Diffusion Weighted Imaging in Pediatric Neuroradiology Massachusetts General Hospital, Boston, MA • Harvard Medical School, Boston, MA
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Pallavi Sagar, M.D.; P. Ellen Grant, M.D. Diffusion Weighted Imaging in Pediatric Neuroradiology Massachusetts General Hospital, Boston, MA • Harvard Medical School, Boston, MA I. CEREBROVASCULAR DISEASE IV. TOXIC AND METABOLIC DISORDERS V. DEMYELINATING DISORDERS 1) Arterial Ischemic Stroke (AIS) 3) Global Hypoxia and Hypoperfusion 1) Methotrexate Neurotoxicity 1) Multiple Sclerosis (MS) INTRODUCTION Pediatric AIS is less common and almost 50% of the pediatric AIS are Perinatal Hypoxic Ischemic Brain Injury Intrathecal or intravenous methotrexate can cross blood brain barrier and cause diffuse or multifocal Figure 9. Methotrexate toxicity. Axial (a) T2 and (b) DWI. There is MS is an inflammatory demyelinating process, Diffusion-weighted magnetic resonance idiopathic. Pediatric strokes can be classified as perinatal (between 28 weeks white matter changes typically in the periventricular region. Alteration in myelin metabolism faint T2 hyperintensity in the left posterior centrum semiovale. which can be reversible due to reparative imaging (DWI) provides image contrast DWI is more sensitive in demonstrating increased signal in this of gestation and 28 days of postnatal life) or childhood (between 30 days and Hypoxic ischemic brain injury results from a combination of global cerebral hypoxia and hypoperfusion. Two patterns have causing axonal swelling and intramyelinic edema has been proposed. In acute encephalopathy region and an additional lesion on the right side presumably remyelination or become irreversible with that is dependent on the molecular motion 18 year of life) ( Figure 1) . been described. Partial asphyxia or peripheral pattern with bilateral white matter injury and a profound or central pattern with transient and reversible lesions with decreased diffusion can be observed. (Figure 9) due to intramyelinic edema which can be reversible. tissue loss. Destruction of myelin sheath and of water. This gets substantially altered corticospinal tract, VL thalamus, and perirolandic involvement. Conventional imaging may be negative until 3-7 days after the axonal loss leads to expansion of extracellular by many CNS diseases . It has become a insult. DWI provides a means of earlier detection of injury especially in the first hours after the insult (Figures 3 and 4). 2) Heroin Induced Leukoencephalopathy space with a quantitative increase in water useful tool for probing tissue physiology diffusion. Occasionally acute MS lesions may at the cellular level. It enables detection Figure 3. Neonatal Profound hypoxic ischemic injury with central asphyxia pattern. Axial (a) T2 , (b) DWI and (c) ADC. Inhaled or intravenous heroin vapor causes spongiform vacuolar degeneration of cerebral white have decreased ADC values presumably due of otherwise subtle abnormalities, narrows Loss of the normal low T2 signal is noted in the posterior limb matter. This results in DWI hyperintensity with reduced ADCs due to vacuolar white matter to more rapid demyelination. (Figure 17) a b c d the differential diagnosis and provides of the internal capsule and VL thalamus. Bright DWI signal and degeneration. (Figure 10) a b Figure 17. Multiple sclerosis. Axial (a) T2, (b) post contrast increased diffusion, but also shows that the region with additional relevant information when decreased ADCs are seen in these regions presumably due to enhanced T1, (c) DWI and (d) ADC. There are multiple foci of T2 brightest DWI signal has decreased diffusion. The region of cytotoxic edema. 2) Acute disseminated encephalomyelitis combined with routine MR imaging. As hyperintensites in the centrum semiovale, the largest lesion on decreased ADC does not match the area of enhancement and 3) Hypoglycemia (ADEM) the right with partial enhancement. DWI shows heterogenous may represent a subtype of active demyelination. a result, DWI plays an important role increased signal and the ADC map demonstrates predominantly in pediatric neuroimaging in better Excitotoxic brain damage can occur with ADEM is also an inflammatory demyelinating characterizing the disease process. a b c severe hypoglycemia with a blood glucose disease that develops in close temporal Figure 1. Neonatal Stroke. Axial (a) T2, (b) DWI lesion with low ADCs in a vascular distribution concentration below 30mg/dl. Decrease diffusion relationship to a viral illness or vaccination. The In this poster we will demonstrate the and (c) ADC performed on day 2. There is loss of consistent with acute arterial ischemic infarct a b c grey white matter differentiation in the left MCA and associated cytotoxic edema. with a posterior predominance involving the neurologic picture of ADEM usually reflects a expanded clinical applications of DWI in a Figure 4. Neonatal Hypoxic ischemic injury with peripheral territory. DWI there is a sharply marginated bright parieto-occipital lobes is typically observed, multifocal but often monophasic involvement. number of pediatric brain disorders. partial asphyxia pattern. Axial (a) T2, (b)DWI and (c) ADC. Faint loss of grey white matter differentiation is noted in the hypothesized secondary to excitotoxic neuronal Mostly elevated ADC values in acute lesions 2) Sinus Venous Infarction (SVT) posterior and parasagittal occipital lobes which can be easily injury from glutamate and aspartate on the are seen. Although decreased ADC values due overlooked. Diffuse bilateral hyperintense DWI signal with NMDA receptors. (Figure 11) to aggressive demyelination has also been PATHOPHYSIOLOGY decreased ADCs are easily identified involving primarily the SVT can occur due to infections, extrinsic compression of the venous sinus by occipital cortex and white matter. reported. (Figure 18) a b c d intracranial mass, dehydration, trauma, and hypercoagable. Venous occlusion a b c a b c DWI provides a more direct way to assess Figure 18. ADEM. Axial (a) T2, (b) Flair, (c) DWI and (d) ADC. The ADC map shows signal heterogeneity with decreased ADC causes regional venous hypertension with breakdown of the blood brain Figure 10. Heroin induced encephalopathy. Axial (a) T2, (b) DWI and (c) ADC. There is Figure 11. Neonatal hypoglycemia. Axial (a) T2, (b) DWI and (c) ADC. There is subtle loss of grey 3) Wallerian degeneration There are multiple bilateral scattered foci of T2 and flair values around the periphery of the lesion possibly secondary the extent of tissue injury by measuring T2 prolongation in the centrum semiovale bilaterally. DWI shows bright DWI signal and white matter differentiation posteriorly. Bright DWI signal and decreased ADC values are noted in barrier causing vasogenic edema. (Figure 2). hyperintensities involving the subcortical white matter. On DWI, to a subtype of active demyelination. the apparent diffusion coefficient (ADC) of reduced ADCs presumably due to spongiform degeneration of the white matter with the bioccipital cortex and subcortical white matter. This is secondary degeneration of axons the lesions are bright, predominantly due to T2 shine through. water within the imaged voxel. In the brain, a b c 4) Mitochondrial encephalopathy, lactic intramyelinic edema that is known to occur in this disorder. Figure 2. Neonatal Deep Vein and myelin sheaths of the descending white factors contributing to the measured ADC thrombosis. Axial (a) T2, (b) acidosis and stroke like syndromes (MELAS) Susceptibility, (c) DWI, (d) ADC. matter tracts, due to cortical or subcortical include true random diffusion, tortuosity There is extensive thrombosis of the Hypoxic Ischemic Injury in the Young Child injury. Cortical injury leads to cellular energy of the diffusion space, cytosolic streaming, internal cerebral veins with edema MELAS is a heterogeneous group of disorders Figure 12. MELAS. Axial (a) Flair, (b) DWI (c) ADC and (d) Single voxel MR spectroscopy at TE 135 ms depletion of the cell bodies of neurons exchange times between compartments of the basal ganglia. There is diffuse Most of the hypoxic or anoxic injuries in young child affecting the CNS and skeletal muscles. This is diffusion signal abnormality of the on the abnormality. A transient lesion in a patient resulting in axonal swelling. This results in and restriction by cell membranes. caused by defect in mitochondrial respiratory with MELAS presenting with seizures. Note the white matter with a combination of are a result of choking or near drowning. The initial myelin fragmentation and vacuolization into vasogenic (arrowhead) and cytotoxic DWI hyperintensities start in the posterior lentiform chain leading to cellular energy depletion involvement of the crest of the gyrus of the right frontal lobe on Flair, with corresponding bright ellipsoids and spheres causing decreased ADC edema (arrows) due to venous nucleus and VL thalamus and can progress over resulting in anaerobic glycolysis with lactate hypertension. DWI and isointense cortical ADCs in addition values. This process occurs within 4 weeks CLINICAL APPLICATIONS time. Imaging studies performed on the 3-4 day after production. MRI shows signal change both there is elevated subcortical ADCs. Targeted MR a b in the grey and white matter in a nonvascular Spectroscopy identified lactate. (arrow) of injury, during which conventional MRI is insult best correlate with clinical outcome. Therefore usually negative. (Figure 19) a b c d The practical applications of DWI are in distribution. MRS usually demonstrate a lactate if the initial imaging in the first 1-2 days is negative, Figure 19. Neonatal Wallarian degeneration. Axial (a & b) DWI brain stem, on the left side along the course