http://www.jorsm.com/~binstock/vin.htm
VACCINATION-INDUCED NEUROPATHIES
Infection, Autoimmunity, and Autism
by Teresa Binstock
Researcher in
Developmental and Behavioral Neuroanatomy
My writings do not constitute medical advice.
Instead, they represent a seeking to understand
autism-spectrum disorders
and their causes and associated traits.
>>> Posting number 384,
dated 3 Jan 1997 21:16:41
.....PRELUDE.....
I have written a short paper that, including this announcement, shall be posted in
four sections to bit.listserv.autism. The paper is copyrighted 1997 by Teresa C.
Binstock, and persons wishing to share the paper may do so if shared in its
entirety. The views expressed in the above-entitled document are those of Teresa C.
Binstock and of no other person or institution. Persons wishing to cite the paper
in correspondence or in other academic papers may use the following internet
citation:
Binstock, T. Hypothesis: Infection, antibiotics, vaccination-induced neuropathies:
Mechanisms of pathogenesis in some cases of autism, ADHD, Tourette's, OCD, and other
neurological disorders. Bit.listserv.autism January 3 1997.
>>> Posting number 383,
dated 3 Jan 1997 21:24:58
.....ABSTRACT.....
Cytokines are released in response to vaccination (i) as part of the processes by
which vaccinations induce antibody formation, and (ii) as indicated by the
occurrence of fever and, in many children, lethargic behavior. The cytokines so
released are causally associated with two other processes: (i) edema within the cns,
and (ii) clonal expansions of T-cell and B-cell subsets already activated by
specific antigens from recent processes within the central nervous system (cns).
Of significance to autism, OCD, Tourette's, ADHD, etc, is that some T-cells
and B-cells in peripheral circulation may be encoded with neuron-derived epitopes
(NdEs) subsequent to various infections and/or various treatments with antibiotics.
In children having such NdE-encoded T-cells, B-cells, and antibodies,
vaccination-induced clonal expansions of those T-cells and B-cells may, in some
cases, initiate further neuronal damage. In other words, brain regions whose
pre-vaccination neuronal damage had been relatively insignificant may, via
vaccination-induced clonal expansions, suffer additional damage.
The sequence is as follows: individuals primed with NdE-encoded immunological
cells may, given cytokines-release induced by one or more vaccinations, experience
clonal expansions of those T-cells and B-cells, which can re-cross the bbb into the
brain and then induce additional damage, ie, resulting in vaccination-enhanced
neuropathy presenting clinically as autism, tics, Tourette's syndrome, OCD, ADHD,
etc.
>>> Posting number 385,
dated 3 Jan 1997 21:39:23
.....RATIONALE.....
1. In his book VACCINATION, SOCIAL VIOLENCE, AND CRIMINALITY, Harris Coulter
makes an important observation: in many children, post-vaccination traits appear to
be similar to those described as sequelae to various CNS infections (15). This
paper's hypothesis presents molecular mechanisms that may account for the
similarities in sequelae to various CNS infections and, in some children, to
vaccinations.
2. Based upon the facts (i) that fever is a vaccination reaction experienced by
many individuals (9), and (ii) that fever and edema are stimulated by similar
cytokines (34, 43, 57), a subset of vaccinated children -- as a direct result of
vaccination-induced cytokines release -- may be likely to experience both
encephalitis and subsequent encephalopathy.
3. For instance, recent research findings are instructive regarding autistic
children for whom -- as neonates, infants or toddlers -- medical records show a
history of infections, antibiotic treatments, vaccinations, and temporally
associated onset of autistic traits (eg, 3, 15).
4. As suggested by Coulter (15) a range of mild but significant post-vaccination
neuropathies may occur, and the following rationale applies not only to autism but
also to traits such as tics, ADHD, OCD (obsessive-compulsive disorder), etc.
A. Fever is strongly associated with interleukin-1, interleukin-6, and
tumor necrosis factor alpha (IL-1, IL-2, TNF-alpha; ref 34).
B. Brain inflammation is strongly associated with those same cytokines (6,
12).
C. IL-1 and IL-6 are among primary components in inflammatory expansions
of B-cells and T-cells, which can migrate to tissues from which, for instance, the
antineural epitopes are derived (19, 20, 24, 35, 37, 40). Furthermore, because the
very mechanism of vaccination-induced immunity derives from clonal expansions of
B-cells (1), cytokines needed for B-cell clonal expansions are induced and present
as a causally related response to vaccination.
D. If, prior to or immediately subsequent to vaccination, any neuronal
damage, however slight, has occurred in response to the child's infections and/or
antibiotic treatments (2, 23, 28, 45, 50, 51), then the child probably has some
activated microglia and some anti-neuronal antibodies, as well as activated T-cells
and B-cells whose epitopic focus is derived from neurons that were injured either
(i) during the prior infections and treatment (17, 30, 39, 42, 46, 54), or (ii) as
a result of vaccination-induced edema (22).
E. Not only do inflammatory cytokines modulate blood-brain barrier (bbb)
permeability (5), but perivascular microglial cells of the bbb can become
antigen-presenting cells encoded with epitopes from the injured tissue within the
brain, and these perivascular cells allow activated T-cells to pass from peripheral
circulation, across the bbb, into csf wherein additional autoimmune- like damage can
ensue (4, 10, 27, 33, 44). A similar crossing of the bbb occurs with activated
B-cells (16).
5. If, from the child's prior infection(s) and/or from vaccination-induced edema,
activated T-cells and B-cells exist with neuronally derived epitopes, at least in
some individuals during their response to vaccination, the following sequence may
ensue: (i) clonal expansions of existing T-cells and B-cells having neuronally
derived epitopes, (ii) further activation of microglia in brain regions already
damaged, (iii) increases in bbb permeability, thereby allowing activated T-cells,
etc, to enter the brain. (iv) Furthermore, as the clonally expanding T-cells, etc,
travel toward brain cells having sequences similar to the NdEs, encephalitis would
be one result of these events and, more importantly, additional sequelae would
include increased autoimmune-like damage to neurons that, prior to the vaccination,
had been only mildly, perhaps even unnoticeably damaged by the prior infections.
6. In extreme cases of individuals having vaccination-induced clonal expansions
of immunological cells with neuron-based epitopes, autism might be a result; and,
as suggested by Coulter (15) milder cases might appear as ADHD, Tourette's,
impulsivity, OCD, and other traits often presumed to be "genetic".
7. Nearly any vaccine may have the potential for inducing neuronal damage in
persons with NdEs. In other words, any vaccination that induces strong antibody
responses (i) would appear to be capable of inducing fever-generating cytokines and,
therefore at least hypothetically, (ii) could simultaneously induce clonal
expansions of pre-existing T- and B-cells encoded with neuronally derived epitopes
(NdEs), thereby leading to increased neuronal damage in varying degrees across
individuals.
8. That vaccinations are helpful to society is without question; however, that
some individuals suffer permanent and damaging sequelae to vaccinations is also well
documented. My purpose with this letter is not to rail against all vaccinations, but
instead is to offer a mechanism by which vaccination- induced neuronal damage in
some individuals can be understood.
9. Three additional concepts are helpful for understanding inflammation- related
pathologies of the cns: (i) molecular mimicry -- whereby epitope sequences are
virtually identical between an immunogenic pathogen and a naturally occurring
molecular sequence (8), (ii) cross-reactivity -- eg, when a lipopolysaccharide
amidst a cellular bilipid layer induces a wider range of immunological responses
involving self-membrane sequences (52), and (iii) epitope-spreading or "determinant
spreading", ie, a process that also describes spontaneously occuring widening ranges
of immungenicity (7, 38, 53). Each of these three processes illustrates ways that
autoimmune neuronal damage may be induced and the range of neuronal targets expanded
in response to fever-related levels of cytokines release that occur in response to
vaccinations. These process would be more likely in some children if, due to
infections and/or antibiotics, the child has T- and/or B-cell subsets encoded with
NdEs.
10. In extreme cases, sufficient interleukin-2 levels in damaged areas of the cns
could mobilize lymphokine-activated killer cells (LAKs), which then might induce a
more general damage (21, 25), thereby yielding increasingly severe neurological
deficits.
11. Additional factors may augment the mechanisms of neuronal damage outlined
hereinabove:
A. Targeting the cerebellum and temporal lobe: Swartz (1984) mentions that
the temporal lobe and cerebellum are likely targets for edema-induced neuronal
damage (49). Furthermore, certain hippocampal regions as well as Purkinje cells of
the cerebellum have a relative deficit of apoptosis-related protein Bcl-2, thereby
inclining cells in those regions toward apoptosis if and as edema- induced injury
occurs (26).
B. Cerebellum: Discrete lesions of the cerebellum are associated with
mania, depression, bipolar disorders, and OCD (31); and more than thirty bacterial,
fungal, and viral infectious agents are known to be able to affect the cerebellum
(13). Therefore, mechansisms presented in this paper (eg, in 11A and 11B, etc) could
even account for multiple and varied occurrences of these traits across individuals
within families.
C. Gastrointestinal tract: Many infections are known to begin in the
gastrointestinal tract, oftentimes after antibiotic regimens have eliminated
naturally occurring and beneficial microflora (18, 36, 41). Occasionally, the
infectious agent can translocate through the GI-tract and affect other organs and
occasionally become systemtic (11). Occasionally, neurological ramifications ensue
and can be modulated by glutamate and aspartate (47, 48, 56, 58).
D. Other inflammatories: In addition to IL-1, IL-6, and TNF-alpha, the
following are additional factors influencing brain inflammation: Platelet-activating
factor, prostaglandins E2 and I2, leukotriene B4, and polymorhpnuclear neutophil
leukocytes (47).
12. As stated in a recent guideline for physicians, vaccination-induced
inflammation ought be treated aggressively (22), and better understanding of
pathogenic processes, of risk factors, and of preventive or corrective measures are
worthwhile goals.
* * *
After writing this paper, a newly published study about the MMR and its induction
of interferon gamma suggested other ways that vaccinations can induce neurologic
and/or gastrointestinal effects.
MMR and
interferon-gamma
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>>> Posting number 386,
dated 3 Jan 1997 21:58:52
>>> Posting number 387,
dated 3 Jan 1997 22:05:37
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(c) 1997
Teresa C. Binstock,
Researcher in Developmental & Behavioral Neuroanatomy
Denver
POSTING HISTORY
>>> Posting number 384, dated 3 Jan 1997 21:16:41
Sender: SJU Autism and Developmental Disablities List
From: Teresa Binstock
Organization: University of Colorado, Health Sciences Center
Subject: 1: INFECTION ANTIBIOTICS VACCINATION NEUROPATHIES: AUTISM, etc.
>>> Posting number 383, dated 3 Jan 1997 21:24:58
Sender: SJU Autism and Developmental Disablities List
From: Teresa Binstock
Subject: 2: INFECTION ANTIBIOTICS VACCINATION NEUROPATHIES: AUTISM,
>>> Posting number 385, dated 3 Jan 1997 21:39:23
Sender: SJU Autism and Developmental Disablities List
From: Teresa Binstock
Subject: 3: INFECTION ANTIBIOTICS VACCINATION NEUROPATHIES: AUTISM,
>>> Posting number 386, dated 3 Jan 1997 21:58:52
Sender: SJU Autism and Developmental Disablities List
From: Teresa Binstock
Subject: 4a: INFECTION ANTIBIOTICS VACCINATION NEUROPATHIES: AUTISM,
>>> Posting number 387, dated 3 Jan 1997 22:05:37
Sender: SJU Autism and Developmental Disablities List
From: Teresa Binstock
Subject: 4b: INFECTION ANTIBIOTICS VACCINATION NEUROPATHIES: AUTISM,
return to: Contents
e-mail to: Teresa Binstock
copyright 1997
ALL INFORMATION, DATA, AND MATERIAL
CONTAINED, PRESENTED, OR PROVIDED HERE IS FOR GENERAL INFORMATION PURPOSES ONLY
AND IS NOT TO BE CONSTRUED AS REFLECTING THE KNOWLEDGE OR OPINIONS OF THE
PUBLISHER, AND IS NOT TO BE CONSTRUED OR INTENDED AS PROVIDING MEDICAL OR LEGAL
ADVICE. THE DECISION WHETHER OR NOT TO VACCINATE IS AN IMPORTANT AND
COMPLEX ISSUE AND SHOULD BE MADE BY YOU, AND YOU ALONE, IN CONSULTATION WITH
YOUR HEALTH CARE PROVIDER.