Biomedical subjects
Publications and source records attributed to G Di Chiro.
Cerebral glucose metabolic rate (CMRGlu), measured by positron emission tomography, was bilaterally and symmetrically reduced in two patients with autosomal dominant Alzheimer's disease. Supramarginal gyri and temporal lobes were most severely affected. An isolated reduction of CMRGlu in the left supramarginal gyrus was observed in one asymptomatic at-risk subject.
A significant rank correlation between rigidity and putaminal signal dropout on magnetic resonance imaging (MRI) in patients with multiple system atrophy suggests that putaminal degeneration may cause this clinical finding. Absence of putaminal abnormalities on MRI in patients with pure autonomic failure may prove useful in differentiating these two autonomic disorders.
Seventeen patients with intracranial meningiomas were studied with positron emission tomography and fluorine-18-2-fluorodeoxyglucose (PET-FDG) to assess the glucose utilization of these tumors. Four meningiomas followed for 3-5 years after PET-FDG and surgery showed no evidence of recurrence. These tumors had significantly lower glucose utilization rates (1.9 mg/dl/min +/- 1.0) than 11 recurrent or regrowing meningiomas (4.5 mg/dl/min +/- 1.96) (P less than .01). The glucose metabolic rates of meningiomas correlated with tumor growth, as estimated from changes in tumor size on repeated computed tomographic scans. Histopathologically, a syncytial (atypical) meningioma had the highest glucose utilization rate, followed by a papillary meningioma and an angioblastic meningioma. Individual transitional and syncytial (typical) meningiomas showed marked differences in glucose metabolism despite similar microscopic appearance. Glucose utilization rate appears to be at least as reliable as histologic classification and other proposed criteria for predicting the behavior and recurrence of intracranial meningiomas.
Cerebral glucose metabolic rates were measured in 23 normal volunteers by studying the uptake of 18F-deoxyglucose with positron emission tomography (PET). These values were correlated against a brain-size index obtained from the PET images by measuring the lateral and anteroposterior brain diameters. There was a significant negative correlation (p less than 0.001), which corresponds, within the statistical uncertainty, to an inverse proportionality of glucose metabolic rate and brain volume. The variation with brain size accounted for approximately one-half of the total intersubject variance. Measurements on phantoms of different sizes and analyses of instrumental errors failed to uncover any artifactual reason for the correlation.
Magnetic resonance imaging (MRI) was performed on 12 patients with spinal arteriovenous malformations (AVM's). Six lesions were intramedullary, five were dural, and one was in a posterior extramedullary location. Serpentine filling defects similar to the classic myelographic findings were demonstrated within the high-signal cerebrospinal fluid on T2-weighted coronal scans. The intramedullary nidus was identified by MRI as an area of low-signal intensity within the cord in all six intramedullary AVM's. Neither the dural nor the posterior extramedullary lesions showed intramedullary components. It is concluded that MRI may noninvasively provide the initial diagnosis of a spinal AVM and distinguish intramedullary from dural and extramedullary lesions.
Glucose utilization by normal and neoplastic cerebral tissue can be measured in humans using positron emission tomography (PET) with fluorine-18-labeled 2-deoxy-D-glucose (FDG). Malignant gliomas are known to exhibit hypermetabolic glucose consumption compared to normal brain. Barbiturate-sensitive cerebral glucose utilization is coupled to neuronal activity, and lesions lacking neuronal activity should be relatively insensitive to barbiturate suppression of glucose utilization. In a study to examine this phenomenon, three patients with cerebral gliomas underwent FDG-PET while awake and during deep barbiturate coma. Cerebral glucose utilization was measured in normal brain, tumor, and a homologous, non-neoplastic control site in the contralateral hemisphere. A glucose utilization ratio for tumor/control tissue was calculated. The mean reduction of glucose utilization during barbiturate coma was: gray matter 67%, white matter 47%, basal ganglia 66%, thalamus 57%, cerebellar cortex 55%, tumor 32%, and the contralateral control site 64%. The mean tumor glucose utilization ratio was 1.48:1 in the awake state and 2.69:1 during barbiturate coma. The changes in gray matter, basal ganglia, thalamus, cerebellar cortex, and tumor/control tissue ratio were significant (p less than 0.05). In one patient, deep tumor invasion not evident on computerized tomography, magnetic resonance imaging, or baseline FDG-PET was apparent during barbiturate-enhanced FDG-PET scanning. The study findings suggest that gliomas resist suppression of glucose utilization by barbiturates; this supports the hypothesis that barbiturates reduce neuronal metabolism by blocking synaptic activity. This differential effect on normal brain and gliomas enhances the capability to assess the extent of neoplastic tissue in brain and may represent the basis for novel therapeutic strategies.
The medical records and arteriograms of 81 patients with spinal arteriovenous malformations (AVM's) were reviewed, and the vascular lesions were classified as dural arteriovenous (AV) fistulas or intradural AVM's. Intradural AVM's were further classified as intramedullary AVM's (juvenile and glomus types) and direct AV fistulas, which were extramedullary or intramedullary in location. Dural AV fistulas were defined as being supplied by a dural artery and draining into spinal veins via an AV shunt in the intervertebral foramen. Intramedullary AVM's were defined as having the AV shunt contained at least partially within the cord or pia and receiving arterial supply by medullary arteries. Of the 81 patients, 27 (33%) had dural AV fistulas and 54 (67%) had intradural AVM's. Several dissimilarities in clinical and radiographic findings of the two subgroups were evident. The patients with intramedullary AVM's were younger; the age at onset of symptoms averaged 27 years compared to 49 years for dural AV fistulas. The most common initial symptom associated with dural AV fistulas was steadily progressive paresis, whereas hemorrhage was the most common presenting symptom in cases of intramedullary lesions. No patients with dural AV fistulas had subarachnoid hemorrhage. Activity exacerbated symptoms more frequently in patients with dural lesions. Associated vascular anomalies occurred only in cases of intradural AVM's. In 96% of the dural lesions the AV nidus was in the low thoracic or lumbar region; in only 15% did the intercostal or lumbar arteries supplying the AVM also provide a medullary artery which supplied the spinal cord. In contrast, most intradural AVM's (84%) were in the cervical or thoracic segments of the spinal cord and all of them were supplied by medullary arteries. Transit of contrast medium through the intradural AVM's was rapid in 80% of cases, suggesting high-flow lesions. Forty-four percent of the patients with AVM's of the spinal cord had associated saccular arterial or venous spinal aneurysms. No dural AV fistulas displayed these characteristics. A good outcome occurred in 88% of patients with dural AV fistulas after nidus obliteration, while 49% of patients with intramedullary AVM's did well after surgery or embolization. These findings suggest that dural and intradural AVM's differ in etiology (acquired vs. congenital) and that they have different pathophysiology, radiographic findings, clinical presentation, and response to treatment.
To assess the effect of extra-occipital lesions on the local cerebral glucose utilization of the primary and associative visual cortex, 29 patients were studied in the unstimulated state by positron emission tomography and [18F]2-deoxyglucose. Quantitative Goldmann perimetry was done in each patient at the time of the positron emission tomographic study. Nine patients showed homonymous defects, either hemianopsia or quadrantanopsia, whereas nine patients had heteronymous defects. Eleven control subjects, free of any neurological symptoms and with normal visual fields, were also studied with [18F]2-deoxyglucose positron emission tomography. In the normal control subjects and in patients with a heteronymous defect, left-to-right differences in the local cerebral metabolic rate for glucose of the visual cortex varied less than 10%. In patients with hemianopic defects, differences ranged from 8 to 38%, with the hypometabolic cortex always contralateral to the field defect. In patients with quadrantanopic defects, the visual cortex contralateral to the field defect demonstrated differences from 14 to 24% above and below the calcarine fissure, the cortex that received greater input from the affected field being hypometabolic.
In studies using [18F]deoxyglucose (FDG), one often wants to compare metabolic rates following stimulation (drug or motor-sensory) with the baseline values. However, because of reproducibility problems with baseline variations of 25% in the same individual not uncommon, the global effect of the stimulation may be difficult to see. One approach to this problem is to perform the two studies sequentially. This means that, with the 110-min half-life of 18 F, one must take into account the residual activity from the first study when calculating metabolic rates for the second. We performed TEST-RETEST baseline studies on four subjects, with a 1-hr interval between injections. These studies were done without stimulation, in order to validate the repeatability of the method. To reduce the amount of residual activity from the first study, the first injection was only 2 mCi in three cases, and only 1 mCi in one case, out of a total injected dose of 5 mCi. A correction for residual activity was included in the RETEST calculation of metabolic rate. The results showed a global metabolic shift between the two studies of 2% to 9%. An error analysis shows that the shift could be further reduced if anatomically comparable scans are done at comparable postinjection times.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The Shy-Drager syndrome (SDS) is a form of progressive autonomic nervous system failure (PAF) with orthostatic hypotension and associated extrapyramidal involvement that is often mistaken for Parkinson disease. SDS includes olivopontocerebellar atrophy and striatonigral degeneration which is attended by PAF. Eight patients with SDS were studied on a 0.5-T superconducting system utilizing T1-weighted inversion recovery (IR) and T2-weighted spin-echo pulse sequences and also on a 1.5-T system using spin-echo sequences. With IR sequences, atrophy of the putamina was demonstrated in patients with SDS that is consistent with findings of neuronal loss in these nuclei reported on postmortem examinations. An abnormal decrease in signal intensity of the putamina, particularly along their lateral and posterior portions, was also detected, predominantly on T2-weighted sequences, and in three cases on T1-weighted spin-echo sequences. Abnormalities were detected on both imagers but were shown with greater clarity on the 1.5-T device. SDS is the first disease in which convincing basal ganglia changes have been shown in vivo exclusively by MR imaging.
Canine cerebrospinal fluid rhinorrhea, which occurs frequently in purebred beagles, was demonstrated in two dogs on magnetic resonance images after cisternal introduction of gadolinium-DTPA dimeglumine.
Explore the source record for details and available documents.
The dynamic changes in ventricular dimensions related to the cardiac cycle were evaluated by analyzing gated magnetic resonance images in normal volunteers and in several patients with ventriculomegaly. Small variations in dimensions of the lateral and third ventricles were observed shortly after cardiac systole.
Explore the source record for details and available documents.
The dural type of spinal arteriovenous malformation (AVM) can be cured by excision or by embolization of the nidus. The common origin of the blood supply to the malformation and to the cord from the same segmental artery would profoundly affect therapeutic choices. This anatomic situation was encountered in two of nine such lesions. The angiographic appearance and the importance of recognizing this common origin is discussed.
A number of surgical clips and other metallic materials embedded within patients have ferromagnetic properties that present a potential hazard when in the strong fields associated with magnetic resonance imaging. Several types of magnetometers and metal detectors were investigated as possible pre-imaging screening devices. The sensitivities and costs of these devices are given.