Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report palilalia and acquired stuttering in a 60-year-old Japanese male with Parkinson's disease. At the age of 54, he presented with resting tremor in the hand and foot on the left, and gradual slowness in voluntary movements. Two years later, resting tremor involved the right foot, and an expressionless face and frozen gait occurred. A diagnosis of Parkinson's disease was made and treatment with L-dopa and carbidopa resulted in conspicuous improvement. At the age of 57, he developed compulsive repetitions of syllables, words and phrases, and sentences infrequently when he spoke. They have been persisting for four years. Repetitions increased in spontaneous speech while they decreased in oral reading and repetition of sentences. These repetitions in speech were symptomatologically diagnosed as palilalia and acquired stuttering. Brain CT showed slight brain atrophy, and brain MRI disclosed a few lesions indicating lacunae in the left substantia nigra, left putamen, and right internal capsule. SPECT showed a slight decrease in blood flow in the frontal lobes and basal ganglia bilaterally. Full IQ on WAIS was 105, and neither agnosia nor apraxia was detected. Palilalia and acquired stuttering, though the pathomechanism has not been clarified, have been reported to occur usually secondary to cerebral vascucular lesions and very rarely in Parkinson's disease. In the present case, they may have been produced by the parkinsonian nigro-striatal lesions. Alternatively, they may have been induced by the small vascular lesions demonstrated by MRI.
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PMID:[Palilalia and acquired stuttering in a case of Parkinson's disease]. 149 Mar 13

Thirty-six patients with Parkinson's disease and medically refractory tremor underwent stereotactic ventrolateralis thalamotomy at the Mayo Clinic between 1984 and 1989. All patients had been or were being treated with carbidopa/levodopa but with unsatisfactory tremor control. Modern stereotactic techniques, including microelectrode recording, were used to treat 36 patients, of whom 31 (86%) had complete abolition of tremor and three patients (5%) had significant improvement. Tremor recurred in two patients within 3 months of surgery; however, the remaining patients suffered no recurrence of tremor during follow-up periods ranging from 14 to 68 months (mean 33 months). Persistent complications (arm dyspraxia, dysarthria, dysphasia, or abulia) were noted in five patients but were a source of disability in only two. It is concluded that thalamotomy in carefully selected patients is a beneficial operation for the control of medically refractory parkinsonian resting tremor.
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PMID:Stereotactic ventrolateralis thalamotomy for medically refractory tremor in post-levodopa era Parkinson's disease patients. 156 56

Cognitive disturbances are frequently encountered in advancing Parkinson's disease (PD). Typically there are visuo-spatial disorders, memory impairment and bradyphrenia, defined as 'subcortical dementia' to distinguish it from the dementia that occurs in Alzheimer's disease, where the most prominent dysfunctions are agnosia, apraxia and aphasia. An electrophysiological test to study cognitive processing is the P300 (or P3) of the Event Related Potentials; in particular the latency of the P3 seems to correlate with cognitive decline. Thirty patients affected with idiopathic PD were investigated using a classic auditory "oddball" paradigm (rare tone--"target"--3000 Hz, frequent tone--"non target"--1000 Hz; the patients were instructed to recognize and keep a mental count of the number of rare tones). Electrophysiological findings were compared with those obtained in twenty normal subjects, age and sex matched with the patient's group. The parameters of P300 were correlated with patient's age, duration of the disease, motor and cognitive impairment levels and L-Dopa therapy. The P300 was loss in 16.6% (5 p.) and delayed in 33.3% (10 p.). Significative correlations were found only with age and cognitive impairment scores, but not with other variables analyzed. These results suggest that P300 could be a useful test to identify demented patients among those with PD, despite different motor disabilities.
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PMID:[P300 and Parkinson disease. The role of cognitive changes]. 210 48

Apraxia of lid opening is a nonparalytic motor abnormality characterized by difficulty in initiating the act of lid elevation. It has been reported with extrapyramidal disorders, including Parkinson's disease, Huntington's chorea, progressive supranuclear palsy, and Shy-Drager syndrome. We found seven cases (7%) of functionally disabling apraxia of lid opening in 100 consecutive blepharospasm patients studied. It is important for physicians treating blepharospasm to be aware of the association between these two visually debilitating disorders.
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PMID:Apraxia of lid opening in blepharospasm. 238 54

Seven patients, aged 65-72 years, are described with dementia and cortical Lewy bodies. In one patient a Parkinsonian syndrome was followed by dementia and motor neuron disease. In the remaining six patients dementia was accompanied by dysphasia, dyspraxia and agnosia. One developed a Parkinsonian syndrome before the dementia, in three cases a Parkinsonian syndrome occurred later, and in two cases not at all. All patients showed Lewy bodies and cell loss in the substantia nigra, locus coeruleus and dorsal vagal nucleus, as in Parkinson's disease. The severity of cell loss in the nucleus basalis varied from mild to severe. Lewy bodies were also present in the parahippocampus and cerebral cortex, but Alzheimer-type pathology was mild or absent, and insufficient for a diagnosis of Alzheimer's disease. Patients with moderate or severe dementia, some with temporal or parietal features, may have cortical Lewy body disease, Alzheimer's disease, or a combination of the two. Cortical Lewy body disease may be associated with dementia in Parkinson's disease more often than realised, but is not necessarily associated with extensive Alzheimer pathology.
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PMID:Cortical Lewy body dementia: clinical features and classification. 246 66

Three patients with clinical and pathological features of corticobasal degeneration are described. They presented with a progressive disease bearing some clinical resemblance to Steele-Richardson-Olszewski syndrome and displaying some pathological features of Pick's disease. Their illness began at the age of 59 to 66 yrs with focal dystonia and myoclonus of an arm, the 'alien hand' sign, or an akinetic-rigid syndrome. They developed a supranuclear gaze palsy, parkinsonian features and mild cerebellar signs. Two patients showed constructional dyspraxia when using the arms. The duration of disease to death was 4 to 6 yrs. Pathological examination showed frontoparietal atrophy with cortical cell loss, gliosis and Pick cells, but there was no significant hippocampal disease or Pick bodies in this region. There was nerve cell loss and gliosis in the thalamus, lentiform nucleus, subthalamic nucleus, red nucleus, midbrain tegmentum, substantia nigra and locus coeruleus. Neuronal inclusions in the substantia nigra, termed corticobasal inclusions, were reminiscent of the globose neurofibrillary tangle of Steele-Richardson-Olszewski syndrome, and other pale inclusions resembled the pale body of Parkinson's disease, but Lewy bodies and neurofibrillary tangles were generally absent. Some nigral inclusions were similar to those in Pick's disease. Despite some pathological similarities to Pick's disease we suggest that the distribution of nerve cell loss and the corticobasal inclusion are unique to corticobasal degeneration.
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PMID:Corticobasal degeneration. 2059 45

The question of whether dementia of the Alzheimer type and dementia associated with Parkinson's disease are clinically separable is controversial. We examined possible neuropsychological differences in these two patient groups matched for overall severity of dementia. Patients with dementia of the Alzheimer type had more severe impairment on measurements of memory, language, and orientation, and, unlike patients with Parkinson's disease, there was evidence of apraxia. Patients with Parkinson's disease had more severe impairment related to speed of information processing, and, unlike patients with dementia of the Alzheimer type, they also had disturbance of mood. The nature of visuospatial abnormalities also differentiated the two groups. The pattern of neuropsychological differences is consistent with the cortical-subcortical hypothesis.
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PMID:Neuropsychological differences between the dementias of Alzheimer's and Parkinson's diseases. 259 12

A study of clinical features and an analysis of gait with floor reaction forces and EMG of leg flexors and extensors were made in patients with multiple cerebral infarction or patients with Parkinson's disease having frozen gait. A case with occlusion of the bilateral anterior cerebral arteries resulting in massive infarction of the infero-medial part of the frontal lobes was also studied as he showed a unique disorder characterized by apraxia of gait. Frozen gait is characterized by shuffling steps, broad-based stance, positive foot grasp, kinesia paradoxa and disturbance of postural reflexes. The vector angle which shows foot pressure in forward locomotion was decreased in patients with frozen gait. EMGs of lower leg muscles in frozen gait were grouping of potentials corresponding to the shuffle and reciprocity between flexors and extensors was preserved. The patient with infarction of the bilateral anterior cerebral arteries showed a peculiar disorder of gait which was characterized by an inability to initiate stepping. It is considered as "apraxia of gait" in a classical sense, which differs from frozen gait. Observation of this patient suggests that the infero-medical part of the frontal lobe plays an important role in the initiation of gait. Furthermore, common features of frozen gait in patients with Parkinson's disease and in patients with multiple cerebral infarction involving the frontal lobe suggest that the nigrostriatal structures and the frontal lobe are important in CNS mechanisms subserving smooth locomotion.
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PMID:[Clinical and physiological study of apraxia of gait and frozen gait]. 275 55

Four patients with severe dementia and a parkinsonian syndrome are described. Dysphasia, dyscalculia, dyspraxia, visual and verbal memory disturbance and psychosis, usually of depressive type, occurred early in the course of the illness. Pathologically they were characterized by the presence of numerous Lewy bodies throughout both the cerebral cortex and brainstem. Three cases also had severe neurofibrillary tangle change or senile plaques in the neocortex, compatible with Alzheimer's disease, but the cortical tangle distribution did not always match that of the Lewy bodies. This disorder may form part of the spectrum of pathology in Parkinson's disease, where it may be one possible cause of dementia.
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PMID:Clinical and pathological features of diffuse cortical Lewy body disease (Lewy body dementia). 282 57

The subcortical dementias such as progressive supranuclear palsy, Huntington's disease, and Parkinson's disease are said to be characterized by the presence of slowed mentation, apathy, and the absence of aphasia, agnosia, and apraxia, symptoms that are claimed to be more common in cortical dementias such as Alzheimer's disease. Conceptual problems (such as vagueness of terms and difficulties with symptom definition) and methodological problems (such as improper matching of comparison groups and inadequate assessment techniques) found in currently available studies require a reappraisal of this classification of dementias into cortical and subcortical forms. A review of recent clinical, neuropathological, and neurochemical studies offers little support for this classification system, although adequate systematic studies have not been performed.
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PMID:The concept of subcortical and cortical dementia: another look. 286 89


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