Histopathologic basis of clinical findings in poliomyelitis

摘要: Abstract 1.1. Experimental evidence indicates that the onset of CNS pathologic changes occurs in preparalytic period and is closely associated with earliest virus activity any particular region involved. 2.2. The cytopathologic are diffuse chromatolysis Nissl substance cytoplasm nerve cells mild cellular exudate consisting polymorphonuclear mononuclear leukocytes. 3.3. Nerve cell may be present stages without inflammatory reaction vicinity therefore not necessarily result latter, but rather direct action. 4.4. either lead to rapid destruction or arrest stage cytoplasmic chromatolysis, following which complete morphologic recovery generally over a about month less, depending upon severity injury. 5.5. Virus activity, localized only certain susceptible regions CNS, largely due specific differences susceptibility cells. intensity reaction, however, quite variable different centers individuals. Severe usually always extensive destruction. damage occur infiltration cord. 6.6. Lesions cerebral cortex confined motor area precentral gyrus even here lesions rarely severe enough suggest they produce clinical symptoms. 7.7. "Encephalitic" symptoms such as restlessness, stupor, disorientation coma brainstem often small softenings this region. They unusual involvement cortex. 8.8. Brainstem principally involved most instances reticular formation hind-brain, vestibular nuclei roof cerebellum. Resulting functional disturbances discussed. 9.9. Widespread dissemination among spinal cord enlargements experimental poliomyelitis early first day paralysis. Motor affected destroyed very quickly during few days disease undergo slower leading within month. After time it can shown degree paralysis atrophy correlated number destroyed. In acute stage, correlation high other factors must also play role producing An important factor reversible injury Less from human material suggests similar situation obtains poliomyelitis. 10.10. work three possible determine variation infection. These are, first, variations difference strains virus, second, reduction previous paralytic non-paralytic infection, third, host unrelated immunizing experience virus.