Книги по МРТ КТ на английском языке / MR Imaging in White Matter Diseases of the Brain and Spinal Cord - K Sartor Massimo Filippi Nicola De Stefano Vincent Dou

be an early finding. After about 3 weeks, enlargement of the cerebral sulci and basal cisterns and dilatation of the ventricles can be seen with well-defined foci of hypointensity in the white matter (Zimmerman et al. 1978). Sasiadek et al. (1991) reported that the typical CT findings of DAI were small hemorrhagic lesions, most often in the cerebral white matter and internal capsule. Hemorrhagic lesions resulting from shearing injury in the cerebral white matter and graywhite matter junction are easily identified on CT in the acute stage. However, CT is limited in the evaluation of DAI. Mittl et al. (1994) found abnormalities compatible with DAI on MRI (spin-echo T2-weighted and T2*-weighted gradient echo images) in 30% of patients with normal head CT scans following minor head trauma (Fig. 29.2).

29.2

Magnetic Resonance Imaging in Traumatic Brain Injury

MRI has rapidly become the imaging modality of choice for most neurological disease. In the arena of TBI, MRI has become an important adjunct to CT in the evaluation of patients with DAI, cortical contusion, subcortical gray matter injury, and primary brainstem injury (Gentry et al. 1988). DAI most frequently involves the white matter of the frontal and temporal lobes, the corpus callosum, and corona radiata (Figs. 29.3, 29.4). Cortical contusions most commonly involve the inferior, lateral, and anterior portions of the frontal and temporal lobes where they are exposed to the rough bony surface of the frontal

and temporal fossa. Primary brainstem injury occurs in the dorsolateral aspects of the midbrain.

Several different MR sequences have been studied in the evaluation of head trauma. The utility of fluidattenuated inversion-recovery sequences in the evaluation of head trauma has been reported by several authors, who found the sensitivity of FLAIR images to be equal or superior to conventional T2-weighted spin-echo images. MRI is indicated when there is a significant discrepancy between the patient’s clinical condition and the CT findings, which could be unremarkable in some instances. Gradient echo images further enhance the sensitivity in detecting hemorrhagic shearing injury in the acute phase (deoxyhemoglobin) and chronic phase (hemosiderin) of the injury (Fig. 29.5). This is due to the shortening of T2* by the heterogeneous local magnetic field arising from paramagnetic blood breakdown products. These changes can persist for months to years after the head trauma. T2*-weighted images are critical in the evaluation of patients with chronic head injury. Yanagawa et al. (1978) found that there is a correlation between the lesions seen on gradient echo images and the Glasgow Coma Score and the duration of unconsciousness. They also found the number of hemorrhagic lesions detected by gradient echo sequences per patient was significantly higher than those seen by T2-FSE.

Magnetization transfer (MT) imaging is based on the principle that protons bound in macromolecules exhibit T1 relaxation coupling with protons in the aqueous phase. Application of an off-resonance saturation pulse can effectively saturate bound protons selectively. Subsequent exchange of longitudinal magnetization with free water protons reduces the signal

a

Fig. 29.5a–c. Diffuse axonal injury demonstrated by gradient echo images. a Axial T1-weighted sequence reveals a tiny hyperintense petechial hemorrhage in the right frontal white matter. b Axial FLAIR sequence demonstrates small hyperintense areas in the right frontal white matter. c Coronal gradient echo sequence clearly shows several hypointense areas of petechial hemorrhage, consistent with diffuse axonal injury

intensity detected from these free protons. The magnetization transfer ratio (MTR) provides a quantitative index of this MT effect and may be a quantitative measure of the structural integrity of the tissue (Bagley et al. 2000). Experimental models of DAI in pigs showed reduced MTR values in regions of histologically proven axonal injury. McGowen et al. (2000) found that the MTR in the splenium of the corpus callosum was lower in patients who suffered minor head injury compared with a control group, but no significant reduction in MTR was found in the pons. All the patients demonstrated impairment of at least three measures on neuropsychological tests, and in two cases a significant correlation was found between regional MTR values and neuropsychological performance. McGowen et al. also found that quantitative MT can be used to detect lesions of DAI even when conventional T2-weighted MRI is negative.Bagley et al.(2000) found that average MTR values were higher in all areas of white matter in patients without persistent neurological deficit than in patients with deficits. They concluded that detection of

b

c

an abnormal MTR in normal-appearing white matter may suggest a poor prognosis.

Magnetic resonance spectroscopy (MRS) provides a noninvasive method of evaluating microscopic injury of the white matter in patients with DAI and may help to predict outcome. MRS is a sensitive tool in detecting DAI and may be particularly useful in evaluating patients with mild TBI with unexplained neurological and cognitive deficits. Since DAI disturbs the balance of chemicals that exist in the brain, such as N-acetyl aspartate (NAA), lactate, choline and high-energy phosphates,MRS can provide an index of neuronal and axonal viability by measuring levels of NAA.A majority of mildly brain injured patients, as well as those severely injured, showed a reduction in NAA levels and NAA/ creatine ratio in the splenium of the corpus callosum compared with normal controls. Reduced NAA levels, corresponding to neuronal injury,were observed in patients with elevated lactate up to 24 h following the TBI. Marked reduction of NAA in the white matter continues into the subacute phase. However, in some patients

normal NAA levels may be detected 6 months following the trauma (Brooks et al. 2001). Elevated lactate levels on MRS in normal-appearing tissues on MRI correlates with poor clinical outcome (Condon et al. 1998).

Animal studies of diffusion-weighted imaging demonstrated conflicting results in the change of apparent diffusion coefficient (ADC) due to DAI (Alsop et al. 1996; Hanstock et al. 1994; Ito et al. 1996). Liu et al. (1999) reported the first clinical study of diffu- sion-weighted imaging in DAI. They performed dif- fusion-weighted imaging in patients with acute and subacute DAI and demonstrated that a significant decrease in ADC values can be seen in areas of DAI up to 18 days following head injury. This probably reflects cellular swelling or cytotoxic edema in the

acute stage. The authors hypothesize that very low ADC values, compared with acute ischemia, might be due to the presence of blood products and ruptured axons with membrane fragmentation, which restrict the free movement of water molecules. In the first few hours following traumatic brain injury, DAI is characterized by disruption of the cytoskeletal network and axonal membranes. Histological abnormalities seen in association with DAI decrease the diffusion along axons and increase the diffusion in directions perpendicular to them. White matter structures with reduced diffusion anisotropy are detected in the first 24 h in patients suffering from DAI after TBI. A fol- low-up study revealed several regions that might have recovered from the injury 1 month later (Fig. 29.6).

dence of brainstem injury on MRI. Traumatic injury to the brainstem involving the dentato-rubro-olivary pathway can result in unilateral or bilateral olivary hypertrophy, which is readily detected by MRI as a focal area of enlargement with high signal intensity on T2-weighted images in the region of the inferior olivary nucleus (Birbamer et al. 1993).

29.4

Cerebral Swelling

Traumatic cerebral swelling can occur secondary to cerebral hyperemia or cerebral edema. Cerebral hyperemia results from a loss of normal autoregulation of cerebral blood flow, which is secondary to elevation of systemic blood pressure. The cerebral blood flow then passively follows systemic blood pressure. Loss of autoregulation of cerebral blood flow is more common in children. Cerebral edema results from an increase in water content. Diffuse brain injury can cause generalized cerebral swelling (Yoshino et al. 1985). Infarction, secondary to intracranial and extracranial vascular injury, is seen with edema. On CT, the edematous brain is hypodense due to increased water content and there is subsequent loss of the normal differentiation between gray and white matter. Ventricular compression and sulcal effacement are also seen. In children, diffuse cerebral edema and subarachnoid hemorrhage are frequently seen as a result of closed head trauma (Segall et al. 1980). When diffuse cerebral swelling is predominantly due to cerebral hyperemia, initial CT scans may show a slight increase in overall density of the brain. This is particularly common in children. Unilateral cerebral swelling is seen frequently with ipsilateral subdural hematoma, less frequently in ipsilateral epidural hematoma, and occasionally as an isolated finding (Lobato et al. 1980).

29.5

Post-traumatic Atrophy of Cerebrum, Cerebellum, and Corpus Callosum

Atrophy of the cerebrum may occur focally or diffusely in patients with previous head trauma (Bakay and Glassauer 1980; Tsai et al. 1978). In such cases, both CT and MRI will show both widening of the cortical sulci and concordant ventriculomegaly in the affected areas. Cerebellar atrophy is demonstrated by

the prominence of subarachnoid and cisternal space in the posterior fossa. Time-dependent atrophic changes occurring after TBI can be quantified using MR volumetric studies and, in the chronic stages, these studies may be predictive of eventual cognitive outcome (Bakay and Glassauer 1980). Focal atrophy may present as focal areas of encephalomalacia or porencephalic cyst. Sometimes, it may be difficult to differentiate encephalomalacia from porencephalic cyst on CT as both entities show low density. Since porencephalic cyst contains cerebrospinal fluid, it is generally of lower density than areas of encephalomalacia. On MRI, they can easily be differentiated from each other on the FLAIR sequence, as porencephalic cyst shows low signal intensity whereas encephalomalacia demonstrates high signal intensity.

In patients with long-standing, severe closed head injury and diffuse white matter injury, atrophy of the corpus callosum can occur. The degree of corpus callosal atrophy correlates significantly with the chronicity of the injury. MRI provides an in vivo determination of corpus callosal atrophy which may reflect the severity of DAI. The MRI findings of corpus callosal atrophy following closed head trauma appear to correlate clinically with post-traumatic hemispheric disconnection effects (Benavidez et al. 1999). Reduction in fornix size and hippocampal volume has also been reported in patients with TBI (Tate and Bigler 2000).We have recently observed a case of post-traumatic seizure in a patient with previous temporal lobe injury. MRI of the temporal lobe demonstrated temporal lobe encephalomalacia and bilateral mesial temporal sclerosis.

29.6

Correlation of Neuroimaging and Neurotraumatic Outcome

The role of advanced neuroimaging techniques in TBI management is undergoing a fundamental change.Historically,the radiographic findings in neurotrauma have focused on the descriptive anatomy of lesions with little regard to correlation with clinical outcomes of patients. Given the wide spectrum of traumatic mechanisms coupled with the complexity of neurophysiological autoregulation, prognostication based solely on location, number, and size of lesions has been poor at best. However, recent advances in neuroimaging have opened new opportunities to understanding the biology of neurotrauma as well as stratifying the clinical outcomes based on physiologi-

cal, functional, and anatomical imaging correlates. With the growing widespread use of MRI,single-pho- ton emission CT, and positron emission tomography (PET) scanning, new techniques are being applied to trauma situations which aim to improve clinical diagnosis and prognosis.

With the widespread adoption of advanced neuroimaging studies, neuroradiologists have gained the ability to correlate subtle changes in neurophysiology and map them anatomically. MRI can detect punctate areas of hemorrhage, differentiate between vasogenic and cytotoxic edema, and demonstrate areas of ischemia/infarct with much greater precision and speed than earlier-genera- tion neuroimaging modalities. While several studies have examined the link between TBI and routine MRI findings, these investigations have focused primarily on lesional anatomy (Hofman et al. 2001; Tate and Bigler 2000; Udstuen and Claar

2001). However, with the development of MRS, MT, diffusion/perfusion imaging, and functional imaging, our understanding of the neurophysiology of TBI has been greatly enhanced (Hammound and Wasserman 2002).) For example, both MRS and MT imaging have been shown to quantify damage after TBI, as reported by Sinson et al. (2001). Posttraumatic differences in NAA/Cr ratios between patients with good and poor outcomes were observed but were not statistically significant. Furthermore, McGowan et al. (2000) have reported that quantitative MT imaging can be utilized to detect abnormalities associated with mild TBI which are not detected on routine CT or MRI. Although there was only a weak correlation between the MRI and neurophysiological data, refinements in the technique may allow development of a grading system to predict extent of injury (Zee et al. 2002). In fact, mild TBI is becoming an intense area of focus given its high prevalence in the population and the greater sensitivity of advanced MRI techniques. Hofman et al. (2001) recently reported the largest prospective study to date correlating neuroimaging findings and neurocognitive tests in patients with mild TBI. Their results suggest that even mild trauma to the brain results in abnormalities identified on singlephoton emission CT (SPECT) and MRI which were previously not apparent. Unfortunately, the correlation between the two imaging techniques and neurocognitive tests was poor. Nevertheless, the data would support the further application of MRI and SPECT imaging to patients with head trauma given the sensitivity of these techniques to post-trau- matic brain lesions.

The future of TBI research and neuroimaging is bright.We are no longer limited to simple anatomical descriptive analysis but can extend our involvement into the arena of microscopic imaging and the sphere of outcomes research. The role of the neuroradiologist as prognosticator is becoming more important as the tools at our disposal allow better understanding of the link between what we see and what clinicians observe.

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