Infection of cerebrospinal fluid (CSF) shunts is a common occurrence and can often be difficult to diagnose using standard analysis of shunt fluid. This article presents the first case report on the diagnosis of a CSF shunt infection on FDG PET scan. A 26-year-old female underwent ventriculoperitoneal shunt placement after developing a pseudomeningocele subsequent to a suboccipital craniectomy for Chiari malformation. Two months later, the patient presented with abdominal pain and non-specific symptoms and was found to have a perisplenic abscess for which she was adequately treated. Failure of her symptoms to solve and an initial negative shunt CSF analysis prompted the search for other sources of infection. An FDG PET scan performed a week later found evidence of increase tracer uptake around the distal tip of the catheter and a repeat shunt CSF analysis showed evidence of CSF infection. FDG PET may be useful in diagnosing shunt related infections in case of high clinical suspicion when standard diagnostic modalities fail to diagnose hardware infection.
✓ Previously the authors showed that hypothermia exerts a greater effect on the cerebral metabolic rate for oxygen (CMRO 2 ) that is associated with the maintenance of cellular viability, or “basal” CMRO 2 , than on electroencephalogram (EEG)-associated CMRO 2 or “functional” CMRO 2 . On the basis of their findings, the authors hypothesized that the ratio of CMRO 2 over a 10°C temperature range (Q 10 ) for basal CMRO 2 was greater than that for functional and total CMRO 2 . They tested their hypothesis by determining the Q 10 for basal CMRO 2 from 38°C to 28°C. They measured whole-brain cerebral blood flow (CBF) and CMRO 2 in six rats during progressive hypothermia at a brain temperature of 38°C and, after induction of an isoelectric EEG signal (50 µV/cm) with thiopental sodium, they repeated the measurements at 38°C, 34°C, 30°C, and 28°C. In a control group (five rats), six sequential measurements of CBF and CMRO 2 were made while the animals were anesthetized by 0.5% isoflurane/70% N 2 O/30% O 2 at a brain temperature of 38°C over a time span equivalent to the hypothermic group, that is, approximately 3 hours. The Q 10 for basal CMRO 2 calculated over 38°C to 28°C was 5.2 ± 0.92. However, the decrease in basal CMRO 2 between 38°C and 28°C was nonlinear on a log plot, revealing a two-component response: a high temperature sensitivity component between 38°C and 30°C with a Q 10 of 12.1, and a lower temperature sensitivity component between 30°C and 28°C with a Q 10 of 2.8. The combined overall Q 10 for basal CMRO 2 between 38° and 28°C was 5.2. The energy-requiring processes associated with these high and low temperature sensitivity components of basal CMRO 2 have yet to be identified.
Atherosclerotic lesions of the extracranial carotid arteries are one of the most common cases of stroke.Rarely, a stroke may result from isolated non-stenotic carotid disease in the absence of systemic manifestations of cardiovascular disease or significant cardiovascular risk factors.We present an unusual case of multiple strokes resulting from a solitary finger-like projection within the posterior wall of the carotid artery in an otherwise healthy patient.This small finger-like projection has a propensity to act as a nidus for thrombus formation and a potential source of cerebral embolism.
The cerebral metabolic rate of oxygen (CMRO2) has been functionally compartmentalized using the barbiturate thiopental into active CMRO2, associated with electroencephalographic (EEG) activity, and the balance, basal CMRO2, associated with the maintenance of neuronal viability. Previous measurements of these CMRO2 compartments were made in anesthetized animals. Our aim was to determine whether the same proportions for these compartments applied in unanesthetized monkeys. The active: basal distribution of the cerebral metabolic rate of glucose (CMRG) and cerebral flood flow (CBF) were also determined. Three measurements of whole-brain CBF (H2 clearance), CMRO2, and CMRG were made in six unanesthetized rhesus monkeys (Macaca mulatta). Thereafter, thiopental anesthesia was induced and maintained until an isoelectric EEG was obtained. Three additional measurements of CBF, CMRO2, and CMRG were made. Arterial blood pressure, end-tidal CO2, and arterial blood gas were measured with each set of measurements. Thiopental-induced isoelectric EEG resulted in a 47% reduction in CMRO2 from 5.95 ± 0.54 to 3.10 ± 0.51 ml/100 g/min (mean ± SD); a 36% reduction in CBF from 76 ± 21 to 48 ± 14 ml/100 g/min; and a 61% reduction in CMRG from 8.09 ± 2.78 to 3.13 ± 0.77 mg/100 g/min. The oxygen-glucose index was 0.99 ± 0.10 for the whole brain, 0.87 ± 0.15 for the active, and 1.27 ± 0.25 for the basal compartments. These results indicated an active: basal distribution of ∽50:50 for CMRO2, 40:60 for CBF, and 60:40 for CMRG. The active:basal CMRO2 distribution corroborates earlier data and shows that relative to CMRO2, the active compartment is underperfused with a lower oxygenglucose index compared with the basal compartment.
✓ In this study the authors have examined the effects of transluminal angioplasty on cerebral blood flow (CBF) in the management of intractable vasospasm following aneurysmal subarachnoid hemorrhage (SAH). Fourteen consecutively enrolled patients underwent attempted angioplasty with or without intraarterial infusion of papaverine. Twelve patients underwent pre- and postangioplasty xenon-enhanced computerized tomography (Xe-CT) scanning to measure regional CBF in 55 to 65 regions of interest (ROIs) per patient. Angioplasty was possible in 13 (93%) of 14 patients, with angiographically demonstrated improvement in all 13. Twelve (92%) of the 13 patients were neurologically improved following angioplasty; seven (58%) of the 12 patients who improved had a complete reversal of all delayed ischemic deficits. Angioplasty significantly decreased the mean number of ROIs at risk (11.4 ROIs pre- and 0.9 ROIs postangioplasty) (p < 0.00005, t-test). All patients had a reduction in the number of ROIs at risk after angio...
A noninvasive technique for measuring local cerebral blood flow (CBF) by xenon-enhanced x-ray transmission computed tomography (CT) was developed and reported on extensively in recent years. In this method, nonradioactive xenon gas in inhaled, and the temporal changes in radiographic enhancement produced by the inhalation are measured by sequential computed tomography. Time-dependent xenon concentration within various tissue segments in the brain is used to derive both the local partition coefficient (lambda) and CBF in each tissue volume (voxel) of the CT image. A comprehensive assessment of this method reveals that although it provides functional mapping of blood flow with excellent anatomic specificity and has several other significant advantages, there are distinct and important limitations. The assumptions underlying this methodology are examined and the advantages as well as the problems associated with applications of this technique are reviewed. Laboratory and clinical observations that have been made using this technique in recent years are summarized, and potential improvements as well as possible future directions are discussed.
Object The purpose of this study was to determine whether cerebral blood flow (CBF) measurements in acute stroke could be correlated with the subsequent development of cerebral edema and life-threatening brain herniation. Methods Twenty patients with aggressively managed acute middle cerebral artery (MCA) territory strokes who underwent xenon-enhanced computerized tomography (Xe-CT) CBF scanning within 6 hours of onset of symptoms were retrospectively reviewed. The relationship among CBF and follow-up CT evidence of edema and clinical evidence of brain herniation during the 36 to 96 hours following stroke onset was analyzed. Initial CT scans displayed abnormal findings in 11 patients (55%), whereas the Xe-CT CBF scans showed abnormal findings in all patients (100%). The mean CBF in the symptomatic MCA territory was 10.4 ml/100 g/minute in patients who developed severe edema compared with 19 ml/100 g/minute in patients who developed mild edema (p < 0.05). The mean CBF in the symptomatic MCA territory was 8.6 ml/100 g/minute in patients who developed clinical brain herniation compared with 18 ml/100 g/minute in those who did not (p < 0.01). The mean CBF in the symptomatic MCA territory that was 15 ml/100 g/minute or lower was significantly associated with the development of severe edema and herniation (p < 0.05). Conclusions Within 6 hours of acute MCA territory stroke, Xe-CT CBF measurements can be used to predict the subsequent development of severe edema and progression to clinical life-threatening brain herniation. Early knowledge of the anatomical and clinical sequelae of stroke in the acute phase may aid in the triage of such patients and alert physicians to the potential need for more aggressive medical or neurosurgical intervention.
