Vietnam Veterans with Diagnosed Parkinson’s or Parkinson like symptoms.
Hi to all,
Shelia sent me the following data that is very important to those Vietnam Veterans and families that have been fighting the VA for service-connected disability associated with Parkinson’s and/or Parkinson like neurological symptoms.
You will find below a write up by Mayo Clinic that clearly points to a connection in males that were exposed to herbicides, a request for contact data, as well as two Board of Veterans Appeals cases awarding neurological issues associated to Parkinson’s and/or Parkinson like neurological disorders.
Now they do not differentiate between the massive amounts of militarized herbicides used with the unprecedented toxic TCDD levels nor the 6 to 25 the normal recommended dose rate that was used in Vietnam from the normal farmer or the rail road worker usage, etc.
At this time in our legacy, VA and IOM have both refused to associate military service in the herbicides as a presumptive disorder. Nevertheless, you will also find references of IOM stating the possibility of a connection.
In researching for my book, I also found many references to this neurological disorder as associated to these pesticides and/or herbicides.
The Office of Technology Assessment (OTA) was commissioned by congress in 1991 to get a nationwide consensus on toxic chemical damages. The Department of Veterans Affairs, for the most part, ignored most, if not all of these findings. It also seems congress did not take the data and “apply it” to those Veterans that said and experienced the same issues as OTA had found and pointed out.
The VA's proposal to compensate Vietnam veterans for peripheral neuropathy, as related to exposure to herbicides containing dioxin (Agent Orange), excludes neuropathies under a wide range of conditions. The proposed compensable neuropathies include only those manifested not later than 10 years following the date of exposure, and excludes those related to the effects of aging, alcohol abuse, trauma, other diseases known to be associated with peripheral neuropathy such as diabetes and Parkinson's disease, and exposure to other toxicants known to produce peripheral neuropathy. In making such exclusions, however, the VACEH did not take into consideration relevant information on neurological damage.
Because of a concern over the wide range of neurotoxic effects being induced
in our population by manmade chemicals, the 101st Congress of the United States
commissioned the Office of Technology Assessment to prepare a scientific
consensus document in 1991 (OTA, 1990). As explained below, the VACEH basis for
excluding peripheral neuropathies under its conditions contradicts the OTA's
findings on the biological mechanism of neurotoxic damage such as peripheral
neuropathy.
The VA proposed exclusion of peripheral neuropathies that
only become evident 10 or more years after service in Vietnam, on the assumption
that such a neuropathy could not be associated with Agent Orange exposure, due
to the long interval from exposure. This assumption contradicts the findings of
the OTA, which found that neurological damage is not always detectable
clinically, or noticeable by, the sufferer after exposure to a
neurotoxic substance such as dioxin. As time
progresses or old age approaches, the rate of natural neuronal cell death
accelerates, and the results of earlier neurological damage may first become
evident, or unmasked (OTA, 1990). The availability of alternate neuronal
pathways is reduced, which were formerly responsible for compensating for
earlier toxic damage. The OTA specifically noted the importance of
research showing the
possibility that neurotoxic substances were important in Alzheimer's disease,
the degenerative brain disease of old age.
The VA also proposed exclusion of peripheral
neuropathies which could only be attributed to diseases associated with
neurological deficits (diabetes, Parkinson's disease) or alcohol abuse, under
the assumption that the disease or alcohol abuse, and not dioxin, was the cause
of neuropathy, similarly contradicts the findings of the OTA. The OTA found
that damage to the nervous system from toxicants may first be unmasked by other
conditions, such as diseases associated with neurological disorders or the
voluntary intake of substances capable of neurological damage (alcohol,
prescription drugs).
The OTA
cited evidence that toxic chemicals might even be the
sole causative agents in some cases of
Parkinson's disease, since onset in certain families was at similar ages,
and since Parkinson's disease has increased significantly from 1962 to 1984
along with exposures to toxic chemicals. The OTA also cited evidence that the
substantial increase in the incidence of motor neuron disease and amyotrophic
lateral sclerosis (Lou Gehrig's disease) between 1962 and 1984 was due to
environmental exposures to neurotoxic chemicals.
It is therefore scientifically probable that in the future
a higher incidence than normal of peripheral
neuropathy will be experienced by Vietnam veterans due to Agent Orange exposure,
despite the fact that the peripheral neuropathy was not detected in the 10-year
interval after exposure in Vietnam. The degree or incidence of
neurological damage in those Vietnam veterans suffering from diabetes or
Parkinson's disease is
also predicted to be higher than others suffering from diabetes or Parkinson's
disease, due to earlier aggravating exposures to Agent Orange.
For the same reasons, there is no scientific basis for
presuming that alcohol abuse is the only cause of any peripheral neuropathy in a
Vietnam veteran. The Secretary of Veterans' Affairs, therefore, should not
place any limitations or exclusions on compensation for peripheral neuropathy,
and following the congressional mandate of providing
the benefit of the doubt to the Vietnam veteran.
This so-called mandate as we all know is a joke,
a sick government
joke.
The exclusion of peripheral neuropathy associated with
diabetes as a compensable disease is flawed for another reason. This is because
the VACEH conveniently neglected the results of the Ranch Hand study (Roegner,
et al., 1991) and other epidemiological research, which shows a dose-related
significant association between diabetes and dioxin exposure. The minutes of
the May 23, 1991 VACEH meeting discussed in detail the correlation between serum
dioxin in Ranch Hand veterans and increasing diabetic rates, with Dr. Lathrop
stating, "these are figures which support an association.” For the VA to now
exclude peripheral neuropathy associated with diabetes, when the VA has not been
able to exclude diabetes itself as being caused by dioxin, is spurious.
It is important to add here that Secretary Derwinski took the credibility of ‘any scientific conclusions being valid’ to a new low in medical history. What was a proposed as a 10-year inclusion was reduced to a one (1) year inclusion by Veterans Affairs. This should mean to anyone in science or the medical field that the Derwinski and the VACEH had no idea of the etiology of what was going on with the association; only mandates to make sure that:
A. Veterans would not be able to qualify to the nonsensical time requirements and the two-year time limit to resolution of the neurological disorder(s).
B. If Veterans Affairs admitted a CNS>PNS effect causation then the door would be wide open to even more long-term neurological disorders as well as neuro-psychiatric / neuro-psychological disorders.
NEGLECT OF CENTRAL
NERVOUS SYSTEM (CNS) EFFECTS
The controlling majority of the VACEH, in making its recommendations to
compensate Vietnam veterans for peripheral neuropathy, neglected to evaluate
dioxin's central nervous system (CNS) effects. * Because the available evidence
for CNS damage by dioxin outweighs that for peripheral nervous system (PNS)
among Vietnam veterans, and because of the inseparable relationship between the
biological mechanisms by with dioxin exerts both CNS and PNS effects, this
failure of the VACEH is indefensible.
* The CNS consists of the neurological apparatus of the brain and spinal cord
(including motor neurons), while the peripheral nervous system (PNS) consists of
those nerves in the extremities of the body (arms, legs, etc.).
Peripheral neuropathies are one result of damage to the PNS.
CNS damage by fat soluble (lipophilic) neurotoxicants such as dioxin has always
been found to accompany, and usually precede, any peripheral nervous system
(PNS) damage such as peripheral neuropathy. See the discussions of relevant
studies in the attached affidavit (Jenkins, 1991). The prestigious
International Agency for Research on Cancer (IARC) concluded as early as 1977
that human CNS damage was associated with dioxin exposures (IARC, 1977a,
1977b). In 1986 the IARC clearly restated its’ finding that dioxin was
associated with both peripheral
neuropathies and personality changes, a neuropsychological
consequence of CNS damage (IARC, 1986).
Since the IARC evaluations, many new epidemiological investigations have
established an even stronger casual relationship between dioxin and CNS damage,
including the Air Force investigations of veterans of Operation Ranch Hand.
TOXICOLOGICAL BASIS FOR CNS DAMAGE BY DIOXIN
A discussion of the biological basis for dioxin's neurological is relevant in
demonstrating the inseparability of dioxin's effects on both the CNS and PNS.
Neurotoxic substances may exert their effects by several mechanisms
(Anthony and Graham, 1991). Chemical attack of whole nerve cell structures may
result in cell injury or death (neuropathy). Chemical attack may be
specifically on the axon (long nerve fiber) (axonopathy), or the myelin
sheath of the axon (myelinopathy). Neurotoxicants may also damage or alter the
neurotransmitter system, damage the glial cells, which support the primary
neurons, or damage the blood vessels supplying the nervous system.
The OTA found that degeneration of the axon (axonopathy)
is one of the most frequently determined neurological effects from neurotoxic
chemicals (OTA, 1990). If the axon of a nerve cell dies back, it no longer
reaches the
next nerve cell, muscle, etc., and cannot transmit any message. Because the
longer axons have more targets (larger surface area) for toxic damage, it is
predicted that the longer axons found in CNS are more effected by
neurotoxicants (Anthony and Graham, 1991), assuming the neurotoxicant is
sufficiently lipophilic to cross the blood-brain barrier. A critical difference
between nerve cell damage in the CNS compared to the PNS
is that PNS nerve cells can regenerate, while those of the CNS cannot. Thus,
any toxic damage to the CNS is permanent.
Although the mechanism by which dioxin exerts its neurotoxic effects, have yet
to be fully elucidated, the CNS effects are consistent with destruction of the
nerve axons (axonopathy). Because of the extreme toxicity of dioxin
and the wide range of biological affects, however, the mechanisms of dioxin's
neurotoxicity may not be limited to axonopathies. The hypothesis that dioxin
damages the CNS and PNS by destruction of axons is supported by
the similarity of the neurological symptoms caused by dioxin and many other
lipophilic neurotoxicants causing both CNS and PNS axonopathies, including
carbon disulfide, hexane, methyl n-butyl ketone, trichloroethylene,
polybrominated biphenyls, and polychlorinated biphenyls
(Anthony and Graham, 1991), discusses the enduring CNS
deficits found among populations exposed to these other lipophilic
neurotoxicants.
Lipophilic toxicants such as dioxin are able to cross the blood-brain barrier to
affect the CNS. In addition, since the brain is 50 percent lipid (dry weight),
compared to 6 to 20 percent lipid in other organs (OTA, 1990), the brain may be
particularly vulnerable to accumulating dioxin into its fat content. Nervous
system tissue itself, with its high lipid content, will also act as a selective
repository for dioxin. In addition, the low elimination rate of dioxin from the
body will contribute to its ability to reach equilibrium concentrations in
lipid-rich nervous system
The mechanism by which dioxin exerts its neurotoxic effects may differ from that of 2,4-D alone (Agent White). The higher polarity of 2,4-D (less lipophilic) compared to dioxin suggests that it would be less capable of penetrating the blood-brain.
Neuropsychological damage may be one of the most significant consequences of exposure to Agent Orange. The Office of Technology Assessment (OTA, 1990) concluded that neurotoxic chemicals play a significant casual role in development of psychiatric as well as neurological disorders. Even minor changes in the structure or function of the nervous system were found to have profound consequences for behavioral and other neurological functions.
The OTA found that neurotoxic chemicals can cause or exacerbate anxiety,
depression, mania, and psychosis.
It is simply amazing how
our congress cannot put two and two together and come up with the correct answer
even when they paid for the study results. I guess they figure THEY did the
study; what more do you VETERANS want! Justice and GOVERNMENT ACCOUNTABLY;
----- surly
you jest!!!!!
Mayo Clinic in
Rochester
Wednesday, June 14, 2006
Study Concludes that Pesticide Use Increases Risk of Parkinson's in Men
Additional Resources
For appointments or more information, call the Central Appointment Office at
507-284-2111.
Other Web Resource: Patient's Guide
Journalists:
For more information, contact:
Lisa Lucier
507-284-5005 (days)
507-284-2511 (evenings)
newsbureau@mayo.edu
ROCHESTER, Minn.--Mayo
Clinic researchers have found that using pesticides for farming or other
purposes increases the risk of developing Parkinson's disease for men.
Pesticide exposure did not increase the risk of Parkinson's in women, and no
other household or industrial chemicals were significantly linked to the disease
in either men or women.
Findings will be published in the June issue of the journal Movement Disorders.
"This confirms what has been found in previous studies:
that occupational or other exposure to
herbicides, insecticides and other pesticides increases risk for Parkinson's,"
says Jim Maraganore, M.D., Mayo Clinic neurologist and study investigator.
"What we think may be happening is that pesticide use combines with other risk
factors in men's environment or genetic makeup, causing them to cross over the
threshold into developing the disease. By contrast, estrogen may protect women
from the toxic effects of pesticides."
The investigators identified all those in Olmsted County, Minn., home of Mayo
Clinic, who had developed Parkinson's disease between 1976 and 1995. Each
person with Parkinson's disease was matched for comparison to someone similar in
age and gender who did not have the disease. The researchers conducted
telephone interviews with 149 of those with Parkinson's and 129 of those who did
not have the disease, or a proxy for these people, to assess exposure to
chemical products via farming occupation, non-farming occupation or hobbies.
The investigators were unable to determine through these interviews the exact
exposure levels of these individuals or the cumulative lifetime exposure to
pesticides.
Overall, the study found that the men with
Parkinson's were 2.4 times more likely to have had exposure to pesticides than
those who did not have Parkinson's. Women who had Parkinson's, on the
other hand, had a far lower frequency of exposure to pesticides than men with
the disease.
This study was undertaken due to conflicting results from previous studies of
pesticides and other chemical products and risk for Parkinson's.
Funding for the study is from two grants from the National Institutes of Health.
The medical-records linkage system of the Rochester Epidemiology Project also made this study possible.
Jun 08,2007
The
Elderlaw Forum: Calling all Vietnam veterans with Parkinson’s disease!
Governments lie to their citizens. It is the norm. We have come to expect it. Sometimes we like it that way. Lies can provide psychological comfort.
A senior legal helpline caller has encountered the contradiction of promises versus funding. He is a 62-year-old Vietnam veteran who served with the United States Marine Corp at the Chu Lai Air Base. “We were all exposed to Agent Orange during our tour of duty there,” he said. “I found out in 2000 that I have Parkinson’s disease. I filed a claim in 2001 and was turned down.”
The Veterans Administration ruled “Despite the presumption of in-service herbicide exposure in Vietnam, the Board is not in a position to grant service connection because the veteran’s neurological disorder did not appear within weeks or months of exposure to herbicide agent and resolved within two years of onset.”
Mayo Clinic physicians believe the caller’s Parkinson’s is the result of his exposure to Agent Orange while serving in the Republic of Vietnam. “Mayo researchers have found that using pesticides for farming or other purposes increases the risk of developing Parkinson’s disease for men,” according to the June 2007 issue of Movement Disorders. Veteran’s law judges in two cases have found an Agent Orange-Parkinson’s connection, but their rulings are not binding on the Board of Veterans’ Appeals.
It is unlikely the current administration will add Parkinson’s to the list of Agent Orange residual conditions. A well-executed legal and political strategy is needed. If you or a person you know has Parkinson’s and served in Vietnam, contact me at 1-605-677-6343, or email at mmyers@usd.edu.
(Pro bono legal information and advice is available to persons 55 and older through the USD Senior Legal Helpline, 1-800-747-1895; mmyers@usd.edu. Opinions are solely those of the author and not the University of South Dakota).
Citation Nr: 0519813
Decision Date: 07/21/05 Archive Date: 08/03/05
DOCKET NO. 94-37 191 ) DATE
)
)
On appeal from the
Department of Veterans Affairs (VA) Regional Office (RO)
in Winston-Salem, North Carolina
THE ISSUE
Entitlement to service connection for a neurological
disorder, claimed as due to in-service herbicide exposure.
REPRESENTATION
Appellant represented by: The American Legion
WITNESSES AT HEARING ON APPEAL
The veteran and his son.
ATTORNEY FOR THE BOARD
L. Cryan, Counsel
INTRODUCTION
The veteran had active service from June 1966 to October
1969, with approximately four months of additional prior
service.
This matter comes before the Board of Veterans' Appeals
(Board) from a March 1994 rating decision of the RO, which
denied the veteran's claim seeking entitlement to service
connection for a neurological disorder, claimed as peripheral
neuropathy, due to alleged exposure to Agent Orange while in
Vietnam. The veteran submitted a notice of disagreement with
that rating decision in May 1994. In July 1994, he was
provided with a statement of the case. His substantive
appeal was received in September 1994.
The Board notes that the veteran had previously claimed
entitlement to service connection for a neurological
disorder, claimed as Parkinson's disease, due to alleged
exposure to Agent Orange while in Vietnam, which was denied
by an October 1988 rating decision. The veteran submitted a
notice of disagreement with that rating decision in January
1989. In February 1989, he was provided with a statement of
the case. His substantive appeal was received in March 1989.
The matter was received at the Board in October 1989 but was
referred back to the RO pending review and revision of
herbicide regulations. The RO then also deferred a decision
on the claim pending updated proposed regulations.
As noted in a June 1999 remand by the Board, the RO, in the
currently appealed March 1994 rating decision essentially
considered both the claimed peripheral neuropathy and the
claimed Parkinson's disease. Given that the veteran has
claimed service connection for a neurological disorder,
initially claimed as Parkinson's disease and subsequently
claimed as peripheral neuropathy, and given that the
veteran's claims were essentially one continuous claim for
the same neurological disorder, the Board has simply
characterized the veteran's claim as entitlement to service
connection for a neurological disorder, claimed as due to
Agent Orange exposure. The issue has been so identified on
the title page hereinabove.
The veteran testified at a personal hearing before the
undersigned Veterans Law Judge, sitting at the RO in
September 1997. A transcript of his testimony is associated
with the claims file.
Finally, it is noted that the case was previously twice
before the Board and was remanded to the RO in January 1998
and June 1999 for additional evidentiary development.
Following compliance with the Board's directives on Remand,
the case is now returned to the Board for further appellate
consideration.
FINDINGS OF FACT
1. The veteran had active military service in the Republic
of Vietnam during the Vietnam era, and is therefore presumed
to have been exposed to herbicide agents in service.
2. The veteran has a currently diagnosed neurological
disorder with Parkinson-like characteristics, also referred
to as Parkinsonism.
3. The veteran's neurological disorder may not be
presumptively service connected under the provisions of 38
C.F.R. § 3.309(e).
4. The competent and probative medical opinions of record
have determined that the veteran's currently diagnosed
neurological disorder is at least as likely as not due to in-
service exposure to Agent Orange.
CONCLUSION OF LAW
With resolution of all doubt in the veteran's favor, the
veteran's currently diagnosed neurological disorder, referred
to as Parkinsonism and Parkinson-like syndrome, was incurred
in service as a result of in-service herbicide exposure in
Vietnam. 38 U.S.C.A. §§ 1110, 5103, 5103A, 5107 (West 2002);
38 C.F.R. §§ 3.159, 3.303 3.304 (2004).
REASONS AND BASES FOR FINDINGS AND CONCLUSION
The veteran asserts that service connection is warranted for
his neurological disorder with symptomatology which mirrors
that of Parkinson's disease, which he claims is due to in-
service herbicide exposure in the Republic of Vietnam.
I. Duties to Notify and Assist
At the outset, the Board notes that on November 9, 2000, the
Veterans Claims Assistance Act of 2000 (VCAA) was enacted.
See 38 U.S.C.A. §§ 5103, 5103A (West 2002). Among other
things, the VCAA amended 38 U.S.C.A. § 5103 to clarify VA's
duty to notify claimants and their representatives of any
information and evidence that is necessary to substantiate
the claim for benefits. The VCAA also created 38 U.S.C.A. §
5103A, which codifies VA's duty to assist, and essentially
states that VA will make reasonable efforts to assist a
claimant in obtaining evidence necessary to substantiate a
claim. Implementing regulations for the VCAA were
subsequently enacted, which were also made effective
November 9, 2000, for the most part. See 66 Fed. Reg. 45,620
(Aug. 29, 2001) (codified at 38 C.F.R. §§ 3.102, 3.159). The
intended effect of the implementing regulations was to
establish clear guidelines consistent with the intent of
Congress regarding the timing and scope of assistance VA will
provide to claimants who file a claim for benefits. See 66
Fed. Reg. 45,620 (Aug. 29, 2001). Both the VCAA and the
implementing regulations are applicable in the present case,
and will be collectively referred to as "the VCAA."
Pertinent to the merits of the veteran's claim of entitlement
to service connection for a neurological disorder, the Board
finds that the provisions of the VCAA have been complied
with. In light of the complete grant of benefits sought on
appeal (entitlement to service connection for a neurological
disorder), no further evidence is necessary to substantiate
the veteran's claim for service connection. See 38 U.S.C.A.
§ 5103(a) (West 2002). In this veteran's case, there is no
reasonable possibility that further assistance would aid in
substantiating the claim for VA compensation benefits. See
38 U.S.C.A. § 5103A(a)(1),(2) (West 2002). Also, further
notice to the veteran concerning the evidence necessary to
substantiate his claim or regarding responsibilities in
obtaining evidence would serve no useful purpose.
II. Factual Background
The veteran's service medical records are negative for
complaints, findings, or diagnosis of a neurological disorder
of any kind.
A review of the post-service evidentiary record reveals
numerous medical records clearly indicating that the veteran
has been diagnosed with a neurological disorder, although
there has been some degree of variance in the precise nature
of that diagnosis.
A September 1982 private neurology consultation report
prepared by Dr. K, indicated that the veteran was
experiencing progressive weakness of the left side of the
body and noted that he had a history of having polio of the
left arm and left leg when he was age 22 months. There was
also a history of having served two tours of duty in Vietnam.
Other numerous subsequent private medical records from the
neurological offices of Dr. L as well as from a Duke
University Medical Center doctor indicated that the veteran
began experiencing left sided numbness in 1982 and there are
several diagnoses of Parkinsonism shown from 1983. At one
time, it was thought that the veteran's neurological symptoms
could be attributed to basal ganglia disease. Other doctors
noted that the veteran may not have a pure form of
Parkinsonism, but instead, a Parkinson-plus syndrome such as
a progressive supranuclear palsy.
The veteran underwent a VA neurological examination in July
1988, and he gave a history of having been exposed to dioxins
in service. The veteran reported symptoms to include
slowness of movement, muscle stiffness, poor coordination,
slurred speech, excessive salivation, muscle twitching,
muscle cramps, tremor, and involuntary movements. The
examiner noted that the veteran had many features of
Parkinson's Disease, but noted that his picture was unusual.
First, the examiner pointed out that the veteran was young.
Next, the examiner noted that he could never see the true
resting tremor, and muscle tone was not significantly
increased on testing. On the other hand, he showed a lot of
the variability of muscle function that one did see in
Parkinsonism, and he could never convince himself that the
veteran was functional. Therefore, the examiner diagnosed a
neurological problem that was similar to Parkinson's and may
be a variety of such. He further stated that he was not
aware of the veteran's picture being seen with dioxin
exposure, but would defer that question to those with more
knowledge in that field.
Amongst other medical evidence of record is a July 1990
letter from Dr. R, a PhD and toxicologist, with the State of
North Carolina, Department of Environment, Health, and
Natural Resources, Division of Epidemiology. Dr. R referred
to various scientific literature indicating a possible
relationship between dioxin exposure and various neurological
disorders, indicating that one cannot rule out the possible
role of dioxin as a causal agent for various neurological
disorders, including Parkinson's disease. Dr. R noted that
recent scientific literature had brought to light the
possibility of environmental causes of neurological
disorders, as opposed to genetic causes, and that this may be
the reason why more young people were developing that
disease.
Also of record is a report of Dr. R, dated February 1991 and
titled "[veteran's name] - A Possible Association Between