Answers 141-150

Questions and Answers 141-150 are here, in reverse chronological order.

Please note that no treatment should be altered without prior consultation with your specialist or GP.

Question 150 Answer
Question posted September 10, 2002

My sister just got numbness down the right hand side of her body, she couldn't feel anything. Also she is getting weird headaches ever so often. The numbness is gone now but she doesn't feel 100%. What do you think it is?

Answer posted October 16 2002

Sorry for the delayed reply. I will assume your sister is in her 20s like you. Numbness down one side of the body usually indicates interference with the sensory pathways (from skin to nerve to spinal cord to brain) in the body. She should see her GP who may recommend a referral to a neurologist - we now have 12 consultant neurologists in the public sector in Ireland!!.

Dr Lynch

Question 149 Answer
Question posted September 9, 2002

In 1992 I had an MRI which my then Neurologist did not discuss with me. I am on my 6th Neuro as they come and go where I live. My question is why my tremor becomes much worse when tensing the bladder control muscles when I get a sudden and urgent sensation to urinate. I have had prostate checked after passing blood earlier this year. For the past couple of years I have beeen rather uncomfortable initially in morning but once the discomfort in the right buttock passes, I can feel near normal again. What is relationship between lower back discomfort and PD if any? Thank you.

Answer posted October 16 2002

PD tremor often gets worse when the automatic centre for movement (basal ganglia) in the brain is activated. Most physical and mental activity - thinking, walking, talking, micturition, etc. etc. increases tremor as the basal ganglia is activated. PD can be associated with pain especially as Sinemet/Madopar wears off - usually the pain is down the same side as where the PD symptoms begin. Sometimes patients get cramping, abdominal, chest, back, rectal or vaginal pain as part of wearing off. Usually a dispersible/dissolvable Ldopa pill (e.g. Madopar Dispersible 62.5mg) first thing before getting out of bed blocks/stops the pain.

Dr Lynch

Question 148 Answer
Question posted September 5, 2002

Dear Dr Lynch , I was recently prescribed Sinemet 275mg 3 x a day which helped improve my condition (question 133) . The low dose of Sinemet Plus had no effect . My questions are:

  1. Is the dose I am currently taking classed as a low dose of Sinemet because after 3-4 hours of taking it my symptoms start coming back . Could I take with my doctors approval 4 a day ?
  2. Would it assist me to take Sinemet CR at night to help aid a good nights sleep ?
  3. I still have this shake while I am at rest or find myself in a stressfull situation. Are there any drugs that could help this or should the Sinemet help this ?
  4. With all the information I have now given you I would like your views on whether you think it is PD, as I have to wait a long time to see my neurologist, and the not knowing is worse than being told it is as I have prepared myself for that outcome .

With all the information I have found on your website it would appear that it is in fact PD .

Would you also be able to put me in contact with anybody of my age (34) who also has PD as talking helps me a great deal .

Thanks once again for your invaluable help .

Answer posted October 31, 2002

Sorry for the delayed replies. I will answer both questions 139 and 148.

1. Sinemet 275mg 3/day is a moderate to high dose of levodopa. You could increase to 4/day but I think extending the benefit of the Sinemet by the addition of Selegeline and/or Entacapone would be preferable. In addition taking a siesta early afternoon to recharge the batteries may help to boost the Sinemet effect.

2. Sleep is commonly interrupted in PD. Using a low dose tricyclic antidepressant (e.g. Amitriptyline 10mg or 25mg) is preferable to adding more Sinemet overnight. Being off levodopa overnight in some may allow theh dopamine system to reset itself.

3. Rest tremor is the hardest symptom to treat - it usually reappears with excitement or stress. I often get people to use low dose Diazepam (Valium) e.g. 2mg one to one and a half hours before a stressful/exciting event (e.g. public speaking). Diazepam is a good muscle relaxant and amyiolytic that can suppress tremor. The dose can be adjusted to your needs and usually people with PD do not get addicted as they do not have the addictive neurochemical, dopamine, in the brain.

4. You have rest tremor, stiffness and slowness - 3 of the 6 cardinal features of PD. Also, your symptoms responded to levodopa. Therefore I share your strong suspicion that you may have early PD (young onset PD). There are many people of your age with PD unfortunately. I am sure the PALS group could put you in touch with someone of your age with PD - if not I would be happy to ask someone with YOPD. It is important to be aware that our treatments at present will be surpassed over the next few years, hopefully with agents that can reverse or stop the disease.

Dr Lynch

Question 147 Answer
Question posted September 4, 2002

There is quite a stir througout the Parkinson's community, that being us the Parkinson's patients and not the organizations, concerning initial diagnosis and surgical produres such as DBS.

Many of us are told that the only "positive" way to diagnose Parkinson's is via a brain autopsy

Recent events involving our dear friend Deborah Setzer are prompting us, the patients to demand a change in diagnosis as well as verification of Parkinson's prior to surgeries such as DBS. Deborah was diagnosed nearly 5 years ago, had DBS, took all the brain altering drugs, and today she has been told she never had Parkinson's and never should have had DBS without the f-dopa brain scan prior.

A Positron emission tomography (PET) scan of the brain is a research tool and is not used in standard medical practice to see if there is a deficiency in dopamine (a Fluorodopa (F-dopa) PET scan). Conditions other than PD may have a dopamine deficiency but, the pattern of loss may help differentiate these. Because of the cost ($2300) and inaccessibility for most neurologists, PET scans are usually not performed.

My questions are:

  1. Prior to surgeries such as DBS, is a f-dopa scan recommended?
  2. Understanding the cost of a f-dopa pet scan is around $3000 U.S., the machine cost of $2million, the limited hospitals with this machine, as well as the limited pysicians trained to administer/read the results of this scan---would it not be beneficial to the Neurologist/MDS and the patient to obtain this test even if travel may be involved??
  3. What percentage of accuracy does the f-dopa scan give?
  4. Why is this technology not used routinely?

Thank you for your time.

Answer posted October 16 2002

Sorry for the delayed reply. It is difficult for me to reply to these questions as we are not inserting DBS here in Ireland yet and hence we have not had to deal with these issues. Secondly we have one PET scanner in Ireland that is not doing flurodopa PET yet.

However PD is still primarily a clinical diagnosis - it can be supported by flurodopa PET or a dopamineamino transporter spect. (Tissue diagnosis at autopsy is the definitive method of diagnosis).

Therefore in answer to your questions -

1. Most institutions do not routinely perform a flurodopa PET before DBS surgery.
2. Having a flurodopa PET pre DBS is not an unreasonable thought provided the scan is interpreted in parallel with the clinical history and examination - atypical parkinsonism also have abnormal flurodopa PET but do poorly with DBS.
3. Accuracy of diagnosis? The PET still neds to be interpreted in conjunction with the clinical history and examination as atypical parkinsonism has abnormal PET imaging also.
4. PET is not used routinely because it is expensive, cumbersome, exposes the patient to radioactive isotopes and in the majority of patients the clinical assessment makes a clear diagnosis of PD.

Dr. Lynch

Question 146 Answer
Question posted September 3, 2002

From a physician-psychiatrist:

I have recently begun treating a 44 year old woman with "benign essential tremor." Two neurologists have seen her and can offer little treatment. She is trying inderal and others without result. I treat her for longstanding depression and I have been following Dr. Glenmullen's ideas about Prozac Backlash. If the serotonergics which she has been on for 15 years have contributed to the tremor what possible alternative anti-depressant therapy might I consider. Thank you.

Answer posted October 16 2002

Sorry for the delayed response. There is a nice review of essential tremor in the NEJM 2002 by Elan Louis MD including pathogenesis and treatment options.

The bottom line is that bad ET is difficult to treat. Propranolol can sometimes help. Mysoline is often more effective but has to be titrated very slowly over months and often is not tolerated. If there is a strong family history of ET I suspect discontinuing an SSRI will be of little help. I see more ET-like tremor with Lithium and sodium valporate. Perhaps an old fashioned tricyclic antidepressant might be work trying as the anticholinergic side effect might help the tremor.

Dr Lynch

Question 145 Answer
Question posted September 2, 2002

My father was diagnosed with a familial tremor 12 years ago by a neurologist. Familial tremors run in our family. We sought a second opinion by another neurologist who diagnosed him with Parkinson's Disease. This neurologist began medicating him with Sinimet and other Parkinson's medication.

We sought a third opinion by another neurologist who also diagnosed him with Parkinson's disease. The medication never relieved the tremor in his right hand, therefore, the neurologist continued to increase the medication.

After eight years, my father began to have severe tremors in both hands, arms, legs, face, and internally. He also developed blood clots, ulcers, very low blood pressure and his eyes bulge out. After several trips to the emergency room, the emergency room physician advised us to discontinue his medication. We sought the help of a neurologist to began discontinuing the medication and he is actually doing better without the medication.

He no longer takes any PD medication. We went to a university hospital that specializes in deep brain stiumlation. They would not do the surgery because one doctor says he does not have PD, but, he doesn't know what he has. His tremors are severe and so is his fatigue.

He needs help, but, we don't know what to do or where to go. Please help.

Question 144 Answer
Question posted August 31, 2002

I am a 43 y.o. male, not an athlete, but also not deconditioned. Over the period of the last 3.5 years, sx (symptoms) of visual loss, cognitive problems, & neuro-muscular problems have appeared.

DECEMBER 98- blurred lower visual field(LVF) OD in apparent Optic neuritis(papilladema, no cupping); tx: patching.

MARCH 99: loss of LVF OD, poor light acceptance and blurs in UVF(optic atrophy/no papilladema); tx: oral corticosteroids(CS).

JULY 99-slow progressive losses OD and rapid progressive losses OS(3 weeks from floaters to near total loss, severe anemia, dx as NA AION; tx: IV and 3 mo. 40mg daily oral CS, iron and steroid support.

OCTOBER 99-bone marrow biopsy showed leukoerythroblastic smears in peripheral blood (LE).

AUGUST 00-hemorrhoid surgery, mild hypertension/hyperlipidity.

SEPTEMBER 00-slow worsening OU from CS recovery level; tx: IV and 1 mo. 60mg daily oral CS.

FEBRUARY 01- slight worsening OS from CS recovery ! level, LE and anemia cleared; tx: 6 mo. course of Avonex.

MARCH 01- tremors & fasciculation rt arm.

APRIL 01-bilateral tremors, 5 of 18 FM tender points.

JUNE 01-muscular weakening (MW) noted(decreased weight handling, increased fatigability),constant suprination rt foot, borderline sub-cortical dementia(CP), mild GERD.

AUGUST 01- intermittent myoclonus (IM) rt wrist.

NOVEMBER 01- tonsillectomy/UPPP for chronic tonsillitis/mild sleep apnea, visual loss dx as bilateral optic atrophy.

DECEMBER 01- constant suprination lt foot.

FEBRUARY-MARCH 02- restricted ROM(weak pronation in feet, no suprination in wrists & restricted active/pain-limited passive ROM for all joints); tx: constant wear bilateral wrist & ankle braces prescribed, physical/occupational therapy (> 6X/wk).

MAY02- pulmonary hypertension, REM hypoxemia, aortic/tricuspid regurgitation, systemic IM & tremors, cogwheel effect legs & arms, continued MW, edema & itching, 18 of 18 FM tender points, TMJD & worsening GERD & IBS; tx: 2 l/min supp! lemental oxygen, Zocor & 50mg Elavil nightly, CTM, Zyrtec, Celebrex, T enormin, HCTZ, Aciphex, Zantac & Simethicone daily, and Immodium, Surfak, Ibuprofen, Vicadin & Flexaril PRN.

JUNE 02- lessening progression of MW & CP, near-stability of visual field loss with varying acuity throughout the day. I have had 4 MRIs (latest in MAY02, all clean), 5 LPs (latest in DEC 01, slightly elevated opening pressure on all but last), pulmonary & cardiac exercise studies, 4 sleep studies, 3 Neuro-psych. batteries (showing progressive problems in manual dexterity, multi-processing, processing speed & attention/concentration) & innumerable blood & urine tests(including LHON screening, with no definitive clinical markers). EMG scheduled for 10 SEPTEMBER 02.

Answer posted October 16 2002

Sorry for the delay in replying. I am unclear what the question is as your history is highly complex. I assume you have been given a diagnosis and are attending a neurologist(s).

Dr Lynch

Question 143 Answer
Question posted August 16, 2002

I wonder if you can help. I am on a dose of 6mg of Cabaser once a day and 1.25 mg of Zelapar once a day and have been taking these drugs for about a year and a half.

I am now suffering with quite severe abdominal pains, which extend round my kidney area and round the front of my lower abdomen and is painful when sitting.

I have had a ultra sound examination which has found gall stones, but the pain I am suffering is not typical of Gall Stones.

Have you any knowledge of any one who has suffers this with this type of problem and the cause was the Parkinson Disease drugs.

My Doctor is working on the problem but any help would be very useful

Question 142 Answer
Question posted August 14, 2002

From an Occupational Therapist:

I am currently working with a woman who has a diagnosis of profound MR and CP, and it was recently discovered that there have been ischemic changes in her brain. She has high tone in both her arms, the right more so than the left.

Someone suggested that the use of BOTOX might help with the atrophy. However the only documentation I find is the use of it primarily with face lifts. Is there any information for the use of BOTOX under these circumstances, and do you have any recommendations?

Thank you.

Answer posted August 16, 2002

Botox was first used to treat eye squints in the 1980s. Subsequently it has been used for treatment of dystonia and more recently spasticity. It is commonly used in patients with CP to release spasticity and/or contractures. It can be very helpful in this setting but may need to be repeated every 3-4 months. Botulinum toxin has been a marvelous development for neurological disorders and its use for wrinkles is only of recent development.

T Lynch

Question 141 Answer
Question posted August 10, 2002

Is there any relationship, between Agent Orange and PD. I have read alot of articles on PD caused by exposure to pesticides. I was diagnosed with PD when I was 24 years old. There is no history of PD in my family and the cause of my PD is unknown. My father was exposed to Agent Orange in Vietnam. I was then conceived shortly after his return to the states. I find it highly coincidental that I came down with PD and none of my older siblings have any medical problems.

I thank you for your time and any info that you can provide. Again, thanks

Answer posted August 16, 2002

I don't know of reports of Agent Orange and PD. PD onset at age 24 is often due to autosomal recessive inherited PD, i.e. parents are carriers but not affected and the children have a 1 in 4 risk of getting disease. Mutations in the gene Parkin are commonly found in people with onset of PD before age 30. I do not know if a diagnostic Parkin gene test is available in the USA. It is not available in Ireland yet.

T Lynch

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