In fatal infections, lesions are found in the precentral (motor) gyrus of the brain (usually of insufficient severity to cause symptoms), brainstem, and spinal cord. The brunt of the disease in these cases is borne by the hypothalamus, thalamus, motor nuclei of the brainstem and surrounding reticular formation, vestibular nuclei and roof nuclei of the cerebellum, and mainly the neurons of the anterior and intermediate gray matter of the spinal cord. In these areas, nerve cells are destroyed and phagocytosed by microgliacytes (neuronophagia). A local leukocytic reaction is present for only a few days, but mononuclear cells persist as perivascular accumulations for many months. Inclusion bodies are not seen. The earliest histopathologic changes in the anterior horns of the cord are central chromatolysis of the nerve cells, along with an inflammatory reaction. These changes correlate with a multiplication of virus in the CNS and, in the infected monkey, precede the onset of paralysis by one or several days.
In Bodian’s experimental material, the infected motor neurons continued to function until a stage of severe chromatolysis was reached. Moreover, if damage to the cell had attained only the stage of central chromatolysis, complete morphologic recovery could be expected—a process that took a month or longer. After this time, the degrees of paralysis and atrophy were closely correlated with the number of motor nerve cells that had been destroyed; where limbs remain atrophic and paralyzed, less than 10 percent of neurons survived in corresponding cord segments. Lesions in the motor nuclei of the brainstem are associated with paralysis in corresponding muscles. Disturbances of swallowing, respiration, and vasomotor control are related to neuronal lesions in the medullary reticular formation, centered in the region of the nucleus ambiguus, as mentioned earlier.
Atrophic, areflexic paralysis of muscles of the trunk and limbs relates, of course, to destruction of neurons in the anterior and intermediate horns of the corresponding segments of the spinal cord gray matter. The affected regions can be quite focal or scattered, giving rise, for instance, to permanent paralysis of only one limb. Stiffness and pain in the neck and back, attributed to “meningeal irritation,” are probably related to the mild inflammatory exudate in the meninges and to the generally mild lesions in the dorsal root ganglia and dorsal horns. These lesions also account for the muscle pain and paresthesia in parts that later become paralyzed. Abnormalities of autonomic function are attributable to lesions of autonomic pathways in the reticular substance of the brainstem and in the lateral horn cells in the spinal cord.
It is of interest that poliovirus has been readily isolated from CNS tissue of fatal cases but can rarely be recovered from the CSF during clinical disease. This is in contrast to the closely related Coxsackie and echo picornaviruses, which have been isolated frequently from the CSF during the neurologic illness.
Patients in whom acute poliomyelitis is suspected require careful observation of swallowing function, vital capacity, heart rate, and blood pressure in anticipation of respiratory and circulatory complications. With paralysis of limb muscles, footboards, hand and arm splints, and knee and trochanter rolls prevent foot-drop and other deformities. Frequent passive movement prevents contractures, ankylosis, and pressure sores.
Respiratory failure as a result of paralysis of the intercostal and diaphragmatic muscles or of depression of the respiratory centers in the brainstem calls for the use of a positive-pressure respirator and in most patients, for a tracheostomy as well. It was during the epidemics of the mid-twentieth century that the use of Drinker’s “iron lung” attained widespread use. The management of the pulmonary and circulatory complications does not differ from their management in diseases such as myasthenia gravis and Guillain-Barré syndrome and is best carried out in special respiratory or neurologic intensive care units.