generate barcode c# .net THE ACQUIRED METABOLIC DISORDERS OF THE NERVOUS SYSTEM in Microsoft Office

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THE ACQUIRED METABOLIC DISORDERS OF THE NERVOUS SYSTEM
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Other Metabolic Encephalopathies Limitation of space permits only brief reference to other metabolic disturbances that may present as episodic confusion, stupor, or coma The most important members of this group are summarized below Hypercalcemia This is de ned as an elevation of the serum calcium concentration above 105 mg/dL If the serum protein content is normal, Ca levels greater than 12 mg/dL are required to produce neurologic symptoms However, with low serum albumin levels, an increased proportion of the serum Ca is in the unbound or ionized form (upon which the clinical effects depend), and symptoms may occur with serum Ca levels as low as 10 mg/dL In young persons, the most common cause of hypercalcemia is hyperparathyroidism (either primary or secondary); in older persons, osteolytic bone tumors, particularly metastatic carcinoma and multiple myeloma, are often causative Less common causes are vitamin D intoxication, prolonged immobilization, hyperthyroidism, sarcoidosis, and decreased calcium excretion (renal failure) Anorexia, nausea and vomiting, fatigue, and headache are usually the initial symptoms, followed by confusion (rarely a delirium) and drowsiness, progressing to stupor or coma in untreated patients A history of recent constipation is common Diffuse myoclonus and rigidity occur occasionally, as do elevations of spinal uid protein (up to 175 mg/100 mL) Convulsions are uncommon Hypocalcemia The usual manifestations are paresthesias, tetany, and seizures With severe and persistent hypocalcemia, altered mental status in the form of depression, confusion, dementia, or personality change can occur Anxiety to the point of panic attack is also known Even coma may result, in which case there may be papilledema due to increased intracranial pressure Aside from the raised pressure, the CSF shows no consistent abnormality This increase in intracranial pressure may be manifest by headache and papilledema without altered mentation or with visual obscurations Hypoparathydroidism is discussed again further on, in the section on extrapyramidal syndromes Other Electrolyte and Acid-Base Disorders Severe metabolic acidosis from any cause produces a syndrome of drowsiness, stupor, and coma, with dry skin and Kussmaul breathing The CNS depression does not correlate with the concentration of ketones Possibly, there are associated effects on neurotransmitters It is often not possible to separate the effects of acidosis from those due to an underlying condition or toxic ingestion In infants and children, acidosis may occur in the course of hyperammonemia, isovaleric acidemia, maple syrup urine disease, lactic and glutaric acidemia, hyperglycinemia, and other disorders, which are described in detail in Chap 37 High-voltage slow activity predominates in the EEG, and correction of the acidosis or elevated ammonia level restores CNS function to normal provided that coma was not prolonged or complicated by hypoxia or hypotension In uncomplicated acidotic coma, we have observed no recognizable neuropathologic change by light microscopy Encephalopathy due to Addison disease (adrenal insuf ciency) may be attended by episodic confusion, stupor, or coma without special identifying features; it is usually precipitated in the addisonian patient by infection or surgical stress Hemorrhagic destruction of the adrenals in meningococcal meningitis (Waterhouse Friderichsen syndrome) is another cause Hypotension and diminished cerebral circulation and hypoglycemia are the most readily recognized metabolic abnormalities; measures that correct these conditions reverse the adrenal crisis in some instances The various neurologic syndromes that result from electrolytic disorders are reviewed by Laureno
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Central Pontine Myelinolysis
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In 1950, Adams and Victor observed a rapidly evolving quadriplegia and pseudobulbar palsy in a young alcoholic man who had entered the hospital 10 days earlier with symptoms of alcohol withdrawal Postmortem examination several weeks later disclosed a large, symmetrical, essentially demyelinative lesion occupying the greater part of the base of the pons Over the next 5 years, three additional cases (two alcoholic patients and one with scleroderma) were studied clinically and pathologically, and in 1959 these four cases were reported by Adams et al under the heading of central pontine myelinolysis (CPM) This term was chosen because it denotes both the main anatomic localization of the disease and its essential pathologic attribute: the remarkably unsystematic dissolution of the sheaths of myelinated bers and the sparing of neurons Once attention was focused on this distinctive lesion, many other reports appeared The exact incidence of this disease is not known, but in a series of 3548 consecutive autopsies in adults, the typical lesion was found in 9 cases, or 025 percent (Victor and Laureno) Pathologic Features One is compelled to de ne this disease in terms of its pathologic anatomy, because this stands as its most certain feature Transverse sectioning of the xed brainstem discloses a grayish discoloration and ne granularity in the center of the basis pontis The lesion may be only a few millimeters in diameter, or it may occupy almost the entire basis pontis There is always a rim of intact myelin between the lesion and the surface of the pons Posteriorly it may reach and involve the medial lemnisci and, in the most advanced cases, other tegmental structures as well Very rarely, the lesion encroaches on the midbrain, but inferiorly it does not extend as far as the medulla Exceptionally the extensive pontine lesions may be associated with identical myelinolytic foci symmetrically distributed in the thalamus, subthalamic nucleus, striatum, internal capsule, corpus callosum, amygdaloid nuclei, lateral geniculate body, white matter of the cerebellar folia, and deep layers of the cerebral cortex and subjacent white matter ( extrapontine myelinolysis ; Wright et al) Microscopically, the fundamental abnormality consists of destruction of the myelinated sheaths throughout the lesion, with relative sparing of the axons and intactness of the nerve cells of the pontine nuclei These changes always begin and are most severe in the geometric center of the pons, where they may proceed to frank necrosis of tissue Reactive phagocytes and glial cells are in evidence throughout the demyelinative focus, but oligodendrocytes are depleted Signs of in ammation are conspicuously absent This constellation of pathologic ndings provides easy differentiation of the lesion from infarction and the in ammatory demyelinations of multiple sclerosis and postinfectious encephalomyelitis Microscopically, the lesion resembles that of Marchiafava-Bignami disease (Chap 41), with which it is rarely associated In the chronic alcoholic, Wernicke disease is not infrequently associated with CPM, but the lesions bear no resemblance to one another in terms of topography and histology Clinical Features Central pontine myelinosis occurs only sporadically, with no hint of a genetic factor The two sexes are affected equally, and the patients do not fall into any one age period Whereas the cases rst reported had occurred in adults, there are now many reports of the disease in children, particularly in those with severe burns (McKee et al)
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