Eye problems related to mercury. B Windham(ed)
Studies document that mercury and similar toxic metals accumulate
in endothelial cells such as those in the eye retina, cornea, and macula depleting
glutathione and lipoate by binding to thiols; these are needed to counteract free radicals caused
by such as toxic metals that damage the endothelial layers of the the retina, cornea and macula, as major factors in such conditions(see Pub Med abstracts of studies). Such free radicals generated have been found
to cause cataracts and such conditions that can be prevented, slowed, and even
reversed to some degree by detox and antioxidant eye
drops (according to studies). Mercurialentis (brown discoloration of anterior capsule of
eye lens- caused by mercury, is documented in medical texts as the first sign
of mercury toxicity: It is an indicator
and early sign of further eye damage. Cataracts, retinitis pigmentosa,
iritis, color vision problems, and other eye conditions
are documented to commonly be caused by mercury/metals toxicity.
Medical Dictionary, www.medilexicon.com/medicaldictionary.php
It is commonly caused by systemic poisoning from absorption
of mercury vapor through the respiratory tract or through the gastrointestinal
tract: www.llnl.gov/es_and_h/hsm/supplement_21.11/inorg.html
*****
From my experience I know of 5 eye problems related
to mercury. There are probablymore. One eye problem mercury causes is chronic iritis‑ I don't know much about that but it’s
documented in the medical literature and someone else I know had it. Another is color vision; that’s also
documented in the medical literature and several I know have had color vision
improve after amalgam removal, including me.
I
have Fuch's disease(clouding
of cornea caused by deterioration/ glumping of
endothelial cells in the cornea. Aggressive form of
cataracts. Animal studies and in
vitro studies have shown mercury causes similar damage to endothelial cells in
various parts of the body due to deterioration and free radical effects. Since having my amalgams removed over the
last 2 years, my opthamologist says that the
deterioration of the endothelial layer of my corneas has slowed considerably
compared to 2 years ago. My vision has
also improved so much that I cannot see at all through my glasses that I got 4
years ago. My optomitrist
who did the glasses and reexamined me was really surprised, said my vision had
improved almost 50%. I no longer wear
glasses.
Another
eye problem related to mercury is dry eyes.
Several clinics have had success with improvements after amalgam replacement. The other eye problem known to sometimes
be related to mercury is macula degeneration.
The buildup of mercury in the eye is similar to in Fuch’s,
etc. and causes clouding and degeneration.
Someone I know says a relative got better after amalgam
replacement. The following are a few
abstracts or references I’m aware of.
(B Windham)
&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&
Strabismus
is where one eye moves freely of the other, either inwardly or outwardly to focus
independently. This condition, which was present at an early age in my now
5 year old, was quickly corrected by
supplementing the RDA of vit A in cis
form and cutting out all other vit A sources (Megson protocol).
Pupil dilation was
always a factor in him too. Interestingly, his pupils reacted normally
within the first two doses of DMSA he ever received, but the dilation returned post-round. After 5 months of
chelation, I see VERY normal eye function, with normal
pupil reactivity for the most part. I
believe the dilation is a symptom of mercury toxicity. *************
Dilation,
poor accomodative function (focussing)
and convergence insufficiency - which if severe is strabismus - are
characteristic of mercury poisoning. They are all due to a mild, symmetrical
impairment of the third cranial nerve. Since this nerve connects to the brain
right next to the hypothalamus, where mercury is known to concentrate,
Dr.
A. Cutler, (see his web site)
********************************
macular degenerationDegeneration of the
macula lutea of the eye. Often
caused by free radical or oxidation damage. www.nutritionfocus.com/nutrition_supplementation/glossary/GlossaryM.html
The first
symptom I had of mercury toxicity was double vision, then drooping eyelids. I
also had floaters for years and bright lights blinded me. When I was 42 my keen
eyesight started to go and I had to wear glasses to sew or read. By the time
1998 rolled around I was wearing 250 magnifying glasses. Within a short period
of time after amalgam removal I no longer needed reading glasses, and today I
do not wear glasses and am able to read any size print.
However, I still have very slight double
vision to the extreme right and left, I don't have
floaters any longer but still have some sensitivity to bright lights.
Freya Koss, Frekoss@aol.com
Mercury
has been found to be a factor in retinitis pigmentosa
and retina degeneration.
Olynyk F,
Sharpe DH; Mercury poisoning in paper pica, New Eng J Med, 1982, Apr 29:
306(17):1056-57; & Uchino M, Tanaka Y, Ando M, et al; Neurologic
features of chronic minamata disease(organic mercury poisoning)
J Environ Sci Health B 1995, Sep; 30(5): 699-715.
Distributions
of elements in the human retnal pigment epitheliaum; Arch Ophthalmol,
1990, Jan; 108(1):113-117; Ulshafer RJ, Allen CB,
Rubin ML.
Transport of thiol-conjugates of inorganic mercury in human retinal
pigment epithelial cells, Bridges CC,
Battle JR, Zalups RK. Toxicol Appl Pharmacol. 2007 Jun 1;221(2):251-60. Epub 2007 Mar 23
Division of Basic
Medical Sciences, Mercer University School of Medicine, Macon, GA 31207, USA.
bridges_cc@mercer.edu
Inorganic mercury (Hg(2+))
is a prevalent environmental contaminant to which exposure to can damage rod photoreceptor cells and
compromise scotopic vision. The retinal pigment
epithelium (RPE) likely plays a role in the ocular toxicity associated with Hg(2+) exposure in that it mediates transport of substances
to the photoreceptor cells. In order for Hg(2+) to
access photoreceptor cells, it must first be taken up by the RPE, possibly by
mechanisms involving transporters of essential nutrients. In other epithelia, Hg(2+), when conjugated to cysteine
(Cys) or homocysteine (Hcy), gains access to the intracellular compartment of the
target cells via amino acid and organic anion transporters. Accordingly, the
purpose of the current study was to test the hypothesis that Cys and Hcy S-conjugates of Hg(2+) utilize amino acid transporters to gain access into
RPE cells. Time- and temperature-dependence, saturation kinetics, and
substrate-specificity of the transport of Hg(2+), was assessed in ARPE-19 cells
exposed to the following S-conjugates of Hg(2+): Cys
(Cys-S-Hg-S-Cys), Hcy (Hcy-S-Hg-S-Hcy), N-acetylcysteine
(NAC-S-Hg-S-NAC) or glutathione (GSH-S-Hg-S-GSH). We discovered that only Cys-S-Hg-S-Cys and Hcy-S-Hg-S-Hcy were taken up by
these cells. This transport was Na(+)-dependent and
was inhibited by neutral and cationic amino acids. RT-PCR analyses identified
systems B(0,+) and ASC in ARPE-19 cells. Overall, our
data suggest that Cys-S-Hg-S-Cys
and Hcy-S-Hg-S-Hcy are
taken up into ARPE-19 cells by Na-dependent amino acid transporters, possibly
systems B(0,+) and ASC. These amino acid transporters
may play a role in the retinal toxicity observed following exposure to mercury.
Transport of thiol-conjugates
of inorganic mercury in human retinal pigment epithelial cells, Bridges CC, Battle JR, Zalups RK.
Toxicol Appl Pharmacol. 2007 Jun 1;221(2):251-60. Epub 2007 Mar 23
Division of Basic Medical Sciences, Mercer
University School of Medicine, Macon, GA 31207, USA.
bridges_cc@mercer.edu
Inorganic mercury (Hg(2+))
is a prevalent environmental contaminant to which exposure to can damage rod
photoreceptor cells and compromise scotopic vision.
The retinal pigment epithelium (RPE) likely plays a role in the ocular toxicity
associated with Hg(2+) exposure in that it mediates
transport of substances to the photoreceptor cells. In order for Hg(2+) to access photoreceptor cells, it must first be taken
up by the RPE, possibly by mechanisms involving transporters of essential
nutrients. In other epithelia, Hg(2+), when conjugated
to cysteine (Cys) or homocysteine (Hcy), gains access
to the intracellular compartment of the target cells via amino acid and organic
anion transporters. Accordingly, the purpose of the current study was to test
the hypothesis that Cys and Hcy
S-conjugates of Hg(2+) utilize amino acid transporters
to gain access into RPE cells. Time- and temperature-dependence, saturation
kinetics, and substrate-specificity of the transport of Hg(2+), was assessed in
ARPE-19 cells exposed to the following S-conjugates of Hg(2+): Cys (Cys-S-Hg-S-Cys), Hcy (Hcy-S-Hg-S-Hcy), N-acetylcysteine
(NAC-S-Hg-S-NAC) or glutathione (GSH-S-Hg-S-GSH). We discovered that only Cys-S-Hg-S-Cys and Hcy-S-Hg-S-Hcy were taken up by
these cells. This transport was Na(+)-dependent and
was inhibited by neutral and cationic amino acids. RT-PCR analyses identified
systems B(0,+) and ASC in ARPE-19 cells. Overall, our
data suggest that Cys-S-Hg-S-Cys
and Hcy-S-Hg-S-Hcy are
taken up into ARPE-19 cells by Na-dependent amino acid transporters, possibly
systems B(0,+) and ASC. These amino acid transporters
may play a role in the retinal toxicity observed following exposure to mercury.
Homocysteine, system b0,+
and the renal epithelial transport and toxicity of inorganic mercury, Bridges CC, Zalups RK. Am J Pathol. 2004 Oct;165(4):1385-94
Mercer University School of Medicine,
Division of Basic Medical Sciences, 1550 College St., Macon, GA 31207, USA.
Proximal tubular epithelial cells are major
sites of homocysteine (Hcy)
metabolism and are the primary sites for the accumulation and intoxication of
inorganic mercury (Hg(2+)). Previous in vivo data from
our laboratory have demonstrated that mercuric conjugates of Hcy are transported into these cells by unknown mechanisms.
Recently, we established that the mercuric conjugate of cysteine
[2-amino-3-(2-amino-2-carboxy-ethylsulfanylmercuricsulfanyl)propionic
acid; Cys-S-Hg-S-Cys], is
transported by the luminal, amino acid transporter, system b(0,+). As Cys-S-Hg-S-Cys and the mercuric
conjugate of Hcy
(2-amino-4-(3-amino-3-carboxy-propylsulfanylmercuricsulfanyl)butyric
acid; Hcy-S-Hg-S-Hcy) are
similar structurally, we hypothesized that Hcy-S-Hg-S-Hcy is a substrate for system b(0,+). To test this
hypothesis, we analyzed the saturation kinetics, time dependence, temperature
dependence, and substrate specificity of Hcy-S-Hg-S-Hcy transport in Madin-Darby
canine kidney (MDCK) cells stably transfected with
system b(0,+). MDCK cells are good models in which to
study this transport because they do not express system b(0,+).
Uptake of Hg(2+) was twofold greater in the transfectants than in wild-type cells. Moreover, the transfectants were more susceptible to the toxic effects of
Hcy-S-Hg-S-Hcy than wild-type
cells. Accordingly, our data indicate that Hcy-S-Hg-S-Hcy is transported by system b(0,+)
and that this transporter likely plays a role in the nephropathy induced after
exposure to Hg(2+). These data are the first to implicate a specific, luminal
membrane transporter in the uptake and toxicity of mercuric conjugates of Hcy in any epithelial cell.
(mercury accumulates in cornea endothelial cells and causes
oxidative damage resulting in cataracts, etc.)
********************
SEAFOOD/CATARACTS
Methylmercury in seafood may cause lens
clouding, contributing to cataract development. Optometrist Ben Lane noted that
his cataract patients liked seafood, while those who didn't like fish were
clear-eyed. A study of 17 patients revealed that the cataract patients had
eaten salt water fish or shellfish at least once a week on the average, but
those cataract-free reported using these foods an average of once every five
weeks. The cataract patients showed far higher concentrations of mercury in
their hair. Dr. Lane's study showed that the presence of 2.3 ppm or more of mercury in hair samples was related to a
23-fold increase in the risk of cataracts. Dr. Lane encourages his patients to
eat such foods as garlic and pectin-rich foods such as apples to help remove
the mercury, and to receive adequate, while avoiding excessive, amounts of
vitamins A, C, and E.
Dr, Ben
Lane, O.D., Methylmercury in seafood contributes to
cataract development, Medical World News, December 20, 1982
**********************
I would
look into the possibility of mercury poisoning which is capable of causing both
cataracts and light sensitivity. (So are other things.) I have seen many babies
born with mercury poisoning (further exacerbated by the mercury in
vaccinations.) from their mother's dental amalgams. I would get a Hair Mineral
Analysis right away. Good luck.Steve
Rochlitzrochlitz@wellatlast.com ******************************************************
Cataract
reversal through mercury detox www.digitalnaturopath.com/treat/T33633.html
Mobilization
AND excretion are required for mercury detoxification. Consuming foods high in
sulfur such as garlic, onions, beans, and eggs or supplemental sulfur in the
form of MSM can help move mercury around but it is only bound loosely and
caution is advised. There have been reported cases of reversible cataract development from individuals mobilizing mercury
without excreting it. Consult a qualified doctor for a detoxification
protocol appropriate for you.
Alan Thal, MD
Antioxidant
eye drops (n-acetylcarnosine) have been documented to
prevent and sometimes reverse cataracts (such as Can C drops).
******************************************************************
Rudolph CJ, Samuels RT, McDanagh EW. Cheraskin E. Visual Field Evidence of Macular Degeneration
Reversal Using a Combination of EDTA Chelation
and Multiple Vitamin and Trace Mineral Therapy.In: Cranton EM, ed. A Textbook on EDTA Chelation
Therapy, Second Edition. Charlottesville, Virginia: Hampton Roads
Publishing Company; 2001
*********************************************
Dr. G. E. Poesnecker, Its
Only Natural, 2001, http://www.oneflesh.org/only‑22.html
Disorders that Chelation
Can Help
Following is a
list of conditions successfully treated
by chelation that has been assembled by
physicians who did much of the early research work. Many of these problems are
common and are generally considered incurable: scleroderma; digitalis intoxication;
heavy-metal poisoning (especially acute plumbism); calcinosis (pipestem calcinosis of the vessels, prostatic calcinosis);
vascular atheromatous disorders including
atherosclerosis, atheromatous deposits,
arteriosclerosis obliterans, peripheral vascular
insufficiency with intermittent claudication, and
acute brain syndrome secondary to cerebral ischemia secondary to calcific atherosclerosis; myocardial or coronary
insufficiency; collagenosis; arteriosclerosis
including cerebrovascular arteriosclerosis; arthritis
including hypertrophic and rheumatoid; calcific tendinosis; calculi; diabetic retinopathy; multiple
sclerosis; macular degeneration of the retina; cataracts; Parkinsonism;
emphysema; poisonous snake and insect bites; calcified necrotic ulcers; heart
valve calcification; hemochromatosis; calcific bursitis; calcified granulomas;
and hypertension.
&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&
Mercury accumulates in the uvea and
retina of the eye.
Khayat A, Dencker
L. Whole body and liver distribution of inhaled mercury vapor in the mouse:
influence of ethanol and aminotriazole pretreatment.
J Appl Toxicol.
1983 Apr;3(2):66-74
*********************************************************
|
Inorganic mercury has been found to be associated with cataract formation.Hachet E.
Cataracts,
Bull Soc Ophtalmol Fr. 1985 Nov;Spec No:87-107. &&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&Dr.
Victoria Buntine, Mercury Effects, Healthinasia
Incorporated, 2001www.healthinasia.com/mercury.html
|
The problem with mercury
is that it
affects our nervous system. Mercury accumulates in what we call end organs,
like kidneys, brain, thyroid and eyes, and this is why it is detected on hair
analysis It may contribute to cataracts,
headaches, numbness and tingling, irritability, joint pain and autism in kids,
as well as chronic fatigue syndrome and general allergies. *******************************************************
Dr. D.A. Carroll, O.D.&
Dr. B.C. Lane, Preventing mercury
related cataracts,
www.medicalvisioncenter.com/prevention.html
Vitamin C also helps to pull out the
toxic mercury that results from the consumption of
large fish, such as tuna, swordfish and shark. Dr. Lane said that his 1982
study found that mercury, which would
accumulate in the crystalline lens, resulted in the depression of enzymes such
as superoxide dismutase and glutathione peroxidase.
The latter is the primary enzyme that helps prevent mercury cataracts from
forming. 'Organic mercury is the worst offender because it's able to
penetrate membranes and get into organic tissues,' he said.
&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&
Cavalleri A, Belotti
L, Gobba FM, Luzzana G,
Rosa P & Seghizzi P. Colour vision
loss in workers exposed to elemental mercury vapour. Toxicology Letters 77(1‑3):351‑356
(1995)
ABSTRACT: "We evaluated colour
vision in 33 workers exposed to elemental mercury (Hg) vapour
and in 33 referents matched for sex age, alcohol consumption and cigarette
smoking. The results were expressed as colour
confusion index (CCI). In the workers urinary excretion of Hg (HgU) ranged
from 28 to 287 ug/g
creatinine. Subclinical colour
vision loss, mainly in the blue‑yellow range, was observed in the
workers. This effect was related to exposure, as indicated by the correlation
between HgU and CCI (r=0.488, P<0.001).
& Urban P, Gobba F, Nerudova J, Lukas E, Cabelkova Z, Cikrt M,.Color Discrimination
Impairment in Workers Exposed to Mercury Vapor. Neurotoxicology. 2003 Aug;24(4-5):711-716;
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%
If you want to know something about
retinitis pigmentosa (or retinopathia pigmentosa)
and mercury poisoning,
you should read the following two
articles:
1. Olynyk
F, Sharpe DH: Mercury poisoning in paper pica. (retinitis
pigmentosa)
N Engl
J Med 1982 Apr 29;306(17):1056‑1057
2. Uchino M, Tanaka Y,
Ando Y, Yonehara T, Hara A, Mishima
I, Okajima T,
Ando M: Neurologic features of
chronic minamata disease (organic mercury poisoning) and incidence of
complications with aging. J Environ Sci Health B 1995 Sep;30(5):699‑715
Also: Arch Ophthalmol 1990 Jan;108(1):113‑117
Distributions of elements in the human retinal pigment epithelium.
Ulshafer RJ, Allen CB, Rubin ML
Department of Ophthalmology, College of Medicine, Univ. of
Florida, Gainesville 32610.
Distributions of elements above the atomic number of sodium were mapped
in the retinal pigment epithelia of eight human eyes. X‑ray energy
spectra and maps were collected from cryofixed, freeze‑dried, and epoxy‑embedded
tissues using energy‑dispersive x‑ray microanalysis. All eyes had
high concentrations of phosphorus in the nuclei of retinal pigment epithelial
cells. Melanosomes were rich in sulfur, zinc,
calcium, and iron. Lipofuscin and cytoplasm contained
only phosphorus and sulfur in detectable amounts. Drusen,
when present, contained phosphorus and calcium. Six eyes had a prominent
aluminum peak recorded from melanosomes, nuclei, and
Bruch's membrane. In one pair of 90‑year‑old eyes, small, electron‑dense
deposits
surrounded many melanosomes
and contained mercury and selenium. Retinal pigment epithelial melanosomes may bind and accumulate metals and
other potentially toxic ions over time,
preventing them from reaching the neural retina.
********************************************************************
Journal of Environmental Science and
Health Part B Pesticides Food Contaminants and Agricultural Wastes 30(5):
699-715. 1995
Abstract: Tessier‑Lavigne M, Mobbs P,
Attwell D, Invest Ophthalmol
Vis Sci 1985 Aug;26(8):1117‑1123 “Lead and
mercury toxicity and the rod light response”.
Lead and mercury have been reported to alter selectively the rod
component of the electroretinogram, and to inhibit
the phosphodiesterase in rod outer segments which may
be responsible for generating the rods' light response. The authors have
investigated the effect of lead and mercury on the voltage response to light of
rods, and compared these effects with those of the phosphodiesterase
inhibitor papaverine. Lead and
mercury, like papaverine, slow the light response.
In addition, papaverine increases the light response
amplitude while lead decreases it. Mercury initially increases and then
decreases the amplitude. The late decrease in amplitude “produced by mercury is associated with rod degeneration”: an effect which may mimic degenerative
diseases in which the rod phosphodiesterase is
insufficiently active. These results demonstrate that the changes of electroretinogram induced by lead and mercury can be
accounted for by the changes in receptor potential these heavy metals produce.
The changes in receptor potential seen are consistent with mercury inhibiting
the rod phosphodiesterase, and with lead having an
action in addition to phosphodiesterase inhibition.
PMID: 2991162, UI: 85260515
******************************************************************
God Zb Med Fak
Skopje 1978;24:289‑291
[Changes in the crystalline lens of the eye in workers
occupationally exposed to mercury vapors].
[Article in Serbo‑Croatian (Cyrillic)]
Delivanova S, Popovski
P, Orusev T
PMID: 757176, UI: 80092857
*******************************************************************
Abstract
“Effect of the ophthalmic preservative thimerosal on human and rabbit corneal
endothelium”.
Van Horn DL, Edelhauser HF, Prodanovich G, Eiferman R,
Pederson HF
Widespread use of the mercurial‑containing preservative
thimerosal as an antibacterial agent in ophthalmic drugs and solutions
warranted an investigation into its possible cytotoxic
effects on the functional and ultrastructural
integrity of the corneal endothelium. No changes in corneal thickness were
observed during 5 hours' perfusion of the endothelium of rabbit and human corneas with 0.0001
and 0.0005 percent thimerosal in
glutathione bicarbonate Ringer's solution (GBR). Scanning electron
microscopy (SEM) and transmission electron
microscopy (TEM) of the endothelium of the 0.0001 percent group revealed normal
ultrastructure. SEM and TEM of the endothelium of
corneas perfused with 0.0005 percent thimerosal for 5
hours revealed condensed mitochondria, cytoplasmic
vacuoles, and cytoplasmic flaps at the apical end of
the cellular junctions.
Perfusion of higher concentrations (0.001 and 0.005 perecnt)
of thimerosal
in GBR resulted in increases in corneal thickness after 2 hours
and
irreversible ultrastructural damage to the
endothelial cells by 5 hours. Corneas perfused with
0.01 and 0.1 percent thimerosal in GBR showed a rapid and immediate increase in
corneal thickness and endothelial cell death and necrosis within 1 hour. It is
postulated that the mercury in thimerosal
becomes
bound to the cell membrane protein sulfhydryl groups,
causing an
increase in cellular permeability; These
results suggest that the prolonged exposure of the corneal endothelium to
thimerosal in the accepted antimicrobial dosage of 0.005 to 0.001 percent may
result in functional and “structural damage to the endothelium”. *
PMID: 844986, UI: 77140310
********************************************************************
Garron
LK, Wood IS, Spencer WH, Hayes TL. A clinical pathologic study of mercurlalentis
medicamentosus. Trans Am Ophthalmol
Soc 1977;74:295‑320
Thirty‑one patients who used eye drops containing the
preservative, phenylmercuric nitrate for from 3 to 15
years, developed a brownish pigmentation of the
anterior capsule of the pupillary
area. Light and electron microscopic
studies on two lenses demonstrated deposits of
dense particulate material
resembling melanin pigment on and in the anterior
capsule of the lens in
the area of the pupil. Special studies,
including electron microprobe
analysis and neutron activation analysis
established the presence of mercury in a lens with mercurialentis.
No mercury was found in two lenses used as controls.
PMID: 867632, UI: 77196922
*********************************************************************
Klein,
CL; Kohler, H; Kirkpatrick, CJ.
Increased
Adhesion and Activation of Polymorphonuclear Neutrophil Granulocytes to Endothelial Cells under Heavy
Metal Exposure in Vitro.
Pathobiology. 62(2):90‑98, 1994.
ABSTRACT: Heavy metals have
been implicated in the mechanisms of endothelial damage. Influences of heavy
metal ions on diverse cell types have been studied using a variety of in vitro
and in vivo methods. Polymorphonuclear neutrophil granulocytes (PMNs) have physiological and
pathological functions, including the modulation of adhesion to and destruction of endothelial cells
(ECs).
PMNs were studied during interaction with human umbilical vein ECs
under exposure to zinc, nickel and cobalt using an in vitro model. We studied
adhesion processes with the help of a computer‑controlled image‑analyzing
system and examined the activation of PMNs by quantification of leukotriene
B4 (LTB4) release. The biphasic
effects of the valuated heavy metals on PMN‑EC adhesion, with stimulation
at very high and very low molar concentrations, were observed. The release of LTB4 by PMNs increased during
exposure to very low metal concentrations. The initiation of these important pathogenetic mechanisms of inflammation at very low metal
ion concentrations, which give no
morphologic changes, must be regarded as
potentially significant with respect to the toxic effects of heavy metals. BIO‑PROBE COMMENT: Damage to the inner
lining of blood vessels (endothelium)
is widely regarded to be the initial step
in the disease process that leads to cardiovascular disease. Although mercury
was not included in this study, it is a heavy metal that has previously been
shown to cause endothelial damage. The three metals examined in this study
nickel, cobalt and zinc)
are all used in dental restorative
materials. Research, published in peer‑reviewed dental journals, has
demonstrated the release and bioavailability of nickel (and mercury).
Cardiovascular disease has become widespread only since the 1920's, about the
time of increased use of heavy metals in dental
therapy and long after humans consumed eggs,
meat, milk, butter and cheese.(other studies documenting mercury damage to is
available on the web: use EXCITE search engine or MEDLINE http:///www.nlm.nih.gov/)
Abstract
Exp Eye Res 1993 Nov;57(5):549‑555
Low levels of inorganic mercury damage the corneal endothelium.
Sillman AJ, Weidner WJ
Section of Animal Physiology, University of California,
Davis 95616.
The effect of inorganic mercury on the integrity of the
endothelium of isolated bullfrog (Rana catesbeiana) corneas was
examined by spectrophotometric analysis of corneal
uptake of the vital stain Janus green, and by both transmission (TEM) and scanning (SEM)
electron microscopy. The uptake of
Janus green by the endothelium is dose related between 1.0 and
30.0 microM HgCl2. The effect of
mercury is not altered by changes in external calcium concentration, nor is it
influenced by the calcium ionophore A23187,
indicating that inorganic mercury damages the corneal endothelium through a
mechanism which does not involve competition with external calcium or interaction with
calcium channels. TEM and SEM demonstrate significant ultrastructural
damage to the endothelium exposed to inorganic mercury, including cellular swelling, increased
vacuolization, focal denuding of
Descemet's membrane, and
diminished integrity at the intercellular junctions.
PMID: 8282041, UI: 94109509
&&&&&&&&&&&&&&&&&&&&&&&
Toimela
TA, Tahti H.
Effects of mercuric chloride exposure on the glutamate uptake by cultured retinal
pigment epithelial cells. Toxicol In Vitro 2001 Feb;15(1):7‑12
Tampere University Medical School, FIN‑33014 University of
Tampere, Finland.
The cytotoxicity of mercuric chloride and the effects of
mercuric chloride on glutamate and
calcium uptake and the factors regulating glutamate uptake were studied
in retinal pigment epithelium (RPE)
cell cultures. RPE cells isolated from pig eyes and human RPE cell line (D407) cells were cultured to confluency and further subcultured
according to the test protocol in question. The cytotoxicity
caused by 15 min of exposure to mercuric chloride (0.01‑‑1000 microM) was evaluated by WST‑1 assay based on the
activity of mitochondrial
dehydrogenases. [(3)H]Glutamate
uptake was measured after the cells were exposed to 0.1‑‑100 microM mercuric chloride and the selected regulators of
protein kinase C (PKC) pathway: PKC activator SC10, PKC inhibitor chelerythrine chloride, phospholipase
A(2)/C inhibitor manoalide,
tyrosine kinase inhibitor lavendustin
A, competitive NMDA receptor antagonist
AP7 and IP(3) receptor antagonist heparin. Intracellular calcium was monitored with Fluo‑3
probe starting immediately after the exposure to 1‑‑1000 microM mercuric chloride.
Mercuric chloride showed concentration‑dependent effects on cell
viability, on glutamate uptake and on
intracellular calcium concentration. The results give some support to the concept that
glutamate uptake is affected by PKC. The PKC inhibitor chelerythrine
chloride decreased glutamate uptake by
25%, but the PKC activator SC10 could partly prevent the inhibitory effect of mercuric chloride. Lavendustin A, manoalide and
heparin had smaller, but statistically
significant, effects. All these substances act on mediators which can
regulate the activity of
PKC. However, PKC is not likely to be the only regulator of
glutamate uptake. The rise
observed in [Ca(2+)](i)
may initiate various cellular events during mercury intoxication.
&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&
Hum Toxicol 1987 May;6(3):253‑256
Prenatal
and early postnatal intoxication by inorganic mercury
resulting from the maternal use of mercury containing soap.
Lauwerys R, Bonnier C, Evrard P, Gennart JP, Bernard A.
A case of
slight renal tubular dysfunction associated with cataract and anaemia was diagnosed in a 3‑month‑old black boy
in whom high levels of mercury were found in blood and urine. Several arguments suggest that the renal,
ocular and haematological defects may have resulted from
exposure to mercury during foetal life and the 1‑month
lactation period due to the extensive
use of inorganic mercury containing cosmetics by the mother.
**********************************************************
1: Bull Soc Belge Ophtalmol
1978;181:21‑37
[Cataract of toxic origin(mercury)] [Article in French]
Michiels J.
&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&
Bull Soc Ophtalmol Fr 1985 Nov;Cataracts:87‑107
[Cataracts(mercury)].
[Article
in French]
Hachet E.
&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&
Oftalmol Zh 1974;29(7):501‑503
[Eye manifestations of chronic mercury poisoning].
[Article
in Russian]
Fomicheva IV.
&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&7
Bull Environ Contam Toxicol
1991 Feb;46(2):230‑236
Inhibition of corneal epithelial cell migration by cadmium
and mercury.
Ubels JL, Osgood TB
Mount Desert Island Biological Laboratory, Salsbury Cove, Maine 04672.
PMID: 2018869, UI: 91208463
**********************************************************
Klein,
CL; Kohler, H; Kirkpatrick, CJ.
Increased Adhesion and
Activation of Polymorphonuclear Neutrophil Granulocytes to Endothelial
Cells under Heavy Metal Exposure in Vitro.
Pathobiology.
62(2):90‑98, 1994.
ABSTRACT: Heavy metals have
been implicated in the mechanisms of endothelial damage. Influences of heavy
metal ions on diverse cell types have been studied using a variety of in vitro
and in vivo methods. Polymorphonuclear neutrophil granulocytes (PMNs) have physiological and
pathological functions, including the modulation of adhesion to and destruction
of endothelial cells (ECs).
PMNs were studied during interaction with human umbilical vein ECs
under exposure to zinc, nickel and cobalt using an in vitro model. We studied
adhesion processes with the help of a computer‑controlled image‑analyzing
system and examined the activation of PMNs by quantification of leukotriene
B4 (LTB4) release. The biphasic
effects of the valuated heavy metals on PMN‑EC adhesion, with stimulation
at very high and very low molar concentrations, were observed. The release of LTB4 by PMNs increased during
exposure to very low metal concentrations. The initiation of these important pathogenetic mechanisms of inflammation at very low metal
ion concentrations, which give no
morphologic changes, must be regarded as
potentially significant with respect to the toxic effects of heavy metals.
BIO‑PROBE COMMENT: Damage to the inner lining of blood
vessels (endothelium) is widely regarded to be the initial step in the disease
process that leads to cardiovascular disease. Although mercury was not included
in this study, it is a heavy metal that has previously been shown to cause
endothelial
damage. The three metals examined in this
study nickel, cobalt and zinc) are all used in dental restorative materials.
Research, published in peer‑reviewed dental journals, has demonstrated
the release and bioavailability of nickel (and mercury). Cardiovascular disease
has become widespread only
since the 1920's, about the time of
increased use of heavy metals in dental therapy and long after humans consumed
eggs, meat, milk, butter and cheese.
&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&
Toxicology 1996 Mar 18;107(3):189‑200
Mercury accumulation in the squirrel monkey eye
after mercury vapour exposure.
Warfvinge K, Bruun A
Department of Ophthalmology, University Hospital of Lund, Sweden.
Squirrel monkeys were exposed to mercury vapour
at different concentrations and for different numbers of days. The calculated
total mercury absorption ranged between 1.4‑2.9 mg (range of daily
absorption 0.02‑0.04 mg). The monkeys were killed at different intervals
after the end of exposure (range 1 month ‑ 3 years) and the eyes were
enucleated. Eyes from four un‑exposed monkeys were used as control
material. Mapping of the mercury distribution in the eye revealed that the non‑myelin‑containing
portion of the optic disc was densely loaded with mercury deposits, which are
mostly confined to the capillary walls and the glial
columns. The white matter of the brain does not accumulate mercury at these
exposure levels, which might suggest that the myelinization
process inhibits the accumulation of mercury. The pigmented epithelium of the
pars plicata of the ciliary
body and of the retina contained a considerable amount of mercury. This finding
indicates that mercury is trapped within the melanocytes,
which keeps potentially dangerous material from reaching the neural retina. In
addition, the retinal capillary walls were densely loaded with mercury
deposits, even 3 years after exposure. It was also found that the inner layers
of the retina accumulated mercury during a 3‑year period. It is known
that the biological half‑time of mercury in the brain may exceed years.
This seems also to be the case for the ocular tissue.
PMID: 8604479, UI: 96180636
***************************************************************
Toxicology 1988 Sep;51(1):67‑76
Enhanced electroretinogram in cats
induced by exposure to mercury acetate.
Gitter S, Pardo A, Kariv N, Yinon U
Institute for Occupational Health, Maurice and Gabriela Goldschleger Eye Research Institute, Chaim
Sheba Medical Center, Tel‑Hashomer, Israel.
The present study was undertaken in order to verify whether, and
how, retinal functions are affected by subacute
poisoning with organic mercury. Mercury
acetate in various concentrations (0.025‑0.25 mg/kg per day) was injected
subcutaneously every second day to adult cats (N = 20) throughout a 2.5‑4.0‑week
period. The electroretinogram (ERG) was recorded and
the Hg2+ concentrations in the blood were determined. In nearly 90% of the
intoxicated cats an enhanced electroretinogram (scotopic b‑wave amplitude)
was found as compared to its level in the normal control cats (N = 10). The
latency of the ERG was found to be appropriately shorter, up to a maximal
difference of nearly 20% in comparison to the controls. Hg2+ was present in the blood of the
exposed cats during a 2.5‑month period following the exposure. It is
concluded that exposure to mercury acetate
induces a permanent increase in the excitability level of the cat's
retina.
**************************************************************************
Toxicology 1983 Jan;26(1):1‑9
A cell aggregation model for the protective effect of selenium and
vitamin E on
methylmercury toxicity.
Kleinschuster SJ, Yoneyama
M, Sharma RP
Histotypic aggregation of embryonic neural
retinal cells was chosen as a test model to evaluate mercury toxicity. After 24
h rotational culture with methylmercury
(CH3HgCl) at 4 microM, aggregation was completely
inhibited. A dose‑response relationship between concentrations of methylmercury and final sizes of aggregates was found.
Selenium (Na2SeO3) at concentrations of 1, 3 and 5 microM
provided a protective effect for methylmercury (1 microM) toxicity. Vitamin E (DL‑alpha‑Tocopherol
acetate) at concentrations 5, 7 and 10 microM also
provided protection against the same concentration of methylmercury;
however, it was less effective than selenium. Histotypic
embryonal retinal cell aggregation may be a useful
assay system for in vitro neurotoxic studies in
morphogenesis.
PMID: 6829026, UI: 83147085
***********************************************************************
Science 1979 Oct 5;206(4414):78‑80
Heavy metals affect rod, but not cone, photoreceptors.
Fox DA, Sillman AJ
Low concentrations of lead, mercury, or cadmium depress the
amplitude of the rod receptor potential in the perfused
bullfrog retina. Responses from the cones were not affected. The data implicate
the rods as a lesion site in animals exhibiting scotopic
vision deficits as a result of heavy metal poisoning.
PMID: 314667, UI: 80014468
K.Warfvinge et al, "mercury accumulation in
the monkey eye after mercury vapour exposure. Toxicology, 1996, 107: 189‑200.
mercury
from vapor exposure accumulates over time in the various parts of the eye.
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%
Kishimoto T, Ohno M, Yamabe S, Tada M
Methylmercury Injury of Cultured Human Vascular Endothelial Cells
Journal of Trace Elements in Experimental Medicine. 6(4):155‑162,
1993
Abstract The
effect of methylmercury chloride (MeHg)
on cultured human vascular endothelial (HVE) cells was investigated.
Umbilical vein‑derived HVE
cells were collected by enzymatic digestion with collagenase.
At concentrations of 0‑50 mu M, MeHg had only
barely detectable effects on cell
viability. However, the viability of HVE cells decreased dose‑dependently
at concentrations >100 mu M.
Morphologic
examination by phase‑contrast microscopy revealed a markedly damaging
effect of MeHg at concentrations exceeding 500 mu M. The cytotoxic effect of MeHg on DNA synthesis was also concentration‑dependent.
These results suggest that HVE cells are susceptible to concentration‑dependent
MeHg cytotoxicity and that MeHg could induce vascular endothelial injury, which may be
involved in the pathogenesis of arteriosclerosis. (C) 1993 Wiley‑Liss,
Inc. [References: 34]
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%
I have seen several
abstracts related to eye degeneration and mercury ,
due to my friends father's eye degeneration, I researched abstracts for my friend to give to his father. I do not have any of them handy yet
anymore, but I found 1‑2 from Sam Queen's Chronic Mercury Toxicity book(see anotated bibliog.) , and
I found quite a few more when I researched glutathione and lipoic
acid, in addition to mercury, and it has been proven that mercury depletes
glutathione and lipoate by binding to the thiols in these 2 as well as inhibiting various important
glutathione system enzymes.
I found the abstracts
from Medline, additionally, some where in the Life Extension Foundation
Magazine abstract sections, and the same can be found also from Medline. I am sorry that these days I do not have
enough time to go fetch the abstracts for you.
But, what I found from tbe abstracts, lipoate, NAC, GSH, E‑vitamin and C‑vitamin have
the greatest potential to be used as a protective treatment against mercury
also in all eye disease that are due to oxidative damage and thiol‑binding by mercury.
Plaase
go to Medline at www.medscape.com, join them free, and
then seach with "mercury" and
"macular" or "lipoate" and
"macular" or "glutathione" and "macular" and
cross all the years down to 1980 at least, and you will fork many abstracst to read.
Hope this helps,Ray
&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&
From: "Amy L. Riskedahl,
O.D." <ariskedahl@seanet.com>
Subject: Re: Vision
Cataracts and macular degeneration are the two eye diseases most
often
attributed to oxidative damage. Cataracts can be taken out surgically but
macular
degeneration
often can't be helped. The progression
can be slowed with
large amounts of certain anti‑oxidants
such as lutein.
The macula is the part of
the eye that has the
highest number of cones and
thus the sharpest vision and the best color vision. Mercury and other things that cause oxidative
damage can damge the macula over time.
Generally what you do to
heal the body, heals the eye. Get rid of the mercury. Vit. C, Vit. E, essential fatty
acids, proanthocyanadins and several of the carotenoids
are things that have been proven to heal the eye. Keep the cardiovascular system healthy. The retinal artery is a branch off of the carotid artery so plaques thrown off the carotids can
cause strokes in the eye just as
they do in the brain.
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%
Cavalleri A, Gobba
F. Reversible color
vision loss in occupational exposure to metallic mercury. Environ Res 1998 May;77(2):173‑7
Sezione di
Medicina Preventiva dei Lavoratori, Universita di Pavia, Pavia,
Italy.
Color vision was
evaluated in twenty‑one mercury exposed workers and referents matched for
sex, age, tobacco smoking, and alcohol habits. The Lanthony
15 Hue desaturated panel (D‑15 d) was applied.
In the workers, mean urinary Hg (HgU) was 115+/‑61.5
microg/g creatinine; in all
but one the values exceeded the biological limit (BEI) proposed by the American
Conference of Governmental Industrial Hygienists. A dose‑related subclinical color vision impairment
was observed in Hg‑exposed workers compared to the referents. Just after
the survey, working
conditions were improved. Twelve
months later the workers were reexamined. Mean HgU
was 10.0 microg/g creatinine and in no subjects was the BEI exceeded.
Color perception was significantly improved compared to the first examination
and, furthermore, no differences were observed between exposed workers and
referents. The results add evidence that the color vision loss observed during
the first part of the study was related to Hg exposure and, moreover, show that
this effect is reversible. These data indicate that metallic Hg can induce a
reversible impairment in color perception. This suggests that color vision
testing should be included in studies on the early effects of Hg. The
possibility of applying the D‑15 d as an early effect index in the
biological monitoring of Hg exposed workers should also be
entertained. Copyright 1998
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I do not know of any direct science references tying mercury with
Macular Degeneration. However, from
indirect information there appears to be a connection.
Dr. Johnathon Wright and Alan Gaby have
developed a nutritional protocol that is quite
effective.
It is interesting to note that the nutrients are all those that mercury
reduces in the body. ie Taurine, Vit E, Selenium, and
Zinc. I am sure most ACAM physicians
would be happy to get the formula (if it isn't already included in their data)
and administer it. It is given by IV,
except the Vit E.
‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑
Sam Ziff
<bpinfo@bioprobe.com>
<http://www.bioprobe.com/>
Myasthenia Gravis
Quite common with mercury poisoned, relates to antibodies against
acetylcholine receptors, mercury has major effects of impairing acetylcholine
metabolism and neural transmission, and bindind to
the receptors. Quite a few abstracts is available of
that, so the linking of myastenia gravis to the
changes mercury cause is not that great jump to make. I know numerous people
that had myastenic
symptoms, and continue to have from amalgams, I
am one of those, and Freya on the list has similar, and it was quite frequent
when I used to go to amalgam poisoned's meetings in
the early part of
the decade, we had meetings of up to 50 poisoned in Tampere
Finland and even more in Helsinki, and discussed diagnosises
and symptoms each had from amalgams, and myastenia
was one fairly common in addition to MS/ALS , autoimmunities, thyroid, prostata,
liver, kidney, fibromyalgia, chronic fatique and
various other symptoms/ conditions resulting or contributed by the mercury and
copper leaking from the amalgams en masse.
Ray Sarela
++++
Washington University Medical School
Neuropothyhttp://www.neuro.wustl.edu/neuromuscular/nother/toxic.htm
>(another source of eye mercury
& eye problems)
> Mercury is still used in eye makeup as a preservative. From
the FDA site:
>
> http://vm.cfsan.fda.gov/~dms/cos-hdb3.html
>
> Mercury compounds (21 CFR 700.13).
> The use of mercury compounds as cosmetic ingredients is
limited to eye
> area cosmetics at concentrations not
exceeding 65 parts per million
> (0.0065%) of mercury calculated as the metal (about 100 ppm or 0.01%
> phenylmercuric acetate or nitrate)
and provided no other effective and
> safe preservative is available for
use.
>
> Mercury compounds are readily absorbed through the skin on
topical
> application and have the tendency to
accumulate in the body. They may
> cause allergic reactions, skin irritation, or neurotoxic
> manifestations.
>
> List members may be interested to note that information on
this subject
was published in the American Journal of Clinical Pathology in 1973 (Vol. 59,
> 515-7) by my colleagues in the Department of Forensic
Medicine, University
> of Glasgow, Scotland following
research in Africa.
> It is surprising that such a toxic metal should continue to
be used in
> cosmetics.
> Ian Dale
> Occupational Hygienist
> Glasgow Occupational Health
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„Conjunctivitis sicca“ or „dry eye study“
_ Conjunctivitis sicca (dry eyes) is a major
health problem for about 4 million people in Germany.
The „dry eye study“ with 36 patients has
shown that people with heavy metals like amalgam or palladium used in their
goldcrowns often have fungi in the large intestine and also food allergies.
Patients which have been treated had very good results. Other visual problems
(spectacles) have shown to be highly correlated with the number of amalgam
fillings as well.
Marburg Amalgam Study. (there also is a
published version)
From:
"Dr.B. Weber, Amalgaminformation Marburg,
http://home,t‑online.de/home/Institut_f._Naturheilverfahren/patinf.htm"
<b.weber@FIREMAIL.DE>
Subject:
Information about treatment of 3000 patients with amalgam‑problems
in german and englisch
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Dr. D.A. Carroll, O.D.&
Dr. B.C. Lane, Preventing mercury
related cataracts,
www.medicalvisioncenter.com/prevention.html; & Alan Thal, MD, Cataract reversal through mercury detox,
www.digitalnaturopath.com/treat/T33633.html; & Dr, Ben Lane,
O.D., Methylmercury in seafood contributes to
cataract development, Medical World News, December 20, 1982; &
Dr. Victoria Buntine, Mercury Effects, Healthinasia
Incorporated, 2001, www.healthinasia.com/mercury.html,
& Dr. G. E. Poesnecker,
Its Only Natural, 2001, www.oneflesh.org/only‑22.html;
Iritis,
Inflammation of the Eye, (autoimmune condition, can be caused by
mercury)
Syphilitic iritis
after treatment with mercury common; likewise use of thimerosal
eyedrops
Photophobia often
accompanies mercury poisoning, http://www.causeof.org/sensitivity.htm#TreatIritis
************
Astaxanthin, a natural supplement has been
documented to relieve eye fatigue and improve visual acuity and accommodative
amplitude. Reduces inflammation.
Life Extension Foundation Life Extension Jan 2009
Mercury ‑ inorganic
òToxicity òElemental metal òUsually
airborne exposure òOften produces neural disease
without systemic disorders òSalts: GI absorption òProduce systemic & neural effects Organic mercurials: Methyl mercury òLittle
peripheral nerve toxic toxicity òEarly paresthesias & ataxia related to CNS effects òConverted from inorganic mercury by microorganisms òThen enters food chain Outbreaks of toxicity
Minimata Bay: Spillage of HgCl
into sea òIraq: Ethyl Hg fungicide in grain used for
baking bread òSubacute: Metallic mercury vapor òNeuropathy òMotor òAxonal òMyokymia ò
Encephalopathy òOther: Mouth
inflammation; GI; Fetid breath òChronic ò
CNS: Encephalopathy; Psychosis; Extrapyramidal;
Ataxia òNeuropathy:
Sensory & Motor; Pain & paresthesias
ò
Children: Acrodynia òEncephalopathy
òAutonomic: Tachycardia; Hypertension;
Sweating on trunk òInsomnia; Weight
loss; Constipation
òDiagnosis: 24 hour urinary excretion òInorganic
toxicity only ò
Treatment: ?Chelation;
Spironolactone
Optic Nerve & Eye
òAtaxias òFriedreich òMitochondrial
‑ NARP Syndrome: (Neuropathy; Ataxia; Retinitis Pigmentosa)
òPosterior column ataxia + Retinitis pigmentosa òHMSN VI òToxic òCarbon disulfide òDisulfiram òMercury (Hg) òNutrition: Cuban neuropathy òVernant's
disease
3. Cerebellum
òA‑beta‑lipoproteinemia òAtaxia telangectasia
òFriedreich Ataxia ò
Paraneoplastic: Hu; CV2 òInfantile Onset Spinocerebellar
Ataxia (IOSCA) òMetachromatic Leukodystrophy
òRefsum òSCA 2, 3, 4
4. Supratentorial òHereditary
òCowchock Syndrome òFabry's
òHexosaminidase A (Late Onset) òMulti‑Infarct
Dementia (CADASIL) òPorphyria òPrion
protein (PrP27‑30)
mutation: Glu200Lys òPolyglucosan
body syndromes òFamilial ALS: Higher prevalence of
dementia (~15%) than sporadic ALS òInfections òHIV òLyme disease òRabies òSyphilis òInflammatory & Immune òSarcoid
òVasculitis òMetabolic òThyroid òVitamin B12 deficiency òHypophosphatemia òMitochondrial:
òMELAS (Mitochondrial Encephalomyopathy;
Lactic Acidosis; Stroke)
òMERRF (Myoclonic Epilepsy; Ragged Red Fibers
òMNGIE Syndrome (Myopathy and external ophthalmoplegia; Neuropathy; Gastro‑Intestinal;
Encephalopathy) òMotor neuron disorders with dementia
(Sporadic) òWestern Pacific ALS òFrontal Dementia followed by motor system disease òUpper motor neuron: Especially bulbar òLower
motor neuron: Fasciculations; Less prominent weakness
ò? Atypical Creutzfeld‑Jacob syndromes òNeoplastic: Lymphoma (angiotropic
large‑cell); Carcinomatous
meningitis òParaneoplastic (anti‑Hu)
òToxic: Alcohol; Anticholinergic;
Arsenic; Lead; Mercury; Podophyllin; Thallium; Vacor
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