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About malexander

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  1. malexander

    Vagus Nerve

    I have had motor symptoms of tremor-dominant medication-recalcitrant PD for almost 10 years. The tremors and dystonia are now well controlled by STN-DBS. While I had anosmia for decades prior to motor symptoms, I have never had what I considered to be GI symptoms. I realize that there is not agreement as to the origin of PD. But, while PD might start in the gut for many patients, and perhaps have an oral origin, I had thought that it might have a nasal origin in my case. I had thought the olfactory bulb to be quite anterior to the distribution of the vagus nerve, but if this is not the case, perhaps I should reconsider my gut.
  2. malexander

    LSVT Loud

    I lead a large support group in California, and I want to offer the best resources to help our members--many of whom have problems with soft speech. I am familiar with LSVT LOUD, but I understand that there is another therapy available: SPEAK OUT. I want to know how this program compares with the LSVT program. Do we have any data that can be used to compare them?
  3. malexander


    I have noticed for the last several years that my exhalations have not been smooth. Actually, I am not aware of this in general activity throughout the day. I notice it when I practice meditation or yoga or any time I attempt a long smooth exhalation. I can maintain a smooth even inhalation easily over 10 seconds, but the exhalation often gets broken up after about 3 seconds. Before PD, I had previously had no such problem. My question is whether this can be a PD symptom--affecting the diaphragm muscle, and, if so, is there any way of treating it. I have had tremor-dominant PD for 9 years and DBS for 5 years.
  4. malexander


    I wonder what you can tell us about the recent report of 700 deaths associated with this new drug. Is the risk of death any greater with Nuplazid than with the older anti-psychotics. I feel some responsibility for allowing Acadia Pharmaceuticals access to a large support group to direct market their drug via a contracted speaker.
  5. malexander

    Safety Criteria

    I wonder what you can say about the criteria you use to determine whether an activity is safe for a particular patient. I understand that you often recommend that DBS patients should not climb ladders. I imagine that this is not an absolute recommendation. For instance I have had STN DBS for four years, and have no problem on ladders. Where I do wonder about my safety is riding my bike up and down mountains. Actually going up the mountains is no problem; it is the fact that what goes up has to come down again. Herein lies to problem: When descending (even with considerable breaking) it is easy to go speeds that require reaction speeds that test my limits. On the other hand, I love biking up hills and it is good exercise for me. How should I determine when to hang up my biking shoes. Perhaps I should mention that I broke my collar bone in a fall five years ago. I was descending one of my favorite mountains and hit a pothole I thought I could maneuver around. Since then I have been more cautious. st
  6. malexander

    Tremor-dominant subtype

    I am sorry, but I am still confused: Do you mean that 20-40% of all PD patients who have tremor (some percentage of PD patients--perhaps as high as 40%--do not manifest tremor) find their tremors to be medication recalcitrant? Some percentage (I don't know how many) of PD patients are tremor dominant (TD). Are you saying that 20-40% of these TD patients find their tremors to be medication recalcitrant? In other words, is medication recalcitrance more common in TD patients than in other PD subtypes?
  7. malexander

    Tremor-dominant subtype

    I am afraid I am still confused: Is that 20-40% of all PD patients with tremor have some levodopa resistance. Or 20-40% of all tremor dominant PD patients are medication resistant. (AND is not this about the same percentage of all PD patients that are tremor dominant.) Do autopsies show similar areas of the brain affected in "garden variety" PD, tremor dominant PD, and medication resistant PD. If so, what begins to explain these differences?
  8. malexander

    Tremor-dominant subtype

    I was diagnosed 6 years ago with tremor-dominant PD (following 3 years of misdiagnosis of essential tremor). I was quite resistant to levodopa (or any other medication), and I had DBS performed a few years ago. The STN DBS is quite successful in controlling my motor symptoms, and I am currently on no PD meds. At this point I have a number of questions concerning the projected course of my disease. I am particularly interested in what information may be gleaned from the study of PD subtypes. For instance, I do not—and have never had--problems with constipation. However, my anosmia predates my motor symptoms by more than a decade. Is this typical and imply a nasal route of tremor dominant PD? I currently have mild problems with voice volume, urinary urgency, balance, and mental sharpness. What else should I expect? Also, I wonder what an autopsy of my brain would show. Where would Lewy bodies be concentrated? I would think that some systems other than dopaminergic would by responsible for my tremors. After all, I had been experimenting with up to 900mg./day of levodopa with little tremor relief prior to DBS. I would greatly appreciate any references to literature or comments you may have.
  9. malexander


    For the last couple of years, I have been taking atorvastatin 20 mg daily. With the new research showing increased PD risk with statin use, I wonder if I should talk with my doctors about switching to a hydrophilic statin. What do you recommend?
  10. malexander


    Do you think the recent study suggesting that low fat dairy increases PD risk is significant enough to recommend dietary changes?
  11. malexander

    gut microbiome

    I understand that Caltech has found that gut bacteria from PD patients encourages PD symptoms in mice. What do you think of this study and its potential to help find a disease modifying agent. Also, could you comment on the possible spread of PD from the gut to the brain via the vagus nerve and also the possibility of an nasal route (given that some Parkinson patients have olfactory loss--without gut symptoms--decades prior to motor symptoms).
  12. malexander

    DBS and balance issues

    I am a 70 year old man, diagnosed with tremor dominant PD diagnosed 8 years ago. My right arm tremor completely resolved following DBS 2 years ago. This year, I began developing symptoms on my left side and I had DBS surgery performed on my right brain last week. It has not been turned on yet (I am scheduled for that in 2 weeks). One symptom I notice since the surgery is a loss of balance. While I have not fallen, it feels like I am lurching and not getting my feet correctly planted as I walk. Could this be a temporary symptom from the surgery?
  13. malexander

    Loss of power

    I ran the above experiment many times--peddling with each leg individually and together--with DBS on and off--with no Sinemet, with 3 tabs/day, with 6 tabs/day. I charted the results with graphs which I would like to show you, but I do not know how to paste them onto this post. My questions include: Are there any researcher using individual leg power as a diagnostic measure in PD? Sinemet slightly increases power only with my left leg individually when DBS is on, and on both legs when it is off. It does not seem to effect balance, voice volume, or fatigue. Does this suggest that systems other than dopaminergic neurons have a greater share of responsibility for my symptoms? Does it suggest that DBS overrides most of the dopamine deficiency? My neurologist has not ordered a gastric emptying test, but she does not believe that explains my poor response to Sinemet. In fact, when I was testing Sinemet up to 9 tabs/day prior to DBS, I started to have some dyskinesia.
  14. malexander

    Loss of power

    I am a 70 year old man, and I have had motor symptoms of tremor dominant PD for 7.5 years. Medications (I have been on Sinemet up to 9 tabs/day, Requip, and Zonisamide) have never had much benefit and I am currently on none. I had unilateral DBS performed on the left side of my brain 2 years ago with immediate and long lasting relief of symptoms. Concern about continuing loss of power, however, lead me to conduct the following experiment: Using a stationary bike with the resistance set at 14 (a moderate hill) I measured the average power output of each leg individually when cycling for one minute. My right leg produced 136 Watts, and my left leg produced 108 Watts. I then turned off my DBS and repeated the experiment: the right leg power dropped to 60 while the left stayed at 107. During the last year, I have developed (for the first time) a significant tremor in the left arm. I wonder if the fact that my left leg now trails my right is due to rigidity and slowness in muscles on that side now, and if I should consider DBS on the right side of my brain at this time. More than three years ago, prior to my DBS, I noticed a significant loss in performance when cycling. I could no longer keep up with my riding partners. This loss seemed constant no matter how much Sinemet (if any) I was taking. At that time, I noticed I could generate a peak of 135 Watts with my left foot, but only 70 Watts with my right. This was the case in spite of the fact that I could push equal weight with both legs individually on the hamstring curl and quad extension machines . ​I have two questions: ​1) Is it reasonable to expect DBS to improve my physical performance? ​2) What does it mean that L-dopa has little effect on my PD symptoms (in spite of the fact that they are progressing in a classical manner)? I understand that many systems in addition to the dopaminergic neurons are involved with PD. Does my experience suggest that were I to die today an autopsy of my brain might reveal Lewy bodies in some areas of the brain--but not so many in the dopaminergic neurons?
  15. malexander

    Pesticides and PD

    How solid is the evidence for exposure to pesticides (and other agricultural chemicals) being a risk factor for PD. I am aware of some of the studies by Dr. Ritz at UCLA that suggest that several agents, each increase the susceptibility to PD slightly when being the sole exposure. Yet when combined with each other or with certain genetic factor, they can increase the risk of PD substantially. I have seen reports of this relationship in Scientific American, as well as other resources. ​I am responsible for arranging speakers for a large support group. We recently had a speaker who stirred up some controversy by saying this is a myth resulting from self-reporting and poor epidemiology. What can you tell us?