Sallie Bernard* Albert Enayati, B. S., Ch. E., M. S. M. E. Heidi Roger




НазваниеSallie Bernard* Albert Enayati, B. S., Ch. E., M. S. M. E. Heidi Roger
страница2/17
Дата30.09.2012
Размер0.74 Mb.
ТипДокументы
1   2   3   4   5   6   7   8   9   ...   17

(ii)

Unusual

Stereotyped sniffing (rats)

Stereotyped, repetitive behaviors

Behaviors

ADHD traits

ADHD traits




Agitation, unprovoked crying, grimacing, staring spells

Agitation, unprovoked crying, grimacing, staring spells




Sleep difficulties

Sleep difficulties




Eating disorders, feeding problems

Eating disorders, feeding problems




Self injurious behavior, e.g. head banging

Self injurious behavior, e.g. head banging










Visual

Poor eye contact, impaired visual fixation

Poor eye contact, problems in joint attention

Impairments

“Visual impairments,” blindness, near-sightedness, decreased visual acuity

“Visual impairments”; inaccurate/slow saccades; decreased rod functioning




Light sensitivity, photophobia

Over-sensitivity to light




Blurred or hazy vision

Blurred vision




Constricted visual fields

Not described










Physical Disturbances

Increase in cerebral palsy; hyper- or hypo-tonia; abnormal reflexes; decreased muscle strength, especially upper body; incontinence; problems chewing, swallowing, salivating

Increase in cerebral palsy; hyper- or hypotonia; decreased muscle strength, especially upper body; incontinence; problems chewing and swallowing




Rashes, dermatitis/dry skin, itching; burning

Rashes, dermatitis, eczema, itching




Autonomic disturbance: excessive sweating, poor circulation, elevated heart rate

Autonomic disturbance: unusual sweating, poor circulation, elevated heart rate










Gastro-intestinal

Gastroenteritis, diarrhea; abdominal pain, constipation, “colitis”

Diarrhea, constipation, gaseousness, abdominal discomfort, colitis

Disturbances

Anorexia, weight loss, nausea, poor appetite

Anorexia; feeding problems/vomiting




Lesions of ileum & colon; increases gut permeability

Leaky gut syndrome




Inhibits dipeptidyl peptidase IV, which cleaves casomorphin

Inadequate endopeptidase enzymes needed for breakdown of casein & gluten










Abnormal Biochemistry

Ties up -SH groups; blocks sulfate transporter in intestines, kidneys

Low sulfate levels




Has special affinity for purines & pyrimidines

Purine & pyrimidine metabolism errors lead to autistic features




Reduces availability of glutathione, needed in cells & liver to detoxify heavy metals

Low levels of glutathione; decreased ability of liver to detoxify heavy metals




Causes significant reduction in glutathione peroxidase and glutathione reductase

Abnormal glutathione peroxidase activities in erythrocytes




Disrupts mitochondrial activities, especially in brain

Mitochondrial dysfunction, especially in brain










Immune Dysfunction

Sensitivity due to allergic or autoimmune reactions; sensitive individuals more likely to have allergies, asthma, autoimmune-like symptoms, especially rheumatoid-like ones

More likely to have allergies and asthma; familial presence of autoimmune diseases, especially rheumatoid arthritis; IgA deficiencies




Can produce an immune response in CNS

On-going immune response in CNS




Causes brain/MBP autoantibodies

Brain/MBP autoantibodies present




Causes overproduction of Th2 subset; kills/inhibits lymphocytes, T-cells, and monocytes; decreases NK T-cell activity; induces or suppresses IFNg & IL-2

Skewed immune-cell subset in the Th2 direction; decreased responses to T-cell mitogens; reduced NK T-cell function; increased IFNg & IL-12




CNS Structural Pathology

Selectively targets brain areas unable to detoxify or reduce Hg-induced oxidative stress

Specific areas of brain pathology; many functions spared




Damage to Purkinje and granular cells

Damage to Purkinje and granular cells




Accummulates in amygdala and hippocampus

Pathology in amygdala and hippocampus




Causes abnormal neuronal cytoarchitecture; disrupts neuronal migration & cell division; reduces NCAMs

Neuronal disorganization; increased neuronal cell replication, increased glial cells; depressed expression of NCAMs




Progressive microcephaly

Progressive microcephaly and macrocephaly




Brain stem defects in some cases

Brain stem defects in some cases










Abnormalities in Neuro-chemistry

Prevents presynaptic serotonin release & inhibits serotonin transport; causes calcium disruptions

Decreased serotonin synthesis in children; abnormal calcium metabolism




Alters dopamine systems; peroxidine deficiency in rats resembles mercurialism in humans

Possibly high or low dopamine levels; positive response to peroxidine (lowers dopamine levels)




Elevates epinephrine & norepinephrine levels by blocking enzyme that degrades epinephrine

Elevated norepinephrine and epinephrine




Elevates glutamate

Elevated glutamate and aspartate




Leads to cortical acetylcholine deficiency; increases muscarinic receptor density in hippocampus & cerebellum

Cortical acetylcholine deficiency; reduced muscarinic receptor binding in hippocampus




Causes demyelating neuropathy

Demyelation in brain










EEG Abnormalities/

Causes abnormal EEGs, epileptiform activity

Abnormal EEGs, epileptiform activity

Epilepsy

Causes seizures, convulsions

Seizures; epilepsy




Causes subtle, low amplitude seizure activity

Subtle, low amplitude seizure activities










Population

Effects more males than females

Male:female ratio estimated at 4:1

Charact-eristics

At low doses, only affects those geneticially susceptible

High heritability - concordance for MZ twins is 90%




First added to childhood vaccines in 1930s

First "discovered" among children born in 1930s




Exposure levels steadily increased since 1930s with rate of vaccination, number of vaccines

Prevalence of autism has steadily increased from 1 in 2000 (1940s) to 1 in 500 (1990s)




Exposure occurs at 0 - 15 months; clinical silent stage means symptom emergence delayed; symptoms emerge gradually, starting with movement & sensation

Symptoms emerge from 4 months to 2 years old; symptoms emerge gradually, starting with movement & sensation



Table of Contents


Page

ABSTRACT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . i

Summary Chart of Comparisons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ii


INTRODUCTION
Autism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Mercury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Diagnosing Mercury Poisoning in Autism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2


I. SYMPTOM COMPARISON

a. Affect/Psychological Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

b. Language and Hearing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

c. Sensory Perception . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

d. Movement/Motor Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

e. Cognition/Mental Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

f. Behaviors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

g. Vision . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

h. Physical Presentations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

j. Gastrointestinal Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22


II. BIOLOGICAL ABNORMALITIES

a. Biochemistry . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . 24

b. Immune System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

c. CNS Structure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29

d. Neurons & Neurochemicals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33

e. EEG Activity/Epilepsy . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36


III. MECHANISMS, SOURCES & EPIDEMIOLOGY OF EXPOSURE

a. Exposure Mechanism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

b. Population Susceptibility . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .39

c. Sex Ratio . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

d. Exposure Levels & Autism Prevalence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

e. Genetic Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

f. Course of Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

g. Thimerosal Interaction with Vaccines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 44


IV. DETECTION OF MERCURY IN AUTISTIC CHILDREN

Case Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . .. . . . .. . . .. . . .. . . . . . . 47

Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . 52


DISCUSSION

Diagnostic Criteria Are Met . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54

Unique Form Would be Expected, Implicates Vaccinal Thimerosal. . . . . . . . . . . . . 54

Historical Precedent Exists . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55

Barriers Preventing Earlier Discovery Are Removed . . . . . . . . . . . . . . . . . . . . . . . . 56


MEDICAL & SOCIETAL IMPLICATIONS
Affected Population . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57
Other Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57

Vaccination Programs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57


INTRODUCTION


Autism

Autism, or Autistic Spectrum Disorder (ASD), is considered a neurodevelopmental syndrome, emerging early in life and exhibiting a constellation of seemingly unrelated features and a wide variation in symptom expression and level of severity by individual (Filipek et al, 1999; Bailey et al, 1996). The diagnostic criteria for autism are qualitative impairments in social relatedness, deficits in verbal and nonverbal communication, and the presence of repetitive and restricted behaviors or interests (APA, 1994). As will be cited below, other traits associated with autism are movement disorder, sensory dysfunction, and cognitive impairments as well as gastrointestinal difficulties and immune abnormalities (Gillberg & Coleman, 1992; Warren et al, 1990; Horvath et al, 1999). Onset must occur before age 36 months (APA, 1994); although in some instances deficits are apparent at birth, in the great majority of cases there are at least several months of normal development followed by clear regression or failure to progress normally (Gillberg & Coleman, 1992; Filipek et al, 1999; Bailey et al, 1996). Formerly regarded as a rare disease, autism is now said to affect one in 500 children (Bristol et al, 1996), with some estimates suggesting one in 100 for a broader phenotype often labeled as the “autism-spectrum” of disorders and which includes both higher and lower functioning individuals (Arvidsson et al, 1997; Wing, 1996).


Autism and autistic symptoms can arise from a number of known disorders, most notably tuberous sclerosis, Rhett syndrome, Landau-Kleffner syndrome, Fragile X, Phenylketonuria, purine autism, and other purine metabolic diseases such as PRPP synthetase defects and 5’-nucleotidase superactivity. The etiology and pathogenesis of the vast majority of autism cases – 70% - 90% (Gillberg and Coleman, 1992; Bailey et al, 1996) – remain unexplained, however, despite ASD being “one of the most extensively studied disorders in child psychiatry today” (Malhotra and Gupta, 1999). Nevertheless, there is general agreement that most cases of autism arise “from the interaction of an early environmental insult and a genetic predisposition” (Trottier et al, 1999; Bristol et al, 1996).


Mercury

A heavy metal, mercury (Hg) is widely considered one of the most toxic substances on earth (Clarkson, 1997). Instances of Hg poisoning or “mercurialism” have been described since Roman times. The Mad Hatter in Alice in Wonderland was a victim of occupational exposure to mercury vapor, referred to as “Mad Hatter’s Disease.” Further human data has been derived from instances of widespread poisonings during the 20th Century. These misfortunes include an outbreak in Minamata, Japan, caused by consumption of contaminated fish and resulting in “Minamata Disease;” outbreaks in Iraq, Guatemala and Russia due to ingestion of contaminated seed grains; and, in the first half of the century, poisoning of infants and toddlers by mercury in teething powders, leading to acrodynia or Pink Disease. Besides these epidemics, numerous instances of individual or small group cases of Hg intoxication and subsequent phenotype are described in the literature.


The constellation of mercury-induced symptoms varies enormously from individual to individual. The diversity of disease manifestations derives from a number of interacting variables which are summarized in Table I. The variables which affect phenotype include an individual’s age, the total dosage, dose rate, duration of exposure, type of mercury, routes of exposure such as inhaled, subcutaneous, oral, or intramuscular, and, most importantly, by individual sensitivity arising from immune and genetic factors (Dales, 1972; Koos and Longo, 1976; Matheson et al, 1980; Eto et al, 1999; Feldman, 1982; Warkany and Hubbard, 1953).


Table I: Summary of Mercury Exposure Variables

Leading to Diverse & Non-Specific Symptomatology


Variable

Level of Variable

Exposure Amount

Ranges from high doses, leading to death or near death with severe impairments, to low “safe” doses, leading to subtle neurological and other physical impairments

Duration of exposure

One time vs. multiple times over the course of weeks, months, or years

Dose rate

Bolus dose, daily dose

Individual sensitivity

A function of (a) the age at which exposure occurs, that is, prenatal, infant, child, adolescent, or adult, (b) genetically determined reactivity to mercury, and (c) gender

Common types of mercury

The organic alkyl forms – methylmercury and ethylmercury; and inorganic forms - metallic mercury, elemental (liquid) mercury, and ionic mercury/mercuric salt

Primary routes of exposure

Inhalation of mercury vapors, orally through the intestinal tract, subcutaneous and intramuscular injections, topically through ear drops, teething powders, skin creams and ointments, and intravenously during medical treatments


While these variations in exposure, individual status, and genotype give rise to a diverse clinical phenotype, there are nevertheless obvious commonalities across all mercury-caused disorders. Thus, for example, victims will almost always develop a movement disorder, but in some individuals this may manifest as mere clumsiness, while others will develop severe involuntary jerking movements. Likewise, psychological disturbances are usually present, but in some individuals these might manifest as anxiety while in others it might present as aggression or irritability.


Diagnosing Mercury Poisoning in Autism

Mercury poisoning can be difficult to diagnose and is often interpreted by clinicians as a psychiatric disorder, especially if exposure is not suspected (Diner and Brenner, 1998; Frackelton and Christensen, 1998). The difficulty in diagnosis derives primarily from two notable characteristics of this heavy metal. First, there can be a long latent period between time of exposure and onset of overt symptoms, so that the connection between the two events is often overlooked. The latency period is discussed in more detail below. Second, the diverse manifestations of the disease make it difficult for the clinician to find a precise match of his particular patient’s symptoms with those described in other case reports (Adams et al, 1983, Kark et al, 1971; Florentine and Sanfilippo, 1991; Matheson et al, 1980; Frackelton and Christensen, 1998; Warkany & Hubbard, 1953).


Due to the difficulty of diagnosing mercurialism based on presentation of non-specific symptoms alone, clinicians have come to rely on the following criteria (Warkany & Hubbard, 1953; Vroom and Greer, 1972).


1. Observation of impairments in many but not all of the following domains: (a) movement/motor disorder, (b) sensory abnormalities, (c) psychological and behavioral disturbances, (d) neurological and cognitive deficits, (e) impairments in language, hearing, and vision, and (f) miscellaneous physical presentations such as rashes or unusual reflexes (Adams et al, 1983; Snyder, 1972; Vroom & Greer, 1972).


2. Known exposure to Hg (a) at a level that has been documenting as causing impairment in similar individuals under similar circumstances, and (b) at approximately the same time as the symptoms emerge, with allowances given for the latency period (Ross et al, 1977; Amin-Zaki et al, 1978). It should be noted that the dose which is considered “toxic” vs. “safe” is unresolved among toxicologists; some researchers feel that any amount of exposure is “unsafe” (see EPA, 1997, pp.6-47 to 6-59, for dose discussion).


3. Detectable levels of mercury in urine, blood, or hair (Florentine and Sanfilippo, 1991; Frackelton and Christensen, 1998; EPA, 1997, p.ES-2). Importantly, because mercury can clear from biologic samples before the patient feels symptoms or is tested, the lack of detectable mercury is not cause for ruling out mercury poisoning; and conversely, detectable levels have been observed in unaffected individuals (Adams et al, 1983; Warkany & Hubbard, 1953; Cloarec, 1995).


4. Improvement in symptoms after chelation. While many patients’ symptoms resolve with chelation, some clearly poisoned individuals do not improve. Other exposed subjects have also been known to improve without intervention (Vroom & Greer, 1972; Warkany & Hubbard, 1953).


Thus, none of these criteria is sufficient on its own for a certain diagnosis. Rather, observed effects within two or three domains are generally required. This paper, which reviews and compares the extensive literature available on both ASD and mercury, provides citations documenting that, based on these four diagnostic criteria, many if not most cases of autism meet the requirements for mercury poisoning. In fact, this review and its citations (i) delineate a single mechanism for inducing all of the primary domains of impairment and biological abnormalities in autism, including its genetic component, prevalence levels, and sex ratios; and (ii) identify that mechanism as arising from the “environmental insult” of early childhood exposure to mercury. Furthermore, the route of exposure is thimerosal, which is 50% ethylmercury by weight and which is a preservative used in many childhood vaccines.


We are not suggesting that the previous reports of mercurialism described in the literature are in fact cases of autism; rather, we claim that autism represents its own unique form of Hg poisoning, just like acrodynia, Minamata disease, and Mad Hatter's disease represent distinct yet closely related presentations of mercurialism. A unique expression would be expected in cases of autism, given that the effects of repeated vaccinal administration of ethylmercury to infants and toddlers have never been described before in mercury-related literature. We maintain that the diverse phenotype that is autism matches the diverse phenotype that is mercurialism to a far greater degree that could reasonably be expected to occur by chance. Given the known exposure to mercury via vaccination of autistic children and the presence of mercury found in biologic samples from a number of autistic subjects, also described here, we are confident that our claim is substantiated. Our paper discusses some important medical and societal ramifications of this conclusion.


I. SYMPTOM COMPARISON


The overt symptoms of ASD and mercury poisoning, described in the literature and presented here, are strikingly similar. Summary tables have been provided after each section to aid in symptom comparisons.


a. Affect/Psychological Presentation

Since its initial description in 1943 by Leo Kanner, a psychiatrist, autism has been defined primarily as a psychiatric condition. One of the three requirements for diagnosis is a severe deficit in social interactions (APA, 1994). Self and parental reports describe children and adults who prefer to be alone and who will withdraw to their rooms if given the chance (MAAP, 1996-1999). Even high functioning autistics tend to be aloof, have poor social skills, are unable to make friends, and find conversation difficult (Tonge et al, 1999; Capps et al, 1998). Face recognition and what psychologists call "theory of mind" are impaired (Klin et al, 1999, Baron-Cohen et al, 1993). Poor eye contact or gaze avoidance is present in most cases, especially in infancy and childhood (Bernabei et al, 1998).


The second psychobehavioral diagnostic characteristic of autism is the presence of repetitive, stereotyped activities and the need for sameness (APA, 1994). Traits in this domain strongly resemble obsessive-compulsive tendencies in both thought and behavior (Lewis, 1996; Gillberg & Coleman, 1992, p.27), especially as the individual becomes more high functioning (Roux et al, 1998): "it [is] very difficult…to distinguish between obsessive ideation and the bizarre preoccupations so commonly seen in autistic individuals" (Howlin, 2000). Serotonin uptake inhibitors known to be effective for OCD also reduce repetitive behaviors in some autistic patients (Lewis, 1996). Most autistic subjects - 84% in one study - show high levels of anxiety and meet diagnostic criteria for anxiety disorder (Muris et al, 1998).


ASD has been linked to depression, based on symptoms, familial history of depression and the positive response to SSRIs among many autistics (Clarke et al, 1999; DeLong, 1999; Piven and Palmer, 1999). One subset of autistics has been described as “passive”, with flat affect, “absence of facial expression,” lack of initiative, and diminished outward emotional reactions. Some autistics have a strong family history of manic depression and mood swings, and, among those who are verbal, psychotic talk is frequently observed (Plioplys, 1989). Autism is also said to strongly resemble childhood schizophrenia. In the past it was often misdiagnosed as such (Gillberg & Coleman, 1992, p.100), and there are a number of instances of dual ASD-schizophrenia diagnoses in the literature (Clarke et al, 1999). Furthermore, irrational fears, aggressive behaviors, and severe temper tantrums are common (Muris et al, 1998; McDougle et al, 1994), as are chronic hyperarousal and irritability (Jaselskis et al, 1992). “Inexplicable changes of mood can occur, with giggling and laughing or crying for no apparent reason” (Wing & Attwood, 1987).


Mercury poisoning, when undetected, is often initially diagnosed as a psychiatric disorder in both children and adults (Fagala and Wigg, 1992). Common psychiatric symptoms are (a) depression, including “lack of interest” and “mental confusion;” (b) "extreme shyness," indifference to others, active avoidance of others or “a desire to be alone”; (c) irritability in adults and tantrums in children; and (d) anxiety and fearfulness. Neurosis, including schizoid and obsessive-compulsive traits, has been reported in a number of cases (Fagala and Wigg, 1992; Kark et al, 1971; O’Carroll et al, 1995; Florentine and Sanfilippo, 1991; Amin-Zaki, 1974 and 1979; Matheson et al, 1980; Joselow et al, 1972; Smith, 1972; Lowell, 1996; Tuthill, 1899; Clarkson, 1997; Camerino et al, 1981; Grandjean et al, 1997; Piikivi et al, 1984; Rice, 1996; Vroom & Greer, 1972; Adams et al, 1973; Hua et al, 1996).


Juvenile monkeys prenatally exposed to mercury exhibit decreased social play and increased passive behavior (Gunderson et al, 1986, 1988), as well as impaired face recognition (Rice, 1996). Humans exposed to mercury vapor also perform poorly on face recognition tests and may present with a “mask face” (Vroom & Greer, 1972); emotional instability can occur in children and adults exposed to Hg. For instance, Iraqi children poisoned by methylmercury had a tendency “to cry, laugh, or smile without obvious provocation” (Amin-Zaki et al, 1974 & 1979), like the autistic group described by Wing and Attwood (1987).


Table II: Summary of Psychiatric Disturbances
Found in Autism & Mercury Poisoning



Mercury Poisoning

Autism

Extreme shyness, social withdrawal, feeling overly sensitive, introversion

Social deficits, social withdrawal, self reports of extreme shyness, aloofness

Mood swings; flat affect; mask face; laughing or crying without provocation; episodes of hysteria

Mood swings; flat affect in some; no facial expression; laughing or crying without reason

Anxiety; nervousness; tremulousness; somatization of anxious feelings

Anxiety, nervousness; anxiety disorder

Schizoid tendencies, neurosis, obsessive-compulsive traits, repetitive dreams

Schizophrenic traits; OCD traits; repetitive behaviors and thoughts

Lack of eye contact; being less talkative; hesitancy to engage others

Lack of eye contact, gaze avoidance; avoids conversation

Depression, lack of interest in life, lassitude, fatigue, apathy; feelings of hopelessness; melancholy

Association with depression; lack of initiative, diminished outward emotions

On the one hand, less overtly active, unwilling to go outside or be with others; on the other hand, increased restlessness

Tendency to withdraw, especially to own rooms, prefer to be alone; hyperactivity

Irrational fears

Irrational fears

Irritability, anger, and aggression; in children this may manifest as frequent and severe temper tantrums

Irritability and aggression; severe temper tantrums in children

Psychotic episodes; hallucinations, hearing voices; paranoid thoughts

Psychotic talk, paranoid thoughts

Impaired face recognition

Impaired face recognition


Since traditionally autism has been characterized and studied by researchers primarily in psychiatric terms, providing case studies illustrating the psychiatric aspects of ASD and of mercurialism are necessary in establishing the similarities of the two disorders on this critical domain. Also included is a comparison of "Lenny," an autistic adult described by Rhea Paul (1987), and the Mad Hatter from Alice in Wonderland, considered to be an accurate portrayal of victims of the disease. Of particular relevance in all these cases are social withdrawal and deficits in social communication, traits (i) always prominent in autism and (ii) clearly associated with mercurialism.

Case Studies: Autism


“I am 18 years old. My parents found out I was autistic when I was 18 months old. My parents said I banged my head a lot when I got frustrated when I was young. Head banging motions help me deal with nervousness. I also take 2 medications to help me cope with stress. I have very few friends. It is also somewhat painful for me to look people in the eye. This sometimes makes people think I am not paying attention” (The MAAP, Vol. II, 1997).


“I have a high-functioning autistic eight-year-old boy. My mistake was putting him in the second grade with a teacher who was determined to ‘socialize’ him. After three months, the anxiety proved to be too great for him. He spent a lot of time crying, withdrawing to his room, becoming compulsive and belligerent. In another era, he would have been seen as having a ‘nervous breakdown’” (The MAAP, Vol. II, 1997).


“I am writing regarding our 25 year old son who was diagnosed only a few months ago as having Asperger’s Syndrome. All his life he displayed the ‘classic’ symptoms of Asperger’s (lack of social skills, disorganization, anxiety, etc.). A few months ago, he became clinically depressed, phobic about being around people for fear of more rejection or being laughed at. He now has obsessive thoughts that our home is electronically ‘bugged’ and all his actions are being observed and belittled” (The MAAP, Vol. II, 1997).


“Several people have asked me what it’s like to have Asperger’s Syndrome. Today, I still prefer to work on my computer or with electronics rather than socialize. I’ve never been able to tolerate any kind of physical contact or intimacy. I like wrestling and rough-housing, but I hate being caressed or held.” (The MAAP, Vol. II, 1997).


“My son Brian is a 6-year-old with high functioning autism. Our main problem now is his rigidity and obsessive/compulsive behaviors. He gets extremely upset when activities don’t go as he thinks they should. He first gets mad, screaming and yelling, then begins to obsessively talk about how he can remedy the situation, then often begins to cry uncontrollably. These tantrums can go on for hours” (The MAAP, Vol. IV, 1996).


“[I’m] age 12½. I have Autism/PDD. I don’t really know any real social skills, though my brother Isaiah says I am a social outcast. I do have trouble making new friends because I get real shy and nervous” (The MAAP, Vol. IV, 1997).


“I am the mother of three autistic boys. Nate was considered very shy. Poor eye contact but very smart and doing well in school. Nate was also diagnosed with Hypotonia of the face (which answered all the mumbling he did wasn’t just shyness) and extremities” (The MAAP, Vol. III, 1999)


“I spent many hours sitting in the trees or under the bed or in a dark closet. I had a loud flat voice. Socialization has always been beyond me” (The MAAP, Vol. II, 1998).


“I sit in my room a prisoner to my autism. Mom and sis doing their loving best to get me out. I wanted to get out – really get out. I wanted to love, to feel, to connect. But, I couldn’t. I was stuck. I was slowly dying. There were days I truly wanted to end it all. If any days were good, I didn’t deserve it. I shouldn’t be happy. Autism teaches you that – because it’s a life sentence” (The MAAP, Vol. VI, 1996).

1   2   3   4   5   6   7   8   9   ...   17

Похожие:

Sallie Bernard* Albert Enayati, B. S., Ch. E., M. S. M. E. Heidi Roger iconArrizabalaga, Heidi Pattern and Palette Sourcebook a complete Guide to Choosing the Perfect Color and Pattern in Design / Heidi Arrizabalaga. Rockport
Цветочный орнамент / textes Clara Schmidt, Helene Franchi; William Wheeler; O. L. and Co.; Najjia Zegoudh; Olga Nazarova. L'Aventurine,...
Sallie Bernard* Albert Enayati, B. S., Ch. E., M. S. M. E. Heidi Roger iconThe ghost of Roger Casement Is beating on the door. W. B. Yeats, “The Ghost of Roger Casement” What symbol are you in this dance of death? What is your relevance?

Sallie Bernard* Albert Enayati, B. S., Ch. E., M. S. M. E. Heidi Roger iconC. V. of Roger L. Boyell, Page of Roger L. Boyell, electronics analyst

Sallie Bernard* Albert Enayati, B. S., Ch. E., M. S. M. E. Heidi Roger iconPygmalion by George Bernard Shaw

Sallie Bernard* Albert Enayati, B. S., Ch. E., M. S. M. E. Heidi Roger iconChakats © Bernard Doove/Chakat Goldfur used with permission

Sallie Bernard* Albert Enayati, B. S., Ch. E., M. S. M. E. Heidi Roger iconThe Project Gutenberg ebook of George Bernard Shaw, by Gilbert K. Chesterton

Sallie Bernard* Albert Enayati, B. S., Ch. E., M. S. M. E. Heidi Roger iconTake a look at Roger Ebert's 2002

Sallie Bernard* Albert Enayati, B. S., Ch. E., M. S. M. E. Heidi Roger icon) stars as a very animated Heidi who is unfairly separated from her loving grandfather (Burl Ives), and forced to live with a gaggle of despicable relatives in

Sallie Bernard* Albert Enayati, B. S., Ch. E., M. S. M. E. Heidi Roger iconRoger Stelljes. Smashwords Edition

Sallie Bernard* Albert Enayati, B. S., Ch. E., M. S. M. E. Heidi Roger iconTranslated by Albert Tezla

Разместите кнопку на своём сайте:
Библиотека


База данных защищена авторским правом ©lib.znate.ru 2014
обратиться к администрации
Библиотека
Главная страница