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Autism: a Novel
Form of Mercury Poisoning S. Bernard, B.A.,
A. Enayati, M.S.M.E., L. Redwood, M.S.N., H. Roger, B.A., T. Binstock
Sallie Bernard, ARC Research, 14 Commerce Drive, Cranford, NJ 07901 USA, 908 276-6300,
fax 908 276-1301
INTRODUCTION
Autistic Spectrum Disorder (ASD) is a neurodevelopmental syndrome with onset prior to
age 36 months. Diagnostic criteria consist of impairments in sociality and communication
plus repetitive and stereotypic behaviors (1). Traits strongly associated with autism
include movement disorders and sensory dysfunctions (2). Although autism may be apparent
soon after birth, most autistic children experience at least several months, even a year
or more of normal development -- followed by regression, defined as loss of function or
failure to progress (2,3,4).
The neurotoxicity of mercury (Hg) has long been recognized (5). Primary data derive
from victims of contaminated fish (Japan – Minamata Disease) or grain (Iraq,
Guatemala, Russia); from acrodynia (Pink Disease) induced by Hg in teething powders; and
from individual instances of mercury poisoning (HgP), many occurring in occupational
settings (e.g., Mad Hatter's Disease). Animal and in vitro studies also provide
insights into the mechanisms of Hg toxicity. More recently, the Food and Drug
Administration (FDA) and the American Academy of Pediatrics (AAP) have determined that the
typical amount of Hg injected into infants and toddlers via childhood immunizations has
exceeded government safety guidelines on an individual (6) and cumulative vaccine basis
(7). The mercury in vaccines derives from thimerosal (TMS), a preservative which is 49.6%
ethylmercury (eHg) (7).
Past cases of HgP have presented with much inter-individual variation, depending on the
dose, type of mercury, method of administration, duration of exposure, and individual
sensitivity. Thus, while commonalities exist across the various instances of HgP, each set
of variables has given rise to a different disease manifestation (8,9,10,11). It is
hypothesized that the regressive form of autism represents another form of mercury
poisoning, based on a thorough correspondence between autistic and HgP traits and
physiological abnormalities, as well as on the known exposure to mercury through vaccines.
Furthermore, other phenomena are consistent with a causal Hg-ASD relationship. These
include (a) symptom onset shortly after immunization; (b) ASD prevalence increases
corresponding to vaccination increases; (c) similar sex ratios of affected individuals;
(d) a high heritability rate for autism paralleling a genetic predisposition to Hg
sensitivity at low doses; and (e) parental reports of autistic children with elevated Hg.
TRAIT COMPARISON
ASD manifests a constellation of symptoms with much inter-individual variation (3,4). A
comparison of traits defining, nearly universal to, or commonly found in autism with those
known to arise from mercury poisoning is given in Table I. The characteristics defining or
strongly associated with autism are also more fully described.
Autism has been conceived primarily as a psychiatric condition; and two of its three
diagnostic criteria are based upon the observable traits of (a) impairments in sociality,
most commonly social withdrawal or aloofness, and (b) a variety of perseverative or
stereotypic behaviors and the need for sameness, which strongly resemble
obsessive-compulsive tendencies. Differential diagnosis may include childhood
schizophrenia, depression, obsessive-compulsive disorder (OCD), anxiety disorder, and
other neuroses. Related behaviors commonly found in ASD individuals are irrational fears,
poor eye contact, aggressive behaviors, temper tantrums, irritability, and inexplicable
changes in mood (1,2,12-17). Mercury poisoning, when undetected, is often initially
diagnosed as a psychiatric disorder (18). Commonly occurring symptoms include (a)
"extreme shyness," indifference to others, active avoidance of others, or
"a desire to be alone"; (b) depression, "lack of interest" and
"mental confusion;" (c) irritability, aggression, and tantrums in children and
adults; (d) anxiety and fearfulness; and (e) emotional lability. Neuroses, including
schizoid and obsessive-compulsive traits, problems in inhibition of perseveration, and
stereotyped behaviors, have been reported in a number of cases; and lack of eye contact
was observed in one 12 year old girl with mercury vapor poisoning (18-35).
The third diagnostic criterion for ASD is impairment in communication (1).
Historically, about half of those with classic autism failed to develop meaningful speech
(2), and articulation difficulties are common (3). Higher functioning individuals may have
language fluency but still show semantic and pragmatic errors (3,36). In many cases of
ASD, verbal IQ is lower than performance IQ (3). Similarly, mercury-exposed children and
adults show a marked difficulty with speech (9,19,37). In milder cases scores on language
tests may be lower than those of unexposed controls (31,38). Iraqi children who were
postnatally poisoned developed articulation problems, from slow, slurred word production
to an inability to generate meaningful speech; while Iraqi babies exposed prenatally
either failed to develop language or presented with severe language deficits in childhood
(23,24,39). Workers with Mad Hatter's disease had word retrieval and articulation
difficulties (21).
Nearly all cases of ASD and HgP involve disorders of physical movement (2,30,40).
Clumsiness or lack of coordination has been described in many higher functioning ASD
individuals (41). Infants and toddlers later diagnosed with autism may fail to crawl
properly or may fall over while sitting or standing; and the movement disturbances
typically occur on the right side of the body (42). Problems with intentional movement and
imitation are common in ASD, as are a variety of unusual stereotypic behaviors such as toe
walking, rocking, abnormal postures, choreiform movements, spinning; and hand flapping
(2,3,43,44). Noteworthy because of similarities to autism are reports in Hg literature of
(a) children in Iraq and Japan who were unable to stand, sit, or crawl (34,39); (b)
Minamata disease patients whose movement disturbances were localized to one side of the
body, and a girl exposed to Hg vapor who tended to fall to the right (18,34); (c) flapping
motions in an infant poisoned from contaminated pork (37) and in a man injected with
thimerosal (27); (d) choreiform movements in mercury vapor intoxication (19); (e) toe
walking in a moderately poisoned Minamata child (34); (f) poor coordination and clumsiness
among victims of acrodynia (45); (g) rocking among infants with acrodynia (11); and (h)
unusual postures observed in both acrodynia and mercury vapor poisoning (11,31). The
presence of flapping motions in both diseases is of interest because it is such an unusual
behavior that it has been recommended as a diagnostic marker for autism (46).
Virtually all ASD subjects show a variety of sensory abnormalities (2). Auditory
deficits are present in a minority of individuals and can range from mild to profound
hearing loss (2,47). Over- or under-reaction to sound is nearly universal (2,48), and
deficits in language comprehension are often present (3). Pain sensitivity or
insensitivity is common, as is a general aversion to touch; abnormal sensation in the
extremities and mouth may also be present and has been detected even in toddlers under 12
months old (2,49). There may be a variety of visual disturbances, including sensitivity to
light (2,50,51,52). As in autism, sensory issues are reported in virtually all instances
of Hg toxicity (40). HgP can lead to mild to profound hearing loss (40); speech
discrimination is especially impaired (9,34,). Iraqi babies exposed prenatally showed
exaggerated reaction to noise (23), while in acrodynia, patients reported noise
sensitivity (45). Abnormal sensation in the extremities and mouth is the most common
sensory disturbance (25,28). Acrodynia sufferers and prenatally exposed Iraqi babies
exhibited excessive pain when bumping limbs and an aversion to touch (23,24,45,53). A
range of visual problems has been reported, including photophobia (18,23,34).
COMPARISON OF BIOLOGICAL ABNORMALITIES
The biological abnormalities commonly found in autism are listed in Table II, along
with the corresponding pathologies arising from mercury exposure. Especially noteworthy
similarities are described.
Autism is a neurodevelopmental disorder which has been characterized as "a
disorder of neuronal organization, that is, the development of the dentritic tree,
synaptogenesis, and the development of the complex connectivity within and between brain
regions" (54). Depressed expression of neural cell adhesion molecules (NCAMs), which
are critical during brain development for proper synaptic structuring, has been found in
one study of autism (55). Organic mercury, which readily crosses the blood-brain barrier,
preferentially targets nerve cells and nerve fibers (56); primates accumulate the highest
Hg-levels in the brain relative to other organs (40). Furthermore, although most cells
respond to mercurial injury by modulating levels of glutathione (GSH), metallothionein,
hemoxygenase, and other stress proteins, neurons tend to be "markedly deficient in
these responses" and thus are less able to remove Hg and more prone to Hg-induced
injury (56). In the developing brain, mercury interferes with neuronal migration,
depresses cell division, disrupts microtubule function, and reduces NCAMs (28,57-59).
While damage has been observed in a number of brain areas in autism, many nuclei and
functions are spared (36). HgP’s damage is similarly selective (40). Numerous studies
link autism with neuronal atypicalities within the amygdala, hippocampi, basal ganglia,
the Purkinje and granule cells of the cerebellum, brainstem, basal ganglia, and cerebral
cortex (36,60-69). Each of these areas can be affected by HgP (10,34,40,70-73). Migration
of Hg, including eHg, into the amygdala is particularly noteworthy, because in primates
this brain region has neurons specific for eye contact (74) and it is implicated in autism
and in social behaviors (65,66,75).
Autistic brains show neurotransmitter irregularities which are virtually identical to
those arising from Hg exposure: both high or low serotonin and dopamine, depending on the
subjects studied; elevated epinephrine and norepinephrine in plasma and brain; elevated
glutamate; and acetylcholine deficiency in hippocampus (2,21,76-83).
Gillberg and Coleman (2) estimate that 35-45% of autistics eventually develop epilepsy.
A recent MEG study reported epileptiform activity in 82% of 50 regressive autistic
children; in another study, half the autistic children expressed abnormal EEG activity
during sleep (84). Autistic EEG abnormalities tend to be non-specific and have a variety
of patterns (85). Unusual epileptiform activity has been found in a number of mercury
poisoning cases (18,27,34,86-88). Early mHg exposure enhances tendencies toward
epileptiform activity with a reduced level of seizure-discharge amplitude (89), a finding
consistent with the subtlety of seizures in many autism spectrum children (84,85). The
fact that Hg increases extracellular glutamate would also contribute to epileptiform
activity (90).
Some autistic children show a low capacity to oxidize sulfur compounds and low levels
of sulfate (91,92). These findings may be linked with HgP because (a) Hg preferentially
binds to sulfhydryl molecules (-SH) such as cysteine and GSH, thereby impairing various
cellular functions (40), and (b) mercury can irreversibly block the sulfate transporter
NaSi cotransporter NaSi-1, present in kidneys and intestines, thus reducing sulfate
absorption (93). Besides low sulfate, many autistics have low GSH levels, abnormal
GSH-peroxidase activity within erythrocytes, and decreased hepatic ability to detoxify
xenobiotics (91,94,95). GSH participates in cellular detoxification of heavy metals (96);
hepatic GSH is a primary substrate for organic-Hg clearance from the human (40); and
intraneuronal GSH participates in various protective responses against Hg in the CNS (56).
By preferentially binding with GSH, preventing absorption of sulfate, or inhibiting the
enzymes of glutathione metabolism (97), Hg might diminish GSH bioavailability. Low GSH can
also derive from chronic infection (98,99), which would be more likely in the presence of
immune impairments arising from mercury (100). Furthermore, mercury disrupts purine and
pyrimidine metabolism (97,10). Altered purine or pyrimidine metabolism can induce autistic
features and classical autism (2,101,102), suggesting another mechanism by which Hg can
contribute to autistic traits.
Autistics are more likely to have allergies, asthma, selective IgA deficiency (sIgAd),
enhanced expression of HLA-DR antigen, and an absence of interleukin-2 receptors, as well
as familial autoimmunity and a variety of autoimmune phenomena. These include elevated
serum IgG and ANA titers, IgM and IgG brain antibodies, and myelin basic protein (MBP)
antibodies (103-110). Similarly, atypical responses to Hg have been ascribed to allergic
or autoimmune reactions (8), and genetic predisposition to such reactions may explain why
Hg sensitivity varies so widely by individual (88,111). Children who developed acrodynia
were more likely to have asthma and other allergies (11); IgG brain autoantibodies, MBP,
and ANA have been found in HgP subjects (18,111,112); and mice genetically prone to
develop autoimmune diseases "are highly susceptible to mercury-induced
immunopathological alterations" even at the lowest doses (113). Additionally, many
autistics have reduced natural killer cell (NK) function, as well as immune-cell subsets
shifted in a Th2 direction and increased urine neopterin levels, indicating immune system
activiation (103,114-116). Depending upon genetic predisposition, Hg can induce immune
activation, an expansion of Th2 subsets, and decreased NK activity (117-120).
POPULATION CHARACTERISTICS
In most affected children, autistic symptoms emerge gradually, although there are cases
of sudden onset (3). The earliest abnormalities have been detected in 4 month olds and
consist of subtle movement disturbances; subtle motor-sensory disturbances have been
observed in 9 month olds (49). More overt speech and hearing difficulties become
noticeable to parents and pediatricians between 12 and 18 months (2). TMS vaccines have
been given in repeated intervals starting from infancy and continuing until 12 to 18
months. While HgP symptoms, may arise suddenly in especially sensitive individuals (11),
usually there is a preclinical "silent stage" in which subtle neurological
changes are occuring (121) and then a gradual emergence of symptoms. The first symptoms
are typically sensory- and motor-related, which are followed by speech and hearing
deficits, and finally the full array of HgP characteristics (40). Thus, both the timing
and nature of symptom emergence in ASD are fully consistent with a vaccinal Hg etiology.
This parallel is reinforced by parental reports of excessive amounts of mercury in urine
or hair from younger autistic children, as well as some improvement in symptoms with
standard chelation therapy (122).
The discovery and rise in prevalence of ASD mirrors the introduction and spread of TMS
in vaccines. Autism was first described in 1943 among children born in the 1930s (123).
Thimerosal was first introduced into vaccines in the 1930s (7). In studies conducted prior
to 1970, autism prevalence was estimated, at 1 in 2000; in studies from 1970 to 1990 it
averaged 1 in 1000 (124). This was a period of increased vaccination rates of the
TMS-containing DPT vaccines among children in the developed world. In the early 1990s, the
prevalence of autism was found to be 1 in 500 (125), and in 2000 the CDC found 1 in 150
children affected in one community, which was consistent with reports from other areas in
the country (126). In the late 1980s and early 1990s, two new TMS vaccines, the HIB and
Hepatitis B, were added to the recommended schedule (7).
Nearly all US children are immunized, yet only a small proportion develop autism. A
pertinent characteristic of mercury is the great variability in its effects by individual,
so that at the same exposure level, some will be affected severely while others will be
asymptomatic (9,11,28). An example is acrodynia, which arose in the early 20th
Century from mercury in teething powders and afflicted only 1 in 500-1000 children given
the same low dose (28). Studies in mice as well as humans indicate that susceptibility to
Hg effects arises from genetic status, in some cases including a propensity to autoimmune
disorders (113,34,40). ASD exhibits a strong genetic component, with high concordance in
monozygotic twins and a higher than expected incidence among siblings (4); autism is also
more prevalent in families with autoimmune disorders (106).
Additionally, autism is more prevalent among boys than girls, with the
ratio estimated at 4:1 (2). Mercury studies in mice and humans consistently report greater
effects on males than females, except for kidney damage (57). At high doses, both sexes
are affected equally; at low doses only males are affected (38,40,127).
DISCUSSION
We have shown that every major characteristic of autism has been exhibited in at least
several cases of documented mercury poisoning. Recently, the FDA and AAP have revealed
that the amount of mercury given to infants from vaccinations has exceeded safety levels.
The timing of mercury administration via vaccines coincides with the onset of autistic
symptoms. Parental reports of autistic children with measurable mercury levels in hair and
urine indicate a history of mercury exposure. Thus the standard primary criteria for a
diagnosis of mercury poisoning - observable symptoms, known exposure at the time of
symptom onset, and detectable levels in biologic samples (11,31) - have been met in
autism. As such, mercury toxicity may be a significant etiological factor in at least some
cases of regressive autism. Further, each known form of HgP in the past has resulted in a
unique variation of mercurialism – e.g., Minamata disease, acrodynia, Mad
Hatter’s disease – none of which has been autism, suggesting that the Hg source
which may be involved in ASD has not yet been characterized; given that most infants
receive eHg via vaccines, and given that the effect on infants of eHg in vaccines has
never been studied (129), vaccinal thimerosal should be considered a probable source. It
is also possible that vaccinal eHg may be additive to a prenatal mercury load derived from
maternal amalgams, immune globulin injections, or fish consumption, and environmental
sources.
CONCLUSION
The history of acrodynia illustrates that a severe disorder, afflicting a small but
significant percentage of children, can arise from a seemingly benign application of low
doses of mercury. This review establishes the likelihood that Hg may likewise be
etiologically significant in ASD, with the Hg derived from thimerosal in vaccines rather
than teething powders. Due to the extensive parallels between autism and HgP, the
likelihood of a causal relationship is great. Given this possibility, TMS should be
removed from all childhood vaccines, and the mechanisms of Hg toxicity in autism should be
thoroughly investigated. With perhaps 1 in 150 children now diagnosed with ASD,
development of HgP-related treatments, such as chelation, would prove beneficial for this
large and seemingly growing population.
Table I: Summary Comparison of Traits
of Autism & Mercury Poisoning
(ASD references in bold; HgP references in italics)
Psychiatric Disturbances |
| Social deficits, shyness, social withdrawal (1,2,130,131;
21,31,45,53,132) |
| Repetitive, perseverative, stereotypic behaviors;
obsessive-compulsive tendencies (1,2,43,48,133; 20,33-35,132) |
| Depression/depressive traits, mood swings, flat affect;
impaired face recognition (14,15,17,103, 134,135; 19,21,24,26,31) |
| Anxiety; schizoid tendencies; irrational fears (2,15,16;
21,27,29,31) |
| Irritability, aggression, temper tantrums (12,13,43;
18,21,22,25) |
| Lacks eye contact; impaired visual fixation (HgP)/
problems in joint attention (ASD) (3,36,136,137; 18,19,34) |
| Speech and Language Deficits |
| Loss of speech, delayed language, failure to develop
speech (1-3,138,139; 11,23,24,27,30,37) |
| Dysarthria; articulation problems (3;
21,25,27,39) |
| Speech comprehension deficits (3,4,140;
9,25,34,38) |
| Verbalizing and word retrieval problems (HgP); echolalia,
word use and pragmatic errors (ASD) (1,3,36; 21,27,70) |
| Sensory Abnormalities |
| Abnormal sensation in mouth and extremities (2,49;
25,28,34,39) |
| Sound sensitivity; mild to profound hearing loss (2,47,48;
19,23-25,39,40) |
| Abnormal touch sensations; touch aversion (2,49;
23,24,45,53) |
| Over-sensitivity to light; blurred vision (2,50,51;
18,23,31,34,45) |
| Motor Disorders |
| Flapping, myoclonal jerks, choreiform movements, circling,
rocking, toe walking, unusual postures (2,3,43,44; 11,19,27,30,31,34,39) |
| Deficits in eye-hand coordination; limb apraxia; intention
tremors (HgP)/problems with intentional movement or imitation (ASD) (2,3,36,181;
25,29,32,38,70,87) |
| Abnormal gait and posture, clumsiness and incoordination;
difficulties sitting, lying, crawling, and walking; problem on one side of body (4,41,42,123;
18,25,31,34,39,45) |
| Cognitive Impairments |
| Borderline intelligence, mental retardation – some
cases reversible (2,3,151,152; 19,25,31,39,70) |
| Poor concentration, attention, response inhibition
(HgP)/shifting attention (ASD) (4,36,153; 21,25,31,38,141) |
| Uneven performance on IQ subtests; verbal IQ higher than
performance IQ (3,4,36; 31,38) |
| Poor short term, verbal, and auditory memory (36,140;
21,29,31,35,38,87,141) |
| Poor visual and perceptual motor skills; impairment in
simple reaction time (HgP)/ lower performance on timed tests (ASD) (4,140,181;
21,29,142) |
| Deficits in understanding abstract ideas & symbolism;
degeneration of higher mental powers (HgP)/sequencing, planning & organizing (ASD);
difficulty carrying out complex commands (3,4,36,153; 9,18,37,57,142) |
| Unusual Behaviors |
| Self injurious behavior, e.g. head banging (3,154;
11,18,53) |
| ADHD traits (2,36,155; 35,70) |
| Agitation, unprovoked crying, grimacing, staring spells (3,154;
11,23,37,88) |
| Sleep difficulties (2,156,157; 11,22,31) |
| Physical Disturbances |
| Hyper- or hypotonia; abnormal reflexes; decreased muscle
strength, especially upper body; incontinence; problems chewing, swallowing (3,42,145,181;
19,27,31,32,39) |
| Rashes, dermatitis, eczema, itching (107,146;
22,26,143) |
| Diarrhea; abdominal pain/discomfort, constipation,
"colitis" (107,147-149; 18,23,26,27,31,32) |
| Anorexia; nausea (HgP)/vomiting (ASD); poor appetite
(HgP)/restricted diet (ASD) (2,123; 18,22) |
| Lesions of ileum and colon; increased gut permeability (147,150;
57,144) |
Table II: Summary Comparison of Biological Abnormalities
in Autism & Mercury Exposure
Mercury Exposure |
Autism |
| Biochemistry |
|
| Binds -SH groups; blocks sulfate transporter
in intestines, kidneys (40,93) |
Low sulfate levels (91,92) |
| Reduces glutathione availability; inhibits
enzymes of glutathione metabolism; glutathione needed in neurons, cells, and liver to
detoxify heavy metals; reduces glutathione peroxidase and reductase (97,100,161,162) |
Low levels of glutathione; decreased ability
of liver to detoxify xenobiotics; abnormal glutathione peroxidase activity in erythrocytes
(91,94,95) |
| Disrupts purine and pyrimidine metabolism
(10,97,158,159) |
Purine and pyrimidine metabolism errors lead
to autistic features (2,101,102) |
| Disrupts mitochondrial activities, especially
in brain (160,163,164) |
Mitochondrial dysfunction, especially in brain
(76,172) |
| Immune System |
|
| Sensitive individuals more likely to have
allergies, asthma, autoimmune-like symptoms, especially rheumatoid-like ones
(8,11,18,24,28,31,111,113) |
More likely to have allergies and asthma;
familial presence of autoimmune diseases, especially rheumatoid arthritis; IgA
deficiencies (103,106-109,115) |
| Can produce an immune response in CNS; causes
brain/MBP autoantibodies (18,111,165) |
On-going immune response in CNS; brain/MBP
autoantibodies present (104,105,109,110) |
| Causes overproduction of Th2 subset;
kills/inhibits lymphocytes, T-cells, and monocytes; decreases NK T-cell activity; induces
or suppresses IFNg & IL-2 (100,112,117-120,166) |
Skewed immune-cell subset in the Th2
direction; decreased responses to T-cell mitogens; reduced NK T-cell function; increased
IFNg & IL-12 (103,108,114-116,173,174) |
| CNS Structure |
|
| Selectively targets brain areas unable to
detoxify or reduce Hg-induced oxidative stress (40,56,161) |
Specific areas of brain pathology; many
functions spared (36) |
| Accummulates in amygdala, hippocampus, basal
ganglia, cerebral cortex; damages Purkinje and granule cells in cerebellum; brain stem
defects in some cases (10,34,40,70-73) |
Pathology in amygdala, hippocampus, basal
ganglia, cerebral cortex; damage to Purkinje and granule cells in cerebellum; brain stem
defects in some cases (36,60-69) |
| Causes abnormal neuronal cytoarchitecture;
disrupts neuronal migration, microtubules, and cell division; reduces NCAMs
(10,28,57-59,161) |
Neuronal disorganization; increased neuronal
cell replication, increased glial cells; depressed expression of NCAMs (4,54,55) |
| Progressive microcephaly (24) |
Progressive microcephaly and macrocephaly
(175) |
| Neuro-chemistry |
|
| Prevents presynaptic serotonin release and
inhibits serotonin transport; causes calcium disruptions (78,79,163,167,168) |
Decreased serotonin synthesis in children;
abnormal calcium metabolism (76,77,103,179) |
| Alters dopamine systems; peroxidine deficiency
in rats resembles mercurialism in humans (8,80) |
Either high or low dopamine levels; positive
response to peroxidine, which lowers dopamine levels (2,177,178) |
| Elevates epinephrine and norepinephrine levels
by blocking enzyme that degrades epinephrine (81,160) |
Elevated norepinephrine and epinephrine (2) |
| Elevates glutamate (21,171) |
Elevated glutamate and aspartate (82,176) |
| Leads to cortical acetylcholine deficiency;
increases muscarinic receptor density in hippocampus and cerebellum (57,170) |
Cortical acetylcholine deficiency; reduced
muscarinic receptor binding in hippocampus (83) |
| Causes demyelinating neuropathy (22,169) |
Demyelination in brain (105) |
| Neurophysiology |
|
| Causes abnormal EEGs, epileptiform activity,
variable patterns, e.g., subtle, low amplitude seizure activities (27,31,34,86-89) |
Abnormal EEGs, epileptiform activity, variable
patterns, including subtle, low amplitude seizure activities (2,4,84,85) |
| Causes abnormal vestibular nystagmus
responses; loss of sense of position in space (9,19,34,70) |
Abnormal vestibular nystagmus responses; loss
of sense of position in space (27,180) |
| Results in autonomic disturbance: excessive
sweating, poor circulation, elevated heart rate (11,18,31,45) |
Autonomic disturbance: unusual sweating, poor
circulation, elevated heart rate (17,180) |
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