Hypoxic-Ischemic Brain Damage

Chapter 1 Hypoxic-Ischemic Brain Damage



Alejandro A. Rabinstein, Steven J. Resnick


The 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 defined 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 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 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 hypoxic-ischemic brain damage.


Computed tomography (CT) scan has limited sensitivity to diagnose the extent of brain damage after a 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 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.


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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 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 fluid-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 confirmed the diagnosis of cardiac arrest and initiated full advanced cardiac life support. Electrical defibrillation resulted in return of spontaneous circulation. Initial neurological examination at the hospital revealed that the patient was comatose but with intact brainstem reflexes. 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.


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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).



♦ 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 first 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 identification of areas of laminar necrosis unrecognizable by CT scan.5

♦ MRI findings, 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

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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).



ADDITIONAL EXAMPLES OF GLOBAL BRAIN EDEMA



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 coefficient (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).
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Jul 23, 2016 | Posted by in NEUROLOGICAL IMAGING | Comments Off on Hypoxic-Ischemic Brain Damage

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