1. Rev Neurol. 2002 Oct 16-31;35(8):741-2.

[Hypothyroidism concealed by Parkinson's disease]

[Article in Spanish]

García-Moreno JM, Chacón J.

Servicio de Neurología, Hospital Universitario Virgen Macarena, Sevilla, España.
sinue@arrakis.es

AIMS: Although it is commonly recognised that diseases of the thyroids can
simulate extrapyramidal disorders, a review of the causes of Parkinsonism in the
neurology literature shows that they are not usually mentioned or, if so, only
very briefly. The development of hypothyroidism in a patient with Parkinson s
disease can go undetected, since the course of both diseases can involve similar
clinical features. Generally speaking there is always an insistence on the need
to conduct a thyroidal hormone study in any patient with symptoms of Parkinson,
but no emphasis is put on the need to continue to rule out dysthyroidism
throughout the natural course of the disease, in spite of the fact that the
concurrence of both pathological conditions can be high and that, in the same way
hypothyroidism can simulate Parkinson s disease, the latter can also conceal
hypothyroidism. CASE REPORT: We report the case of a female patient who had been
suffering from Parkinson s disease for 17 years and started to present on off
fluctuations that did not respond to therapy. Hypothyroidism was observed and the
hormone replacement therapy used to resolve the problem allowed the Parkinsonian
fluctuations to be controlled. CONCLUSIONS: We believe that it is very wise to
suspect hypothyroidism in patients known to be suffering from Parkinson s
disease, and especially so in cases where the clinical condition worsens and
symptoms no longer respond properly to antiparkinsonian treatment. These
observations stress the possible role played by thyroid hormones in dopaminergic
metabolism and vice versa.

PMID: 12402227 [PubMed - indexed for MEDLINE]

-------------------


1. Arch Gerontol Geriatr. 2001 Nov-Dec;33(3):295-300.

Subclinical thyroid disease in patients with Parkinson's disease.

Tandeter H, Levy A, Gutman G, Shvartzman P.

Department of Family Medicine, Health Sciences Faculty, Ben-Gurion University of
the Negev, PO Box 653, Beer-Sheva 84105, Israel. howard@bgumail.bgu.ac.il

The objective of this study was to determine whether hypothyroidism is more
common in Parkinson patients than in a control group without Parkinson, as
suggested in the past. We performed a retrospective file review of all admissions
to the geriatric ward during a 1-year period. Concentrations of thyroid
stimulating hormone (TSH) and thyroxine (T4) from 92 Parkinson patients were
compared with those of 225 randomly selected controls from the same ward.
Hypothyroidism was not found to be more common in patients with Parkinson disease
as previously suggested. Incidentally, we found an unexpected increase in the
prevalence of abnormal thyroid laboratory tests in this group. Statistically
significant differences were found in two subgroups, (1) men with Parkinson were
more likely to have abnormal thyroid laboratory tests as compared with controls;
and (2) 'subclinical' hyperthyroidism was found to be more prevalent in Parkinson
patients than in controls. Further research in this field is warranted in
non-hospitalized patients.

PMID: 15374026 [PubMed]

---------------------------

1. Ann Endocrinol (Paris). 1990;51(1):43-5.

[Dysthyroidism and Parkinson's disease]

[Article in French]

Guerin V, Guyot C, Hartemann P.

Clinique Médicale et Endocrinologique, CHU Nancy.

Associations between hyperthyroidism and Parkinson disease have been reported.
The treatment of the hyperthyroid state seems to improve the extrapyramidal
symptomatology. We report a case of a woman suffering from Parkinson disease and
hypothyroidism. The treatment with thyroxine increased parkinsonian tremor.
Dopamine regulation of TSH circadian and pulsatile release is not clear. These
observations stress the possible role of thyroid hormones in regulating
dopaminergic metabolism.

PMID: 2221822 [PubMed - indexed for MEDLINE]

--------------------------


1. Med Hypotheses. 1987 Nov;24(3):249-63.

Disease family trees: the possible roles of iodine in goitre, cretinism, multiple
sclerosis, amyotrophic lateral sclerosis, Alzheimer's and Parkinson's diseases
and cancers of the thyroid, nervous system and skin.

Foster HD.

Department of Geography, University of Victoria, British Columbia, Canada.

Geographical distribution patterns of incidence and mortality for a wide variety
of diseases display strong positive and negative correlations when analyzed
statistically. It is argued that these relationships do not occur by chance, but
reflect the causal role of surpluses and/or deficiencies of various bulk and
trace elements. This concept is explored for one such "disease family tree", that
of iodine. Deficiencies of this essential trace element appear to be associated
with many diseases, or birth defects, including goitre, cretinism, multiple
sclerosis, amyotrophic lateral sclerosis and cancer of the thyroid and nervous
system. Although the evidence is weaker, iodine deficiency may also be implicated
in Alzheimer's and Parkinson's diseases. In contrast, too much iodine may be
linked to elevated mortality from cancer of the skin and melanoma. Rat studies
indicate that iodine deficiencies can cause reduced brain weight, limited myelin
formation, retarded neuronal maturation, a lowering of the production of various
enzymes and slowing of the rates of protein and R.N.A. synthesis. Similar
processes appear to occur in many of the diseases identified above.

PMID: 3320695 [PubMed - indexed for MEDLINE]

-------------------------

1. Ann N Y Acad Sci. 2004 Nov;1033:158-67.

Effects of carnitine on thyroid hormone action.

Benvenga S, Amato A, Calvani M, Trimarchi F.

Sezione di Endocrinologia, Dipartimento Clinico Sperimentale di Medicina e
Farmacologia, University of Messina School of Medicine, 98125 Messina, Italy.
s.benvenga@me.nettuno.it

By experiments on cells (neurons, hepatocytes, and fibroblasts) that are targets
for thyroid hormones and a randomized clinical trial on iatrogenic
hyperthyroidism, we validated the concept that L-carnitine is a peripheral
antagonist of thyroid hormone action. In particular, L-carnitine inhibits both
triiodothyronine (T3) and thyroxine (T4) entry into the cell nuclei. This is
relevant because thyroid hormone action is mainly mediated by specific nuclear
receptors. In the randomized trial, we showed that 2 and 4 grams per day of oral
L-carnitine are capable of reversing hyperthyroid symptoms (and biochemical
changes in the hyperthyroid direction) as well as preventing (or minimizing) the
appearance of hyperthyroid symptoms (or biochemical changes in the hyperthyroid
direction). It is noteworthy that some biochemical parameters (thyrotropin and
urine hydroxyproline) were refractory to the L-carnitine inhibition of thyroid
hormone action, while osteocalcin changed in the hyperthyroid direction, but with
a beneficial end result on bone. A very recent clinical observation proved the
usefulness of L-carnitine in the most serious form of hyperthyroidism: thyroid
storm. Since hyperthyroidism impoverishes the tissue deposits of carnitine, there
is a rationale for using L-carnitine at least in certain clinical settings.

PMID: 15591013 [PubMed - indexed for MEDLINE]

----------------

1. Altern Med Rev. 2005 Dec;10(4):268-93.

Neurodegeneration from mitochondrial insufficiency: nutrients, stem cells, growth
factors, and prospects for brain rebuilding using integrative management.

Kidd PM.

University of California, Berkeley, USA. dockidd@dockidd.com

Degenerative brain disorders (neurodegeneration) can be frustrating for both
conventional and alternative practitioners. A more comprehensive, integrative
approach is urgently needed. One emerging focus for intervention is brain
energetics. Specifically, mitochondrial insufficiency contributes to the
etiopathology of many such disorders. Electron leakages inherent to mitochondrial
energetics generate reactive oxygen free radical species that may place the
ultimate limit on lifespan. Exogenous toxins, such as mercury and other
environmental contaminants, exacerbate mitochondrial electron leakage, hastening
their demise and that of their host cells. Studies of the brain in Alzheimer's
and other dementias, Down syndrome, stroke, Parkinson's disease, multiple
sclerosis, amyotrophic lateral sclerosis, Huntington's disease, Friedreich's
ataxia, aging, and constitutive disorders demonstrate impairments of the
mitochondrial citric acid cycle and oxidative phosphorylation (OXPHOS) enzymes.
Imaging or metabolic assays frequently reveal energetic insufficiency and
depleted energy reserve in brain tissue in situ. Orthomolecular nutrients
involved in mitochondrial metabolism provide clinical benefit. Among these are
the essential minerals and the B vitamin group; vitamins E and K; and the
antioxidant and energetic cofactors alpha-lipoic acid (ALA), ubiquinone (coenzyme
Q10; CoQ10), and nicotinamide adenine dinucleotide, reduced (NADH). Recent
advances in the area of stem cells and growth factors encourage optimism
regarding brain regeneration. The trophic nutrients acetyl L-carnitine (ALCAR),
glycerophosphocholine (GPC), and phosphatidylserine (PS) provide mitochondrial
support and conserve growth factor receptors; all three improved cognition in
double-blind trials. The omega-3 fatty acid docosahexaenoic acid (DHA) is
enzymatically combined with GPC and PS to form membrane phospholipids for nerve
cell expansion. Practical recommendations are presented for integrating these
safe and well-tolerated orthomolecular nutrients into a comprehensive dietary
supplementation program for brain vitality and productive lifespan.

PMID: 16366737 [PubMed - indexed for MEDLINE]

(Note: Full text is available for that last one and recommended. )

I'm tired and should probably know the answer - even if it is unknown - but I'm drawing a blank. The dates of your research say that they have dropped the ball? Dare I wonder if it's because hormonal abnormalities are perceived as a woman's disease? i noticed erectile dysfunction was swiftly "supplemented".

Laura - i should know more about this condition but as much as i read about pd, this is the first time I have looked at the thyroid. When you talked about it first being hyper and then turning hypo- i understood that my doctor had not made a mistake. of course i believed doctors knew all the answers then and didn't question it when it changed to hypothyroid.i just thought the first doctor had made a mistake.

i have heard of thyroids going bad from radiation [Chernobyl] and other toxic environments and eventually assumed that i had drunk a lot of heptachlor in Hawaii's milk...for years.

i think we all know that stress is a major killer and causes much suffering. so if they don't know what causes thyroid problems, and they are associated with pd, and often go undiagnosed or unnoticed....doesn't this sound familiar? so why is your research dated 1990s and still standing today without much progress? Perhaps it's a little more complicated than just taking synthroid and could quickly become life threatening if we couldn't get the med for any reason.

so keep us posted laura.

Rick,

I'll answer directly below and try my best to be brief. lol

When you are dealing with this would you say that your arms and legs were best decribed as weak or as rigid?

extremely weak

At its worst, what happens if you try to force yourself to walk?

I scoot along on my rear- sometimes crawling requires too much coordination

How long does it last?

Up to 3 hours but Friday it short cycled all day with rapid shallow breathing. Either Gatorade or Propanalol helped break cycle.

This was unusual and along with rapid breathing I would get hot then cold, so I almost went to the ER.

The fact that meds were really ineffectual in this short cycling made me start thinking that maybe it is a thyroid disorder and that it is interfering with my meds- a lead provided by you or Paula led to an abstract that said this could very well happen.

My answers are weak, everything locks up immediately, and two to three hours, so that's where I'm coming from.

As to the meds in the system,it is as though time had been suspended and they pick up where they left off.

What made you decide you were hypothyroid? Any testing?

I had mild hypothyroid in my twenties that I did not even recall until similar symptoms emerged around 5 months post delivery of my child. I have no metabolism despite not eating much, fatigue, depression, dry skin, etc. (dry skin is unheard of for me). I took Synthroid the first time around and didn't note any changes; I was young, invincible, and clueless, so I stopped taking the med.

I recently had a complete blood panel after visiting my GP about the above symptoms. I have low normal range T3, but they did not test for T4 levels so back I go Tuesday. I also plan to e-mail my neuro and share some of the references with him to see that he recommend an endocrinologist.

In reading your references along with Paula's, it made sense to me that our thyroid hormone play a part in metabolism of my PD meds hence the sudden decline my last trimester to point now where it can interfere at all wearing off times. Your improvement using l-carnitine rather supports this, and I wonder if this is result in my sudden need for more meds post partum.

It does feel like I am experiencing a periodic paralysis as I never felt so profoundly weak. Though, I am confused because the paralysis is result of hyperthyroidism- I did read that there is a Hashimoto's variant where a person can experience the periodic paralysis.

My triggers are stress, wearing off, and being in relaxed state after a full "on" day of activity ie. winding down after dinner with a book or knittingp.

I'm assuming that I am hyperthyroid with associated periodic paralysis based entirely on my experiences until I can talk my way into an endo's office

Laura

P.S. will try the Carnitine in the interim

Paula,

From www.endocrineweb.com:

Causes of Hypothyroidism
There are two fairly common causes of hypothyroidism. The first is a result of previous (or currently ongoing) inflammation of the thyroid gland, which leaves a large percentage of the cells of the thyroid damaged (or dead) and incapable of producing sufficient hormone. The most common cause of thyroid gland failure is called autoimmune thyroiditis (also called Hashimoto's thyroiditis), a form of thyroid inflammation caused by the patient's own immune system.
The second major cause is the broad category of "medical treatments." The treatment of many thyroid conditions warrants surgical removal of a portion or all of the thyroid gland. If the total mass of thyroid producing cells left within the body are not enough to meet the needs of the body, the patient will develop hypothyroidism


The autoimmune version is what strikes during pregnancy. Did you check you 23andme results on this SNP? I have the genetic variant that gives me a moderately high increased risk for Hashimoto's.

What I find really weird is that in one of the case studies (you are right, they are all old), patients had inflammation of thyroid and then ended up with neurodegenerative disease resembling Ataxia, Parkinsonism, etc. Pardon my ignorance, but how in the world does the inflammation "spread" or "migrate" to one's cerebral cortex or basal ganglia?

Laura

Laura-

I swear that it sounds like we are dealing with identical problems. I am beginning to think that it is less a matter of hypo- vs hyper- than it is a matter of dysregulation or poor control. It is possible that you are moving back and forth between the two states as well

The temptation to head for the ER was a factor for me, too. Watch your blood pressure and body temp but don't get obsessed with it. The endocrine system runs on feedback loops and you can throw yourself into a panic attack.

I'm going to add a little more reading material or you. Remember that we are juggling three balls- PD, thyroid control, and a thyroid driven periodc paralysis. Number three is causing the weakness but number two is the foundation for three and is easier to deal with. Get yourself a bottle of acetyl-l-carnitine and keep it on the shelf for confidence if nothing else. It is common enough that the big pharma chains have it. If you do decide to try it, don't under dose. There is a threshold effect. ALC is considered safe at least up to 4 g/day although if pregnant then common sense advises extra caution.

http://www.lef.org/magazine/mag2007/...thyroid_01.htm
<LEF sells supplements, it is true, but they also turn out high quality research.>

http://www.webmd.com/vitamins-supple...ITINE&source=2

http://www.doctoryourself.com/ames.html
<This one is a little OT but worthwhile. Dr. Ames has led the research into the other aspects of carnitine.>

My only reservations at present are the questions of hypo- vs hyper-. If we think in terms of a shortage of one being a surplus of another, then you have to wonder will it make hypo- symptoms worse. But if you think of it as a shortage in both cases (as seems to be the case) then that should be moot. If there is any real danger I think it would be in a runaway hyper- situation (the "storm") which ALC seems to prevent. Too far in the hypo- direction and one feels like crap but no emergency.

Big to you! I would more than likely have checked into a hospital psych ward by now if it weren't for you or Neuro Talk.

What did you show your neurologist to convince him this was a thyroid issue?

I don't know which abstracts would persuade my MDS. I saw him literally days before we stumbled into the realm of the thyroid.

I am thinking we need a remake of the classic sci fi movie "Fantastic Voyage" featuring our brains and endocrine systems

Laura

Well, now, I didn't say that I convinced him of it...

I've got four players to manage here-

1> My GP of 15 years. He knows I am not a hypochondriac since I show up for my annual physical every two years. He also spotted the low potassium so he knows I have something going on.

2> My neuro is new and has seen me twice. First time I walked in but left in a wheel chair as an attack came on. That along with a low potassium reading in his bloodwork got his attention at least. With him I take the approach of "I don't usually show up with a stack of paper BUT this is important to me and I need your help " He, too, knows something is going on and is going to look into carnitine.

3> My HMO uses my GP as the bottleneck so Tuesday I meet with him to discuss how to justify seeing an endo. I expect more blood work.

4> The endo is an unknown.


Something just occurred to me Laura. If you are in a thyroid episode with hot flashes and all, you are going to be just the opposite of when you are paralytic. Your docs need to understand that.

Also, the reality is that, as a woman, if your doctors are men you have a problem I don't. I don't know their personalities but you might consider meeting the issue head on as in: "I know this is a weird problem but it is ruining my life. I also know that there is a risk of some unconscious stereotyping because I'm a woman. I don't think that will be a problem or I wouldn't be here. However, if at anytime you find that creeping in, let's deal with it even if you need to refer me to someone else." That could help or not. You aren't the "poor little me" type.

Laura, my mother was diagnosed with PD 7 years ago and recently has been experiencing depression, tiredness, etc. They just determined she has an abnormal parathyroid. BTW, also lost her smell years ago....... Your article is very interesting.....