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Background: Multislice proton magnetic resonance spectroscopic imaging (1H-MRSI) permits the simultaneous acquisition of N-acetylaspartate (NA), choline (Cho), creatine/phosphocreatine (Cre), and lactate (Lac) signal intensities from four 15-mm slices divided into 0.84-ml single-volume elements. NA is inferred to be a neuron-specific molecule, whereas Cho mainly reflects glycerophosphocholine and phosphocholine, compounds involved in phospholipid metabolism. Objective: To assess whether 1H-MRSI could detect a regional pattern of cortical and subcortical involvement in the brain of Alzheimer's disease (AD) patients. Methods: 1H-MRSI was performed in 15 patients with probable AD and 15 age-matched healthy controls. Regions of interest (ROIs) were selected from frontal (FC), temporal (TC), parietal (PC), occipital, and insular cortices, subcortical white matter (WM), and thalamus. Results: In AD patients, we found a significant reduction of NA/Cre in the FC, TC, and PC and a significant reduction of Cho/Cre in the WM. Conclusions: This 1H-MRSI study of AD patients shows a regional pattern of neuronal damage in the associative cortices, as revealed by significant reduction of NA/Cre in the FC, TC, and PC, and regional derangement of phospholipid metabolism, as revealed by significant reduction of Cho/Cre in the WM.NEUROLOGY 1996;47: 696-704

Objective To determine if the transneuronal cerebellar hemispheric metabolic asymmetry seen in crossed cerebellar diaschisis, and readily detected with positron emission tomography (PET), is associated with alterations in metabolite signal intensities on [1H]MR spectroscopic (MRS) imaging when compared with the normal pattern and distribution of cerebellar metabolites. Materials and methods The pattern and distribution of metabolites [N-acetyl-aspartate (NAA), choline-containing compounds, creatine, phosphocreatine, and lactate] in the cerebellum, using [1H]MRS imaging, were studied in a patient with documented long-standing (3 years duration) crossed cerebellar diaschisis and seven normal subjects. Cerebellar diaschisis was detected with fluorodeoxyglucose-PET imaging. Single slice [1H]MRS imaging was carried out at 1.5 T. Results There was a marked reduction in NAA signal intensity in the diaschitic cerebellar hemisphere but minimal reduction in choline and creatine signal intensities. The decrease in NAA signal intensity was most marked in the middle cerebellar peduncle and white matter of the diaschitic cerebellar hemisphere. In the normal subjects and in the uninvolved cerebellar hemisphere of the patient the NAA signal intensity was more prominent in the white matter than the cerebellar cortex. Conclusion Our data indicate (a) transneuronal metabolic effects can be detected with [1H]MRS imaging and (b) there is a differential distribution of metabolite signal intensities in the cerebellum with NAA signal intensity predominantly localized to axons of the cerebellar fiber tracts rather than neuronal cell bodies in the cortex and the converse is true for choline and creatinine signal intensities.

A unilateral supratentorial lesion may cause hypometabolism in the contralateral cerebellar hemisphere (crossed cerebellar diaschisis). We analyzed glucose metabolism, measured by PET-FDG, in the posterior fossa in 67 patients (78 PET studies) with primary unilateral supratentorial brain tumors selected for visually obvious metabolic asymmetry in the cerebellar hemispheres. We found that glucose utilization was 17% lower in the contralateral cerebellar cortex (compared with the ipsilateral one), consistent with the selection criterion, and 19% lower in the ipsilateral pons, wherein lie the first order synapses of the corticopontocerebellar pathway. This finding helps to validate the prevalent view that cerebellar diaschisis is due to interruption of afferent input from the corticopontocerebellar pathway. However, glucose metabolism in the contralateral dentate nucleus was relatively preserved--only 2% less than the ipsilateral dentate. This "dentate sparing" suggests preservation of afferent input to the largest of the deep cerebellar nuclei from the Purkinje cells in the cortex, despite interruption of the major excitatory input to the Purkinje cells.

Hypertrophic degeneration of the inferior olivary nuclei is the pathologic substrate for palatal myoclonus, but the physiologic correlate of this finding is uncertain. Using the 2-[ 18 F]fluoro-2-deoxy-d-glucose and PET method, we determined the local cerebral metabolic rate of glucose utilization in seven patients with palatal myoclonus (following stroke or infection, or idiopathic), one patient with oculopalatal myoclonus (following a stroke affecting the brainstem), and nine normal subjects. The metabolism of glucose in the medulla of the patients with palatal myoclonus was significantly greater than that of the normal subjects. This may well have been due to increased metabolism of the inferior olivary nuclei. Glucose metabolism in the medulla of the patient with oculopalatal myoclonus was normal. These findings suggest that the inferior olivary nuclei, or a region of the brainstem encompassing the inferior olivary nuclei, are hypermetabolic in palatal myoclonus and may be the generators of the involuntary movements in palatal myoclonus.

Cryptococcus neoformans is an ubiquitous yeast. As a budding type of fungus, it is also known as Torula histolytica and is a common cause of infection of the central nervous system (CNS), particularly in debilitated and immunodeficient patients. We have examined 12 patients with computed tomography who had well documented cryptococcal CNS infection and will review our findings in this paper. Three of these patients had mass lesions, while nine others had a variety of changes such as ventricular dilatation, cortical atrophy, and focal ischemic changes.

In computer assisted tomography, the slice being imaged is not a uniform slab because (1) the X-rays are not parallel, (2) the source and detector may not have equal dimensions, (3) the source collimator may produce a penumbra region on the detector, and (4) in some machines two slices are scanned simultaneously from a common focal spot. One method of measuring slice thickness, uniformity, and overlap is with a phantom containing an aluminum strip at a 45 degree angle. This provides a direct display, in the viewing plane, of the slice profile. Measurements have been made on seven new tomographic scanners, and photographs and plots of slice geometry are presented. It is suggested that slice thickness be defined as the full width at half maximum sensitivity, but that this measure should not necessarily be used as the desirable increment between scans.

The management of low-grade gliomas represents a challenge to the physician as a significant proportion may undergo malignant degeneration to a high-grade tumor. We present the positron emission tomography (PET) scans, using [18F] fluorodeoxyglucose (FDG), of 12 patients who have histological and/or clinical evidence of malignant degeneration of a low-grade glioma. Each scan displays a focal area of hypermetabolism similar to that of malignant gliomas which arise de novo. Three patients also underwent PET scanning prior to malignant degeneration. When the initial scan is compared with the postmalignant degeneration study, a difference in tumoral glucose uptake can be recognized. A region previously shown to be hypometabolic develops focal hypermetabolism as malignant changes evolve. This study displays the utility of FDG-PET in the evaluation of malignant degeneration of low-grade gliomas. The knowledge that a neoplasm has altered its biological behavior may influence subsequent therapeutic options. If these findings can be confirmed in larger series and by other investigators, it is possible that FDG-PET may be adopted as one of the diagnostic tools for guiding the management of low-grade gliomas.

Positron emission tomography was used to measure local cerebral glucose utilization by the 1-[18F]fluoro-2-deoxy-D-glucose technique in 23 patients with cerebral gliomas. All 10 high-grade (III and IV) astrocytomas demonstrated a region of high activity with a glucose consumption of 7.4 +/- 3.5 (SD) mg/100 gm per minute. The 13 low-grade (I and II) gliomas had a glucose metabolic rate of 4.0 +/- 1.8 mg/100 gm per minute, with no distinctly visible hot spot. Thus, we found a correlation between rate of glycolysis and malignancy in primary cerebral tumors. Cerebral cortical glucose utilization was often depressed in areas adjacent to or neurally connected to the tumor site, and there was focal irregular delta wave EEG activity in these areas.

Three types of test objects were superimposed on noisy backgrounds and observed by 58 subjects: large low-contrast disks to simulate tumors, small disks to simulate calcifications, and bars to simulate blood vessels. Three types of noise were used: random noise, CT noise (reconstructed random noise), and an actual water scan taken with an EMI CT1010 scanner. In addition, each image was smoothed by a factor of two, giving six test patterns altogether. Photographic images were presented to 25 lay observers, while 25 other lay observers and eight radiologists used a viewing console. The photographs produced a slightly lower true positive rate than the console, although the degree of confidence in the identifications was slightly greater. The anticorrelation property of CT noise gives it a "lumpy" structure, which aided the identification of bars but impeded the identification of small disks. Smoothing did not significantly affect the detectability with random noise, but with CT noise, smoothing improved the detectability of bars and large disks.

SUMMARYA case of Foix-Alajouanine disease verified at operation has been described. Thrombosis in a previously studied arteriovenous malformation involving the cervical spinal cord was demonstrated with both contrast radiography and surgical exploration. Except in unusual circumstances, diagnosis requires surgical exploration, although surgery cannot be expected to alter the disease course and care should be exercised not to injure residual vital cord structures. The etiology and prognosis of this disorder are uncertain.