PATH review Flashcards
What is the cystic lesion?
The cystic lesion is a remote infarct.
How does an infarct become cystic? How long does it take for an infarct to undergo cystic change?
The infarct becomes cystic because of phagocytosis of the necrotic, ipid-rich tissue by macrophages, which migrate into the infarct during the first week. Evolution of the infarct to a cystic defect is usually complete by about 6 months. Review: Cell Injury Introductory Image 25 (brain, cystic infarct, gross)
Explain the transient episodes of right-sided weakness and speech difficulty during the year prior to the development of the infarct.
The episodes of transient weakness and speech difficulty likely reflect brief episodes of vascular occlusion by small embolic fragments, originating either from the heart or from atheromatous plaques in more proximal arterial segments. Such episodes are termed transient ischemic attacks (TIAs). The term denotes a self-limited episode of neurological dysfunction lasting from a few seconds to as long as 24 hours (but usually not longer than 30 minutes). Approximately 20 to 25% of patients suffering from TIAs will develop a CNS infarct during the next five years.
How does the appearance of this acute infarct differ from that of the remote infarct?
In contrast to the cavitary defect that characterizes the remote infarct in our patient, in the acute setting, the necrotic tissue is swollen. This swollen appearance is caused by the accumulation of fluid, both within the necrotic cells (cytotoxic edema) and within the interstitium, the latter due to leakage of fluid into the affected tissue from damaged blood vessels (vasogenic edema). In severe cases, this edema may raise the intracranial pressure to life-threatening levels.
Why do the necrotic neurons stain red compared to the viable neurons in the left panel?
The red staining is caused by a combination of protein denaturation and loss of RNA within the cytoplasm of the affected neuron.
How do brain parenchymal infarcts organize?
CNS parenchymal infarcts organize via an influx of macrophages into the area of necrosis. The macrophages ingest the lipid-rich, necrotic parenchyma (see image 7), ultimately converting the area to a fluid-filled cavity (liquefactive necrosis). As noted previously, this process is usually complete by about 6 months after the development of the infarct.
What factors contribute to the hemorrhagic appearance of some infarcts?
Several factors may contribute to the development of significant hemorrhage in CNS infarcts, of which two of the most important are (1) anticoagulation and (2) reperfusion of nonviable tissue.
What is the most common predisposing factor to spontaneous brain parenchymal hemorrhage? What lesion is felt to be the source of such hemorrhages?
Hypertension is the most common cause of spontaneous brain parenchymal hemorrhage. So-called hypertensive hemorrhages are felt to originate in tiny aneurysms, termed Charcot-Bouchard microaneurysms, usually located in small arterial channels in the area of the basal ganglia or thalamus.
Why are epidural hematomas dangerous?
Because they are arterial in origin, epidural hematomas tend to enlarge very rapidly. This is manifested clinically by rapid loss of consciousness after a brief lucid interval, as was the case with this patient. Like any expanding intracranial mass, epidural hematomas cause an increase in intracranial pressure, which is associated, in turn, with decreased perfusion of the brain and potentially catastrophic compression of vital respiratory centers (e.g., the cardiorespiratory centers in the brainstem).
What is the pathogenesis of subdural hematomas?
Subdural hematomas develop between the arachnoid mater and the inner surface of the dura whenever tears occur in the veins (bridging veins) connecting the surface of the brain to one of the dural sinuses (usually the superior sagittal sinus).
Traumatic subarachnoid hemorrhages are usually caused by bruises of the surface of the brain, termed ________.
contusions
What are the important consequences of cerebellar tonsillar herniation?
Cerebellar tonsillar herniation is a potentially catastrophic lesion, due to associated compression and distortion of the adjacent brainstem, which contains vital respiratory centers. Compromise of these areas may cause respiratory arrest, a common terminal event in patients with expanding intracranial lesions. Caudal displacement of the cerebellum and brainstem may also be associated with hemorrhagic necrosis of the cerebellar tonsils, and with secondary hemorrhage within the brainstem (Duret hemorrhage, illustrated in the next image).
What are some common sites for brain contusions?
Although they may occur anywhere on the surface of the brain, contusions are encountered most commonly in the frontal poles, the orbital surfaces of the frontal lobes, the temporal poles, the inferior temporal lobes, and the region of the Sylvian fissure.
What is the most common site for pilocytic astrocytomas? What are some of the major differences between pilocytic astrocytomas and infiltrating astrocytomas?
Pilocytic astrocytomas most commonly occur in the cerebellum. Pilocytic astrocytomas may occur in both children and adults, but are much more common in the pediatric population. In contrast to the infiltrating astrocytomas, pilocytic astrocytomas tend to be comparatively circumscribed and, as such, can sometimes be completely resected. If completely removed, their prognosis is quite good, with survival rates exceeding 90%. In the case of pilocytic astrocytomas arising in areas not amenable to surgical resection (e.g., hypothalamus, thalamus), the prognosis is much more guarded.
What are common sites of primary tumors that metastasize to the brain?
Although any visceral carcinoma can metastasize to the brain parenchyma, the lung is the most common primary site. An estimated 15% to 20% of cases of lung cancer present with neurological abnormalities. Other important primary sites include breast, skin (melanomas), and, less commonly, the gastrointestinal tract.
