Increase in apparent diffusion coefficient in normal appearing white matter following human traumatic brain injury correlates with injury severity

Following diffuse traumatic brain injury, there may be persistent functional or psychological deficits despite the presence of normal conventional MR images. Previous experimental animal and human studies have shown diffusion abnormalities following focal brain injury. Our aim was to quantify changes in apparent diffusion coefficient (ADC) and absolute relaxation times of normal appearing white matter (NAWM) in humans following traumatic brain injury. Twenty-three patients admitted with a diagnosis of head injury (nine mild, eight moderate, and six severe) were scanned an average of 7.6 days after injury using a quantitative echo planar imaging acquisition to obtain co-registered T1, T2, and ADC parametric maps. Mean NAWM values were compared with a control group (n = 13). The patient group showed a small but significant increase in ADC in NAWM, with no significant change in T1 or T2 relaxation times. There was a correlation between injury severity and increasing ADC (p = 0.03) but no correlation with either T1 or T2, suggesting that ADC is a sensitive and independent marker of diffuse white matter tissue damage following traumatic insult. None of the patients had a reduced ADC, making ischaemia unlikely in this cohort. Pathophysiological mechanisms that may explain diffusely raised ADC include vasogenic edema, chronic ischemic phenomena, or changes in tissue cytoarchitecture or neurofilament alignment.     

Cerebral metabolism in experimental hydrocephalus: an in vivo 1H and 31P magnetic resonance spectroscopy study.

OBJECT: Brain damage in patients with hydrocephalus is caused by mechanical forces and cerebral ischemia. The severity and localization of impaired cerebral blood flow and metabolism are still largely unknown. Magnetic resonance (MR) spectroscopy offers the opportunity to investigate cerebral energy metabolism and neuronal damage noninvasively and longitudinally. Previous 1H MR spectroscopy studies have shown an increased lactate resonance that is suggestive of anaerobic glycolysis. The aim of this study was to assess cerebral damage and energy metabolism in kaolin-induced hydrocephalus in adult rats by using in vivo 1H and 31P MR spectroscopy. The presence of lactate was correlated with high-energy phosphate metabolism and intracellular pH. The measurement of relative concentrations of N-acetyl aspartate (NAA), choline (Cho), and total creatine (tCr) served to assess neuronal damage. METHODS: Hydrocephalus was induced in adult rats by surgical injection of kaolin into the cisterna magna. Magnetic resonance studies, using a 4.7-tesla magnet, were performed longitudinally in hydrocephalic animals at 1 (10 rats), 8 (six rats), and 16 weeks (six rats) thereafter, as well as in eight control animals. To evaluate ventricular size and white matter edema T2-weighted MR imaging was performed. The 1H MR spectra were acquired from a 240-microl voxel, positioned centrally in the brain, followed by localized 31P MR spectroscopy on a two-dimensional column that contained the entire brain but virtually no extracranial muscles. The 1H and 31P MR spectroscopy peak ratios were calculated after fitting the spectra in the time domain, intracellular pH was estimated from the inorganic phosphate (Pi) chemical shift, and T2 relaxation times of 1H metabolites were determined from the signal decay at increasing echo times. CONCLUSIONS: In hydrocephalic rats, ventricular expansion stabilized after 8 weeks. White matter edema was most pronounced during acute hydrocephalus. Lactate peaks were increased at all time points, without a decrease in phosphocreatine (PCr)/Pi and PCr/adenosine triphosphate (ATP) peak ratios, or pH. Possibly lactate production is restricted to periventricular brain tissue, followed by its accumulation in cerebrospinal fluid, which is supported by the long lactate T2 relaxation time. Alternatively, lactate production may precede impairment of ATP homeostasis. The NAA/Cho and tCr/Cho ratios significantly decreased during the acute and chronic stages of hydrocephalus. These changes were not caused by alterations in metabolite T2 relaxation time. The decreases in the NAA/Cho and tCr/Cho ratios implicate neuronal loss/dysfunction or changes in membrane phospholipid metabolism, as in myelin damage or gliosis. It is suggested that 1H MR spectroscopy can be of additional value in the assessment of energy metabolism and cerebral damage in clinical hydrocephalus.     

Magnetic resonance imaging of silastic-induced canine hydrocephalus

Nine adult beagle dogs underwent magnetic resonance imaging in a 2-Tesla small-bore unit. Six surviving dogs were followed up serially with magnetic resonance imaging after induction of hydrocephalus by injection of Silastic into the prepontine cistern or fourth ventricle. Ventricular size (Y) measured as percentage cross-sectional area of an anterior frontal slice was related to postoperative day (X) as Y = 1.54 + 4.21 x ln(X), r = 0.9596. Periventricular edema appeared initially in the superlateral angles of the frontal horns in an area that corresponded histologically to the subcallosal fasciculus. T1 relaxation time of normal white matter of 979.32 msec increased to 1813.90 msec in the area of the edema (p less than 0.0001). The T2 relaxation time of normal white matter of 83.39 msec increased to 238.26 msec in the area of the edema (p less than 0.0001). Histological changes included expansion of the extracellular space in an area comparable to the region of increased signal intensity on T2-weighted images, as well as diffuse astrocytosis in the chronically hydrocephalic dogs.     

Proton magnetic resonance studies of triethyltin-induced edema during perinatal brain development in rabbits

To better understand the role of myelin-associated water in the differentiation of white and gray matter in magnetic resonance (MR) imaging, changes in MR relaxation processes were studied in rabbits during myelination and after induction of cytotoxic edema with triethyltin (TET). Normal rabbits were killed at various age intervals ranging from premature (28 days' gestation) to adult, and changes in MR relaxation times (T1 and T2) and in water and electrolyte content were determined for various areas of brain and muscle. Similar measurements were made in rabbits of comparable age exposed to TET. Light and electron microscopy and MR imaging were used to follow myelin development and morphological changes induced by TET. During the first 30 postnatal days, both T1 and T2 declined by 50% in normal rabbits, a fall that paralleled the loss in brain water and sodium that occurred during the same period. Exposure to TET prolonged T1 and T2 in white but not gray matter, reflecting the accumulation of sodium and water (edema fluid) in white matter areas. Multiexponential analysis revealed a second, longer component in T2 magnetization decay of TET-exposed white matter, presumably attributable to accumulation of non-ordered water within intramyelinic vacuoles, a supposition consistent with electron microscopic and MR imaging findings. In contrast to reports by others, changes in T1 (but not T2) closely correlated with alterations in brain water (r = 0.93, df = 39). The absence of tissue disruption in the animals in the present study may account for these differences, but further studies will be required both to resolve this question and to fully understand MR images of white matter edema in mature and immature brain.     

Experimental study on pathophysiology and treatment of congenital hydrocephalus evaluated by magnetic resonance imaging and magnetic resonance spectroscopy]

I. Experimental Study on Pathophysiology of Congenital Hydrocephalus It is well known that the major pathogenic mechanism of hydrocephalus is disturbance in cerebrospinal fluid (CSF) circulation. For this reason, many studies on hydrocephalus were intended from the viewpoint of CSF circulation both experimentally and clinically. However, few studies have yet been done on the correlation between the morphological changes and the changes in cerebral energy metabolism in hydrocephalus in vivo. So, in this study, the correlation between the morphological changes and the changes in cerebral energy metabolism in congenital hydrocephalic rats was evaluated experimentally. The morphological changes were estimated by using magnetic resonance imaging (MRI), and the longitudinal relaxation time (T1) of brain tissue at parietal area was also measured. The cerebral energy metabolism was evaluated by using 31P magnetic resonance spectroscopy (MRS) method, and cerebral phospholipid membrane metabolism was also evaluated by using 31P-MRS method. The region of interest (ROI) giving rise to the 31P spectra was placed at fore-brain and parietal area. The PCr/Pi ratio was used as the chosen indicator of cellular bioenergetic status. The PME/beta-ATP ratio and PDE/beta-ATP ratio were used as the chosen indicator of cerebral phospholipid membrane metabolism. The intracellular pH was also evaluated by using 31P-MRS method. Fifty congenital hydrocephalic rats of the HTX strain were used. The animals were divided into two groups--non-hydrocephalic group (n = 15) and hydrocephalic group (n = 35)--. The rats of hydrocephalic group were subdivided into three smaller groups according to the degree of hydrocephalus--mild (n = 15), moderate (n = 10) and severe (n = 10)--, which was estimated by using the cerebro-ventricular ratio (CVR) in coronal section of MRI. Experimental results were as follows: 1) The T1 values in rats of mild, moderate and severe hydrocephalic groups showed significant elongation in comparison with the value in non-hydrocephalic group (p less than 0.01), which indicated the expansion of interstitial edema in cerebral cortex. 2) The correlation between the T1 value and the CVR was evaluated and the correlation coefficient (r) was 0.932 which indicated high correlation. 3) The PCr/Pi ratios in rats of mild, moderate and severe hydrocephalic groups were decreased significantly in comparison with the value in non-hydrocephalic group (p less than 0.01), which demonstrated the disturbance of cerebral energy metabolism in congenital hydrocephalic rats. 4) The PCr/Pi ratio seemed to give the indicative data concerning the prognosis of congenital hydrocephalus.(ABSTRACT TRUNCATED AT 400 WORDS)     

Magnetic resonance imaging measurement of relaxation and water diffusion in the human lumbar intervertebral disc under compression in vitro.

STUDY DESIGN: Twelve lumbar intervertebral disc specimens were imaged with magnetic resonance imaging to estimate relaxation constants, T1 and T2, and tissue water diffusion, before and after applying compression. OBJECTIVES: The objectives of the study were to measure T1, T2, and water diffusion for differences with loading state, region of the disc (anulus fibrosus or nucleus pulposus), and grade of degeneration. SUMMARY OF BACKGROUND DATA: Magnetic resonance imaging can be used qualitatively to estimate water content and degeneration of the intervertebral disc. Beyond structural information of images, the relaxation times T1 and T2 may contain information on the changes occurring with degeneration. A modified spin-echo sequence can be used to estimate tissue water diffusion in cartilage and disc specimens with the ability to measure anisotropy. METHODS: Specimens were imaged in a 1.5-Tesla clinical scanner. T1, T2, and water diffusion were estimated from midsagittal images. Magnetic resonance imaging parameters were calculated before and after axial loading. The measured T1, T2, and D (diffusion coefficient) were compared before and after compression, and for the diffusion data, also by direction to consider anisotropy. RESULTS: For the T1 data, a significant difference was found by region, nucleus > anulus, and loading state, loaded > unloaded. For the T2 values, there was a significant difference by region, nucleus > anulus, and Thompson grade. For diffusion, significant differences were found by region, nucleus > anulus, Thompson grade, direction of diffusion, and state of compression, loaded > unloaded. CONCLUSIONS: This study demonstrated that magnetic resonance imaging can be used to measure significant changes in T1, T2, or diffusion in intervertebral disc specimens by region, loading condition, or Thompson grade.     

Changes in the components and content of biological water in the brain of experimental hydrocephalic rabbits

Changes in biological water components and their respective content in the cortical gray matter and periventricular white matter were studied in rabbits rendered hydrocephalic by intracisternal kaolin injection. There was no change in either total water content or free or bound water content in the cortical gray matter at the various stages of hydrocephalus development. While there was no significant change in total water content in the periventricular white matter at any stage of hydrocephalus, free water content was significantly elevated and bound water content was decreased at the acute and subacute stages, with a return to relatively normal levels at the chronic stage. It is concluded that in the periventricular white matter, free water enters the brain across the ependymal lining during the acute and subacute stages of experimental hydrocephalus with a simultaneous reduction in the bound water and that there is some recovery at the chronic stage. It is suggested that alternative drainage pathways may develop in chronic hydrocephalus allowing drainage of free water in the periventricular white matter, which in turn permits bound water to return to relatively normal levels.     

Influence of the rate of ventricular enlargement on the ultrastructural morphology of the white matter in experimental hydrocephalus

The influence of the rate of ventricular enlargement on the morphology of hydrocephalic white matter was studied and correlated with previous studies of water content. Different rates of ventricular enlargement were obtained in two groups of cats by opening either the calvaria or the calvaria and the dura mater before injecting kaolin into the cisterna magna. Animals from each group underwent in vivo fixation of brain 2, 3, and 6 weeks after hydrocephalus was induced. Specimens of white matter were taken 1, 2, and 3 mm lateral to the ependymal surface of the lateral ventricles, imbedded, and examined using transmission electron microscopy. The ultrastructural changes associated with ventricular enlargement varied with the model used and the duration of hydrocephalus. Marked expansion of the extracellular space extending 2 mm lateral from the ependyma was found in the craniectomy-durectomy preparations examined 2 to 3 weeks after kaolin injection. Time-matched craniectomy preparations had less enlargement of the extracellular space that was confined to the white matter immediately adjacent to the ventricle. Marked glial reaction was observed in these areas in the early craniectomy preparations. When studied 6 weeks after hydrocephalus induction, both models had less expansion of the extracellular spaces compared to early observations. Glial reaction was found in both models, but was greater in the craniectomy model. The correlation of these morphological findings with the rate of ventricular enlargement and earlier studies of water content are discussed.     

Diffusion-weighted imaging of edema following traumatic brain injury in rats: effects of secondary hypoxia

Hypoxia and edema are frequent and serious complications of traumatic brain injury (TBI). Therefore, we examined the effects of hypoxia on edema formation after moderate lateral fluid percussion (LFP) injury using NMR diffusion-weighted imaging (DWI). Adult Sprague-Dawley rats were separated into four groups: sham uninjured (S), hypoxia alone (H), trauma alone (T), and trauma and hypoxia (TH). Animals in Groups T and TH received LFP brain injury, with Groups H and TH undergoing 30 min of moderately severe hypoxia (FiO2 = 0.11) immediately after surgery or TBI (respectively). DWIs were obtained at 2, 4, and 24 h and at 1 week post injury, and apparent diffusion coefficient (ADC) maps were constructed. Animals in Groups T and TH showed an early decrease (p < 0.001) in ADC values in the cortex ipsilateral to TBI 4 hr post injury, followed by elevated ADCs 1 week later (p < 0.05). No significant differences in ADC values were seen between T and TH groups in the ipsilateral cortex. In contrast, the ipsilateral hippocampus for Group TH showed only increasing ADC values. This hyperintensity in the ADC map began at 2 h after TBI, was significant by 24 h (p < 0.05), and reached a maximum at 1 week. This hyperintensity was not observed in Group T. Histopathology seen in TBI animals corresponded well with the pathology observed with MRI. Midline shifts reflecting edema were only observed in TBI animals with little difference between normoxic (T) and hypoxic animals (TH). In sum, this study demonstrates that the development and extent of brain edema following TBI can be examined in vivo in rats using DWI technology. TBI resulted in an early decrease in ADC values indicating cytotoxic edema in the cortex that was followed at 1 week by an increase in the ADC that was associated with decreased tissue cellularity. Histopathology corresponded well to the regions of brain injury and edema visualized by T2 and DWI procedures. Overall, the addition of hypoxia to brain injury resulted in a small increase in the magnitude of edema in hippocampus and cortex over that seen with trauma alone.     

Neuroprotective effects of the Ras inhibitor S-trans-trans-farnesylthiosalicylic acid, measured by diffusion-weighted imaging after traumatic brain injury in rats

Ras proteins play a role in receptor-mediated signaling pathways and are activated after traumatic brain injury. S-trans-trans-farnesylthiosalicylic acid (FTS), a synthetic Ras inhibitor, acts primarily on the active, GTP-bound form of Ras and was shown to improve neurobehavioral outcome after closed head injury (CHI) in mice. To gain a better understanding of the neuroprotective mechanism of FTS, we used diffusion-weighted imaging (DWI) in a rat model of CHI. Apparent diffusion coefficients (ADC) and transverse relaxation times (T2) were measured in injured rat brains after treatment with vehicle or FTS (5 mg/kg). Neuroprotection by FTS was also assessed in terms of the neurological severity score. One week after injury, significantly better recovery was observed in the FTS-treated rats than in the controls (p = 0.0191). T2 analysis of the magnetic resonance images revealed no differences between the two groups. In contrast, they differed significantly in ADC, particularly at 24 h post-CHI (p < 0.05): in the vehicle-treated rats ADC had decreased to approximately 26% below baseline, whereas it had increased to about 10% above baseline in the FTS-treated rats. As the magnitude of ADC reduction is strongly linked to blood perfusion deficit, these results suggest that the neuroprotective mechanism of FTS might be related to an improvement in cerebral perfusion. We propose that FTS, which is currently being tested in humans for anti-cancer indications, should also be considered as a new strategy for the management of head injury.     

Characterization of periventricular edema in normal-pressure hydrocephalus by measurement of water proton relaxation times

The magnetic resonance longitudinal relaxation time (T1) and transverse relaxation time (T2) of the water proton of the periventricular white and cortical gray matter were measured for 17 control patients and 21 patients with suspected normal-pressure hydrocephalus (NPH). Of the latter group, 14 showed good response to shunting (true-NPH group) and seven showed no response (false-NPH group). In the true-NPH group, both the T1 and the T2 of the periventricular white matter were significantly prolonged compared to the control values, and slowly shortened after cerebrospinal fluid (CSF) shunting. The true-NPH group showed significantly longer T1 and T2 of the white matter than did the false-NPH group. The T1 and T2 of the white matter were longer than those of the gray matter in this group, which was the reverse of the relationship observed in the control patients. In the white matter of the false-NPH group, there was a significant prolongation of T1 only; no difference was seen in the T2 compared to control values. There was no change in either T1 or T2 of this region after CSF shunting. The false-NPH group showed no significant difference in either T1 or T2 between the white and the gray matter. There was no difference in either T1 or T2 of the gray matter between the false-NPH and control groups or between preshunt and postshunt measurements in each patient group. It is suggested that a distinction between true- and false-NPH, which cannot be made from the radiographic appearance alone, may be possible from measurement of relaxation times. The mechanism of varied relaxation behavior between two entities may be explained by a difference in properties of the biological water and its environment.     

Measurement of changes in brain water in man by magnetic resonance imaging

John Hunter was undoubtedly aware of the water content of normal brain tissue, and described cerebral oedema. The advent of nuclear magnetic resonance (NMR) shed new light on brain water, and the derivation of spatial information and hence images from NMR signals, has permitted studies of regional brain water in man in vivo. The initial study described here tested whether NMR longitudinal relaxation time (T1) correlates with brain water content in the cerebral cortex and white matter in man, and significant relationships have been demonstrated in cortex (r = 0.65, P less than 0.002) and white matter (r = 0.94, P less than 0.0001), the latter having narrow 95% confidence limits. The residual variance allows the prediction of water content from the T1 of white matter, measured from the image of a single patient, with an accuracy of +/- 4% of total tissue water with 95% confidence. In the further study described, the effects of dexamethasone and an infusion of 20% mannitol on brain water content has been assessed in patients with intrinsic cerebral tumours. Dexamethasone had no significant effect on the T1 of normal brain, oedematous peritumoural white matter, or tumour tissue. It must be concluded that the water content of these tissues is not changed by dexamethasone and that the clinical improvement seen in patients with cerebral tumours immediately after dexamethasone has to be explained by some mechanism other than a reduction in cerebral oedema. Mannitol did reduce the T1 of oedematous peritumoural white matter, and the T1 of tumour tissue, but did not change the T1 of normal brain significantly.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sodium channel-blocking agents are not of benefit to rats with kaolin-induced hydrocephalus

OBJECTIVE: Hydrocephalus causes damage to periventricular white matter at least in part through chronic ischemia. The sodium channel-blocking agents mexiletine and riluzole have been shown to be of some protective value in various models of neurological injury. We hypothesized that these agents would ameliorate the effects of experimental childhood-onset hydrocephalus. METHODS: Hydrocephalus was induced in 4-week-old rats by injection of kaolin into the cisterna magna. Tests of cognitive and motor function were performed on a weekly basis. In a blinded and randomized manner, mexiletine (0.7, 7, or 42 mg/kg/d) or riluzole (1.4 or 13.6 mg/kg/d) was administered by osmotic minipump for 2 weeks, beginning 2 weeks after induction of hydrocephalus. The brains were then subjected to histopathological and biochemical analyses. RESULTS: Compared with untreated hydrocephalic rats, neither mexiletine nor riluzole was associated with a protective effect on behavioral, structural, or biochemical abnormalities. CONCLUSION: Protection of hydrocephalic brains through pharmacological sodium channel blockade is probably an approach not worth pursuing.     

1H magnetic resonance imaging of normal brain tissue response to photodynamic therapy.

1H Magnetic resonance imaging (MRI) was used to study the effects of photodynamic therapy (PDT) on normal rat brain (n = 5) using T1-, T2-, diffusion-, and proton density (rho)-weighted images. Rats received intraperitoneal injections of 12.5 mg/kg of Photofrin II, and 48 hours later the dural area over the frontal cortex was treated with 35 J/cm2 of light (632 +/- 1 nm). The T1-, T2-, and diffusion-weighted images revealed an evolving high contrast region of brain that corresponded to the PDT-treated area. Lesioned brain exhibited significant increases in T1 and T2 relaxation times at 1 day (P less than 0.01) and 3 days (T1, P = 0.018; T2, P less than 0.01) after treatment, compared with the contralateral equivalent volume of nonlesioned brain. Water proton diffusion coefficient (DW) in the lesioned area decreased at 1 day (P = 0.026) and increased at 3 days (P = 0.012) compared with nonlesioned brain. An increase in the proton density ratio (rho D/rho O) from PDT (rho D) versus nonlesioned side (rho O) was found 3 days after PDT treatment (P = 0.03). The data indicate that the biophysical parameters obtained from magnetic resonance imaging scans, T1, T2, DW, and proton density, can be used to monitor changes in an evolving photochemically induced lesion.     

Hydrocephalus: increased intracranial pressure and brain stem auditory evoked responses in the hydrocephalic rabbit

The auditory evoked response (AER) was used to study the effect of increased intracranial pressure (ICP) on the auditory pathway in normal New Zealand rabbits and in those made hydrocephalic by intracisternal injections of kaolin. AERs were studied: (a) in the normal and then in the hydrocephalic animal; and (b) in the hydrocephalic animal during further ICP elevation by cerebrospinal fluid infusion. The AER was obtained from ongoing electroencephalographic activity after rarefaction auditory clicks presented at 90 dB sound pressure equivalent. In comparing base line normal AERs to those found in hydrocephalic conditions, a statistically significant increase in latency for AER components N2, P2, and P5 was noted in hydrocephalic rabbits. Increased ICP in the hydrocephalic model showed an increase in the latencies of AER components for P0 and P1 at 250 mm H2O, and a prolongation of P3-P5 central conduction time at 700 mm H2O above base line cerebrospinal fluid pressure. In addition, a decrease in the P4/N5 amplitude and an increase in P1-P3 central conduction times at 700 mm H2O was observed. The differences between normal and hydrocephalic rabbit AER base lines may be the result of the chronically increased ICP and presumed chronic anatomical changes within the auditory pathway due to kaolin itself. The differences in the AER from base line hydrocephalus to acute increased ICP may indicate that the hydrocephalic system is more sensitive to acute neuropraxic pressure effects on the brain stem auditory structures than is the normal brain.     

Association of learning and memory impairments with changes in the septohippocampal cholinergic system in rats with kaolin-induced hydrocephalus

OBJECTIVE: The septohippocampal cholinergic (SHC) system plays an important role in the maintenance of normal memory and learning. However, the fact that memory and learning impairments under hydrocephalic conditions are directly related to the SHC system is less well known. We investigated the relationships between pathological changes in SHC neurons and impairments in memory and learning among hydrocephalic rats. METHODS: Rats with kaolin-induced hydrocephalus were prepared with injections of kaolin suspension into the cisterna magna. Learning and memory performance was assessed with the passive avoidance and Morris water maze tests. Ventricular sizes were measured for the lateral and third ventricles. Acetylcholinesterase and choline acetyltransferase immunostaining was performed to investigate degenerative changes in cholinergic neurons in the medial septum and hippocampus. RESULTS: Hydrocephalic rats demonstrated significant learning and memory impairments in the passive avoidance and Morris water maze tests. Decreased hesitation times in the passive avoidance test and markedly increased acquisition times and decreased retention times in the Morris water maze test indicated learning and memory dysfunction among the hydrocephalic rats. The numbers of cholinergic neurons in the medial septum and hippocampus were decreased in the hydrocephalic rats. The decreases in choline acetyltransferase and acetylcholinesterase immunoreactivity were significantly correlated with enlargement of the ventricles. CONCLUSION: Impairment of spatial memory and learning may be attributable to degeneration of SHC neurons. These results suggest that learning and memory impairments in rats with kaolin-induced hydrocephalus are associated with the dysfunction of the SHC system induced by ventricular dilation.     

Discrimination of capsular stage brain abscesses from necrotic or cystic neoplasms using diffusion-weighted magnetic resonance imaging

OBJECT: The authors' aim was to assess the ability of apparent diffusion coefficient (ADC) ratios in distinguishing brain abscesses from cystic or necrotic neoplasms. METHODS: Fifty-three patients with rim-enhancing masses in the brain observed on T1-weighted MR images were included: 26 had abscesses (14 bacterial, six nonbacterial, and six of unknown origin), 11 had glioblastoma multiforme, and 16 had rim-enhancing metastasis. The ADC values, derived from diffusion-weighted imaging, were measured in the most homogeneous portion of the cystic component of the mass. The ADC ratios were calculated by dividing the ADC values from the nonenhancing cystic portion of the mass by the ADC values from contralateral normal-appearing white matter. Lesions were further differentiated based on presence, absence, or incompleteness of a T2 hypointensity rim. The mean (+/- standard deviation) ADC ratios were significantly higher in neoplasms than in abscesses (2.45 +/- 0.91 compared with 1.12 +/- 0:53, p < 0.01). The accuracy of ADC ratios in discriminating abscesses from neoplasms, determined by the area under the receiver operating characteristic curve (Az), was high: 0.91 +/- 0.04 (mean +/- standard error of the mean [SEM]). The threshold of 1.7 was associated with highest efficiency (87%) in discriminating abscesses from neoplasms. If only bacterial abscesses were analyzed compared with neoplasms, the Az increased to 0.96 +/- 0.03 (SEM). Using ADC ratios and T1 rim characteristics, 50 of 53 lesions were correctly classified (efficiency 94.3%). CONCLUSIONS: The accuracy of ADC ratios in discriminating brain abscesses from cystic or necrotic neoplasms is very high and can be further improved using T2 rim characteristics.     

Diffusion-weighted imaging improves outcome prediction in pediatric traumatic brain injury

Diffusion-weighted imaging (DWI) and consequent apparent diffusion coefficient (ADC) maps have been used for lesion detection and as a predictor of outcome in adults with traumatic brain injury (TBI), but few studies have been reported in children. We evaluated the role of DWI and ADC for outcome prediction after pediatric TBI (n=37 TBI; n=10 controls). Fifteen regions of interest (ROIs) were manually drawn on ADC maps that were grouped for analysis into peripheral gray matter, peripheral white matter, deep gray and white matter, and posterior fossa. All ROIs excluded areas that appeared abnormal on T2-weighted images (T2WI). Acute injury severity was measured using the Glasgow Coma Scale (GCS) score, and 6-12-month outcomes were assessed using the Pediatric Cerebral Performance Category Scale (PCPCS) score. Patients were categorized into five groups: (1) controls; (2) all TBI patients; (3) mild/moderate TBI with good outcomes; (4) severe TBI with good outcomes; and (5) severe TBI with poor outcomes. ADC values in the peripheral white matter were significantly reduced in children with severe TBI with poor outcomes (72.8+/-14.4x10(-3) mm2/sec) compared to those with severe TBI and good outcomes (82.5+/-3.8x10(-3) mm2/sec; p<0.05). We also found that the average total brain ADC value alone had the greatest ability to predict outcome and could correctly predict outcome in 84% of cases. Assessment of DWI and ADC values in pediatric TBI is useful in evaluating injury, particularly in brain regions that appear normal on conventional imaging. Early identification of children at high risk for poor outcome may assist in aggressive clinical management of pediatric TBI patients.     

Magnetic resonance imaging detects and predicts early brain injury after subarachnoid hemorrhage in a canine experimental model

Abstract The canine double hemorrhage model is an established model to study cerebral vasospasm, the late sequelae of subarachnoid hemorrhage (SAH). The present study uses magnetic resonance imaging (MRI) to examine the recently reported early brain injury after SAH. Double hemorrhage SAH modeling was obtained by injecting 0.5 mL/kg of autologous arterial blood into the cisterna magna of five adult mongrel dogs on day 0 and day 2, followed by imaging at day 2 and day 7 using a 4.7-Tesla (T) scanner. White matter (WM) showed a remarkable increase in T2 values at day 2 which resolved by day 7, whereas gray matter (GM) T2 values did not resolve. The apparent diffusion coefficient (ADC) values progressively increased in both WM and GM after SAH, suggestive of a transition from vasogenic to cytotoxic edema. Ventricular volume also increased dramatically. Prominent neuronal injury with Nissl's staining was seen in the cortical GM and in the periventricular tissue. Multimodal MRI reveals acute changes in the brain after SAH and can be used to non-invasively study early brain injury and normal pressure hydrocephalus post-SAH. MR can also predict tissue histopathology and may be useful for assessing pharmacological treatments designed to ameliorate SAH.