Dano Cerebral Hipóxico Isquêmico

Chapter
Alejandro A. Rabinstein and Steven J. Resnick
he brain is our most essential organ but also the most sensitive to oxygen deprivation. Diffuse hypoxia and ischemia result in global cerebral damage that follows a typical pattern dened by the selective vulnerability 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 cerebral autoregulation. Whereas moderately severe reductions in cerebral blood 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 examination 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 hypoxicischemic brain damage. Computed tomography (CT) scan has limited sensitivity to diagnose the extent of brain damage after a
PR SA O M PE PL R E TY C O O F N E TE L N SE T V - N IE O R T FI N AL
Hypoxic-Ischemic Brain Damage
diffuse hypoxic insult. Loss of the normal differentiation between cortical gray matter and subcortical white matter and effacement of the delineation of deep gray matter 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 ndings may be subtle and difcult 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., pseudosubarachnoid hemorrhage).35 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 hypoxicischemic 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.511. Figure 1-1 summarizes the main radiological ndings encountered in patients with severe hypoxic-ischemic brain damage. 1

SUMMARY OF HYPOXIC-ISCHEMIC BRAIN DAMAGE Basal ganglia Sequence Cerebral cortex
CT
DWI
T1
T1 with Contrast
FLAIR
Figure 1-1. Imaging 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 indicating laminar necrosis (right). Third row: Axial T1-weighted MRI shows bilateral symmetrical hyperintense signals within the putamen 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 bilaterally (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 uid-attenuated inversion recovery (FLAIR) MRI denoting bilateral symmetrical hyperintense 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).
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 cardiopulmonary resuscitation for nearly 15 minutes. On arrival, paramedics conrmed the diagnosis of cardiac arrest and initiated full advanced cardiac life support. Electrical debrillation resulted in return of spontaneous circulation. Initial neurological examination at the hospital revealed that the patient was comatose but with intact brainstem reexes. 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 unchanged 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).
ADDITIONAL EXAMPLES OF GLOBAL BRAIN EDEMA
Figure 1-3. Additional case illustrating the changes of severe of anoxic brain injury on computed
tomography (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).
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 rst 24 to 48 hours. In the most severe cases, CT scan may actually display reversal of the gray/white matter densities with relatively 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 identication of areas of laminar necrosis unrecognizable by CT scan.5 MRI 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 ganglia in the great majority of our patients, although the time of its appearance may vary. White matter abnormalities tend to manifest in the late subacute and chronic phases (after 10 days from the time of injury).6
Cortical Laminar Necrosis
Cortical laminar necrosis occurs because of the selective 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 excitatory amino acids that are released after the anoxic-
ischemic event, precipitating the mechanism of excitotoxicity. Early cytotoxic edema in these injured cells is responsible for the bright signals seen on DWI and the corresponding low apparent diffusion coefcient (ADC) values7,10,11 (Figures 1-4 and 1-5). The hyperintense signal observed on T1-weighted sequences 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).
Figure 1-4. Diffusion-weighted imaging sequence (left) and corresponding apparent diffusion coefcient 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.
Figure 1-5. Additional example of restricted diffusion affecting extensively the cortex of both cerebral hemispheres in a 58-year-old patient who underwent cardiopulmonary resuscitation after out-of hospital ventricular brillation. Images shown are diffusion-weighted imaging sequence (left) and apparent diffusion coefcient map (right) from a brain magnetic resonance image performed 46 hours after the cardiac arrest.
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 putamen (thick arrows). This MRI scan was performed nearly 3 weeks after a cardiac arrest,
Laminar necrosis may be identied within hours of the anoxic-ischemic event. In this acute phase (particularly the rst 24 hours), DWI is far superior to conventional MRI sequences in its ability to distinguish cortical changes.6,7,11 ADC values are typically 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 become 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 uid-attenuated inversion recovery (FLAIR), injured cortical areas are more prominently hyperintense 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 experience, this sequence offers limited value for the accurate diagnosis of laminar necrosis. Cortical enhancement is 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 visualized on CT scan, either in the form of gyriform high attenuation (likely caused by local hemorrhage) (Figure 1-9) or areas of cortical hypoattenuation (Figure 1-10).
Figure 1-7. Two cases of anoxic brain injury depicted on uidattenuated inversion recovery (FLAIR) sequences. Upper row: FLAIR sequence of a brain magnetic resonance imaging (MRI) scan of a patient with persistent coma 6 days after being resuscitated 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 relatively early stage. Lower row: Another 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.
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 incapacitated and was suspected to be cortically blind. Notice diffuse cortical enhancement predominantly involving the occipital and perirolandic cortical areas. The gure shows enhanced T1-weighted sequences with axial cuts (upper row), sagittal cut (lower left), and coronal cut (lower right).
Figure 1-9. This gure illustrates the changes caused by cortical laminar necrosis on computed tomography 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 magnied view on the upper right) or, less commonly, more manifest as shown in the lower row (arrowheads).
Figure 1-10. Computed tomography scan of the brain shows multifocal areas of severe cortical edema 3 days after cardiac arrest in a patient with persistent coma and myoclonic status. Basal ganglia also exhibit low attenuation.
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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 illustrations, 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 adventitious movements frequently seen in survivors of cardiac arrest and other severe hypoxic-ischemic events.
Figure 1-11. Magnetic resonance imaging (MRI) scans showing evidence of basal ganglia involvement 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.
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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 distribution 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 predominant thalamic lesions in the lower right.
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Watershed Infarctions
Watershed infarctions caused by a diffuse anoxicischemic insult appear to be more common in neonates and children. In adults, we have observed these lesions more often in patients who survive the event. In addition, watershed infarcts are not typically seen in conjunction with extensive laminar necrosis (Figure 1-13).
It is tempting to hypothesize that watershed infarcts occur in cases of severe hypoperfusion without 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: Diffusionweighted 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 uidattenuated inversion recovery sequence. Notice that the changes extend beyond typical watershed territory to affect larger areas of the frontal cortex on the right hemisphere.
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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 manifestation of brain anoxia.17 Presence of diffusion abnormalities or T1 hyperintensity in these cortical areas in a patient with coma of unclear cause should be considered strongly supportive of the diagnosis of hypoxic-ischemic brain damage. Cerebellar lesions may be prominent in certain severe cases, and cerebellar ischemia is probably an extremely poor prognostic indicator (Figure 1-16).
Figure 1-14. This gure illustrates predominant anoxic changes in the perirolandic regions after cardiac arrest. Upper row: Restricted diffusion on diffusion-weighted imaging (left) and corresponding dark signal on the apparent diffusion coefcient map (right) in a 56-year-old man who sustained prolonged ventricular brillation-arrest 5 days before. Lower row: FLAIR sequence shows high-intensity signal outlining the perirolandic cortex (normal view on the left and magnied view on the right).
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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 showing extensive areas of restricted diffusion in both cerebellar hemispheres (left). T2-weighted sequence also shows high signal intensity in these regions (right).
Figure 1-15. Figure demonstrating predominant involvement of changes indicative of laminar necrosis in the occipital cortex (arrows). Diffusion-weighted imaging sequence is shown in the upper left and FLAIR sequence in the rest of the images. Notice selective involvement of medial occipital cortex and relative sparing of mesial temporal structures.
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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 advanced 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 displacement of hypoattenuated cerebrospinal uid, engorgement 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 particularly deceptive in patients with coma of unclear
etiology; in these patients, it may result in unnecessary 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 special 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, patients with severe brain edema may also exhibit the false appearance of unilateral or, most often, bilateral 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.
Figure 1-17. False radiological signs in computed tomography scans after severe brain anoxia: pseudo-subarachnoid hemorrhage and false hyperdense middle cerebral artery sign. Pseudosubarachnoid 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 hyperdense middle cerebral artery signs. Notice extensive brain swelling in all cases.
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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 anoxicischemic brain damage and worsen over time.6,18 (Figure 1-18). It has been suggested that this delayed leukoencephalopathy may be more common after prolonged
hypoxemia combined with hypotension and acidosis,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 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 coefcient (ADC) on the ADC map (not shown). Lower row: Axial FLAIR shows extensive white matter changes in the same patient.
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References
1. Levy DE, Caronna JJ, Singer BH, Lapinski RH, Frydman H, Plum F. Predicting outcome from hypoxic-ischemic coma. JAMA 1985; 253:14201426. 2. Maramattom BV, Wijdicks EF. Postresuscitation encephalopathy. Current views, management, and prognostication. Neurologist 2005; 11:234243. 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; 24:254256. 4. Phan TG, Wijdicks EF, Worrell GA, Fulgham JR. False subarachnoid hemorrhage in anoxic encephalopathy with brain swelling. J Neuroimaging 2000; 10:236238. 5. Wijdicks EF, Campeau NG, Miller GM. MR imaging in comatose survivors of cardiac resuscitation. AJNR Am J Neuroradiol 2001; 22:15611565. 6. Arbelaez A, Castillo M, Mukherji SK. Diffusion-weighted MR imaging of global cerebral anoxia. AJNR Am J Neuroradiol 1999; 20:9991007. 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; 110:361367. 8. Goto Y, Wataya T, Arakawa Y, Hojo M, Chin M, Yamagata S et al. [Magnetic resonance imaging ndings of postresuscitation encephalopathy: sequential change and correlation with clinical outcome]. No To Shinkei 2001; 53:535540. 9. Komiyama M, Nishikawa M, Yasui T. Cortical laminar necrosis in brain infarcts: chronological changes on MRI. Neuroradiology 1997. 39:474479. 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 hypoxicischemic encephalopathy. AJNR Am J Neuroradiol 2004; 25:16591665.
11. Lovblad KO, Wetzel SG, Somon T, Wilhelm K, Mehdizade A, Kelekis A, et al. Diffusion-weighted MRI in cortical ischaemia. Neuroradiology 2004; 46:175182. 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; 10:11911198. 13. Tippin J, Adams HP Jr, Smoker WR. Early computed tomographic abnormalities following profound cerebral hypoxia. Arch Neurol 1984; 41:10981100. 14. Komiyama M, Nakajima H, Nishikawa M, Yasui T. Serial MR observation of cortical laminar necrosis caused by brain infarction. Neuroradiology 1998; 40:771777. 15. Siskas N, Lefkopoulos A, Ioannidis I, Charitandi A, Dimitriadis AS. Cortical laminar necrosis in brain infarcts: serial MRI. Neuroradiology 2003; 45:283288. 16. Barrett KM, Freeman WD, Weindling SM, Brott TG, Broderick DF, Heckman MG, et al. Brain injury after cardiopulmonary arrest and its assessment with diffusionweighted magnetic resonance imaging. Mayo Clin Proc 2007; 82:828835. 17. Konaka K, Miyashita K, Naritomi H. Changes in diffusionweighted magnetic resonance imaging ndings in the acute and subacute phases of anoxic encephalopathy. J Stroke Cerebrovasc Dis 2007; 16:8283. 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 sequential MR imaging. Radiology 1993; 189:449456. 19. Ginsberg MD, Hedley-Whyte ET, Richardson EP Jr. Hypoxicischemic leukoencephalopathy in man. Arch Neurol 1976; 33:514. 20. Chalela JA, Wolf RL, Maldjian JA, Kasner SE. MRI identication of early white matter injury in anoxic-ischemic encephalopathy. Neurology 2001; 56:481485.

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Dano Cerebral Hipóxico Isquêmico

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Chapter

Alejandro A. Rabinstein and Steven J. Resnick

Hypoxic-Ischemic Brain Damage

Hypoxic-Ischemic Brain Damage

Hypoxic-Ischemic Brain Damage

Hypoxic-Ischemic Brain Damage

ADDITIONAL EXAMPLES OF GLOBAL BRAIN EDEMA

Hypoxic-Ischemic Brain Damage

Cortical Laminar Necrosis

Hypoxic-Ischemic Brain Damage

Hypoxic-Ischemic Brain Damage

Hypoxic-Ischemic Brain Damage

Hypoxic-Ischemic Brain Damage

Hypoxic-Ischemic Brain Damage

Basal Ganglia Involvement

Hypoxic-Ischemic Brain Damage

Hypoxic-Ischemic Brain Damage

Hypoxic-Ischemic Brain Damage

Vulnerable Cortical Areas: Perirolandic and Occipital Cortex

Hypoxic-Ischemic Brain Damage

Hypoxic-Ischemic Brain Damage

Hypoxic-Ischemic Brain Damage

Early and Delayed White Matter Changes: Anoxic Leukoencephalopathy

Hypoxic-Ischemic Brain Damage

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