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Mural or arterial wall abnormalities are due to vascular malformations, thickening of the intima, or obliterative arteritis. Obliterative arteritis is probably the cause of cerebral infarcts in infants of cocaine-addicted mothers. Extramural abnormalities such as neoplasms can produce cerebral infarcts but they most frequently produce intracranial bleeding. Asphyxia may produce cerebral infarcts by a combination of endomural and mural factors. Neonates with cerebral infarct should be evaluated by obtaining MRI and MRA of the brain, carotid ultrasonogram, echocardiogram, EKG, CBC with differential and platelets, prothrombin time, partial thromboplastin time, fibrinogen splitting products, proteins S and C activity levels, antithrombine-III activity, antiphospholipid antibody, urine for homocysteine, and factor-V Leidenpolymerase chain reaction (PCR). More about... 244

Hypoxic-Ischemic Encephalopathy
The diagnosis of hypoxic-ischemic encephalopathy should be based on clinical evidence of encephalopathy and perinatal asphyxia. Perinatal asphyxia is diagnosed in the presence of 3 or more of the following findings: (1) intrapartum distress (bradycardia with a heart rate of less than 100 beats per minute, late decelerations, or absence of beat-to-beat variability); (2) thick meconium-stained amniotic fluid, (3) an APGAR score of 6 or less at 5 minutes, (4) a need for resuscitation for more than 1 minute with positive pressure ventilation and oxygen immediately after birth, and (5) an arterial pH value of 7.20 or less or a base deficit of at least 14 mmol per liter within the first hour after birth. A minimal degree of encephalopathy produces lethargy and mild hypotonia with superimposed jitteriness. These findings, if lasting less than 24 hours, are very common after a traumatic delivery. Severe hypoxic-ischemic encephalopathies manifest as coma. Neonates with severe hypoxic-ischemic encephalopathies are hypotonic and have evidence of brainstem dysfunction. Asphyxia should be diagnosed if an event of hypotension and hypoxia is documented by clinical or laboratory findings. The presence of multi-organ involvement (high blood-urea nitrogen, creatine, and creatine phosphokinase) is often present in asphyxiated neonates. The degree of acidemia reflects the severity of the asphyxia. Computed tomography or MRI of the brain may initially demonstrate brain edema and, after 14 days, laminar cortical necrosis and status marmoratus (Figure 55.1).

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Figure 55.1. Hypoxic ischemic encephalopathy. [A] T1- weighted sagittal image of the brain demonstrates laminar necrosis and diffuse hyperintensity of the basal ganglia and thalami. [B] T1- weighted axial image of the brain demonstrates laminar necrosis (especially in the occipital region) and diffuse hyperintensity of the thalami.

 

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cerebellum occipital horn of the lateral ventricle hyperintensity in the lateral thalamus laminar necrosis (depth of the sulci) laminar necrosis (depth of sulci) area of laminar necrosis area of laminar necrosis habernula ventriculus III sylvian fissure sylvian fissure diffuse hyperintensity in the thalamus diffuse hyperintensity in the thalamic area Harum, 2000 Huang, 1999 Click on figure for animated labels.  Pause pointer on different areas of the figure for labels. Figure must be centered.