|ECR 2018 / C-0153||
|Hypoxic-ischemic encephalopathy review: mechanisms of injury and patterns of cerebral involvement in both children and adults|
Findings and procedure details
PRETERM HYPOXIC-ISCHEMIC ENCEPHALOPATHY
Hypoxic-ischemic injury is more common in preterm neonates than in term neonates. At least 5% of infants born before 32 weeks gestational age and up to 9% of infants born before 28 weeks develop cerebral palsy.
Due to the immadurity of the preterm neonatal brain, imaging findings of hypoxic-ischemic injury in preterm neonates differ from those seen in term neonates.
• SEVERE ASPHYXIA
Profound hypoxic-ischemic events in preterm neonates manifestates predominantly as damage to the deep gray matter structures and brainstem, with the THALAMI, ANTERIOR VERMIS and DORSAL BRAINSTEM being most frequently involved Fig. 6 .
The areas of most advanced myelination in the brain generally correspond to the areas of greatest metabolic activity. These are the areas that are expected to be most susceptible to damage in the setting of oxygen deprivation.
The perirolandic cortex is more likely to be spared in premature neonates than in term neonates.
Germinal matrix hemorrhages and periventricular white matter injury may be seen.
MRI performed within the first day after injury may be normal or show only subtle abnormalities:
- Diffusion abnormalities are usually evident in the thalamus within 24 hours, but are more apparent around days 3-5 after injury.
- After 2 days, T2 prolongation can be seen in the thalami and basal ganglia.
- By the 3rd day following injury, T1 shortening will be seen and persists into the chronic stage.
- T2 shortening develops in the injured areas at approximately 7 days Fig. 7 .
• MILD TO MODERATE ASPHYXIA: INTRAVENTRICULAR HEMORRHAGE
Prevalence is inversely related to gestational age and weight at birth. Bleeding occurs in the majority of cases within the first 24 hours of life.
The majority of intraventricular hemorrhages in preterm are associated with GERMINAL MATRIX HEMORRHAGES. Germinal matrix corresponds to a zone of cells lining the walls of the lateral ventricles in fetal life and ultimately gives rise to the neurons and glia of the brain.
By 34 weeks gestation, the germinal zones have nearly completely involuted, which explains why hemorrhages are infrequent after this time.
The last portion of the germinal matrix to involute (GANGLIONIC EMINENCE) is located deep to the ependyma in the caudothalamic notch, a groove between the head of the caudate nucleus and the thalamus. IT IS WHERE MOST GERMINAL MATRIX HEMORRHAGES ORIGINATE Fig. 8 .
Grades of germinal matrix-intraventricular hemorrhage Fig. 9 :
- Grade I: subependymal hemorrhage with no or minimal intraventricular extension.
- Grade II: hemorrhage extending from the germinal matrix into the ventricle without ventricular enlargement.
- Grade III: hemorrhage extending from the germinal matrix into the ventricles with ventricular enlargement.
- Periventricular parenchymal hemorrhagic infarction.
• MILD TO MODERATE ASPHYXIA: PERIVENTRICULAR LEUKOMALACIA
(White matter injury of prematurity)
Prevalence of injury appears to be inversely related to gestational age at birth.
Periventricular leukomalacia is probably related to:
- Selective vulnerability of cells of oligodendrocyte linage to changes in hypoxia-ischemia.
- Damage to subplate neurons.
The declining prevalence of periventricular leukomalacia after 32 weeks gestation coincides with oligodendrocyte maduration in the periventricular white matter.
It is most frequently observed adjacent to the trigones of the lateral ventricles and adjacent to the foramina of Monro Fig. 10 .
Stages of periventricular leukomalacia at ultrasonography: Fig. 11
1. CONGESTION: globular areas of increased echogenicity ("flares") in the periventricular regions in the first 48 hours.
2. TRANSIENT PERIOD OF RELATIVE NORMALIZATION: 2nd to 4th weeks of life.
3. PERIVENTRICULAR CYSTS DEVELOPMENT: 3 - 6 weeks of life
4. END-STAGE: by 6 months of age. Resolution of cysts and ventricular enlargement with irregular ventricular outline.
At MRI, early white matter injury will manifest as periventricular foci of T1 shortening within larger areas of T2 prolongation. These foci are usually evident by 3-4 days, subsequently giving way to mild T2 shortening at 6-7 days.
HYPOXIC-ISCHEMIC ENCEPHALOPATHY IN THE TERM INFANT
In the term infant, the most common mechanism of hypoxic injury is intrauterine asphyxia brought by circulatory problems (clotting of placental arteries, placental abruption or inflammatory processes). This asphyxia leads to perinatal depression with diminished exchange of oxygen and carbon dioxide and severe lactic acidosis.
• SEVERE ASPHYXIA
Includes selective injury to the putamen, thalamus, brainstem and PERIROLANDIC CEREBRAL CORTEX.
Bilateral basal ganglia and thalamic lesions are strongly associated with the development of motor impairment. Extension of the lesions related to the severity of the impairment.
In most infants, white matter is relatively spared, although a transient increase in the T2WI signal is often seen in the posterior internal capsule soon after injury.
Cortical abnormality frequently accompanies the classic lesions of the basal ganglia and thalami. Cortical injury are usually seen along the CENTRAL SULCUS and along THE MEDIAL ASPECT OF THE INTERHEMISPHERIC FISSURE Fig. 12 . It is due to the relative high metabolic rate in the tissue around the central sulcus related to maduration and early myelination.
Cortical abnormalities observed on MRI represent laminar necrosis in the deep layers of the cortex.
• PARTIAL ASPHYXIA
Results in more extensive cortical injury Fig. 13 .
HYPOXIC-ISCHEMIC ENCEPHALOPATHY IN POSNATAL INFANTS AND YOUNG CHILDREN
Hypoxic-ischemic injuries in infants and young children are mainly due to drowning and nonaccidental trauma.
• SEVERE ASPHYXIA
Severe insults between 1 and 2 years of age result in injuries to the corpora striata, lateral geniculate nuclei, hippocampi and cerebral cortex (particularly the anterior frontal and parieto-occipital cortex), with RELATIVE SPARING OF THE THALAMI AND PERIROLANDIC CORTEX.
Injuries occurring after the immediate perinatal period but before 1 year of age demonstrate FEATURES OF BOTH BIRTH ASPHYXIA AND LATER INFANTILE ASPHYXIA with involvement of the basal ganglia (posteriorly), lateral thalami, dorsal midbrain and cortex.
These differences are due to physiologic and biochemical changes that occur with brain maturation, and based on different patterns of activity and regional energy requirements.
Ultrasonography ceases to be an imaging option once the anterior fontanelle has closed. Then, CT BECOMES THE INITIAL IMAGING STUDY OF CHOICE Fig. 14 :
- Early CT within 24 hours may be negative or demonstrate subtle hypoattenuation of the deep gray matter structures.
- Subsequent CT: diffuse basal ganglia abnormalities with diffuse cerebral edema (cortical hypoattenuation, loss of "gray-white" differentiation, cisternal and sulcal effacement)
- Hemorrhagic infarctions of he basal ganglia may be evident by 4-6 days.
- Chronic phases reveal diffuse atrophy with sulcal and ventricular enlargement.
Within the first 24 hours a small number of patients will demonstrate the "REVERSAL SIGN" (reversal of normal attenuation of gray and white matter). It has been proposed that this finding is due to the distention of deep medullary veins secondary to partial obstruction of venous outflow secondary to the elevated intracranial pressure caused by diffuse edema.
Another CT sign of severe hypoxic-ischemic injury if the "WHITE CEREBELLUM SIGN" (described as a component of the reversal sign). There is diffuse edema and apparent hyperattenuation of the posterior fossa relative to the hypoattenuation of the cerebral hemispheres. This sign is due to the redistribution of blood to the posterior fossa occurring during anoxic events Fig. 15 .
DWI will usually be abnormal within the first 12-24 hours, initially demonstrating bright signal intensity in the posterolateral lentiform nuclei. Thalamic involvement will involve the ventrolateral nuclei. T1WI and T2WI are oftern normal.
Over the next 48 hours, hypoxic-ischemic injury progresses to include the remainder of the basal ganglia and the cortex. T2WI demonstrate diffuse basal ganglia and cortical signal intensity abnormality (edema).
There may be relative sparing of the perirolandic cortex and thalami Fig. 16 .
• MILD TO MODERATE ASPHYXIA
Milder anoxic events will generally result in watershed zone injuries involving the cortex and subcortical white matter.
White matter lesions are more common in children under the age of 1 year.
There is RELATIVE SPARING OF THE PERIVENTRICULAR WHITE MATTER Fig. 17 .
HYPOXIC-ISCHEMIC ENCEPHALOPATHY IN OLDER CHILDREN AND ADULTS
In adult population, the most common causes of hypoxic-ischemic encephalopathy are cardiac arrest or cerebrovascular disease with secondaty hypoxemia. In older children, drowning and asphyxiation are the most frequent causes of hypoxic-ischemic injury.
• SEVERE HYPOXIC-ISCHEMIC INJURY
Primarily affects the gray matter structures: the basal ganglia, thalami, cerebral cortex (in particular sensorimotor and visual cortices, although often diffuse), cerebellum and hippocampi Fig. 18 .
Predominance of GRAY MATTER INJURY is related to the fact that contains most of the dendrites where postsynaptic glutamate receptors are located.
Cerebellar injury tends to be more common in older patients.
CT is generally the first imaging study performed in older patients and shows:
- Diffuse edema.
- Effacement of the CSF-containing spaces.
- Decreased cortical and basal ganglia attenuation.
- Loss of gray-white matter differentiation.
Diffusion is the earliest imaging modality to become positive, usually within the first few hours.
During the first 24 hours, DWI may demonstrate increased signal intensity in the cerebellar hemispheres, basal ganglia or cerebral cortex (in particular, perirolandic and occipital) Fig. 19 .
Thalami, brainstem or hippocampi may also be involved.
Pseudonormalization of DWI occurs by the end of the first week Fig. 20 .
Early subacute period (24 hours - 2 weeks): T2WI typically become positive and demonstrate hyperintensity and swelling of the injured gray matter structures.
Chronic stages: T2WI show residual hyperintensity and T1WI may show cortical necrosis (areas of high signal intensity in the cortex) Fig. 21 .
• MILD TO MODERATE GLOBAL ISCHEMI ISCHEMIC INSULTS
Results in watershed zone infarcts Fig. 22 .
DELAYED WHITE MATTER INJURY
Postanoxic leukoencephalopathy is an uncommon syndrome of delayed white matter injury that occurs weeks after the hypoxic-ischemic insult.
Affects 2-3% of patients following a global hypoxic injury.
It is characterized by a period of relative clinical stability or improvement, followed by an acute neurologic decline, usually 2-3 weeks after the initial insult.
In young children, postanoxic white matter injury occurs sooner and can be observed by as early as 2 days.
At DWI appears as confluent areas of restricted diffusion throughout the cerebral white matter that corresponds to subtle hyperintensity on T2WI Fig. 23 .
Surviving patients may develop diffuse atrophy at follow-up in a process similar to wallerian degeneration.
THE ROLE OF MR SPECTROSCOPY IN HYPOXIC-ISCHEMIC INJURIES
Spectroscopy is more sensitive to injury and more indicative of the severity of injury in the first 24 hours after a hypoxic-ischemic episode, when conventional MRI and DWI may underestimate the extent of injury.
Neonates with asphyxia have statistically significant correlation between proton spectroscopy results and both neurologic and cognitive status by 12 months of age.
The optimal regions for determining the abnormalities associated to hypoxic-ischemic injury include the occipital cortex, the basal ganglia and the watershed zones.
LACTATE is an early observation within the first 12 or 24 hours after insult. It is the best prognostic indicator in the early stage and is related to poor outcome. However, it is important to remember that a small amount of lactate can be observed in watershed regions of the preterm infant.
In the late stage, N-ACETYL-ASPARTATE is the preferred prognostic indicator. It is also important to remember that a reduction of NAA levels is a normal finding in the brain of the preterm children Fig. 24 .
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