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The brain is our most essential organ but also themost 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 minimallevels required for sustaining effective brain metabolismand energy production. Physiologically, this occurs whenmean arterial pressure falls below the lower limit of cere-bral autoregulation. Whereas moderately severe reduc-tions in cerebral blood flow and oxygen supply result indepression or suppression of brain tissue metabolism,critically severe reductions cause irreversible disruptionof cellular membranes (responsible for the developmentof cytotoxic edema) and cell death.

The most characteristic example of hypoxic-ischemicbrain damage is produced by cardiac arrest. Attempts toprognosticate outcome accurately after cardiac arresthave generated abundant research. Although clinical ex-amination remains the preeminent tool to predict thechances of recovery after cardiac resuscitation, a numberof electrophysiological and neuroimaging techniquesprovide valuable aid.1,2 This chapter summarizes the mostimportant and useful features of neuroimaging in thediagnosis 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 differentiationbetween 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 hypoxiaon CT scan. They represent early stages of brain swelling,

mostly due to cytotoxic edema. However, these findingsmay be subtle and difficult to recognize. Additionally, CTscans can be deceiving, showing little change in patientswith severe hypoxic damage or presenting signs thatmay be confused with other conditions (i.e., pseudo-subarachnoid hemorrhage).35 In patients who developareas of infarction, CT scans may fail to reveal any focalhypodensities until 24 to 48 hours after the episode.

In contrast, magnetic resonance imaging (MRI)scans are extremely useful to recognize the severity ofstructural damage even very shortly after a hypoxic-ischemic event. The prognostic usefulness of MRIscans is becoming increasingly well established. Theadvent of diffusion-weighted imaging (DWI) has addeda new dimension to the role of MRI in the workup ofpatients with acute global brain hypoxia-ischemia. Thissequence allows good visualization of laminar necrosisand other characteristic signs of hypoxic injury, and itoffers reliable information of prognostic importancewith unsurpassed promptness.511.

Figure 1-1 summarizes the main radiological findingsencountered in patients with severe hypoxic-ischemicbrain damage.

Chapter 1

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


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2 Hypoxic-Ischemic Brain Damage

CT

DWI

T1

T1 with Contrast

FLAIR

Sequence

Basal ganglia Cerebral cortex

SUMMARY OF HYPOXIC-ISCHEMIC BRAIN DAMAGE

Figure 1-1. Imaging findings 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 fluid-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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Hypoxic-Ischemic Brain Damage 3

Case Vignette

A 29-year-old, previously healthy man collapsed after alightning strike. A bystander at the scene noted absence ofpulse and audible heartbeat and performed basic cardiopul-monary resuscitation for nearly 15 minutes. On arrival, para-

medics confirmed the diagnosis of cardiac arrest and initi-ated full advanced cardiac life support. Electrical defibrillationresulted in return of spontaneous circulation. Initial neuro-logical examination at the hospital revealed that the patientwas comatose but with intact brainstem reflexes. He had aGlasgow coma scale sum score of 4 and exhibited frequent

myoclonic jerks (myoclonic status). He subsequently failed toregain consciousness. Five days later, he was transferred to atertiary 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 afterthe 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 invegetative state 2 months later.

Figure 1-2. Computed tomography (CT) scan of the brain showing effacement ofthe 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-ischemicevent, CT may show signs of cerebral edema such aseffacement of sulci, loss of differentiation betweencortical gray matter and underlying white matter,blurring of the insular ribbon, and loss of distinctionof the margins of the deep gray nuclei (particularlythe lenticular nucleus). Watershed infarctions may

be evident after the first 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 associatedwith an ominous prognosis (Figure 1-3).

Although CT scan may occasionally show earlychanges,13 it is most often normal hours after theinsult and may remain unremarkable at laterstages, even in patients with extensive neurologicaldamage.5

MRI is far more sensitive in the depiction ofhypoxic-ischemic damage. It allows prompt andreliable identification of areas of laminar necrosisunrecognizable by CT scan.5

MRI findings, especially extensive cortical laminarnecrosis and presence of changes in the brainstemand 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. Cerebellarchanges are often inconspicuous. Conversely, wehave found an abnormal signal in the basal gan-glia in the great majority of our patients, althoughthe time of its appearance may vary. White matterabnormalities tend to manifest in the late sub-acute and chronic phases (after 10 days from thetime 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-efficient 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 toanoxia and ischemia. In addition to neurons, glialcells and blood are also damaged, resulting in apan-necrosis. The selective vulnerability of gray

matter may be due to higher metabolic demandand denser concentration of receptors for excit-atory amino acids that are released after the anoxic-

ischemic event, precipitating the mechanism ofexcitotoxicity.

Early cytotoxic edema in these injured cells is re-sponsible for the bright signals seen on DWI andthe 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 accumulationof denatured proteins in dying cells and does notrepresent 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 corticalhyperintensity 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 exampleof 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 fibrillation. Im-

ages shown are diffusion-weighted

imaging sequence (left) and appar-

ent diffusion coefficient 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 anoxicbrain injury depicted on fluid-

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 identified within hours ofthe anoxic-ischemic event. In this acute phase (par-ticularly the first 24 hours), DWI is far superiorto conventional MRI sequences in its ability todistinguish 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 lateas 2 years after the insult.

On fluid-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 FLAIRwithin a few days of the anoxic insult (Figure 1-7).

Affected cortex tends to appear isointense to slightlyhyperintense on T2-weighted sequence. In our ex-perience, this sequence offers limited value for theaccurate diagnosis of laminar necrosis.

Cortical enhancement is first seen after 2 weeks,

peaks after 1 to 2 months, and is usually resolvedafter 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 localhemorrhage) (Figure 1-9) or areas of corticalhypoattenuation (Figure 1-10).


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Figure 1-8. Magnetic resonance imaging scan of the brain with gadolinium performed for prognosticpurposes 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 figure shows enhanced T1-weighted sequenceswith axial cuts (upper row), sagittal cut (lower left), and coronal cut (lower right).


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Figure 1-9. This figure illustratesthe 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-fied 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 restricteddiffusion 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 mostcases of anoxic-ischemic brain damage.

Bilateral thalami, lenticular nuclei, and caudatenuclei may be involved. As exhibited by the illus-trations, the distribution of lesions is not uniform

across patients and may change over time in eachpatient (Figures 1-11 and 1-12).

Lesions may be seen in association with corticallaminar changes or in isolation.

Although signal changes are often present early, thetime of appearance varies. The factors determiningthe timing and extent of these lesions remain to beestablished.

Basal ganglia injury may be the anatomicalsubstrate that accounts for the various adventi-tious movements frequently seen in survivors of

cardiac arrest and other severe hypoxic-ischemicevents.


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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 oftenin patients who survive the event. In addition, water-

shed infarcts are not typically seen in conjunctionwith 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 bycarotid occlusion or critical stenosis with systemichypotension), whereas laminar necrosis resultsfrom 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 fluid-

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 figure 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 coefficient map (right) in a 56-year-old man who sustained prolonged

ventricular fibrillation-arrest 5 days before. Lower row: FLAIR sequence shows high-intensity signal

outlining the perirolandic cortex (normal view on the left and magnified 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 extentthan other cortical areas. In our experience, themedial 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 areasmost susceptible to anoxia, radiological evidence ofdamage to these structures is seen much less com-

monly after cardiac arrest than are lesions in themedial occipital lobes and perirolandic regions.However, it has been suggested that the damage tothe hippocampus (along with the corpus callosumand 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 comaof unclear cause should be considered strongly sup-portive of the diagnosis of hypoxic-ischemic braindamage.

Cerebellar lesions may be prominent in certain se-vere cases, and cerebellar ischemia is probably anextremely 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 resonanceimage 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 radiologicalsigns in computed tomography

scans after severe brain anoxia:

pseudo-subarachnoid hemorrh-

age and false hyperdense middle

cerebral artery sign. Pseudo-

subarachnoid hemorrhage thickarrows 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 causedby anoxia-ischemia4 (Figure 1-17, upper row).

The most plausible explanation for the occurrenceof this phenomenon is a combination of displace-ment of hypoattenuated cerebrospinal fluid, en-gorgement of pial compliance vessels, and edemain the adjacent cortex.3

As displayed in our cases, increased attenuationwithin the falx, tentorium, and, most remarkably,the basal cisterns is responsible for the possiblemisdiagnosis 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 patientswith global edema may be avoided by being aware ofthis possibility. When in doubt, it is useful to pay spe-cial attention to the attenuation values in the basalcisterns, 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 thefalse appearance of unilateral or, most often, bilat-eral middle cerebral artery (MCA) signs, whichwould suggest bilateral stroke rather than diffuseanoxia-ischemia. Close attention to the presence ofsigns of diffuse swelling beyond the boundaries ofrestricted arterial vascular territories helps avoidthis misdiagnosis.


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Early and Delayed White Matter Changes:

Anoxic Leukoencephalopathy

White matter lesions typically become visible in thelate 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 thisform of leukoencephalopathy has been reported inthe literature.

Early white matter changes have been observed insome patients.20 The actual prevalence of this findingis unclear, but from our experience, it is probably

quite low.

Figure 1-18. Seventy-year-old man with poor recovery 2 weeks after prolonged cardiorespiratoryarrest 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 coefficient (ADC) on the ADC map (not shown).

Lower row:Axial FLAIR shows extensive white matter changes in the same patient.


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