Acute Postviral Encephalopathy: Pathologic and Radiologic Correlation in an Atypical Case

Abstract

The authors report a case of fatal acute encephalopathy following influenza infection, with slightly atypical pathological and imaging findings. A healthy 8-year-old boy with probable recent influenza A/B infection admitted for refractory seizures was placed on phenobarbital coma and later developed hemodynamic instability. Magnetic resonance imaging revealed bilateral cerebral and cerebellar white matter lesions and microhemorrhages. Following his demise, the autopsy revealed a large area of necrosis in the right centrum semiovale with similar lesions in the temporal and cerebellar regions. Microscopically, there was extensive coagulative necrosis, compatible with necrotizing white matter encephalopathy, and neuronal loss suggesting superimposed hypoxic-ischemia. The acute progressive neurologic deterioration was partly reminiscent on acute necrotizing encephalopathy, a condition recently associated with influenza A. In acute necrotizing encephalopathy, typical brain findings are characterized by bilateral thalamic necrosis/petechiae with variable white matter edema. The somewhat atypical findings in our case can relate to superadded cardiovascular collapse and hypoxic-ischemic effects.

Keywords: acute necrotizing encephalopathy; influenza-associated encephalopathy; postviral.

Figure 1.

Noncontrast head computed tomography (CT) images. A, Extensive white matter hypodensity in the right centrum semiovale (black arrows). B, Hypodensity in the right caudate head and anterior lentiform nucleus (white arrows) and cerebral white matter (black arrows). C, Patchy hypodensity in the bilateral cerebellar white matter (black arrows).

Figure 2.

Brain magnetic resonance imaging (MRI). A, T2-weighted axial image showing heterogeneous signal in the right centrum semiovale (black arrows). B, T2-weighted axial image showing patchy T2 hyperintensity in the right basal ganglia (white arrows) and bilateral posterior thalami (black arrows). C, T2-weighted axial image shows bilateral cerebellar patchy T2 hyperintensity (black arrows). D, T1-weighted axial image showing faint hyperintensity in the right basal ganglia (white arrows) and posterior left thalamus (black arrow) consistent with hemorrhage. E and F, Susceptibility weighted images showing scattered hypointensities in the right cerebral hemisphere and bilateral cerebellar hemispheres, right greater than left (black arrows), consistent with petechial hemorrhages.

Figure 3.

Sections of the brain showing (A) right frontoparietal white matter necrosis; (B) bilateral cerebellar white matter necrosis; and (C) right basal ganglia and thalamus with areas of necrosis.

Figure 4.

Microscopic images showing (A) abrupt necrosis (N, bottom left) in the white matter (W, middle) and uninvolved cortical gray matter (G, top right; hematoxylin–eosin stain ×40); (B) smooth opaque, “mummified” central necrosis without cavitation and preserved vasculature (hematoxylin–eosin stain ×100); (C) necrosis with peripheral macrophage clustering in an angiocentric fashion (hematoxylin–eosin stain ×100); (D) perivascular calcification—linear rows (hematoxylin–eosin stain × 100).

Figure 5.

Microscopic images showing (A) hippocampus—massive neuronal loss within the CA1 and proximal CA2 regions (arrow approximately at the CA2/3 interface with neuronal losses and reactive vascular prominence to the right and viable CA3 neurons to the left of arrow; hematoxylin–eosin stain ×20 [inset ×40]); (B) cerebellum—selective, extensive Purkinje cell loss (hematoxylin–eosin stain ×100; M, molecular layer; P, Purkinje cell layer; G, [internal] granule cell layer); (C) spinal cord with myelin pallor, vacuolation, and fiber loss in the lateral corticospinal tract (hematoxylin–eosin stain ×100); (D) skeletal muscle with extensive atrophy (hematoxylin–eosin stain ×100).