Securing of suctions drains in head and neck surgery.
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Head↗
Biomedical subjects
Y Stern
Publications and source records attributed to Y Stern.
Depression in Parkinson's disease: a biochemical model.
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Brain↗
Measurement and prediction of functional capacity in Alzheimer's disease.
Functional loss in Alzheimer's disease is difficult to measure or predict. The Blessed Dementia Rating Scale (Part 1) correlates well with postmortem changes but is not an effective antemortem index of functional change since disparate behavioral domains are assessed. We performed a factor analysis of the Blessed items in 187 patients with clinically diagnosed Alzheimer's disease and identified 4 independent factors: (I) cognitive, (II) personality, (III) apathy, and (IV) basic self-care. An endpoint, consisting of a score indicative of moderate disability, was determined for each factor. We then used life table analyses to compare the probability of reaching these endpoints over time in longitudinally followed patients. Patients with extrapyramidal signs at their initial visit reached the factor IV endpoint sooner, and those with psychosis or no family history of dementia also reached the factor I endpoint faster. These data illustrate the utility of a multifactorial approach to the assessment of functional capacity in Alzheimer's disease, and also indicate that extrapyramidal symptoms and psychosis are powerful predictors of the rate of decline in basic self-care activities and cognition.
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An estimate of the incidence of dementia in idiopathic Parkinson's disease.
The proportion of patients with idiopathic Parkinson's disease (PD) who are considered demented ranges from 10% to 15%. Because dementia may affect survival in PD, the incidence rate of dementia, rather than proportion, would be a more accurate measure of disease frequency. We previously estimated the proportion of patients with PD and dementia to be 10.9% from the records of a cohort with the idiopathic form of PD in a major medical center. We reviewed the clinical records of this cohort after 4 years and 9 months to estimate the incidence rate of dementia. We identified 65 new cases of dementia from the 249 patient-records available. Using the number of person-years of follow-up for each case as the denominator, we estimated the overall incidence rate to be 69 per 1,000 person-years of observation. The mean age of this cohort was 71.4 years. The cumulative incidence of dementia increased with age. By 85 years of age, over 65% of the surviving members of the cohort were demented. The age-specific incidence rates for dementia in this cohort of PD were significantly greater than for a similarly aged cohort of healthy elderly people. The age-specific standard morbidity ratios indicated that, compared with people of similar ages, patients with PD have the highest increase in risk for dementia between ages 65 and 75.
Age Factors↗
Cognitive change following MPTP exposure.
In a previous study, we demonstrated that patients with MPTP-induced parkinsonism (MPTP-IP) had a pattern of cognitive change similar to that in nondemented patients with idiopathic Parkinson's disease (PD). The present study addressed cognitive change in MPTP-exposed but relatively asymptomatic (MPTP-AS) individuals. We examined them for general intellectual function, construction, language, memory, executive function, attention, and reaction time, and compared their performance with data obtained in the previous study from patients with MPTP-IP and drug addict controls. Each MPTP-AS individual had some subtle parkinsonian signs, but in no case would these be sufficient for a diagnosis of PD. PET studies showed that these individuals had significantly reduced uptake of labeled 6-fluorodopa into the striatum. MPTP-AS and MPTP-IP groups performed comparably and were significantly worse than controls on tests of construction and category naming. The MPTP-AS group performed at a level between the other 2 groups on a test of executive function. The 3 groups performed comparably on all other measures. The similarity of the pattern of intellectual change in MPTP-AS to that seen in MPTP-IP and idiopathic PD supports the idea that the dopamine system mediates a specific set of cognitive functions and suggests that cognitive change can occur in the presence of few or no motor signs of parkinsonism.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
Coexisting dementia and depression in Parkinson's disease.
Dementia and depression in patients with Parkinson's disease have been reported separately, but their prevalence is controversial. This study examines the coexistence of these two problems and suggests a common underlying biochemical system. We examined these two entities by retrospective chart review and cerebrospinal fluid biochemistry. We found a prevalence of 10.9% for dementia, 51% for depression, and 5.4% for coincident depression and dementia. In a prospective study of patients with Parkinson's disease we found a continuum of cerebrospinal fluid 5-hydroxyindoleacetic acid concentrations. Patients who were either depressed or demented had lower concentrations of this metabolite than other patients with Parkinson's disease, but patients who were depressed and demented had the lowest levels. These results suggest that the coexistence of dementia and depression represents a unique clinical entity in Parkinson's disease. The serotonergic system may be involved in depression and dementia because evidence of a cumulative effect on this biochemical system is present.
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Gray-matter degeneration in presenile Alzheimer's disease.
Previous comparisons between presenile Alzheimer's disease (AD) and senile dementia of the Alzheimer type (SDAT) did not control for disease severity and duration. In the current study, 18 patients with each diagnosis were matched for disease duration, cognitive dysfunction, and behavioral symptoms (using the modified Mini-Mental Status [mMMS] examination and the Blessed Dementia Rating Scale [BDRS] ). Regional cerebral blood flow (rCBF) was quantified by the 133xenon inhalation technique, and several indices of tissue perfusion were examined. The two variables of primary interest were relative gray-matter relative weight (35% in presenile patients versus 39% in senile patients and healthy control subjects, p = 0.006), with neither perfusion nor disease severity differences between the two dementia samples. This loss of gray matter was significantly related to both severity and duration of disease in the patients with presenile AD, but not in patients with SDAT. These findings lend support ot previous suggestions of greater degenerative process in presenile AD and confirm the need to examine and control age of onset in future investigations of AD. Further, correlation analysis suggests greater proportion of common variance among clinical and physiological indices in presenile AD.
Age Factors↗
Slow changes in the flexion reflex of the rat following arthritis or tenotomy.
(1) The flexor reflex was measured in control decerebrate spinal rats by recording the motor axon activity in the nerve to biceps femoris evoked by a pressure stimulus to the hindpaw. A brief (1 Hz, 20 s) conditioning stimulus to peripheral nerves with sufficient strength to activate C fibres results in a prolonged increase in this flexor reflex. If the conditioning stimulus is applied to a cutaneous nerve, the sural, the facilitation lasts 5 (5.0 +/- 1.6, n = 28) min. However, if the same conditioning stimulus is applied to the muscle nerve to gastrocnemius, the facilitation lasts up to an hour (54.0 +/- 8.3 min, n = 16). (2) Ankle joint urate arthritis was induced by the injection of 1.25 mg sodium urate crystals into one ankle joint. Two hours after the injection, conditioning of the flexor reflex by brief stimulation of the sural or gastrocnemius nerves produced the same effect as in control animals. However, 24 h after the injection, sural nerve conditioning produced the same effect on the flexor reflex as in controls but gastrocnemius nerve conditioning produced only 8 min (8.3 +/- 1.6, n = 8) of facilitation instead of the expected 54 min. (3) The decreased ability of the muscle nerve to produce prolonged facilitation was not dependent on a saturation of the flexor reflex since the reflex could still be enhanced briefly by the conditioning stimuli. It was also not dependent on a continuous input from the arthritic ankle since the decrease is still apparent when the ankle has been denervated 24 h after the beginning of the arthritis.(ABSTRACT TRUNCATED AT 250 WORDS)
Achilles Tendon↗
An estimate of the prevalence of dementia in idiopathic Parkinson's disease.
A review of the records for evidence of dementia using criteria adapted from the third edition of the Diagnostic and Statistical Manual of Mental Disorders in every patient (hospitalized and outpatient) with parkinsonism at a major medical center during an 18-month period revealed an overall prevalence of 10.9% in 339 patients with idiopathic Parkinson's disease. Demented patients were older, had a later age at onset of motor manifestations, and a more rapid progression of physical disability than nondemented patients. Duration of illness and levodopa use and the presence of tremor or depression were similar in demented and nondemented patients. Demented patients more often responded poorly or developed adverse effects to levodopa than nondemented patients. When Parkinson's disease began after age 70 years, dementia was noted over three times more frequently than when the disease began at an earlier age. The age-specific prevalence rate of dementia for patients older than 70 years was more than twice that for younger patients. Moreover, the number of records with evidence for dementia with idiopathic Parkinson's disease was 3.75 times greater than expected in comparison with data from a study of the prevalence of dementia in the elderly.
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The relationship of serotonin to depression in Parkinson's disease.
We have previously reported a correlation between depression in patients with idiopathic Parkinson's disease and decreased concentrations of the cerebrospinal fluid content of the serotonin metabolite, 5-HIAA. To further examine this relationship, we repeated the study in a new cohort of patients while they remained on dopaminergic medications, conducted follow-up interviews and examinations in our original cohort, and conducted an open trial of the serotonin precursor, 5-hydroxytryptophan in a group of new patients with depression. We were again able to demonstrate a significant reduction in cerebrospinal 5-HIAA in depressed patients in comparison to controls and patients without depression. Demented patients with Parkinson's disease, particularly those with concurrent depression, had the lowest values of 5-HIAA. No new cases of depression occurred in our original cohort after 2 1/2 years of follow-up, and depression remitted following conventional or experimental treatment in four patients. Depression improved in six of the seven new patients following oral 5-hydroxytryptophan. Three of these patients allowed a repeat lumbar puncture, and the concentration of 5-HIAA increased following 5-hydroxytryptophan. These three studies support our hypothesis that depression in idiopathic Parkinson's disease is associated with a reduction in brain serotonin. However, it also suggests that other factors, biological or environmental, may be causal factors.
5-Hydroxytryptophan↗
Prism adaptation in Parkinson's disease.
Prism adaptation is impaired by lesions in the basal ganglia in non-human primates, suggesting that this area is involved in this form of visuomotor learning. We investigated the ability of patients with Parkinson's disease to prism adapt. Patients and controls wore prisms which deflected vision laterally by 11 degrees. After baseline testing with a localisation task that permitted no feedback about performance accuracy, prism adaptation was tested at 4 minute intervals over a 28 minute trial. All subjects erred initially, reaching too far to the left of the target, but a separate pointing task encouraged adaptation and reaching error decreased at a similar rate in Parkinsonians and controls. Immediately after the prisms were removed, all subjects reached to the right of the target. This negative after effect was present in controls but not patients when assessed 4 minutes later, suggesting that the patients could not maintain the new sensorimotor relationship imposed by the prisms after their removal. This is similar to performance on visuospatial and executive tasks in Parkinsonians, where ongoing behaviour cannot be modulated without external guidance.
Adaptation, Ocular↗
Long-term administration of oral physostigmine in Alzheimer's disease.
Minimal short-term benefits with oral physostigmine have been reported in Alzheimer's disease. We examined long-term oral physostigmine therapy in 14 patients with probable Alzheimer's disease in an extended double-blind crossover trial in which they received physostigmine for five intervals of 4 to 6 weeks in length and placebo for one interval determined at random. At each interval a Selective Reminding Test was administered and three indexes were examined: total recall, long-term recall, and intrusions. As a group, patients' memory test scores were significantly better during the drug period. Two patients who previously had performed worse on drug than on placebo in a short-term trial continued to do so. Nine of the remaining 12 patients performed better on two or more measures on physostigmine compared with placebo. In some cases scores improved up to 50% over placebo values. This improvement was not predicted by response to medication in the earlier short-term trial. Seven patients completed an additional six-interval crossover trial. All but one continued to have improved performance with oral physostigmine and, in grouped data, memory measures remained significantly improved. These results suggest that long-term administration of physostigmine in Alzheimer's disease may be more effective than short-term. This benefit can be sustained for up to a year in some patients.
Administration, Oral↗
Cerebral perfusion as a diagnostic marker of early Alzheimer's disease.
Clinical diagnosis of Alzheimer's disease (AD) is not fully satisfactory, and laboratory markers of this disease are not yet established. We report substantial regional Cerebral Blood Flow (rCBF) abnormalities in patients with documented early stages of the disease, when differential diagnosis is most critical. Thirty-six patients with carefully documented clinical diagnosis of early AD (mean disease duration, 3.25 +/- 1.80 years) and 12 elderly healthy controls participated in rCBF studies using the 133Xe inhalation method. Whole-brain perfusion was significantly (p less than 0.001) lower in the AD group, and a characteristic perfusion deficit was consistently found in temporoparietal cortex of the AD patients. Discriminant analyses demonstrated over 90% correct classification of the two groups. Two subgroups of patients with mildest disease manifestations were equally well discriminated. The similarity of these findings to those in late stages, which have been validated neuropathologically, offers indirect confirmation of validity and specificity. These results suggest that rCBF procedures may provide an accurate and sensitive laboratory marker for early AD.
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Effects of oral physostigmine in Alzheimer's disease.
Previous studies of oral physostigmine in the treatment of Alzheimer's disease have: (1) assumed physostigmine is effective only in mildly affected patients; (2) relied on an initial "dose-finding" phase to determine the most effective dose and excluded nonresponders; and (3) primarily assessed memory. We examined the response of 22 patients to six different daily dosages of oral physostigmine, using selective reminding tests that were administered twice daily. Nine patients had a "best" dose/day (mode = 13 mg/day), which was used in a subsequent double-blind crossover study. The other 13 were given the highest tolerated dose. The selective reminding test and a full neuropsychological battery were given during the drug and placebo periods. As a group, the 22 patients improved significantly on the Wechsler Adult Intelligence Scale-Revised Digit Symbol subtest and a shape cancellation task (p less than 0.05). Nine patients showed improved performance on the selective reminding test during physostigmine treatment, and 9 showed no response; 4 patients performed better during placebo treatment. Dose finding did not help in predicting response in the crossover study; only 2 of the 9 who showed improvement had a best dose. Dementia severity did not predict crossover response. This suggests that: (1) physostigmine as administered had no pronounced effect on memory in Alzheimer's disease; (2) oral physostigmine produces no greater benefits on memory in mildly than in moderately demented patients; (3) response in a dose-finding phase does not predict response in double-blind crossover; and (4) Digit Symbol and cancellation tasks may be more sensitive than memory tests to the effects of oral physostigmine.
Administration, Oral↗
The amine transporter from bovine chromaffin granules: photolabeling and partial purification.
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Affinity Labels↗
Predictors of disease course in patients with probable Alzheimer's disease.
The presence of extrapyramidal signs or psychosis may indicate greater disability in patients with probable Alzheimer's disease. We evaluated the ability of these signs, noted at a patient's first visit, to predict one of two specific clinical endpoints: (1) a preselected score on the modified Mini-Mental State examination (cognitive endpoint), and (2) a preselected score on the Blessed Dementia Rating Scale (functional endpoint). Sixty-five patients were followed either until they reached the endpoints or to the end of the study period. Survivorship curves were drawn to predict the distribution of time to onset of an endpoint in patients with and without the clinical signs. Time to reach the cognitive endpoint was shorter for patients with extrapyramidal signs or psychosis compared with those without these signs and symptoms. These clinical signs did not predict the functional endpoint. We conclude that extrapyramidal signs and psychosis may be useful predictors of intellectual decline in Alzheimer's disease.
Activities of Daily Living↗
Clinical and biochemical correlates of bradyphrenia in Parkinson's disease.
Bradyphrenia is considered the mental equivalent of bradykinesia in Parkinson's disease. Patients are described as inattentive and "slow thinking," but not demented. We compared the performance of three groups: parkinsonians age-matched controls, and mildly impaired patients with probable Alzheimer's disease in tests of general intellect, memory reaction time, and in a continuous performance task measuring attention and vigilance. Metabolites of the major biogenic amine in CSF were also measured. The parkinsonians formed two distinct groups. In one, intellectual function and CSF measures were similar to that of controls. The other group of parkinsonians had significantly more omission errors and fewer correct response on the continuous performance task than did controls or patients with Alzheimer's disease. We considered this second group to have bradyphrenia. Their performance on measures of general intellectual and memory function was similar to that of the patients with Alzheimer's disease. CSF-MHPG, the major metabolite of norepinephrine, correlated with the continuous performance task and reaction time in all parkinsonians, and those with bradyphrenia had the highest CSF-MHPG levels. Our data suggest that bradyphrenia is an impairment of attention and vigilance, unique to Parkinson's disease, that may be associated with dementia and with an alteration in norepinephrine metabolism.
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