and 2nd phenotypes within the same sibship suggests that they are variant expressions of the same clinicopathologic disorder. Niemann-Pick disease type C should be considered not only in infants and children who present with organomegaly and a progressive neurodegenerative course, but also in adolescents and adults who have insidiously progressive neurologic dysfunction and only slight organomegaly. Associated with the disease is a marked deficiency in the ability of cultured fibroblasts to esterify exogenously supplied cholesterol. Assay of this deficiency is particularly useful for confirming the diagnosis in patients with atypical presentation.
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PMID:Clinical spectrum of Niemann-Pick disease type C. 276 97

Ten right-handed patients suffering from visuospatial impairment were examined. The impairment was ascertained by a test requiring visual organization (picture completion). The patients did not suffer from other neuropsychological disorders (e.g., aphasia, dementia). Furthermore, psychiatric symptoms and defective oculomotion (gaze paresis, ocular paresis) were controlled. CT scan data revealed that in 4 patients the impairment was associated with lesions of the posterior right hemisphere. All lesions involved the central optic pathways and were accompanied by visual field defects. On the other hand, 6 patients turned out as suffering from damage of the cerebellum or brainstem. The available electronystagmographical data revealed impaired visual fixation, an oculomotor defect characterizing gaze apraxia, the diagnostic marker of Balint's syndrome.
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PMID:Visuospatial disorders and related lesions of the brain. 277 81

We found abnormal supranuclear ocular or lid motility in all of 37 patients with Lytico-Bodig (amyotrophic lateral sclerosis/parkinsonism-dementia complex). Twenty-one patients had pursuit paresis, 18 abnormal vestibulo-ocular reflex (VOR) cancellation, 15 abnormal convergence, 13 abnormal optokinetic nystagmus (OKN), 12 conjugate gaze limitation, nine nystagmus, nine saccadic paresis, and six abnormal fixation. Lid abnormalities included glabellar hyperreflexia in 21, involuntary levator inhibition in three, and blepharospasm in two. Earlier reports have indicated infrequent ocular disturbances in Lytico-Bodig, but we now find supranuclear eye and lid deficits are universal and sometimes very prominent.
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PMID:Supranuclear disturbances of ocular motility in Lytico-Bodig. 319 62

Borrelia spirochetes were directly visualized in autopsy brain tissue from a patient with Alzheimer's disease and were cultured from cerebral cortex in artificial media. The authors propose that, as occurs in tertiary neurosyphilis and general paresis of the insane, Borrelia species may invade the brain, remain in a latent state for many years, and cause dementia in the absence of other focal neurologic deficits. An undetermined fraction of patients with Alzheimer's disease may be shown to have late tertiary neuroborreliosis.
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PMID:Concurrent neocortical borreliosis and Alzheimer's disease. 329 97

Binswanger, in his 1894 dissertation on the differential diagnosis of general paresis of the insane, described a slowly progressive dementia associated with macroscopic loss of white matter. In recent years interest in Binswanger's disease was rekindled with CT demonstration of extensive white matter low densities in some patients. To define the clinical spectrum, we reviewed 22 consecutive cases in which the CT appearances suggested a diagnosis of Binswanger's disease. Two patients had focal neurological deficits at presentation, but recent anoxic or hypoglycaemic insults could not be excluded as the cause of the CT abnormalities. The 20 remaining patients were demented and showed variable combinations of corticobulbar dysfunction and gait dyspraxia. The duration of symptoms ranged from a few months to several years. Sixty per cent of this group gave a history of discrete stroke events and focal cortical and/or lacunar infarcts were a frequent CT finding. Binswanger's disease is probably due to chronic or acute-on-chronic white matter ischaemia. The association with lacunar and cortical infarctions suggests that a combination of large and small vessel disease produces diffuse ischaemia maximal in white matter watershed zones. Binswanger's disease is clinically differentiated from multi-infarct dementia by its time course.
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PMID:Subcortical arteriosclerotic encephalopathy: Binswanger's disease. 366 81

The olivopontocerebellar atrophies (OPCA) can be divided into five disease entities. One of these, dominant OPCA with dementia and extrapyramidal signs, is better defined by the family we studied. Five persons in three generations were affected by progressive ataxia, tremor, rigidity and mental deterioration, beginning in their twenties and thirties. Neurologic examination showed mental deterioration, high-pitched dysarthric voice, gaze paresis, rigidity and coarse tremor. This disease differs from other dominant and recessive OPCAs clinically because of the prominent mental deterioration and extrapyramidal signs, and pathologically because of cortical, lentiform and substantia nigra neuronal loss.
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PMID:Dominant olivopontocerebellar atrophy with dementia and extrapyramidal signs: report of a family through three generations. 517 58

Seven affected individuals from three generations in a kindred having over 250 members were identified as having possible, probable, or definite Creutzfeldt-Jakob disease. Spongiform encephalopathy was found at postmortem examination in two cases. Detailed inpatient neurological examinations were performed on four of the subjects, three of whom were first observed with supranuclear gaze paralysis, gait ataxia, and rapidly progressive dementia. Supranuclear gaze paresis can be seen as an early feature of Creutzfeldt-Jakob disease, although it has been regarded as a late sign. In this, the largest reported kindred of Creutzfeldt-Jakob disease, most of the affected patients were farmers. Possible modes of infection are discussed.
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PMID:Supranuclear gaze palsy in familial Creutzfeldt-Jakob disease. 635 15

Three principal diagnostic problems were encountered in a group of 81 elderly patients with epileptic seizures: Post-ictal paresis (Todd's palsy) occurred in 13 patients (16%), of whom seven had evidence of past or present cerebral infarction, and six no such evidence. The paresis lasted up to 4 days, and could be confused with recurrent infarction or a transient ischaemic episode. Ictal and post-ictal confusional states of 24 h or more duration (up to 7-8 days) were noted in 11 patients (14%). They occurred in association with normal intellectual function as well as with pre-existing dementia, and required to be distinguished from other causes of delirium. Two patients presented paroxysmal sensory phenomena of ictal type. The differential diagnosis of episodic pain in hemiplegic limbs is discussed.
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PMID:Epileptic seizures in the elderly: II. Diagnostic problems. 680 29

From 1972-1974, 228 children began treatment for acute lymphocytic leukemia and were prospectively assessed for neurologic complications. After CNS irradiation (2,400 rad) and intrathecal methotrexate (MTX), they received weekly intravenous maintenance therapy with MTX alone (40-60 mg/m2; 20 patients) or MTX (10-30 mg/m2) with other drugs (208 patients). Signs of leukoencephalopathy appeared in 11 children (nine without CNS leukemia) after 4-15 months of IV MTX alone, and included lethargy, seizures, spasticity, paresis, drooling, and dementia. Before or during the clinical onset, EEG frequencies slowed (all ten patients tested). Radionuclide scans showed periventricular accumulation of 99mTc (9/11 patients) and remained abnormal for greater than or equal to six months in eight patients. Cranial computed tomograms or neuropathology findings (five patients each) demonstrated leukoencephalopathy (nine patients) and radiation-related microangiopathy (ten patients). Severe neurologic and neuropsychologic dysfunctions were present in four long-term survivors.
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PMID:Progression of methotrexate-induced leukoencephalopathy in children with leukemia. 693 56


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