Biomedical subjects

J J Pahl

Publications and source records attributed to J J Pahl.

9 recordsLinked to original sources

PubMed1995

Positron-emission tomography in tardive dyskinesia.

Cerebral glucose metabolic rates were determined in normal control subjects (n = 26) and schizophrenic patients with tardive dyskinesia (n = 14). Globus pallidus and primary motor cortex (precentral gyrus) metabolic values divided by those of the cerebral hemispheres were significantly increased in the patient group. A similar metabolic pattern has not been reported for schizophrenic patients without tardive dyskinesia, and the abnormalities were demonstrated despite the normal appearance of the basal ganglia on X-ray CT. The findings differed markedly from the reduced metabolic rates of the basal ganglia previously identified in other choreiform disorders, including Huntington's and Wilson's diseases. The findings suggest that tardive dyskinesia is characterized by increased pallidal synaptic activity resulting from either altered striatopallidal input or increased pallidal interneuron firing.

Adult↗

PubMed1995

Physical and subjective evaluation of a three-detector (TRIAD 88) SPECT system.

The three-detector TRIAD 88 is a variable cylindrical FOV whole-body SPECT system designed for both brain as well as body organ imaging. The system performance was assessed in terms of physical indices and clinical quality. Measures of low contrast resolution using contrast-detail curves, high contrast resolution using LSFs and associated frequency descriptors, display characteristics, system sensitivity, energy resolution and uniformity analysis were utilized. In addition, images of Carlson phantom, Hoffman brain phantom and clinical brain images were used to compare two collimators subjectively. Measurements and calculations were obtained for two sets of parallel hole collimators, i.e., LEUR_PAR and LEHR_PAR. Of special interest is the consistency among the three detectors. The planar and volume sensitivities for the LEUR_PAR collimator were about 58% of those of the LEHR_PAR collimator. The planar spatial resolution of the two collimators differed by about 14%. The display was characterized by a logistic model H & D curve. The planar contrast-detail curves demonstrated no statistical difference in lesion detectability between the two collimator types, however SPECT phantom and clinical images demonstrated improved performance with the LEUR_PAR collimator. Images of Hoffman single slice brain and Carlson phantoms and Tc-99m (HMPAO) brain images demonstrated excellent image quality. There was similarity in performance parameters of the three detector heads.

Biophysical Phenomena↗

PubMed1994

A method for co-registering three-dimensional multi-modality brain images.

A method has been developed for co-registering three-dimensional multi-modality images of the human brain. The interactive program allows users to specify the interhemispheric fissure plane in three dimensions by identifying the endpoints of the centerline within transaxial slices. Translations and rotations within transaxial and coronal planes are determined to align the interhemispheric fissure planes of the two image sets to be co-registered. After reslicing the two partially co-registered image volumes, the intercommissural lines are detected by using three internal landmarks. A transformation including translation and rotation in the sagittal plane finally co-registers the two image sets in three-dimensional space. Single photon emission computed tomography (SPECT) images and magnetic resonance (MR) images have been used to validate the method for co-registering three-dimensional functional and anatomic brain images. This new co-registration method requires neither special head positioning procedures nor external fiducial markers, thereby making it appropriate for the routine clinical practice.

Brain↗

PubMed1992

Serial changes of cerebral glucose metabolism and caudate size in persons at risk for Huntington's disease.

OBJECTIVE: To determine the rate of change of glucose metabolism and caudate size in persons at risk for Huntington's disease. DESIGN: Eighteen persons at risk for Huntington's disease had two positron emission tomographic glucose metabolic studies and two magnetic resonance imaging scans separated by 42 (+/- 9) months. SETTING: Ambulatory research subjects at a teaching hospital with magnetic resonance imaging and positron emission tomographic technology. SUBJECTS: Seven of the individuals were Huntington' disease gene negative by testing at the polymorphic DNA loci D4S10, D4S43, and D4S125; the remainder were gene positive by genetic testing or onset of chorea after study entry. INTERVENTIONS: None. OUTCOME MEASURES: Onset of chorea and imaging results. RESULTS: The gene-positive group demonstrated a significant 3.1% loss of glucose metabolic rate per year in the caudate nucleus (95% confidence interval [CI], -4.64, -1.48) compared with the gene-negative group. There was a 3.6% per year increase in the magnetic resonance imaging bicaudate ratio (95% CI, 1.81, 5.37), a linear measure of caudate atrophy. The rate of change in caudate size did not correlate with the rate of change in caudate metabolism, suggesting that metabolic loss and atrophy may develop independently. CONCLUSIONS: The results suggest that a reduction in caudate glucose metabolism and atrophy develop rapidly in Huntington's disease. The findings establish a strategy for using serial positron emission tomographic imaging to monitor experimental pharmacologic interventions in presymptomatic individuals who have developed caudate hypometabolism.

Adult↗

PubMed1992

Psychiatric, genetic, and positron emission tomographic evaluation of persons at risk for Huntington's disease.

We examined chorea-free subjects at risk for Huntington's disease (n = 52) for lifetime psychiatric diagnoses, present mood, genetic marker status, and caudate glucose metabolic rates with positron emission tomography. Based on previous work, a caudate-ipsilateral hemisphere ratio less than 1.15 was defined as abnormal and predictive of Huntington's disease. None of three methods used to segregate subjects into groups more and less likely to develop Huntington's disease gave significant group rate differences for any formal psychiatric diagnoses. On present mood testing, however, subjective "anger/hostility" was significantly higher in those likely, compared with those less likely, to develop Huntington's disease, as determined by all three methods.

Adult↗

PubMed1990

A comparison of neurological, metabolic, structural, and genetic evaluations in persons at risk for Huntington's disease.

We compared four diagnostic data sets for the assessment of individuals at risk for Huntington's disease. Fifty-four chorea-free persons were evaluated by neurological examination, positron emission tomography measurement of glucose metabolism, radiographic computerized tomographic measurement of caudate size, and genetic testing at the polymorphic DNA loci D4S10, D4S43, and D4S125. Twelve (22%) persons had abnormal caudate metabolism, 6 (11%) had subtle abnormalities of motor control, and 7 (13%) had computed tomographic evidence of caudate atrophy, compared with an expected gene frequency of 34% for this population. In 20 persons with unambiguous genetic test results or the subsequent phenotypic expression of Huntington's disease (chorea), there was a greater sensitivity of the positron emission tomographic measurement of caudate metabolism (75%) relative to computed tomography (33%) or the clinical examination (17%) for the determination of a subpopulation of probable Huntington's disease gene carriers. Hypometabolism of the putamen and globus pallidus, and hypermetabolism of the precentral gyrus were also associated with a high probability of carrying the Huntington's disease gene. The findings support the hypothesis that abnormalities of cerebral metabolism precede clinical or structural (computed tomographic) abnormalities in gene-positive individuals at risk for Huntington's disease.

Atrophy↗

PubMed1988

Cerebral glucose metabolic rates in nondepressed patients with obsessive-compulsive disorder.

The authors compared 10 nondepressed patients with obsessive-compulsive disorder with 10 normal control subjects of the same sex and similar age for cerebral glucose metabolic rates obtained using positron emission tomography. Obsessive-compulsive patients showed significantly elevated metabolic rates in the whole cerebral hemispheres, heads of the caudate nuclei, orbital gyri, and the orbital gyri relative to the ipsilateral hemisphere (the orbital-hemisphere ratio). These results are similar to those the authors reported previously for another group of obsessive-compulsive patients and normal control subjects.

Adult↗

PubMed1987

Reduced cerebral glucose metabolism in asymptomatic subjects at risk for Huntington's disease.

Symptomatic patients with Huntington's disease may have reduced glucose metabolism in the caudate nuclei. We used positron emission tomography and [18F]fluorodeoxyglucose to study cerebral glucose metabolism in 95 subjects: 58 clinically asymptomatic (chorea-free) subjects at risk for Huntington's disease, 10 symptomatic patients with the disease, and 27 controls. All the symptomatic patients had marked reductions in caudate glucose metabolism. Despite a normal structural appearance on computed tomography, caudate glucose metabolism was bilaterally reduced in 31 percent of the subjects at risk (18 of 58). Using each at-risk subject's age and the sex of the affected parent, we averaged individual risk estimates for the development of Huntington's disease for this group and predicted that the probability of having the clinically unexpressed Huntington's disease gene should be 33.9 +/- 6.0 percent for the group. Thus, there was excellent agreement between the predicted percentage of carriers of the Huntington's disease gene (33.9 +/- 6.0 percent) and the percentage with metabolic abnormalities of the caudate nuclei (31 percent). These results indicate that the measurement of glucose metabolism may allow the observation of the pathophysiologic effects of the Huntington's disease gene during the natural development of the disease. It may also provide a direct means to monitor the response to experimental treatments during both the clinically asymptomatic and the symptomatic phases of the disorder.

Adult↗

PubMed1987

Regional cerebral glucose metabolism in anorexia nervosa measured by positron emission tomography.

Regional cerebral glucose metabolism was measured in five female anorectic patients, during the anorectic state and after weight gain, using the fluorodeoxyglucose method and positron emission tomography. In addition, these results were compared with those of 15 young male normals. During the anorectic state, significant caudate hypermetabolism was found bilaterally, unlike the finding in repeat measurements or in male normals. In some other brain structures (temporal cortex, lentiform nucleus, thalamus, and brainstem), significant hypermetabolism was also found during the anorectic state, but these results were not concordant for both sides and in both comparisons. There was no difference between patients after improvement and young male normals.

Adolescent↗