Feb 4, 2019

Pain in Post-Polio Syndrome



Anne C. Gawne, MD, Roosevelt Warm Springs Institute for Rehabilitation, Post-Polio Clinic, Warm Springs, Georgia

Anne Carrington Gawne, MD received her medical training at the Uniformed Services University in Bethesda, Maryland, and did her residency at the National Rehabilitation Hospital in Washington, DC.
Before moving to Roosevelt Warm Springs Institute for Rehabilitation in Warm Springs, Georgia, Dr. Gawne treated polio survivors at National Rehabilitation Hospital for nine years. She co-authored Post-Polio Syndrome: Pathophysiology and Clinical Management with Lauro S. Halstead, MD, National Rehabilitation Hospital, which was published in Critical Reviews in Physical Medicine and Rehabilitation, Vol. 7, Issue 2, pages 147-188.

Symptoms of post-polio syndrome include fatigue, new weakness and pain in muscle and joints. Chronic pain is the second most prevalent symptom reported and frequently is the most difficult to treat. Improvement in the evaluation and treatment of pain can significantly improve comfort and restore function. The differential diagnosis is extensive, but many of the problems appear to be related to overuse of weak muscles along with abnormal joint and limb biomechanics.
To facilitate the diagnosis and treatment of pain, a classification that divides the pain syndromes into three classes has been developed:
  1. post-polio muscle pain;
  2. overuse pain;
  3. biomechanical pain.
POST-POLIO MUSCLE PAIN occurs only in muscles affected by polio. It is described as either a deep or superficial aching pain, which many survivors say is similar to the muscle pain they experienced during their acute illness. Characterized by muscle cramps, fasciculations or a crawling sensation, it typically occurs at night or the end of the day when one tries to relax. It is exacerbated by physical activity and stress, and cold temperatures.
OVERUSE PAIN includes injuries to soft tissue, muscle, tendons, bursa and ligaments. Common examples are rotator cuff tendinitis, deltoid bursitis and myofascial pain. Myofascial pain in post-polio is similar to that in others. It occurs most frequently in the muscle of the upper back and shoulders and is characterized by bands of taut muscles and discrete trigger points that elicit a jump response when palpated. These occur due to poor posture or improper body biomechanics.
Fibromyalgia with its associated symptoms is another cause of muscle pain that has been recognized by other investigators and has similar symptoms, but is distinctly different from post-polio muscle pain. The classic tender points are uncommon with post-polio muscle pain.

BIOMECHANICAL PAIN presents as a degenerative joint disease (DJD), low back pain or pain from nerve compression syndromes. Weakness induced by polio-affected muscles, as well as poor body mechanics, makes the joints more susceptible to the development of DJD. Survivors who walk develop degenerative joint disease in the lower extremities because years of ambulating on unstable joints and supporting tissue increase the chance of developing further pain and deformity. Those who use wheelchairs or assistive devices such as canes, crutches or walkers are prone to DJD, or overuse syndromes, in their upper extremities, especially the wrist and shoulders. The joint pains are only rarely accompanied by swelling and/or inflammation, but do demonstrate tenderness and abnormal range of motion. X-rays of painful, weight-bearing joints may show degenerative changes proportional with the amount of stress the joints have sustained.
Nerve compression syndromes, including carpal tunnel syndrome (CTS), ulnar mononeuropathy at the wrist or elbow, brachial plexopathy and cervical or lumbosacral radiculopathy, are syndromes that can cause pain as well as neurological deficits in the post-polio individual. Risk factors for the development of focal neuropathies of the median and ulnar nerves include use of an assistive device such as a cane, crutch or wheelchair. These neuropathies can be detected on electrodiagnostic tests (EMG/NCS) before the individual has the characteristic symptoms of CTS.
The evaluation of post-polio individuals with pain requires careful investigation of all aspects of their pain. Among the questions asked are typical ones such as "What makes the pain better?" and "What makes it worse?" The way pain interferes with the survivors' ability to sleep and work is noted. Which treatments are helpful and by whom they are given is also documented.
Pain management in post-polio is based on a few basic principles, supplemented by class-specific recommendations. These basic principles include efforts to:
  1. improve abnormal body mechanics;
  2. correct and minimize postural and gait deviations mechanically;
  3. relieve or support weakened muscles and joints;
  4. promote lifestyle modifications;
  5. decrease the abnormally high work load of muscles relative to their limited capacity.
TREATMENT FOR POST-POLIO MUSCLE PAIN includes decreasing activity throughout the day, applying heat, and stretching. Stretching has a role in maintaining the extensibility of muscle and connective tissue; however, it must be performed judiciously because there are situations in which a polio survivor may derive greater functional benefit and be safer with tighter tendons and reduced joint range of motion.
A variety of medications are used to treat post-polio muscle pain, but the most common ones - such as nonsteroidal anti-inflammatories (NSAIDS), Tylenol, benzodiazepams, and narcotics - are of little use. The use of tricyclic antidepressants (TCAs), especially amitriptyline, can help with pain and also with fatigue.
TREATMENT FOR OVERUSE PAIN includes modification of extremity use, followed by modalities such as ice, heat or ultrasound, transcutaneous electrical nerve stimulation (TENS), and occasionally NSAID medications. Treatment for myofascial pain consists of myofascial release techniques, including spray and stretch and trigger-point injections. Often rest is not possible since many rely on upper extremities for both locomotion and self care. In rare cases, steroid injections or surgery may be needed.

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Jan 29, 2019

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Germs in Your Gut Are Talking to Your Brain. Scientists Want to Know What They’re Saying.



The body’s microbial community may influence the brain and behavior, perhaps even playing a role in dementia, autism and other disorders.



In 2014 John Cryan, a professor at University College Cork in Ireland, attended a meeting in California about Alzheimer’s disease. He wasn’t an expert on dementia. Instead, he studied the microbiome, the trillions of microbes inside the healthy human body.
Dr. Cryan and other scientists were beginning to find hints that these microbes could influence the brain and behavior. Perhaps, he told the scientific gathering, the microbiome has a role in the development of Alzheimer’s disease.
The idea was not well received. “I’ve never given a talk to so many people who didn’t believe what I was saying,” Dr. Cryan recalled.
A lot has changed since then: Research continues to turn up remarkable links between the microbiome and the brain. Scientists are finding evidence that microbiome may play a role not just in Alzheimer’s disease, but Parkinson’s disease, depression, schizophrenia, autism and other conditions.

For some neuroscientists, new studies have changed 


the way they think about the brain.
One of the skeptics at that Alzheimer’s meeting was Sangram Sisodia, a neurobiologist at the University of Chicago. He wasn’t swayed by Dr. Cryan’s talk, but later he decided to put the idea to a simple test.
“It was just on a lark,” said Dr. Sisodia. “We had no idea how it would turn out.”
He and his colleagues gave antibiotics to mice prone to develop a version of Alzheimer’s disease, in order to kill off much of the gut bacteria in the mice. Later, when the scientists inspected the animals’ brains, they found far fewer of the protein clumps linked to dementia.

Just a little disruption of the microbiome was enough to produce this effect. Young mice given antibiotics for a week had fewer clumps in their brains when they grew old, too. 
“I never imagined it would be such a striking result,” Dr. Sisodia said. “For someone with a background in molecular biology and neuroscience, this is like going into outer space.”
Following a string of similar experiments, he now suspects that just a few species in the gut — perhaps even one — influence the course of Alzheimer’s disease, perhaps by releasing chemical that alters how immune cells work in the brain.




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