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L. Yorik, M.A., M.D., Ph.D.

Professor, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo

Others, however, have reported stiffness and awkwardness of the limbs, often with tremor of the hands, "cogwheel" phenomenon, gross rhythmic movements of the trunk and head, and retropulsive and propulsive gait. Progressive weakness, fatigability, and sleepiness as well as psychiatric symptoms (manganese madness) are other clinical features. Rarely, severe axial rigidity and dystonia, like those of Wilson disease, are said to have been the outstanding manifestations. Neuronal loss and gliosis, affecting mainly the pallidum and striatum but also the frontoparietal and cerebellar cortex and hypothalamus, have been described, but the pathologic changes have not been carefully studied. Treatment the neurologic abnormalities have not responded to treatment with chelating agents. In the chronic dystonic form of manganese intoxication, dramatic and sustained improvement has been reported with the administration of L-dopa; patients with the more common parkinsonian type of manganese intoxication have shown only slight if any improvement with L-dopa. Among the organic compounds, methyl mercury gives rise to a wide array of serious neurologic symptoms that may be delayed for days or weeks after exposure, including tremor of the extremities, tongue, and lips; mental confusion; and a progressive cerebellar syndrome, with ataxia of gait and arms, intention tremor, and dysarthria. Changes in mood and behavior are prominent, consisting at first of subjective weakness and fatigability and later of extreme depression and lethargy alternating with irritability. This delayed form of subacute mercury poisoning has been reported in chemical laboratory workers after exposure to methyl mercury compounds. These agents, particularly dimethyl mercury, are extremely hazardous because they are absorbed transdermally and by inhalation, allowing severe toxicity to occur with even brief contact. In a fatal case of a chemist reported by Nierenberg et al, a rapidly progressive ataxia and stupor progressing to coma developed 154 days after exposure. The pathologic changes are characterized by a striking degeneration of the granular layer of the cerebellar cortex, with relative sparing of the Purkinje cells and neuronal loss and gliosis of the calcarine cortex and to a lesser extent of other parts of the cerebral cortex similar to the Minamata cases described later. The chronic form of inorganic mercury poisoning occurs in persons exposed to large amounts of the metal used in the manufacture of thermometers, mirrors, incandescent lights, x-ray machines, and vacuum pumps. Since mercury volatilizes at room temperature, it readily contaminates the air and then condenses on the skin and respiratory mucous membranes. Nitrate of mercury, used formerly in the manufacture of felt hats ("mad hatters"), and phenyl mercury, used in the paper, pulp, and electrochemical industries, are other sources of intoxication. Paresthesias, lassitude, confusion, incoordination, and intention tremor are characteristic, and, with continued exposure, a delirious state occurs. Headache, various bodily pains, visual and hearing disorders, and corticospinal signs may be added, but their pathologic basis is unknown. The term erethism was coined to describe the timidity, memory loss, and insomnia that were said to be characteristic of chronic intoxication. If the exposure is more than a minimal degree over a long period, gastrointestinal disturbances are prone to occur (anorexia, weight loss), as well as stomatitis and gingivitis with loosening of the teeth. Acute exposure to inorganic mercury in larger amounts is even more corrosive to the gastrointestinal system and produces nausea, vomiting, hematemesis, abdominal pain, and bloody diarrhea as well as renal tubular necrosis. Isolated instances of polyneuropathy associated with exposure to mercury have also been reported (Albers et al, Agocs et al) and may be responsible for the paresthesias that accompany most cases as well as the acrodynic syndrome described below. The polyneuropathy associated with mercury poisoning is discussed on pages 1130 and 1132. The inhalation of vaporized mercury as a result of extensive dental work, or simply the presence of a large number of fillings ("amalgam illness"), is alleged to affect the peripheral nerves or to cause fatigue, but the connection is highly doubtful. The presence of mercury in industrial waste has contaminated many sources of water supply and fish, which are ingested by hu- mans and cause mercurial poisoning. Between 1953 and 1956, a large number of villagers living near Minamata Bay in Kyushu Island, Japan, were afflicted with a syndrome of chronic mercurialism, traced to the ingestion of fish that had been contaminated with industrial wastes containing methyl mercury. Concentric constriction of the visual fields, hearing loss, cerebellar ataxia, postural and action tremors, and sensory impairment of the legs and arms and sometimes of the tongue and lips were the usual clinical manifestations. Pathologically there was diffuse neuronal loss in both cerebral and cerebellar cortices, most marked in the anterior parts of the calcarine cortex and granule cell layer of the cerebellum. A painful neuropathy of children (acrodynia) has been traced to mercury exposure from interior latex paint, to calomel (mercurous chloride), to teething powders, and to a mercuric fungicide used in washing diapers (Agocs et al, Clarkson).

Syndromes

• Swollen tongue (glossitis)
• Tetralogy of Fallot is a heart defect that exists from birth (congenital). It usually includes four defects in the heart and causes the baby to turn a bluish color (cyanosis).
• Change in mental status, such as: Anxiety, confusion, decreased alertness, decreased ability to concentrate, fatigue, restlessness, sleepiness, stupor, lethargy
• May get worse with activity
• Tiny organisms that can cause disease (microorganisms)
• Test lung function in people with advanced pulmonary disease, such as COPD
• Problems with erections
• Widespread red rash that looks like a sunburn -- skin peeling occurs 1 or 2 weeks after the rash, particularly on the palms of the hand or bottom of the feet
• Weight loss
• Dry skin

Etiology and Pathogenesis A number of factors- socioeconomic, psychologic, and pharmacologic- contribute to the genesis of opioid addiction. In our culture, the most susceptible subjects are young men or delinquent youths living in the economically depressed areas of large cities, but significant numbers are now found in suburbs and in small cities as well. The onset of opioid use is usually in adolescence, with a peak at 17 to 18 years; fully two-thirds of addicts start using the drugs before the age of 21. Almost 90 percent of addicts engage in criminal activity, often to obtain their daily ration of drugs, but most of them have a history of arrests or convictions antedating their addiction. Also, many of them have psychiatric disturbances, conduct disorder and sociopathy being the most common ("dual-diagnosis," in psychiatric jargon). Monroe and colleagues, using the Lexington Personality Inventory, examined a group of 837 opioid addicts and found evidence of antisocial personality in 42 percent, emotional disturbance in 29 percent, and thinking disorder in 22 percent; only 7 percent were free of such disorders. One addict recruits another person into addiction, and the new recruit does likewise. In this sense opioid addiction is contagious, and partly as a result of this pattern, heroin addiction has attained epidemic proportions. A small, almost insignificant proportion of addicts are introduced to drugs by physicians in the course of an illness. Therefore, there has been a regrettable tendency not to prescribe opiates to patients with acute or chronic pain. Opioid addiction consists of three recognizable phases: (1) episodic intoxication, or "euphoria," (2) pharmacogenic dependence or drug-seeking behavior (addiction), and (3) the propensity to relapse after a period of abstinence. In patients with severe pain or pain-anticipatory anxiety, the administration of opioids produces a sense of unusual well-being, a state that has traditionally been referred to as morphine euphoria. It should be emphasized that only a negligible proportion of such persons continue to use opioids habitually after their pain has subsided. The vast majority of potential addicts are not suffering from painful illnesses at the time they initiate opioid use, and the term euphoria is probably not an apt description of Opioid Overdose Because of the common and particularly the illicit use of opioids, poisoning is a frequent occurrence. This happens also as a result of ingestion or injection with suicidal intent, errors in the calculation of dosage, the use of a substitute or contaminated street product, or unusual sensitivity. Children exhibit an increased susceptibility to opioids, so that relatively small doses may prove toxic. This is true also of adults with myxedema, Addison disease, chronic liver disease, and pneumonia. Acute poisoning may also occur in addicts who are unaware that available opioids vary greatly in potency and that tolerance for opioids declines quickly after the withdrawal of the drug; upon resumption of the habit, a formerly well-tolerated dose can be fatal. Varying degrees of unresponsiveness, shallow respirations, slow respiratory rate. In the most advanced stage, the pupils dilate, the skin and mucous membranes become cyanotic, and the circulation fails. The immediate cause of death is usually respiratory depression, with consequent asphyxia. Patients who suffer a cardiorespiratory arrest are sometimes left with all the known residua of anoxic encephalopathy. Mild degrees of intoxication are revealed by anorexia, nausea, vomiting, constipation, and loss of sexual interest. Treatment of Overdose this consists of the administration of naloxone (Narcan), or the longer acting nalmefene, both specific antidotes to the opiates and also to the synthetic analgesics. In cases of opioid poisoning, the improvements in circulation and respiration and reversal of miosis are usually dramatic. In fact, failure of naloxone to produce such a response should cast doubt on the diagnosis of opioid intoxication. If an adequate respiratory and pupillary response to naloxone is obtained, the patient should nonetheless be observed for up to 24 h and further doses of naloxone (50 percent higher than the ones previously found effective) can be given intramuscularly as often as necessary. Naloxone has less direct effect on consciousness, however, and the patient may remain drowsy for many hours. Although nalmefene has a plasma halflife of 11 h, compared to 60-90 min for naloxone, it has no clear advantage in emergency practice.

Infant mortality rates-Infant deaths in this report are tabulated by the race and Hispanic origin of the decedent. Live births, the denominators of infant mortality rates, are tabulated by race and Hispanic origin of mother. In 2017, multiple race was reported on the revised birth certificates of all 50 states, District of Columbia, Puerto Rico, U. Infant mortality rates for the Hispanic-origin population are based on numbers of resident infant deaths reported to be of Hispanic origin and numbers of resident live births by Hispanic origin of mother for the United States. In computing infant mortality rates, deaths and live births of unknown origin are not distributed among the specified Hispanic and non-Hispanic groups. In the United States in 2017, the percentage of infant deaths of unknown origin was 0. Small numbers of infant deaths for specific Hispanic-origin groups result in infant mortality rates subject to relatively large random variation (see "Random variation"). Infant mortality rates calculated from the general mortality file for specified race and Hispanic origin contain errors because of reporting problems that affect the classification of race and Hispanic origin on the birth and death certificates for the same infant. Infant mortality rates by specified race and Hispanic origin are more accurate when based on the linked file of infant deaths and live births (33). The linked file computes infant mortality rates using the race and Hispanic origin of the mother from the birth certificate in both the numerator and denominator of the rate. Life tables the life table provides a comprehensive measure of the effect of mortality on life expectancy. It is composed of sets of values showing the mortality experience of a hypothetical group of infants born at the same time and subject throughout their lifetime to the age-specific death rates of a particular time period, usually a given year. In addition, the age range for these life tables was limited to 5-year age groups ending with age group 85 and over. Beginning with final data reported for 2008 (68), the life table methodology was refined by changing the smoothing technique used to estimate the life table functions at the oldest ages. Beginning with the 2008 data year, the methodology used to produce the life tables does not model the probabilities of death beginning at age 66, but rather at ages above 85 or so. See "United States Life Tables, 2008" for a detailed description of the new methodology (69). Life expectancy values in this report for 2016 were revised using final Medicare data; therefore, these values may differ from those previously published (3). These methods that adjust for misclassification are applied to the production of the life tables, but not to the death rates shown throughout this report. Life tables by race and ethnicity are shown in this report with trend data from 2006 through 2017 (Table 4). Causes of death contributing to changes in life expectancy A life table partitioning technique was used to estimate causes of death contributing to changes in life expectancy in this report. In this framework, cause-of-injury deaths are organized principally by mechanism. The number of deaths for selected causes in this framework may differ from those shown in tables that use the standard mortality tabulation lists. For additional information on injury data presented in this framework, see the report, "Deaths: Injuries, 2002," available from. There are two sources of infant mortality data: a) the general mortality file and b) the linked file of live births and infant deaths.

The action potential produced by each motor unit is seen in the upper right: its duration is measured between the two vertical lines. In this myopathic unit, only two fibers remain active; the other three (shrunken) have been affected by one of the primary muscle diseases. Four fibers which originally belonged to other motor units and had been denervated have now been reinnervated by terminal sprouting from an undamaged axon. Note that only under these abnormal circumstances do fibers in the same unit lie next to one another. Complex repetitive discharges- formerly referred to as bizarre high-frequency discharges and, even earlier, as pseudomyotonia- consist of repetitive spontaneous potentials often having A B C D Figure 45-10. Calibrations: 5 ms (horizontal) and 1 mV in A and B; 5 mV in C; 100 mV in D (vertical). The Motor Unit Potential in Myopathy Diseases such as polymyositis, the muscular dystrophies, and other myopathies that randomly destroy muscle fibers or render them nonfunctional obviously reduce the population of muscle fibers per motor unit, as shown in. Both types of alterations produce a characteristic high-pitched crackling sound from the audio monitor that has been likened to rain falling on a tin roof. As mentioned earlier, fibrillation potentials, while typical of denervation, are sometimes seen in the myositides, inclusion-body myopathy, and the rapidly progressive muscular dystrophies, perhaps because of segmental necrosis of muscle fibers that isolates a segment of the fiber from its nerve supply. Electromyographic recordings of single muscle fibers belonging to the same motor unit disclose varying interpotential intervals on successive discharges; this phenomenon is called "jitter" and increases to the point of actual block, with deficits in neuromuscular transmission within a motor unit (see below and Chap. Abnormalities of the Interference Pattern Diseases that reduce the population of functional motor neurons or axons within the peripheral nerve decrease the number of motor units that can be recruited in the affected muscles. The decreased number of motor units available for activation then produce an incomplete interference pattern, which is manifest by a decreased number of units firing at a moderate to rapid rate. A severe reduction in the interference pattern may result in the recruitment of only a single unit. Structural damage to nerve as well as demyelinating block can produce this pattern of reduced recruitment; indeed a reduced recruitment pattern coupled with the absence of denervation indicates a conduction block. Nonetheless, each motor unit will consist of fewer muscle fibers than normal, so more motor units must be activated to reach a certain degree of force. A modest effort can thus produce a full interference pattern despite marked weakness (increased recruitment). Because fewer muscle fibers are firing, the amplitude of the pattern will be reduced from normal. This type of full, highly complex interference pattern of less than usual amplitude in the face of dramatic weakness is the hallmark of myopathy. Motor Unit Counting this experimental technique, developed by McComas and colleagues, estimates the size of motor units and is thus exquisitely sensitive to changes of denervation and reinnervation. It is carried out by applying a weak stimulus to a motor nerve or motor point and increasing it gradually as the evoked muscle response is recorded. Each quantal increase in the compound evoked response is presumed to be due to the addition of a single motor unit. In reinnervated muscles the additional units are reduced in number and are abnormally large. When a normal number and configuration of motor units is found, it has been helpful in distinguishing benign fasciculations from those of serious diseases. Fiber density is an index of the number and distribution of muscle fibers within a motor unit. Jitter is the variability of the interpotential interval of successive discharges of two single-muscle-fibers belonging to the same motor unit. This phenomenon is due largely to the very slight variability of delay at the branch points in the distal axon and by synaptic delay at the neuromuscular junction. Fiber density and jitter may, however, also be increased in neuropathic disorders that cause denervation with reinnervation. Testing for jitter is carried out by having the patient voluntarily contract a muscle to the slightest degree possible in order to activate only one motor unit (requiring a great deal of cooperation by the patient) or by stimulating an intramuscular nerve twig (requiring great patience on the part of the examiner). If the oscilliscope sweep is triggered by the firing of the first fiber, a fluctuating latency of the second fiber potential can be seen on the screen as a movement (jitter) of the second peak. The degree of jitter can be quantitated by measuring the interval between the activation of the two muscle fibers (the result of slightly differing lengths of the terminal axons) from which a mean interpeak interval is determined. Approximately 20 fiber pairs are sampled, and an average of the mean consecutive intervals can be derived. In a muscle such as the extensor digitorum communis, the average variation should be no more than 34 ms.