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By: W. Kliff, M.B.A., M.B.B.S., M.H.S.
Associate Professor, Mercer University School of Medicine
Coarse fasciculations are seen frequently as the muscles weaken; they are transient as a rule erectile dysfunction and diabetes ppt discount malegra dxt 130 mg visa, but occasionally they persist erectile dysfunction 70 year olds generic 130mg malegra dxt fast delivery. Tendon reflexes are diminished and lost as the weakness evolves and paralyzed muscles become flaccid erectile dysfunction treatment in unani buy malegra dxt with mastercard. Patients frequently complain of paresthesias in the affected limbs, but objective sensory loss is seldom demonstrable. Retention of urine is a common occurrence during the early phase in adult patients, but it does not persist. Atrophy of muscle can be detected within 3 weeks of onset of paralysis, is maximal at 12 to 15 weeks, and is permanent. Bulbar paralysis is more common in young adults, but usually such patients have spinal involvement as well. The most frequently involved cranial muscles are those of deglutition, reflecting involvement of the nucleus ambiguus. The other great hazards of bulbar disease are disturbances of respiration and vasomotor control- hiccough, shallowness and progressive slowing of respiration, cyanosis, restlessness and anxiety (air hunger), hypertension, and ultimately hypotension and circulatory collapse. Pathologic Changes and Clinicopathologic Correlations 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 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, giving the illness its name, 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 leukocytic reaction is present for only a few days, but mononuclear cells persist as perivascular accumulations for many months. The earliest histopathologic changes are central chromatolysis of the nerve cells, along with an inflammatory reaction. 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, but only if severe in degree. The 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. 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. 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. Probably these lesions also account for the muscle pain and paresthesias 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. Treatment Patients in whom acute poliomyelitis is suspected require careful observation of swallowing function, vital capacity, pulse, and blood pressure in anticipation of respiratory and circulatory complications. With paralysis of limb muscles, foot boards, hand and arm splints, and knee and trochanter rolls prevent foot drop and other deformities. Respiratory failure, due to paralysis of the intercostal and diaphragmatic muscles or to 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. The management of the pulmonary and circulatory complications does not differ from their management in diseases such as myasthenia gravis and the Guillain-Barre ґ syndrome and is best carried out in special respiratory or neurologic intensive care units. The authors know of no systematic study of the potency of antiviral agents in this disease. Prevention Prevention, of course, has proved to be the most significant aspect and one of the outstanding accomplishments of modern medicine. The cultivation of poliovirus in cultures of human embryonic tissues and monkey kidney cells- the achievement of Enders and associates- made possible the development of effective vaccines. The first of these was the injectable Salk vaccine, containing formalin-inactivated virulent strains of the three viral serotypes. This was followed by the Sabin vaccine, which consists of attenuated live virus, administered orally in two doses 8 weeks apart; boosters are required at 1 year of age and again before starting school. Since 1965, the reported annual incidence rate of poliomyelitis in the United States has been less than 0. The only obstacle to complete prevention of the disease is inadequate utilization of the vaccine.
In addition to acupuncture protocol erectile dysfunction generic 130mg malegra dxt with mastercard overt and covert strokes erectile dysfunction treatment austin tx malegra dxt 130mg on line, a degree of cognitive decline and depression is to guaranteed erectile dysfunction treatment malegra dxt 130mg generic be expected in a proportion of patients undergoing coronary artery bypass grafting. The frequency of these changes is reported to be between 40 and 70 percent (see page 363). It is our impression that many of these neurologic complications, both small strokes and cognitive abnormalities, pass unnoticed in many cardiac surgical units. This was emphasized in the study by McKhann and colleagues, who extensively tested several neuropsychologic areas and found that only 12 percent of patients escaped some type of early cognitive problem. However, several other studies, such as the one by Mulges and colleagues, have sugЁ gested that only a small proportion (13 percent in their series) have permanent effects 5 years after operation. Others have reported Stroke in Pregnancy and the Postpartum Period In addition to the eclamptic state, there is an increased incidence of cerebrovascular events during pregnancy and the postpartum period. The risk of both cerebral infarction and intracerebral hemorrhage appears to be mainly in the 6-week period after delivery rather than during the pregnancy itself (Kittner et al). Fisher has reviewed the literature and has himself analyzed 12 postpartum, 9 puerperal, and 14 contraceptive cases, as well as 9 patients receiving estrogen therapy; arterial thrombosis was demonstrated in half of the group. Most of the focal vascular lesions during pregnancy were due to arterial occlusion in the second and third trimesters and in the first week after delivery. Included in most series are cases of cardiac disease, particularly valve-related embolism. It is perhaps surprising that subarachnoid hemorrhage is not more frequent during the Valsalva activity of childbirth. Carotid artery dissection may also be encountered late in pregnancy or soon after delivery. The occurrence of paradoxical embolus is always a consideration in pregnancy because of a tendency to form clots in the pelvic and leg veins, coupled with increased right heart pressures. The special stroke problems relating to prosthetic heart valves- mainly infective endocarditis causing embolic strokes and anticoagulant-related cerebral hemorrhage- are described in appropriate sections of this chapter. Although more than a dozen causes of nontraumatic intracranial hemorrhage are listed in Table 34-9, primary or hypertensive ("spontaneous") intracerebral hemorrhage, ruptured saccular aneurysm and vascular malformation, and hemorrhage associated with the use of anticoagulants or thrombolytic agents account for the majority. The small brainstem hemorrhages secondary to temporal lobe herniation and brainstem compression (Duret hemorrhages), hypertensive encephalopathy, and brain purpura might be included in this group, but they do not simulate a stroke. Primary (Hypertensive) Intracerebral Hemorrhage this is the mundane "spontaneous" brain hemorrhage. It is due predominantly to chronic hypertension and degenerative changes in cerebral arteries. In recent decades, with increased awareness of the need to control blood pressure, the proportion of hemorrhages attributable to causes other than hypertension has greatly increased; more than half such hemorrhages on our services now occur in Table 34-9 Causes of intracranial hemorrhage (including intracerebral, subarachnoid, ventricular, and subdural) 1. Hemorrhagic disorders: leukemia, aplastic anemia, thrombocytopenic purpura, liver disease, complication of anticoagulant or thrombolytic therapy, hypofibrinogenemia, hemophilia, Christmas disease, etc. Miscellaneous rare types: vasopressor drugs, cocaine, moyamoya, herpes simplex encephalitis, vertebral artery dissection, acute necrotizing hemorrhagic encephalitis (Hurst disease), tularemia, anthrax, etc. Nevertheless, the hypertensive cerebral hemorrhage serves as a paradigm for understanding and managing the cerebral hemorrhage. In order of frequency, the most common sites of a cerebral hemorrhage are (1) the putamen and adjacent internal capsule (50 percent); (2) the central white matter of the temporal, parietal, or frontal lobes (lobar hemorrhages, not strictly associated with hypertension); (3) the thalamus; (4) a cerebellar hemisphere; and (5) the pons (see Weisberg et al). The vessel involved is usually a penetrating artery that originates from a larger trunk vessel. The problem is one of bleeding that occurs within brain tissue; rupture of arteries lying in the subarachnoid space is practically unknown apart from aneurysms and some vascular malformations. The extravasation of blood forms a roughly circular or oval mass that disrupts the tissue and grows in volume as the bleeding continues. If the hemorrhage is large, midline structures are displaced to the opposite side and reticular activating and respiratory centers can be compromised, leading to coma and death in the manner described in Chap. Both the size and the location of the clot determine the degree of upper brainstem compression (Andrew et al). However, a hemorrhage of this type almost never ruptures through the cerebral cortex. The third ventricle and ipsilateral lateral ventricle are compressed and displaced by the expanding mass (12 h after onset of stroke).
