Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the existence, clinical symptoms, and brain pathology of cerebrovascular parkinsonism. In this study, clinicopathological criteria of cerebrovascular parkinsonism was defined as follows: 1) at least 2 or more symptoms from the following 4 symptoms: tremor, rigidity, akinesia or bradykinesia, and short stepped gait or freezing, 2) no depigmentation, no Lewy body at the substantia nigra, no other degenerative disease, and 3) existence of cerebrovascular lesions. Among consecutive 4,000 autopsy series in the elderly, clinicopathologically confirmed cerebrovascular parkinsonism was found in 24 patients with mean age of 80 years. Cerebrovascular parkinsonism was characterized by the short-stepped gait as initial symptoms, absence of the resting tremor, lead-pipe rigidity, the symmetry of findings, and negative response to levodopa. Pseudobulbar palsy was observed in 54%, pyramidal findings in 63% of the cases. Most cases had multiple vascular lesions of the basal ganglia, but the distribution of lesions was not different from that in the cases of progressive subcortical vascular encephalopathy of Binswanger type without parkinsonism. Diffuse pallor and the loss of oligodendrocytes in the frontal white matter observed in the cerebrovascular parkinsonism suggested that the symptoms of parkinsonism resulted from the white matter damages in the frontal lobe.
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PMID:[Cerebrovascular parkinsonism--clinicopathologic study]. 875 29

We report a 83 year-old woman with dementia. She was apparently well until December of 1993 when she was 81-year-old. At that time, she was operated or her cataract. Her post operative course was uneventful, however, shortly after her operation, she had an onset of memory loss and abnormal behavior. She showed a fluctuating course in her mental disturbance. In 1995, her dementia worsened with nocturnal agitation. She was admitted to our service on June 12, 1995. She was alert and her blood pressure was 140/100 mmHg. She showed recent memory loss and disorientation to time. Motor wise, she was unable to stand unsupported. Her gait with support showed small steps and a wide base. She was bradykinetic and ataxic in her finger-to-nose and heel-to-knee test, however, no rigidity or tremor was noted. Her MRI showed T2-high signal lesions in both medial thalamic areas, in the right occipital lobe, and in the bilateral cerebral white matters as well as in the basal ganglia. She was discharged for out-patient follow up on July 3, 1995. Four days after the discharge, she showed declining responses to stimuli and she developed dyspnea on July 14, 1995. She was admitted again on the same day. Her body temperature was 38.5 degrees C and moist rales were heard in the left lung field. She appeared drowsy and no verbal response was obtained; no apparent motor palsy was noted. Blood count showed leukocytosis (14,300/ml). Blood gas analysis under 61 of oxygen inhalation through a mask was as follows: pH 7.460, PCO2 39.6 mmHg, PO2 67 mmHg, and HCO3-28.5 mEq/l. Two days after admission, she developed a convulsion in her left arm and she became unconscious. Her EEG showed periodically recurring lateralized epileptic discharges on the right fronto-central areas. Her subsequent course was complicated by status epilepticus and respiratory distress. She died on July 26, 1995. She was discussed in a neurological CPC. The chief discussant arrived at a conclusion that she suffered from multi-infarct dementia. Bilateral thalamic infarctions were considered to have played a significant role in her dementia. Post-mortem examination revealed subcortical leukoencephalopathy of Binswanger's type and cerebral infarctions in the thalamic and basal ganglia regions and in the right occipital lobe. In addition, she showed isolated angitis of the central nervous system involving mainly in the small arteries located in the superficial areas of the brain and the spinal cord. This patient was interesting in that despite relatively mild leukoaraiosis in MRI, post-mortem examination revealed profound pathologic changes in the subcortical white matters. In addition, she showed the isolated angitis of the CNS. The cause and the clinical correlates of her angitis were unclear.
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PMID:[A 83 year-old woman with dementia, gait disturbance, and convulsion]. 904 33

Freezing of gait (FOG), commonly seen in advanced Parkinson's disease (PD), has been classified as its fifth cardinal feature. However, its presence frequently leads to a misdiagnosis of PD. FOG is actually more common in atypical parkinsonism (AP): including vascular Parkinsonism (VP), progressive supranuclear palsy (PSP), multiple system atrophy (MSA), corticobasal degeneration (CBD), dementia with Lewy bodies (DLB), and higher level gait disorders (HLGDs). VP is the result of multiple small vessel infarcts (lacunar state or Binswanger's disease), particularly involving the frontal, parietal, and basal ganglia regions. Approximately 50% have FOG (often referred to as lower body parkinsonism). FOG is also common in neurodegenerative forms of AP, present in 45-57%. Of these, FOG is present in 53% of PSP, 54% MSA, 54% DLB, 25% CBD, and 40% HLGD. It is generally seen in the late stages. There are two syndromes closely associated with AP that are dominated by FOG; pure akinesia (PA) and primary progressive freezing gait (PPFG). PA is characterized by akinesia of gait (including FOG), writing, and speech. Tremor, rigidity, dementia, and response to levodopa are notably absent. PPFG is defined by early FOG (often the initial feature) that progresses to include postural instability. It is accompanied by bradykinesia, rigidity, postural tremor, dementia, and levodopa unresponsiveness. Both syndromes are heterogeneous but PSP seems to be the most common cause. CBD and DLB can also present as PPFG. FOG is a common feature of AP and although typically occurring late in disease may also be an early symptom.
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PMID:The clinical spectrum of freezing of gait in atypical parkinsonism. 1866 24