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The syndrome of impaired consciousness, its general features, the terms used to describe it, and the mechanisms involved are dis959
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Ischemic-Hypoxic (Ischemic-Anoxic) Encephalopathy
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Here the basic disorder is a lack of oxygen and of blood ow to the brain, the result of failure of the heart and circulation or of the lungs and respiration Often both mechanisms and both organ failures are responsible and one cannot say which predominates; hence the dually ambiguous allusions in medical records to cardiores-
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MAJOR CATEGORIES OF NEUROLOGIC DISEASE
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Table 40-1 Classi cation of the acquired metabolic disorders of the nervous system in adults I Metabolic diseases presenting as a syndrome of confusion, stupor, or coma A Ischemia-hypoxia B Hypercapnia C Hypoglycemia D Hyperglycemia E Hepatic failure F Reye syndrome G Azotemia H Disturbances of sodium, water balance, and osmolality I Hypercalcemia J Other metabolic encephalopathies: acidosis due to diabetes mellitus or renal failure (see also inherited forms of acidosis, in Chap 37); Addison disease K Hashimoto disease encephalopathy II Metabolic diseases presenting as a progressive extrapyramidal syndrome A Acquired hepatocerebral degeneration B Hyperbilirubinemia and kernicterus C Hypoparathyroidism III Metabolic diseases presenting as cerebellar ataxia A Hypothyroidism B Hyperthermia C Celiac sprue disease IV Metabolic diseases causing psychosis or dementia A Cushing disease and steroid encephalopathy B Hyperthyroid psychosis and hypothyroidism (myxedema) C Hyperparathyroidism D Pancreatic encephalopathy ( )
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When blood ow is stable, the most important element in the delivery of oxygen is the oxygen content of the blood This is the product of hemoglobin concentration and the percentage of oxygen saturation of the hemoglobin molecule At normal temperature and pH, hemoglobin is 90% saturated at an oxygen partial pressure of 60 mmHg and still 75% saturated at 40 mmHg; ie, as is well known, the oxygen saturation curve is not linear The product of the oxygen content and the cardiac output is the ultimate determinant of the adequacy of oxygen supply to the organs Reduced to the simplest formulation, a de cient supply of oxygen to the brain is due either to a failure of cerebral perfusion (ischemia) or to a reduced amount of circulating arterial oxygen, the result of diminished oxygen saturation, or insuf ciency of hemoglobin (hypoxia) Although they are often combined, the neurologic effects of ischemia and hypoxia are subtly different Physiology of Ischemic and Hypoxic Damage A number of physiologic mechanisms of a homeostatic nature protect the brain under conditions of both ischemia and hypoxia Through a mechanism termed autoregulation, there is a compensatory dilatation of resistance vessels in response to a reduction in cerebral perfusion, which maintains blood ow at a constant rate, as noted in Chap 34 When the cerebral blood pressure falls below 60 to 70 mmHg, an additional compensation in the form of increased oxygen extraction allows normal energy metabolism to continue In total cerebral ischemia, the tissue is depleted of its sources of energy in about 5 min, although longer periods are tolerated under conditions of hypothermia Also, energy failure due to hypoxia is counteracted by an autoregulatory increase in cerebral blood ow; at a PO2 of 25 mmHg, the increase in blood ow is approximately 400 percent A similar increase in ow occurs with a decrease in hemoglobin to 20 percent of normal In most clinical situations in which the brain is deprived of adequate oxygen, as already commented, there is a combination of ischemia and hypoxia, with one or the other predominating The pathologic effects of ischemic brain injury from systemic hypotension differ from those due to pure anoxia Under conditions of ischemia, the main damage takes the form of incomplete infarctions in the border zones between major cerebral arteries With anoxia, neurons in portions of the hippocampus and the deep folia of the cerebellum are particularly vulnerable More severe degrees of either ischemia or hypoxia lead to selective damage to certain layers of cortical neurons, and if more profound, to generalized damage of all the cerebral cortex, deep nuclei, and cerebellum The nuclear structures of the brainstem and spinal cord are relatively resistant to anoxia and hypotension and stop functioning only after the cortex has been badly damaged The cellular pathophysiology of neuronal damage under conditions of ischemia is discussed in Chap 34 Essentially, the mechanism of injury is an arrest of the aerobic metabolic processes necessary to sustain the Krebs (tricarboxylic acid) cycle and the electron transport system Neurons, if completely deprived of their source of energy, proceed to catabolize themselves in an attempt to maintain their activity and in so doing are damaged to a degree that does not permit their survival ie, they undergo necrosis The accumulation of catabolic products (particularly lactic acid) in the interstitial tissue contributes to the parenchymal damage Ultimately, the accumulated injury leads to cell death, probably through more than one mechanism The most acute forms of cell death are characterized by massive swelling and necrosis of neuronal and nonneuronal cells (cytotoxic edema) Short of immediate
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piratory failure and in neurologic notations to ischemic-hypoxic encephalopathy Ischemic-hypoxic encephalopathy in various forms and degrees of severity is one of the most frequent and disastrous cerebral disorders encountered in the emergency departments and recovery rooms of every general hospital The medical conditions that most often lead to it are as follows: 1 A reduction in cerebral blood ow as a result of myocardial infarction or ventricular arrhythmia, external or internal blood loss, and septic or traumatic shock in all of which circumstances cardiac function fails before that of respiration Hypoxia from suffocation due to drowning, strangulation, or aspiration of vomitus, food, or blood; from compression of the trachea by a mass or hemorrhage; or from tracheal obstruction by a foreign body Carbon monoxide (CO) poisoning, in which respiration fails rst and then the cardiovascular system Diseases that paralyze the respiratory muscles (GuillainBarre syndrome, amyotrophic lateral sclerosis, myasthenia, and, in the past, poliomyelitis) or damage the central nervous system (CNS) diffusely but the medulla speci cally, again with respiratory failure being the initial factor, followed by cardiac failure A general anesthesia accident during which the patient is exposed to inspired gas that is oxygen-de cient
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