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Vrablik M, Zlatohlavek L, Stulc T, et al: Statin-associated myopathy: from genetic predisposition to clinical management, Physiol Res 63(Suppl 3):S327, 2014. [A discussion of the risk factors for statininduced myopathy and its therapy.]
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Edema,Herniation,andHydrocephalus
Hypoxia, Ischemia, and Infarction
Degenerative, inflammatory, infectious, vascular, and neoplastic disorders of the central nervous system (CNS) are some of the most serious diseases of mankind. These diseases have many unique features that reflect the highly specialized structure and functions of the CNS. The principal functional unit of the CNS is the neuron. Neurons of different types and in different locations have distinct properties, including functional roles, distribution of their connections, neurotransmitters used, metabolic requirements, and levels of electrical activity at a given moment. A set of neurons, not necessarily clustered together in a region of the brain, may thus show selective vulnerability to various insults because it shares one or more of these properties. Since different regions of the brain participate in different functions, the pattern of clinical signs and symptoms that follow injury depend as much on the region of brain involved as on the pathologic process. Mature neurons are incapable of cell division, so destruction of even a small number of neurons essential for a specific function may leave the individual with a neurologic deficit. In addition to neurons the CNS contains other cells, such as astrocytes and oligodendrocytes, which make up the glia. The components of the CNS are affected by a number of unique neurologic disorders and also respond to common insults (e.g., ischemia, infection) in a manner that is distinct from other tissues.
Before delving into specific disorders, we will briefly review the characteristic morphologic changes that are often seen in the CNS in the setting of injury or infection.
Features of Neuronal Injury. Inresponsetoinjury,anumberofchangesoccurinneuronsandtheirprocesses(axonsanddendrites).Within12hoursofanirreversiblehypoxic-ischemicinsult,neuronal injury becomesevidentonroutinehematoxylinandeosin(H&E)staining(
Fig.23.1A ).Thereisshrinkageofthecellbody,pyknosisofthenucleus,disappearanceofthenucleolus,lossofNisslsubstance,andintenseeosinophiliaofthecytoplasm(“redneurons”).Axonalinjuryalsoleadstocellbodyenlargementandrounding,peripheraldisplacementofthenucleus,enlargementofthenucleolus,andperipheraldispersionofNisslsubstance(central chromatolysis). Inaddition,acuteinjuriestypicallyresultinbreakdownoftheblood-brainbarrierandvariabledegreesofcerebraledema(discussedlater).