Brain - Necrosis

Appearance of a thalamic infarct at low magnification, identified by pallor within the zone of the black arrows, in an F344/N rat. The dentate gyrus of the hippocampus is identified by a white arrow. This infarct was the result of an arterial embolus (arrowhead), shown at higher magnification in Figure 2.
Figure 1 of 12

Acute necrosis of the posterior colliculus, a bilaterally symmetrical lesion (arrows), in the whole mount of a section in a male F344/N rat from a 4-day study. This resulted from the selective vulnerability of this brain region to toxin-induced impaired energy metabolism. The arrowhead identifies necrosis of the nucleus of the lateral lemniscus.
Figure 3 of 12

Similar regionally selective bilateral brain necrosis of the parietal cortex area 1 (blue arrow), thalamus (arrowhead), and retrosplenial cortex (white arrow) in a treated male F344/N rat from a 4-day study, all resulting from the same toxic compound as used in Figure 3.
Figure 4 of 12

Unusual form of malacia (total regional necrosis) of the spinal cord in the dorsal spinal funiculi (arrow) in a female F344/N rat from a chronic study.
Figure 5 of 12

A cortical infarct with gliosis and capillary hyperplasia (arrow) from a male B6C3F1 mouse in a chronic study.
Figure 6 of 12

A more advanced stage of cortical infarction (arrows) in a treated female B6C3F1 mouse from a chronic chronic inhalation study.
Figure 7 of 12

Morphology of an infarct of known duration (arrow) in an F344/N rat with experimental infarction.
Figure 8 of 12

Later stage of cortical infarction, with loss of tissue and collapse of the cortical structure creating a depression at the meningeal surface (arrows), in a male F344/N rat from a chronic study.
Figure 9 of 12

Detail of the cellular responses in cortical infarction of known 72-hour duration in an F344/N rat with experimental infarction. Note the hypertrophic and hyperplastic state of the capillary endothelium and the prominent macrophage presence (arrows).
Figure 10 of 12

Olfactory bulb necrosis in a male B6C3F1 mouse from a chronic study. Note that the substance of the olfactory bulb is lost (arrows) as a result of marked tissue necrosis, leaving only cellular debris and hemorrhage.
Figure 11 of 12
comment:
This section focuses on the morphology of brain necrosis caused by differing processes and the nature of the responses. In NTP studies, infarcts are diagnosed as necrosis, and the term “malacia” is reserved for gross lesions in the brain.Figure 1




Figure 3


Figure 5

Figure 6

In Figure 7

Figure 8

Depicted in Figure 9

Figure 10

Figure 11


Figure 12

recommendation:
In NTP studies, multifocal infarction and malacia are diagnosed as Brain, Multiple sites, Necrosis. If necrosis is focal, the diagnosis should include the subsite. Severity grading is based on the extent of the lesion. When individual neurons are affected, the diagnosis should be Brain, Neuron, Necrosis. Pertinent features of the necrosis should be included in the narrative. In advanced lesions of necrosis, where gliosis and inflammation, tissue collapse, and cyst formation are also seen, lesions with the most severity are typically diagnosed. Other concurrent lesions may be diagnosed separately, if warranted by the severity.references:
Calloni RL, Winkler BC, Ricci G, Poletto MG, Homero WM, Serafini EP, Corleta OC. 2010. Transient middle cerebral artery occlusion in rats as an experimental model of brain ischemia. Acta Cir Bras 25:428-433. Abstract: http://www.ncbi.nlm.nih.gov/pubmed/20877953
Sicard KM, Henninger V, Fisher V, Duong V, Ferris CF. 2006. Long-term changes of functional MRI-based brain function, behavioral status, and histopathology after transient focal cerebral ischemia in rats. Stroke 37:2593-2600. Abstract: http://www.ncbi.nlm.nih.gov/pubmed/16946164
Web page last updated on: January 02, 2014