Well, here we are on our way to another spring in a new millennium. Our Annual General Meeting is fast approaching, preparations have been made for Dr. Ming Chan from University of Alberta to speak. His topic will be "The Management of Fatigue in Post-Polio Patients." This is on Saturday, April 15, 2000 at 10:00 am. Though the AGM is for members in good standing, our speaker session is open to anyone interested, upon receipt of registration.
This year British Columbia (PPASS) held an International Conference in Richmond. As funds were limited, we were not able to extend registration to all. We did, however, assist two members to represent S.A.P.P. and return with the newest information available.
The Saskatoon PPS Support Group once again is selling car raffle tickets for the Canadian Paraplegic Association (Sask) Inc. This is not only a good local fundraiser, but the exposure is priceless (as a rule we register two to four new polio survivors at each mall). If your local PPS support group would like to get involved in this fund-raising program, call Betty at 306-652-6502 or email her at: email@example.com.
How many of you are aware of the benefits available to polios' in a CPA membership? It will pay you to call 306-652-9644 and enquire.
We would like to pass along our condolences to Connie and family on the passing of her husband Hugh Cyr. He will truly be missed.
Nearly two-thirds of polio survivors report abnormal movements in sleep (AMS), with 52% reporting that their sleep is disturbed by AMS. Sleep studies were performed in seven polio survivors to objectively document AMS. Two patients demonstrated Generalized Random Myoclonus (GRM), brief contractions and even ballistic movements of the arms and legs, slow repeated grasping movements of the hands, slow flexion of the arms and contraction of the shoulder and pectoral muscles. Two other patients demonstrated Periodic Movements in Sleep (PMS) with muscle contractions and ballistic movements of the legs, two had PMS plus Restless Leg Syndrome (RLS) and one had sleep starts involving only contraction of the arm muscles. AMS occurred in Stage II sleep in all patients, in Stage I in some, and could significantly disturb sleep architecture even though patients were totally unaware of muscle contractions. Poliovirus-induced damage to the spinal cord and brain is presented as a possible cause of AMS. The diagnosis of post-polio fatigue, evaluation AMS and management of AMS using benzodiazepines or dopamimetic agents is described.
Despite numerous late-onset symptoms reported by polio survivors -- fatigue, muscle weakness, pain, cold intolerance, swallowing and breathing difficulties -- one symptom was totally unexpected: abnormal movements in sleep (AMS). As early as 1984 our post-polio patients were reporting muscle contractions as they fell asleep. The 1985 National Post Polio Survey included two questions about AMS: "Do your muscles twitch or jump as you fall asleep and "Is you sleep disturbed by muscle twitching? (1) It was surprising that 63% of the 676 respondents reported that their muscles did twitch and jump during sleep and that 52% -- a third of the entire sample -- said that their sleep was disturbed by twitching.
These percentages are markedly elevated as compared to the incidence of AMS in the general population. In one survey only 29% of those without neurological disease who were at least 50 years old reported AMS, versus 63% of surveyed polio survivors who were 52 years old on average. (2) In another survey only 34% of those older than 64 reported AMS, slightly more than half the incidence of AMS in the younger post-polio sample. (3) Given the apparent increased prevalence of AMS in polio survivors, and with daytime fatigue the most commonly reported Post-Polio Sequelae (PPS), we were interested in objectively documenting AMS, relating them to possible disturbances in sleep architecture and identifying an effective treatment for AMS. (1)
Seven polio survivors were referred for sleep studies to a sleep disorders center. This was a sample of convenience, in that the subjects were patients presenting with PPS who themselves knew (three patients) or whose bed mates knew (four patients) that AMS were occurring. Patients were on average 54 years old and 44 years post acute polio which occurred at age 10. The patients had had AMS for a mean of eight years which was on average 35 years post acute polio. Patients reported moderate-to-severe difficulty sleeping at night and moderate-to-severe daytime fatigue that did not respond to the treatments of choice for post-polio fatigue (i.e., pacing of activities, daytime rest periods, energy conservation and use of appropriate assistive devices. (4) In addition to fatigue, patients reported an average of two limbs having late-onset muscle weakness.
Patients underwent a standard polysomnographic evaluation with EEG and facial EMG recorded for sleep staging. (5) Blood oxygen saturation, measured using a finger pulse oxymeter, chest and abdominal wall excursion and nasal air temperature were also recorded; video monitoring of sleep was also performed. Surface EMG was recorded from patients legs as well as from limbs in which AMS were reported.
Four types of AMS were seen: Two patients presented with what has been called Generalized Random Myoclonus (GRM) (1,6), two patients had Periodic Movements in Sleep (PMS), two had PMS plus Restless Leg Syndrome (RLS) and one had Sleep Starts (also called hypnogogic massive myoclonic jerks ).
Generalized Random Myoclonus.
GRM was seen in two patients. One had had bulbar polio with little or no arm or leg involvement acutely, while the other has been diplegic since polio but had no bulbar or respiratory symptoms acutely. These patients had random contractions of muscles throughout their bodies. One had such violent contractions of the trunk muscles that she was pulled into the fetal position during the night. This patient had been very aware of GRM for about 10 years.
However, the other patient had been completely unaware of GRM until they were noticed by her husband (Figure 1). Random, rapid muscle contractions were noted in all four limbs, jaw and pectoral muscles, in addition to slow repeated grasping movements of the hands, slow flexion of the arms and movement of the shoulders. The presence of bilateral toe flexion was notable since the patient s right leg has always been totally paralyzed except for a minimal ability to flex her toes; the toes of her right foot contracted numerous times the during the night.
In both patients, GRM occurred during Stage II sleep; the latter patient also had GRM in Stage I. The patient with violent trunk flexion had muscle contractions, causing a severe disturbance of sleep architecture, only during the first third of the night. She also had a few episodes of obstructive apnea that were not related to the muscle contractions but did disturb her sleep. She was prescribed clonazepam, 0.5 mg B.I.D., which eliminated her GRM. The other patient had GRM throughout the night but had no disturbance of sleep architecture and was not treated pharmacologically.
Periodic Movements in Sleep.
Two patients demonstrated PMS with contractions only of the leg muscles of which neither patient was aware. Both had limb and respiratory involvement with the acute polio and had PMS during Stage II sleep with one patient also having muscle contractions during Stage I. The former patient had nearly continuous EMG activity in his legs throughout the night and had a severe disturbance of sleep architecture (Figure 2). He also had some central episodes of apnea early in the night as he was falling asleep that did not disturb his sleep. The latter patient had PMS occurring only during the first half of the night which caused no disturbance of sleep architecture. However, he had frequent hypopneas which did severely disturb his sleep. Both patients were prescribed lorazepam, 1.0 mg H.S., which eliminated the PMS.
PMS plus Restless Leg Syndrome.
Two patients had PMS plus Restless Legs Syndrome. RLS is characterized by the subjective feeling that the legs must be moved. This feeling increases during the evening, often preventing sleep onset because patients feel as if they must get up and walk. The patients with PMS plus RLS had been very little affected by the acute polio, one having no polio residual and the other having one leg weakened. PMS were seen in both legs and occurred during Stage II in both patients and during Stage I in one patient. One patient s leg muscle contractions were so violent that she was propelled one to two inches off the surface of the bed. Although her PMS occurred only during the first half of the night, her sleep was severely disturbed and she was very aware that she had had PMS for about 5 years. She was prescribed L-dopa/carbidopa (Sinemet) 200/50 mg, 1/2 tablet B.I.D., and clonazepam, 0.5 mg H.S. and at 3 A.M., which reduced the RLS and PMS by about 80% and allowed her to have a restful nights sleep.
The other patient did not know he had PMS which were continuous throughout the night and did moderately disturb his sleep architecture. He was prescribed L-dopa/carbidopa, 200/50 mg H.S., which eliminated his RLS and PMS.
One patient was diagnosed as having a Sleep Start, her arms ballistically abducting as she began to fall asleep. She was very mildly affected by the acute polio and had no AMS in the legs, even in the leg in which she reported new muscle weakness. The patient s sleep was markedly disturbed since her arms would move as she started to fall asleep and prevent sleep onset. She was prescribed alprazolam, 0.125 mg H.S., which eliminated her AMS.
Sleep studies in this sampling of post-polio patients objectively documented three different types of AMS. Whether other types or combinations of AMS occur in polio survivors cannot be determined from this study, nor can this study or the 1985 National Post-Polio Survey state the actual incidence of AMS in polio survivors, since neither sample was random or population-based. However, the objective documentation of AMS in these post-polio patients, and the Post-Polio Survey finding that 63% of polio survivors reported muscle twitching or jumping as they fell asleep, suggest that AMS may in some way be related to the pathophysiology of the original poliovirus infection.
In 1964, Loeb coined the phrase hypnic myoclonus to describe muscle contractions during sleep onset in healthy individuals without neurological disease. (7) Loeb described the contractions as rapid (less 0.5 seconds long), arrhythmic (occurring without a pattern) and causing a variety of movements - finger flexion, thumb adduction, forearm and foot flexion and extension, shoulder elevation and facial twitching during Stages I and II sleep - identical to those seen in the post-polio patients. However, in contrast to the post-polio patients, none of Loeb s subjects demonstrated contractions in more than one muscle group and in none was sleep disturbed by hypnic myoclonus.
Loeb thought that hypnic myoclonus resulted from an abnormality at the level of the brain stem reticular formation causing decreased descending inhibition of anterior horn motor neurons during sleep. Martinelli (8) thought PMS also resulted from an increase in anterior horn cell excitability, with Walters (9) finding that PMS decreased with the administration of an opiate receptor agonist.
Loeb and Askenasy suggested that AMS were also related to abnormal discharges from the thalamus, cerebellum and basal ganglia. (7,10) The implication of the basal ganglia in the generation of AMS is interesting since PMS are common in patients with Parkinson's disease, whose decreased dopamine production impairs basal ganglia functioning, in patients with narcolepsy, who have an increased number and sensitivity of dopamine receptors in the basal ganglia, and have been found to decrease with the administration of dopamine receptor agonists. (9,11,12)
AMS, Polioencephalitis and Poliomyelitis. All of the CNS regions implicated in the pathogenesis of AMS are known to have been lesioned by the poliovirus. The anterior horn motor neurons, cerebellar nuclei and reticular formation were frequently and severely damaged by the poliovirus. (13) The periaquiductal gray, paraventricular hypothalamus and lamina II dorsal horn neurons were all lesioned by the poliovirus (cf. 9;13); damage to these opioid peptide-secreting neurons may be evidenced not only by AMS but also by polio survivor's doubled sensitivity to pain. (14-16) Finally, the thalamus and basal ganglia (the substantia nigra, putamen and globus pallidus) were also damaged by the poliovirus, damage that has been implicated in the pathogenesis of post-polio fatigue. (16-18) Given the distribution and extent of poliovirus lesions in all of the CNS areas implicated in the pathogenesis of AMS, we should not have been surprised in 1985 that a majority of polio survivors reported muscles that twitch and jump during sleep.
PPS remains a diagnosis of exclusion. All possible causes for new symptoms in polio survivors, especially causes for late-onset fatigue, must be ruled out before the diagnosis of PPS is made. Therefore, it is important to rule out a sleep disorder as a cause of late-onset fatigue. Clinicians need to take a thorough sleep history from their post-polio patients, asking not only about symptoms of sleep apnea, which occurs frequently in polio survivors, but also about AMS. (20) The patient s bed partner must also be asked about AMS since the majority of polio survivors will not know that they have AMS.
Patients are referred for a sleep study if sleep apnea or AMS is suspected. The lowest dose of a short acting benzodiazepine will be prescribed before sleep by the Post-Polio Institute physiatrist if a patient has AMS, since these medications seem to virtually eliminate GRM and PMS in our post-polio patients. Treatment of sleep apnea is deferred to the sleep disorders center as is treatment for RLS, since a dopamimetic agent in combination with a benzodiazepine may be required. However, there is a caveat to prescribing dopamimetics for polio survivors. One of our PPS patients developed vasovagal syncope with cardiac asystole during the administration of a dopamine receptor agonist. (21) We consider a history of vasovagal syncope or unexplained faints a contraindication to prescribing dopamimetics for polio survivors with AMS or RLS. (22)
1) Bruno RL, Frick NM: Stress and "Type A" behavior as precipitants of Post-Polio Sequelae: The Felician/Columbia Survey, in Halstead LS, Wiechers DO (eds): Research and Clinical Aspects of the Late Effects of Poliomyelitis. White Plains, NY, March of Dimes Research Foundation, 1987, pp 145-155.
2) Lugaresi E, Cirinotta F, Zucconi M, et al.: Good and poor sleepers: An epidemiological survey, in Guilleminault C, Lugaresi E (eds): Sleep/wake disorders: Natural history, epidemiology, and long-term evolution. NY, Raven, 1983, pp 265-295.
3) Ancoli-Israel S, Kripke DF, Mason W, Kaplan OJ: Sleep apnea and periodic movements in an aging sample. J Gerontol 1985; 40 419-425.
4) Creange SJ, Bruno RL: Compliance with treatment for Post-Polio Sequelae: Effect of Type A behavior, self- concept and loneliness. Am J PM&R 1997; 76:378-382.
5) Rectschaffen A, Kales A: A manual of standardized terminology, techniques and scoring system for sleep stages of human subjects, Los Angeles, UCLA Brain Information Service/Brain Research Institute, 1968.
6) Bruno RL, Frick NM, Creange SJ: Nocturnal generalized myoclonus as a post-polio sequelae. Arch PM&R 1995; 76:594.
7) Loeb C: Etude polygraphique des Myoclonies hypniques chez l'homme. Rev Neurol 1964;110:258-268.
8) Martinelli P, Coccagna G, Lugaresi E: Nocturnal myoclonus, restless legs syndrome and abnormal electrophysiological findings. Ann Neurol 1987;21:515.
9) Walters A, Henning W, Cote L, et al.: Dominantly inherited restless legs with myoclonus and periodic movements in sleep: A syndrome related to endogenous? Adv Neurol 1986; 43:309-319.
10) Askenasy JJM, Weitzman ED, Yahr MD: Are periodic movements in sleep a basal ganglia dysfunction? J Neural Transm 1987;70:337-347.
11) Weiner WJ, Lang AE: Myoclonus and related syndromes, in Weiner WJ, Lang AE: (eds): Movement Disorders. Mount Kisco, Futura, 1989, pp 457-529.
12) Boivin DB, Lorrain D, Montplasir J: Effects of bromocriptine on periodic limb movements in human narcolepsy. Neurol 1993; 43:2134-2136.
13) Bodian D: Histopathological basic of clinical findings in poliomyelitis. Am J Med 1949;6:563-578.
14) Bruno RL, Johnson JC, Berman WS: Motor and sensory functioning with changing ambient temperature in post-polio subjects, in Halstead LS, Wiechers DO (eds): Late Effects of Poliomyelitis. Miami, Symposia Foundation, 1985.
15) Bruno RL, Johnson JC, Berman WS: Vasomotor abnormalities as Post-Polio Sequelae. Orthopedics 1985;8: 865-869.
16) Bruno RL, Frick NM, Cohen, J: Polioencephalitis, stress and the etiology of Post-Polio Sequelae. Orthopedics 1991; 14:1269-1276.
17) Bruno RL, Sapolsky R, Zimmerman JR, Frick NM: The pathophysiology of a central cause of post-polio fatigue. Ann NY Acad Sci 1995;753:257-275.
18) Bruno RL, Frick NM, Creange SJ, et al.: Polioencephalitis and the brain fatigue generator model of post-viral fatigue syndromes. J Chronic Fatigue Syndrome 1996;2:5-27.
19) Bruno RL, Creange SJ, Zimmerman JR, Frick NM: Elevated plasma prolactin and EEG slow wave power in post-polio fatigue: Implications for a dopamine deficiency underlying chronic fatigue syndromes. J Chronic Fatigue Syndrome , 1998 (in press).
20) Bach JR, Alba AS: Pulmonary dysfunction and sleep disordered breathing as post-polio sequelae: Evaluation and management. Orthopedics 1991;14:1329-1337
21) Bruno RL, Zimmerman JR, Creange SJ, et al.: Bromocriptine in the treatment of post-polio fatigue: A pilot study with implications for the pathophysiology of fatigue. Am J PM&R 1996; 75:340-347.
22) Bruno RL: Chronic fatigue, fainting and autonomic dysfunction: Further similarities between post-polio Fatigue and Chronic Fatigue Syndrome? J Chronic Fatigue Syndrome 1997; 3:107-117.
The Symposium was held in Richmond B.C., at the Executive Inn. The accommodations and accessibility were excellent and the staff of the Executive Inn were super.
PPASS of B.C. had everything well-organized and ready to roll as participants arrived. All participants were warmly welcomed.
The activities began Thursday evening with a superb supper buffet, a welcoming introduction from VP Dr. Ruth Heron, of PPASS of B.C., and a welcoming message from Dr. Feldman
Friday's agenda began with the keynote address from Dr. Neil Cashman on the Pathogenesis and Experimental Treatment of Postpoliomyelitis Syndrome. In the area of experimental treatment, Dr. Cashman mentioned strategies for preventing or slowing down loss of terminal axons. One possible treatment, that might be explored in the future, is the use of Nerve Growth Factor targeted to motor nerve cells. At present Dr. Cashman is attempting to redo the clinical trial of mestinone. The results of the first trial may have been flawed due to the fact that the participants may have inadvertently increased their exercise and/or activity level while taking mestinone, which would have negated the positive effects of fatigue reduction by mestinone.
The two workshops given by Dr. Michelle Toshima on Stress and Coping and Spousal and Interpersonal Relationships were highly informative. I brought back copies of her lecture outlines and exercise handouts. In my opinion, they are recommended reading as both workshops have ideas and tips in them for reducing stress in our 'so easily stressed lives'.
The session on dealing with the medical profession given by Dr. Chen and Dr. Feldman gave some very practical strategies and useful advice for obtaining the optimum medical care from medical doctors who do not believe in or do not understand post-polio syndrome. Some tips:
1. If your present doctor does not believe in the existence of PPS, find another one.
2. If your present doctor tells you have had x number of good years and to just accept the inevitable, find another one.
3. Always begin your search for a new doctor at the frontline, the doctor's receptionist or secretary.
4. Establish a good relationship with the receptionist at the beginning by calling ahead. Let the receptionist know that you want to meet the doctor and that you want to seek a consultation from him. The receptionist will then book the appropriate amount of time for your visit(s).
5. Do not make the diagnosis for the doctor, let the doctor make the diagnosis for you.
6. Come to the consultation appointment on time and with an organized list that gives specific symptoms and times of fatigue, weakness and pain. Do not ramble!
The panel of the closing plenary session on Sunday consisted of Dr. Cashman, Dr. Feldman, Dr. Dean, Dr. Travlos, Dr. Yarnell, Dr. Toshima and Dr. Fisher. At the end of the panel discussion, each member was requested to leave us with some parting advice or wisdom.
Dr. Dean-listen to your body, self-monitor
Dr. Cashman-educate, work with and be patient with your health care professionals
Dr. Toshima-treat not only the physical body but the whole person [the mind and the emotions]
Dr. Feldman- You have an enemy-fatigue-deal with it effectively.
Dr. Fisher-keep in mind that not all of your problems are related to polio; there are other reasons or factors that can account for pain and weakness.
Dr. Travlos-take time to rest, be active and then take it easy.
The Symposium ended on Sunday afternoon with closing remarks by the President of PPASS B.C., Joan Toone.
After 15 years of searching, archaeologists from The Post-Polio Institute have unearthed the "commandments" for treating Post-Polio Sequelae (PPS)...
1. Listen to Yourself!
Polio survivors often turned themselves off from the neck down after they got polio. The first step in treating PPS is to listen to yourself: to what you feel, physically and emotionally, when you feel it and why. Our most powerful tool in treating PPS is the daily logs our patients keep that relate activities to their symptoms. However, polio survivors sometimes listen too much: to vitamin salesmen saying some herb or spice will "cure" PPS, to other polio survivors who warn that you will eventually have every possible PPS symptom, and to friends and family members (and the voices in your own head) saying you're lazy and that you must "use it or lose it." Polio survivors need to listen to their own bodies, not to busybodies.
2. Activity is Not Exercise!
Polio survivors believe that if they walk around the block five times a day, spend an hour on the exercise bike and take extra trips up and down stairs, their muscle weakness will go away. The opposite is true: the more you overuse your muscles the more strength you lose. Muscles affected by polio lost at least 60% of their motor neurons, even limbs you thought were not affected by polio lost about 40%. Most disturbing is that polio survivors with new muscle weakness lose on average 7% of their motor neurons per year, while survivors with severe weakness can lose up to 50% per year! You need to substitute a "conserve it ti preserve it" lifestyle for the "use it or lose it" philosophy. Stretching may help pain and non-fatiguing exercise for specific muscles can prevent you from losing the strength you have after you get a brace. But polio survivors need to work smarter, not harder.
3. Brake, Don't Break.
The follow-up study of our patients showed that taking two 15 minutes rest breaks per day - that's doing absolutely nothing for 15 minutes - was the single most effective treatment for PPS symptoms. Another study showed that polio survivors who paced activity - that is worked and then rested for an equal amount of time - could do 240% more work than if they pushed straight through. Our patients who took rest breaks, paced activities and conserved energy had up to 22% less pain, weakness and fatigue. But polio survivors who quit or refused therapy had 21% more fatigue and 76% more weakness. For polio survivors, slow and steady wins the race.
4. A Crutch in Not a Crutch...
...and a brace is not a sign of failure or of "giving up." You use three times less energy (and look better walking) using a short leg brace on a weakened leg. Overworked muscles and joints hurt and nerves die after decades of doing too much work with too few motor neurons. So why not use a brace, cane, crutches (dare we say a wheelchair or a scooter) if they decrease your symptoms and make it possible to finally take that trip to Disney World? We know, you'll slow down and take care of yourself "when you're ready." And you'll use a wheelchair "when there's no other choice." Well, you don't drive your car until it's out of gas. Why drive your body until it's out of neurons?
5. Just Say "No" to Drugs, Unless...
Five studies have failed to find any drug to treat PPS. And there have been no studies showing that herbal remedies or magnets reduce symptoms. Polio survivors shouldn't think that they can run themselves ragged, apply a magnet or pop a pill, and their PPS will disappear. Pain, weakness and fatigue are not-so-subtle messages from your body telling you that damage is being done! Masking symptoms - with magnets or morphine - will not cure PPS. However, two studies have shown that polio survivors are twice as sensitive to pain as everyone else and usually need more pain medication for a longer time after surgery or an injury (see 10 below).
6. Sleep Right All Night.
The majority of polio survivors have disturbed sleep due to pain, anxiety or sleep disorders, such sleep apnea (not breathing) or muscles twitching and jumping all over your body during the night. However, polio survivors are usually not aware that they stop breathing or twitch! You need a sleep study if you awaken at night with your heart pounding, anxiety, shortness of breath, choking, twitching, or awaken in the morning with a headache or not feeling rested. "Post-Polio fatigue" may be due to a treatable sleep disorder.
7. Some Polio Survivors Like it Hot.
Polio survivors have cold and purple "polio feet" because the nerves that control the size of blood vessels were killed by the poliovirus. Actually, polio survivors' nerves and muscles function as if it's 20 degrees colder than the actual outside temperature! Cold is the second most commonly reported cause of muscle weakness and is the easiest to treat. Dress in layers and wear socks made of the silk-like plastic fibre polypropylene (sold as Gortex or Thinsulate) that holds in your body heat.
8. Breakfast if Definitely the Most Important Meal of the Day.
For once Mom was right. Many polio survivors eat a Type A diet: no breakfast, coffee for lunch and cold pizza for dinner. A recent study shows that the less protein polio survivors have at breakfast the more severe their fatigue and muscle weakness during the day. When our patients follow a hypoglycemia diet (have 16 grams of low-fat protein at breakfast and small, non-carbohydrate snacks throughout the day) they have a remarkable reduction in fatigue. Protein in the morning does stop your mid-day yawning.
9. Do Unto Yourself as You Would For Others. Many polio survivors were verbally abused, slapped or even beaten by therapists or family members when they had polio to "motivate" them to get up and walk. So polio survivors took control, becoming Type A super-achievers, "the best and the brightest, "doing everything for everyone except themselves. Many polio survivors do for others and don't ask for help because they are afraid of being abused again. Isn't it time that you got something back for all you've done for others? Accepting assistance is not the same as being dependent. Accepting assistance can keep you independent. But appearing "disabled," by not doing for others, asking for help or using a scooter, will be frightening. Remember: If you don't feel guilty or anxious you are not taking care of yourself and managing your PPS.
10. Make Doctors Cooperate Before They Operate.
Polio survivors are easily anaesthetized because the part of the brain that keeps them awake was damaged by the poliovirus. Polio survivors also stay anaesthetized longer and can have breathing trouble with anaesthesia. Even nerve blocks using local anaesthetics can cause problems. All polio survivors should have lung function tests before having a general anaesthetic. Your complete polio history and any new problems with breathing, sleeping and swallowing should be brought to the attention of your surgeon or dentist - and especially your anesthesiologist - long before you go under the knife. Polio survivors should NEVER have same-day surgery or outpatient tests (like an endoscopy) that require anaesthetic.
The Golden Rule for Polio Survivors:
If anything causes fatigue, weakness, or pain, Don't Do It! (Or do a lot less of it).
I have been having a bit of blood pressure problem, so my specialist in Internal Medicine has requested the Dipyridamole Myocardial Imaging Study. Is their anything I should be aware of in regard to PPS and this procedure to stimulate the heart muscle?
This is the heart stress test we recommend for polio survivors. Many polio survivors are asked to get on a tread mill or bicycle and pump their hearts out (only figuratively speaking) to get their heart rates way up and see if there is enough blood supply to the heart muscle. Two problems with exercise stress tests:
1) if polio survivors can pump their legs enough to get their hear rates up, they can't walk very well when they finish the test cause they have stressed their polio-damaged motor neurons maybe more than their heart. Talk about overuse-abuse!
2) Many polio survivors can't pump their legs enough to get their hear rates up and have an inadequate stress tests or a false negative test. They wasted their time and definitely stressed their polio-damaged motor neurons more than their heart. Talk about needless overuse-abuse!
So using a drug like dipyridamole to chemically turn on you heart and stress its muscle -- without stressing your leg muscles and motor neurons--- is a good idea.
Now, there are contraindications to having any drug and you need to talk to you doctor about those. But there shouldn't be PPS-related problems with dipyridamole.
Thought you might enjoy this one: Here's a story about true love...
The little old couple walked slowly into McDonalds that cold winter evening. They looked out of place amid the young families and young couples eating there that night. Some of the customers looked admiringly at them. You could tell what the admirers were thinking. "Look, there is a couple who has been through a lot together, probably for 60 years or more!" The little old man walked right up to the cash register, placed his order with no hesitation and then paid for their meal. The couple took a table near the back wall and started taking food off of the tray. There was one hamburger, one order of french fries and one drink. The little old man unwrapped the plain hamburger and carefully cut it in half. He placed one half in front of his wife. Then he carefully counted out the french fries, divided them in two piles and neatly placed one pile in front of his wife. He took a sip of the drink, his wife took a sip and then set the cup down between them.
As the man began to eat his few bites of hamburger the crowd began to get restless. Again you could tell what they were thinking. "That poor old couple. All they can afford is one meal for the two of them." As the man began to eat his french fries one young man stood and came over to the old couples table. He politely offered to buy another meal for the old couple to eat. The old man replied that they were just fine. They were used to sharing everything.
Then the crowd noticed that the little old lady hadn't eaten a bite. She just sat there watching her husband eat and occasionally taking turns sipping the drink. Again the young man came over and begged them to let him buy them something to eat. This time the lady explained that no, they were used to sharing everything together.
As the little old man finished eating and was wiping his face neatly with a napkin the young man could stand it no longer. Again he came over to their table and offered to buy some food. After being politely refused again he finally asked a question of the little old lady. "Ma'am, why aren't you eating. You said that you share everything. What is it that you are waiting for?" She answered, "the teeth".
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