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1 T he brain is our most essential organ but also the most sensitive to oxygen deprivation. Diffuse hy- poxia and ischemia result in global cerebral damage that follows a typical pattern defined by the selective vul- nerability of brain regions. Irreversible injury occurs when systemic blood pressure drops below the minimal levels required for sustaining effective brain metabolism and energy production. Physiologically, this occurs when mean arterial pressure falls below the lower limit of cere- bral autoregulation. Whereas moderately severe reduc- tions in cerebral blood flow and oxygen supply result in depression or suppression of brain tissue metabolism, critically severe reductions cause irreversible disruption of cellular membranes (responsible for the development of cytotoxic edema) and cell death. The most characteristic example of hypoxic-ischemic brain damage is produced by cardiac arrest. Attempts to prognosticate outcome accurately after cardiac arrest have generated abundant research. Although clinical ex- amination remains the preeminent tool to predict the chances of recovery after cardiac resuscitation, a number of electrophysiological and neuroimaging techniques provide valuable aid. 1,2 This chapter summarizes the most important and useful features of neuroimaging in the diagnosis and prognosis of patients with global hypoxic- ischemic brain damage. Computed tomography (CT) scan has limited sensi- tivity to diagnose the extent of brain damage after a diffuse hypoxic insult. Loss of the normal differentiation between cortical gray matter and subcortical white mat- ter and effacement of the delineation of deep gray mat- ter structures are the best known signs of global hypoxia on CT scan. They represent early stages of brain swelling, mostly due to cytotoxic edema. However, these findings may be subtle and difficult to recognize. Additionally, CT scans can be deceiving, showing little change in patients with severe hypoxic damage or presenting signs that may be confused with other conditions (i.e., pseudo- subarachnoid hemorrhage). 3–5 In patients who develop areas of infarction, CT scans may fail to reveal any focal hypodensities until 24 to 48 hours after the episode. In contrast, magnetic resonance imaging (MRI) scans are extremely useful to recognize the severity of structural damage even very shortly after a hypoxic- ischemic event. The prognostic usefulness of MRI scans is becoming increasingly well established. The advent of diffusion-weighted imaging (DWI) has added a new dimension to the role of MRI in the workup of patients with acute global brain hypoxia-ischemia. This sequence allows good visualization of laminar necrosis and other characteristic signs of hypoxic injury, and it offers reliable information of prognostic importance with unsurpassed promptness. 5–11 . Figure 1-1 summarizes the main radiological findings encountered in patients with severe hypoxic-ischemic brain damage. Chapter 1 Hypoxic-Ischemic Brain Damage Alejandro A. Rabinstein and Steven J. Resnick PROPERTY OF ELSEVIER SAMPLE CONTENT - NOT FINAL

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The brain is our most essential organ but also the most sensitive to oxygen deprivation. Diffuse hy-poxia and ischemia result in global cerebral damage

that follows a typical pattern defi ned by the selective vul-nerability of brain regions. Irreversible injury occurs when systemic blood pressure drops below the minimal levels required for sustaining effective brain metabolism and energy production. Physiologically, this occurs when mean arterial pressure falls below the lower limit of cere-bral autoregulation. Whereas moderately severe reduc-tions in cerebral blood fl ow and oxygen supply result in depression or suppression of brain tissue metabolism, critically severe reductions cause irreversible disruption of cellular membranes (responsible for the development of cytotoxic edema) and cell death.

The most characteristic example of hypoxic-ischemic brain damage is produced by cardiac arrest. Attempts to prognosticate outcome accurately after cardiac arrest have generated abundant research. Although clinical ex-amination remains the preeminent tool to predict the chances of recovery after cardiac resuscitation, a number of electrophysiological and neuroimaging techniques provide valuable aid.1,2 This chapter summarizes the most important and useful features of neuroimaging in the diagnosis and prognosis of patients with global hypoxic-ischemic brain damage.

Computed tomography (CT) scan has limited sensi-tivity to diagnose the extent of brain damage after a

diffuse hypoxic insult. Loss of the normal differentiation between cortical gray matter and subcortical white mat-ter and effacement of the delineation of deep gray mat-ter structures are the best known signs of global hypoxia on CT scan. They represent early stages of brain swelling, mostly due to cytotoxic edema. However, these fi ndings may be subtle and diffi cult to recognize. Additionally, CT scans can be deceiving, showing little change in patients with severe hypoxic damage or presenting signs that may be confused with other conditions (i.e., pseudo-subarachnoid hemorrhage).3–5 In patients who develop areas of infarction, CT scans may fail to reveal any focal hypodensities until 24 to 48 hours after the episode.

In contrast, magnetic resonance imaging (MRI) scans are extremely useful to recognize the severity of structural damage even very shortly after a hypoxic-ischemic event. The prognostic usefulness of MRI scans is becoming increasingly well established. The advent of diffusion-weighted imaging (DWI) has added a new dimension to the role of MRI in the workup of patients with acute global brain hypoxia-ischemia. This sequence allows good visualization of laminar necrosis and other characteristic signs of hypoxic injury, and it offers reliable information of prognostic importance with unsurpassed promptness.5–11.

Figure 1-1 summarizes the main radiological fi ndings encountered in patients with severe hypoxic-ischemic brain damage.

Chapter 1

Hypoxic-Ischemic Brain DamageAlejandro A. Rabinstein and Steven J. Resnick

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CT

DWI

T1

T1 with Contrast

FLAIR

Sequence

Basal ganglia Cerebral cortex

SUMMARY OF HYPOXIC-ISCHEMIC BRAIN DAMAGE

Figure 1-1. Imaging fi ndings in patients with hypoxic-ischemic brain damage affecting the basal ganglia and cerebral cortex. First row: Axial computed tomography (CT) of the basal ganglia showing symmetrical hypodensity in the caudate nuclei (left). Axial CT scans of the brain without contrast revealing linear hyperdensity outlining the cortex (right). Second row: Axial diffusion-weighted imagery (DWI) magnetic resonance imaging (MRI) scan demonstrates bilateral symmetrical hyperintensity within the stratiocapsular regions (left). Axial DWI MRIs show diffuse hyperintense signal change in the cerebral cortex indicat-ing laminar necrosis (right). Third row: Axial T1-weighted MRI shows bilateral symmetrical hyperintense signals within the puta-men bilaterally (left). Axial T1-weighted MRIs show bilateral areas of cortical hyperintensity representing laminar necrosis (right). Fourth row: Axial T1-weighted MRI with contrast discloses bilateral symmetrical enhancement in the external putamen bilater-ally (left). Axial and sagittal T1-weighted MRI with contrast show linear enhancement outlining the cortex, predominantly located in the occipital lobes (right). Fifth row: Axial fl uid-attenuated inversion recovery (FLAIR) MRI denoting bilateral symmetrical hy-perintense signals in the lenticular nuclei (left). Examples of axial FLAIR MRI showing diffuse and focal cortical hyperintensities distributed throughout the cerebral cortex or preferentially in the medial occipital cortex (right).

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Case Vignette

A 29-year-old, previously healthy man collapsed after a lightning strike. A bystander at the scene noted absence of pulse and audible heartbeat and performed basic cardiopul-monary resuscitation for nearly 15 minutes. On arrival, para-medics confi rmed the diagnosis of cardiac arrest and initi-ated full advanced cardiac life support. Electrical defi brillation resulted in return of spontaneous circulation. Initial neuro-logical examination at the hospital revealed that the patient was comatose but with intact brainstem refl exes. He had a Glasgow coma scale sum score of 4 and exhibited frequent

myoclonic jerks (myoclonic status). He subsequently failed to regain consciousness. Five days later, he was transferred to a tertiary care center. That day, an electroencephalogram (EEG) showed a very low-amplitude, slow (delta, occasional theta) background. A brain CT scan disclosed severe diffuse edema (Figure 1-2, upper row). A brain MRI performed 13 days after the insult displayed signs of extensive laminar necrosis (Figure 1-2, lower row). A second EEG was essentially un-changed almost 1 month after the arrest. He remained in vegetative state 2 months later.

Figure 1-2. Computed tomography (CT) scan of the brain showing effacement of the perimesencephalic cisterns (thin arrows) and areas of parenchymal low attenuation (thick arrows, upper left). Lower cut of the same CT scan reveals diffuse sulcal effacement with decreased differentiation between gray and white matter (upper right). T1-weighted magnetic resonance imaging scan showing high-intensity signals in the lenticular nuclei (arrows, lower left). Fluid-attenuated inversion recovery sequence disclosing hyperintense signal in the medial occipital cortices indicative of laminar necrosis (arrows, lower right).

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❖ As illustrated by this case, after an anoxic-ischemic event, CT may show signs of cerebral edema such as effacement of sulci, loss of differentiation between cortical gray matter and underlying white matter, blurring of the insular ribbon, and loss of distinction of the margins of the deep gray nuclei (particularly the lenticular nucleus). Watershed infarctions may be evident after the fi rst 24 to 48 hours.

❖ In the most severe cases, CT scan may actually display reversal of the gray/white matter densities with rela-tively increased density of the thalami, brainstem, and cerebellum (“reversal sign”).12 This is associated with an ominous prognosis (Figure 1-3).

❖ Although CT scan may occasionally show early changes,13 it is most often normal hours after the insult and may remain unremarkable at later stages, even in patients with extensive neurological damage.5

❖ MRI is far more sensitive in the depiction of hypoxic-ischemic damage. It allows prompt and reliable identifi cation of areas of laminar necrosis unrecognizable by CT scan.5

❖ MRI fi ndings, especially extensive cortical laminar necrosis and presence of changes in the brainstem and white matter, are associated with poor chances of recovery.5,7,11

❖ Apart from cortical necrosis, MRI may exhibit changes in the cerebellum and basal ganglia, which may be present quite early. Cerebellar changes are often inconspicuous. Conversely, we have found an abnormal signal in the basal gan-glia in the great majority of our patients, although the time of its appearance may vary. White matter abnormalities tend to manifest in the late sub-acute and chronic phases (after 10 days from the time of injury).6

ADDITIONAL EXAMPLES OF GLOBAL BRAIN EDEMA

Figure 1-3. Additional case illustrating the changes of severe of anoxic brain injury on computedtomography (CT) scan. A 55-year-old man had a cardiac arrest after surgery. CT scan 12 hours after the arrest shows effacement of the cortical sulci, loss of distinction of gray white matter junction, and slit-like lateral ventricles suggestive of diffuse cerebral edema (left). Higher cut displays multiple areas of decreased attenuation due to diffuse cerebral edema in a gyriform distribution over the hemispheric convexities (right).

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Figure 1-4. Diffusion-weighted imaging sequence (left) and corresponding apparent diffusion co-effi cient maps (right) of a brain magnetic resonance image from a 51-year-old woman obtained 16 hours after resuscitation from prolonged cardiac arrest. Note restricted diffusion in the lenticular nuclei and throughout the cortex of both cerebral hemispheres. The patient remained comatose and expired 3 days later after withdrawal of life support.

Cortical Laminar Necrosis ❖ Cortical laminar necrosis occurs because of the se-

lective vulnerability of cortical layers 3, 4, and 5 to anoxia and ischemia. In addition to neurons, glial cells and blood are also damaged, resulting in a pan-necrosis. The selective vulnerability of gray matter may be due to higher metabolic demand and denser concentration of receptors for excit-atory amino acids that are released after the anoxic-

ischemic event, precipitating the mechanism of excitotoxicity.

❖ Early cytotoxic edema in these injured cells is re-sponsible for the bright signals seen on DWI and the corresponding low apparent diffusion coeffi -cient (ADC) values7,10,11 (Figures 1-4 and 1-5).

❖ The hyperintense signal observed on T1-weighted se-quences is believed to be caused by the accumulation of denatured proteins in dying cells and does not represent presence of hemorrhage14,15(Figure 1-6).

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Figure 1-6. T1-weighted magnetic resonance imaging (MRI) scan showing patchy areas of cortical hyperintensity representing laminar necrosis (thin arrows). Also notice hyperintense signal in the puta-men (thick arrows). This MRI scan was performed nearly 3 weeks after a cardiac arrest,

Figure 1-5. Additional example of restricted diffusion affecting ex-tensively the cortex of both cere-bral hemispheres in a 58-year-old patient who underwent cardiopul-monary resuscitation after out-of hospital ventricular fi brillation. Im-ages shown are diffusion-weighted imaging sequence (left) and appar-ent diffusion coeffi cient map (right) from a brain magnetic resonance image performed 46 hours after the cardiac arrest.

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Figure 1-7. Two cases of anoxic brain injury depicted on fl uid-attenuated inversion recovery (FLAIR) sequences. Upper row: FLAIR sequence of a brain mag-netic resonance imaging (MRI) scan of a patient with persistent coma 6 days after being resusci-tated from a cardiac arrest. It shows diffusely increased signal intensity in the insular, high frontal, parietal, and occipital cortex. The cortex also appears swollen in this rela-tively early stage. Lower row: An-other example of cortical changes on FLAIR but in a later stage. This MRI was obtained 12 days after cardiac arrest. In addition to the high-intensity signal changes in the cortex, the lenticular nuclei also appear hyperintense bilaterally.

❖ Laminar necrosis may be identifi ed within hours of the anoxic-ischemic event. In this acute phase (par-ticularly the fi rst 24 hours), DWI is far superior to conventional MRI sequences in its ability to distinguish cortical changes.6,7,11 ADC values are typi-cally decreased to values ranging from 60% to 80% of normal.11 Cortical diffusion abnormalities are associated with poor outcome after cardiac arrest.16

❖ T1 hyperintensities signaling laminar necrosis be-come evident after 2 weeks, peak at 1 to 3 months, and then fade slowly but can still be visible as late as 2 years after the insult.

❖ On fl uid-attenuated inversion recovery (FLAIR), in-jured cortical areas are more prominently hyperin-tense between 1 month and 1 year after the event.14,15

However, we have observed cortical changes on FLAIR within a few days of the anoxic insult (Figure 1-7).

❖ Affected cortex tends to appear isointense to slightly hyperintense on T2-weighted sequence. In our ex-perience, this sequence offers limited value for the accurate diagnosis of laminar necrosis.

❖ Cortical enhancement is fi rst seen after 2 weeks, peaks after 1 to 2 months, and is usually resolved after 6 months14,15 (Figure 1-8).

❖ Very severe cases of cortical necrosis can be visu-alized on CT scan, either in the form of gyri-form high attenuation (likely caused by local hemorrhage) (Figure 1-9) or areas of cortical hypoattenuation (Figure 1-10).

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Figure 1-8. Magnetic resonance imaging scan of the brain with gadolinium performed for prognostic purposes 1 month after cardiac arrest in a 45-year-old woman with limited recovery. She was fully inca-pacitated and was suspected to be cortically blind. Notice diffuse cortical enhancement predominantly involving the occipital and perirolandic cortical areas. The fi gure shows enhanced T1-weighted sequences with axial cuts (upper row), sagittal cut (lower left), and coronal cut (lower right).

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Figure 1-9. This fi gure illustrates the changes caused by cortical laminar necrosis on computed to-mography scan. Cortical edema (low attenuation) can be combined with small areas of hyperdensity (likely caused by hemorrhage or vascular congestion). These changes can be rather subtle as seen in the upper left (with magni-fi ed view on the upper right) or, less commonly, more manifest as shown in the lower row (arrowheads).

Figure 1-10. Computed tomog-raphy scan of the brain shows mul-tifocal areas of severe cortical edema 3 days after cardiac arrest in a patient with persistent coma and myoclonic status. Basal gan-glia also exhibit low attenuation.

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Figure 1-11. Magnetic resonance imaging (MRI) scans showing evidence of basal ganglia in-volvement after anoxic insults. Upper row: Diffusion-weighted imagery sequence revealing restricted diffusion on bilateral putamen and caudate nuclei (left) and in the caudate nuclei and cortical areas (right). Lower row: T1-weighted sequence showing high-intensity signal in the putamen bilaterally (axial view on the left and coronal on the right). Note associated medial occipital changes on the axial cut.

Basal Ganglia Involvement ❖ Changes in the deep gray nuclei are seen in most

cases of anoxic-ischemic brain damage. ❖ Bilateral thalami, lenticular nuclei, and caudate

nuclei may be involved. As exhibited by the illus-trations, the distribution of lesions is not uniform across patients and may change over time in each patient (Figures 1-11 and 1-12).

❖ Lesions may be seen in association with cortical laminar changes or in isolation.

❖ Although signal changes are often present early, the time of appearance varies. The factors determining the timing and extent of these lesions remain to be established.

❖ Basal ganglia injury may be the anatomical substrate that accounts for the various adventi-tious movements frequently seen in survivors of cardiac arrest and other severe hypoxic-ischemic events.

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Figure 1-12. Magnetic resonance imaging (MRI) scans showing evidence of basal ganglia involvement after cardiac arrest. Upper row: T2-weighted sequence displaying increased signal in lenticular nuclei, caudate nuclei, and throughout the cortical layer. Lower two rows: Various examples of anoxic changes affecting the basal ganglia on FLAIR. Notice that these changes may occur only in the deep structures (middle row) or may also involve cortical areas (lower row). The distri-bution of lesions in the basal ganglia may vary. See predominant putaminal involvement in the middle and lower images of the left column, combined caudate and lenticular involvement on the middle right, and pre-dominant thalamic lesions in the lower right.

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Watershed Infarctions ❖ Watershed infarctions caused by a diffuse anoxic-

ischemic insult appear to be more common in neo-nates and children.

❖ In adults, we have observed these lesions more often in patients who survive the event. In addition, water-shed infarcts are not typically seen in conjunction with extensive laminar necrosis (Figure 1-13).

❖ It is tempting to hypothesize that watershed in-farcts occur in cases of severe hypoperfusion with-out anoxia (as happens when they are caused by carotid occlusion or critical stenosis with systemic hypotension), whereas laminar necrosis results from anoxic injury.

Figure 1-13. Images demonstrate watershed infarctions after cardiac arrest. Upper row: Diffusion-weighted imaging sequence showing restricted diffusion in internal and external watershed distributions 4 days after cardiac arrest in a pediatric patient. Lower row: Early changes already observed in the fl uid-attenuated inversion recovery sequence. Notice that the changes extend beyond typical watershed terri-tory to affect larger areas of the frontal cortex on the right hemisphere.

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Figure 1-14. This fi gure illustrates predominant anoxic changes in the perirolandic regions after car-diac arrest. Upper row: Restricted diffusion on diffusion-weighted imaging (left) and corresponding dark signal on the apparent diffusion coeffi cient map (right) in a 56-year-old man who sustained prolonged ventricular fi brillation-arrest 5 days before. Lower row: FLAIR sequence shows high-intensity signal outlining the perirolandic cortex (normal view on the left and magnifi ed view on the right).

Vulnerable Cortical Areas: Perirolandic and Occipital Cortex ❖ The perirolandic (Figure 1-14) and occipital cortex

(Figure 1-15) are often involved to a greater extent than other cortical areas. In our experience, the medial occipital cortex is the area most commonly affected after anoxic-ischemic brain injury.

❖ The intense baseline metabolic demand of these regions may explain their selective vulnerability.

❖ Although it is commonly held that the hippocampi in the mesial temporal lobes are the cortical areas most susceptible to anoxia, radiological evidence of damage to these structures is seen much less com-

monly after cardiac arrest than are lesions in the medial occipital lobes and perirolandic regions. However, it has been suggested that the damage to the hippocampus (along with the corpus callosum and white matter) may occur as a delayed manifes-tation of brain anoxia.17

❖ Presence of diffusion abnormalities or T1 hyperin-tensity in these cortical areas in a patient with coma of unclear cause should be considered strongly sup-portive of the diagnosis of hypoxic-ischemic brain damage.

❖ Cerebellar lesions may be prominent in certain se-vere cases, and cerebellar ischemia is probably an extremely poor prognostic indicator (Figure 1-16).

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Figure 1-15. Figure demonstrating pre-dominant involvement of changes indicative of laminar necrosis in the occipital cortex (arrows). Diffusion-weighted imaging se-quence is shown in the upper left and FLAIR sequence in the rest of the images. Notice selective involvement of medial oc-cipital cortex and relative sparing of mesial temporal structures.

Figure 1-16. Evidence of cerebellar lesions after brain anoxia is seen in this magnetic resonance image of an 84-year-old woman who had prolonged respiratory arrest. Diffusion-weighted image show-ing extensive areas of restricted diffusion in both cerebellar hemispheres (left). T2-weighted sequence also shows high signal intensity in these regions (right).

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Figure 1-17. False radiological signs in computed tomography scans after severe brain anoxia: pseudo-subarachnoid hemorrh-age and false hyperdense middle cerebral artery sign. Pseudo-subarachnoid hemorrhage thick arrows in the tentorium and sulci in the upper left panel and in the perimesencephalic cisterns in the upper right panel. Thin arrows mark examples of false hyper-dense middle cerebral artery signs. Notice extensive brain swelling in all cases.

False Radiological Signs: Pseudo-Subarachnoid Hemorrhage and False Middle Cerebral Artery Sign ❖ False appearance of subarachnoid hemorrhage

(SAH), or pseudo-SAH, may be seen in cases of ad-vanced diffuse cerebral edema,3 including that caused by anoxia-ischemia4 (Figure 1-17, upper row).

❖ The most plausible explanation for the occurrence of this phenomenon is a combination of displace-ment of hypoattenuated cerebrospinal fl uid, en-gorgement of pial compliance vessels, and edema in the adjacent cortex.3

❖ As displayed in our cases, increased attenuation within the falx, tentorium, and, most remarkably, the basal cisterns is responsible for the possible misdiagnosis of SAH. This appearance may be par-ticularly deceptive in patients with coma of unclear

etiology; in these patients, it may result in unneces-sary testing.

❖ The pitfall of mistakenly diagnosing SAH in patients with global edema may be avoided by being aware of this possibility. When in doubt, it is useful to pay spe-cial attention to the attenuation values in the basal cisterns, because they are much lower in these false cases than those observed in true cases of SAH.3

❖ As clearly shown by the images in Figure 1-17, pa-tients with severe brain edema may also exhibit the false appearance of unilateral or, most often, bilat-eral middle cerebral artery (MCA) signs, which would suggest bilateral stroke rather than diffuse anoxia-ischemia. Close attention to the presence of signs of diffuse swelling beyond the boundaries of restricted arterial vascular territories helps avoid this misdiagnosis.

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Early and Delayed White Matter Changes: Anoxic Leukoencephalopathy ❖ White matter lesions typically become visible in the

late subacute or chronic phase of evolution of anoxic-ischemic brain damage and worsen over time.6,18 (Figure 1-18).

❖ It has been suggested that this delayed leukoen-cephalopathy may be more common after prolonged

hypoxemia combined with hypotension and acido-sis,19 yet surprisingly little research addressing this form of leukoencephalopathy has been reported in the literature.

❖ Early white matter changes have been observed in some patients.20 The actual prevalence of this fi nding is unclear, but from our experience, it is probably quite low.

Figure 1-18. Seventy-year-old man with poor recovery 2 weeks after prolonged cardiorespiratory arrest complicated with renal failure and associated with severe acidosis. Mild initial improvement in alertness was followed by irreversible decline. Upper row: Axial diffusion-weighted imaging sequence shows patchy areas of bright signal within the white matter suggestive of anoxic leukoencephalopathy. These bright spots matched with low apparent diffusion coeffi cient (ADC) on the ADC map (not shown). Lower row: Axial FLAIR shows extensive white matter changes in the same patient.

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H, Plum F. Predicting outcome from hypoxic-ischemic coma. JAMA 1985; 253:1420–1426.

2. Maramattom BV, Wijdicks EF. Postresuscitation encepha-lopathy. Current views, management, and prognostication. Neurologist 2005; 11:234–243.

3. Given CA, Burdette JH, Elster AD, Williams DW III. Pseudo-subarachnoid hemorrhage: a potential imaging pitfall associated with diffuse cerebral edema. AJNR Am J Neuroradiol 2003; 24:254–256.

4. Phan TG, Wijdicks EF, Worrell GA, Fulgham JR. False subarachnoid hemorrhage in anoxic encephalopathy with brain swelling. J Neuroimaging 2000; 10:236–238.

5. Wijdicks EF, Campeau NG, Miller GM. MR imaging in comatose survivors of cardiac resuscitation. AJNR Am J Neuroradiol 2001; 22:1561–1565.

6. Arbelaez A, Castillo M, Mukherji SK. Diffusion-weighted MR imaging of global cerebral anoxia. AJNR Am J Neuro-radiol 1999; 20:999–1007.

7. Els T, Kassubek J, Kubalek R, Klisch J. Diffusion-weighted MRI during early global cerebral hypoxia: a predictor for clinical outcome? Acta Neurol Scand 2004; 110:361–367.

8. Goto Y, Wataya T, Arakawa Y, Hojo M, Chin M, Yamagata S et al. [Magnetic resonance imaging fi ndings of postresusci-tation encephalopathy: sequential change and correlation with clinical outcome]. No To Shinkei 2001; 53:535–540.

9. Komiyama M, Nishikawa M, Yasui T. Cortical laminar necrosis in brain infarcts: chronological changes on MRI. Neuroradiology 1997. 39:474–479.

10. McKinney AM, Teksam M, Felice R, Casey SO, Cranford R, Truwit CL, et al. Diffusion-weighted imaging in the setting of diffuse cortical laminar necrosis and hypoxic-ischemic encephalopathy. AJNR Am J Neuroradiol 2004; 25:1659–1665.

11. Lovblad KO, Wetzel SG, Somon T, Wilhelm K, Mehdizade A, Kelekis A, et al. Diffusion-weighted MRI in cortical ischaemia. Neuroradiology 2004; 46:175–182.

12. Han BK, Towbin RB, De Courten-Myers G, McLaurin RL, Ball WS Jr. Reversal sign on CT: effect of anoxic/ischemic cerebral injury in children. AJNR Am J Neuroradiol 1989; 10:1191–1198.

13. Tippin J, Adams HP Jr, Smoker WR. Early computed to-mographic abnormalities following profound cerebral hypoxia. Arch Neurol 1984; 41:1098–1100.

14. Komiyama M, Nakajima H, Nishikawa M, Yasui T. Serial MR observation of cortical laminar necrosis caused by brain infarction. Neuroradiology 1998; 40:771–777.

15. Siskas N, Lefkopoulos A, Ioannidis I, Charitandi A, Dimitriadis AS. Cortical laminar necrosis in brain infarcts: serial MRI. Neuroradiology 2003; 45:283–288.

16. Barrett KM, Freeman WD, Weindling SM, Brott TG, Broderick DF, Heckman MG, et al. Brain injury after car-diopulmonary arrest and its assessment with diffusion-weighted magnetic resonance imaging. Mayo Clin Proc 2007; 82:828–835.

17. Konaka K, Miyashita K, Naritomi H. Changes in diffusion-weighted magnetic resonance imaging fi ndings in the acute and subacute phases of anoxic encephalopathy.J Stroke Cerebrovasc Dis 2007; 16:82–83.

18. Takahashi S, Higano S, Ishii K, Matsumoto K, Sakamoto K, Iwasaki Y, et al. Hypoxic brain damage: cortical laminar necrosis and delayed changes in white matter at sequen-tial MR imaging. Radiology 1993; 189:449–456.

19. Ginsberg MD, Hedley-Whyte ET, Richardson EP Jr. Hypoxic-ischemic leukoencephalopathy in man. Arch Neurol 1976; 33:5–14.

20. Chalela JA, Wolf RL, Maldjian JA, Kasner SE. MRI identi-fi cation of early white matter injury in anoxic-ischemic encephalopathy. Neurology 2001; 56:481–485.

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