The Framingham study is a large prospective study of over 5,000 men and women living in Framingham, Massachusetts who have been followed every 2 years since 1948. Data from it is used to estimate risk of heart and other diseases. The dementia part of the study began in 1975 using several neuropsychological tests. Recent data from the study reports that people who participate in moderate to heavy physical activity have a 45% lower risk for dementia over time.

"A reduced risk of dementia may be one of the additional health benefits that can actually be derived from maintaining at least moderate physical activity," lead author Zaldy Tan, MD, MPH, from the Brigham and Women's Hospital, VA Boston, and Harvard Medical School, in Massachusetts, concluded. Dr. Tan presented the results at the Alzheimer's Association International Conference on Alzheimer's Disease 2010.

Previous findings from the Framingham have already shown moderate or high physical activity to be associated with a number of positive outcomes, including a reduced risk for stroke and cardiovascular disease, higher high-density lipoprotein cholesterol levels, a reduced risk for colon cancer, and lower overall rates of mortality.

Physical activity is a potential preventive factor that would likely take years to manifest its effect, "so the fact that we've followed them for over 20 years, this is something that suggests that long-term physical activity actually works," Dr. Tan noted. The mechanism is not clear, he added, but reduction of cardiovascular risk factors such as hypertension, or the release of neurotrophic factors, are possible effects.

The Framingham study is not the only one to demonstrate this relationship. A recent review showed that 20 of 24 population-based studies showed a link between physical activity and reduced risk for dementia or cognitive decline. The flip side of this is that four of those studies did not support the correlation. However, the Framingham study is one of the best because it has such well designed, long-term follow-up.

As a back pain sufferer, I was interested to read in the July 7th issue of the Journal of the American Medical Association (JAMA) that glucosamine is not significantly different from placebo for reducing pain-related disability or improving health-related quality of life in patients with chronic low back pain. Years ago I’d tried the dietary supplement without success even though a lot of people swear by it.

Because glucosamine is a precursor molecule involved in building tendons, ligaments, and cartilage it’s widely believed that it helps restore cartilage as well as having anti-inflammatory properties. Despite conflicting data on its efficacy it has been widely used as a treatment for osteoarthritis. Some estimates suggest that more than more than 25% of patients with chronic LBP have tried glucosamine in various forms.

The research was a well-designed clinical study conducted at the Oslo University Hospital Outpatient Clinic using 250 patients with nonspecific chronic pain in the lower back. Patients were randomized to receive either a daily dose of 1500 mg of glucosamine sulfate or identical placebo administered as 3500-mg capsules. (The study design was double-blind cross over). The outcome was measured by a pain scale as well as one to assess quality of life.

Unfortunately low back pain is a significant cause of disability and medical cost in the United States. Too bad it doesn’t seem to have a significant therapeutic effect for relieving the symptoms.

A recently reported study of more than 3,000 people identified 9 modifiable risk factors for reducing more than 90% of all strokes. None of these will come as any big surprise. It’s been known for years that high blood pressure is associated with a higher incidence of brain hemorrhage (intracerebral hematoma) that results in either death of long-term injury. This relationship has been reaffirmed. This finding was based on the definition of hypertension as a systolic blood pressure greater than 150 mm Hg instead of the newer parameter of > 120 mm Hg.

A second, not surprising factor contributing to stroke, is smoking. For years it has been known that smoking increases the risk of both cardiac and stroke disease, mainly because it is associated with increased vascular problems. Diabetes is another factor that leads to vascular problem and stroke.

Two additional factors are obesity (as measured by abdominal girth) and regular exercise. These two have an obvious relationship with each other in that exercise helps maintain weight reduction in most people. Regardless of their interrelationship, they independently factored into the risk of stroke. Excessive alcohol consumption was also identified as a contributing factor.

So, your mother was right when she warned you to eat right, exercise, don’t smoke, and don’t drink excessively. The difference is that we probably didn’t believe our mothers. Now evidence based medicine shows she was correct.

I went to the dentist the other week for a chipped tooth. He used a local anesthetic to numb the nerves to my maxilla, or upper jaw. So I thought I’d write a few words about local anesthetics. When injected near a nerve, these drugs cause reversible loss of function of that nerve. So, if the nerve carries fibers for sensation, blocking it results in anesthesia (lack of sensation).

Nerves transmit information by conducting action potentials, or brief impulses. They do this by allowing sodium and potassium to rapidly flow in and out of the fiber, a process called depolarization and repolarization. If you can chemically block this process, you can block the transmission of action potentials, thus rendering the nerve incapable of sending information. And this is exactly how local anesthetics, such as Novocain work.

All nerve fibers are sensitive to local anesthetics, but generally smaller diameter fiber are more sensitive than larger fibers. Local anesthetics block conduction in the following order: small myelinated axons (e.g. those carrying pain impulses), non-myelinated axons, then large myelinated axons. Because pain fibers are the smallest diameter fibers, a differential block can be achieved (i.e. block pain sensation more readily than other senses, such as light touch).

Permanent nerve damage can occur after a peripheral nerve block but is rare. Symptoms are very likely to resolve within a few weeks. The vast majority of those affected recover within four to six weeks. 99% of these people have recovered within a year. Very few nerve blocks result in some degree of permanent persistent nerve damage.

Nerve fibers are not the only tissues that use potassium and sodium conduction as the basis for their action. So do muscle fibers. For this reason, the amount of anesthetic injected must be carefully monitored. This is also the reason that some local anesthetics are effective in treating some severe types of cardiac arrhythmias.

True allergies to local anesthetics is very rare.

I bought a Kindle the other day. One of the reasons was I found I wasn’t reading as many books as I used to. I thought about why? Well, one reason is eye strain. Without realizing it, I was tiring more when reading printed pages. As a result, I found reasons not to sit down and spend a couple hours reading. But the other week I bought a Kindle and am amazed at the improvement I now have in reading stamina. I had heard Kindles were easier on the eyes than printed books, but really thought it was just marketing hype. Well, for me it isn’t.

So what is eye strain? Several muscles control the eyes, moving them in back and forth and converging to focus at various distances. In addition to the actual muscles that move the eyes are the facial muscles that control the lids. Like any muscle they can fatigue. Our eyes were really designed to see far away and at different focal lengths. But if we look at one focal length for sustained periods of time (as I do during TV football season), we essentially produce a repetitive strain injury to the muscles. This results in aching eye muscles and/or even dry-feeling eyes. A trick I’ve adopted to relieve this problem is to stop every ten minutes or so and look away, at a corner of the room, or at something out the window. The problem, of course, is remembering to do this. In any event, I love my new Kindle. If you’ve ever thought of owning one, seriously consider it. They’re seriously fun.

A strange pain disorder called Causalgia can occur when the nerves that run from the spinal cord to the limbs are partially damaged, especially when the damage involves the bundles of nerves to the arms called the brachial plexus. Partial damage can come from accidents (that stretch the shoulder away from the neck, literally pulling some nerve fibers apart), from hand surgery, or from war injuries. A more recent name for the disorder is Complex Regional Pain Syndrome.
The pain is burning, constant, and usually involves the hand or foot. Sensory stimulation, such as rubbing the area, can worsen the pain. The pain usually is adjacent to any neurological deficit if there is one. Meaning that the pain may not be located in a region of numbness, but adjacent to it.

What makes this pain syndrome so different from other forms of chronic pain is that changes can occur in the skin and bones of the affected limb. The skin can become swollen and red because of loss of the normal tone of the blood vessels. In fact, comparing the temperature of the affected limb compared to the other normal limb is one aid to making the diagnosis (thermography). Abnormal sweating can also be seen. Interestingly, in some case patchy osteoporosis can be shown on X-rays of the limb in as little as three weeks from onset.

The cause is not really understood, but because of the vascular and skin changes, it has been suggested that the sympathetic nervous system is involved. In severe cases nerve blocks to the sympathetic ganglia in the base of neck can provide enough pain relief so that aggressive physical therapy can be started. Cigarette smokes are at much higher risk for developing the painful disorder than non-smokers.

I worked for a couple of medical device companies. One of the was Northstar Neuroscience. It was based a very cool concept. We developed a small battery powered electrode that could be implanted on the motor area of stroke victim’s brain. The system could be turned on to provide a tiny electrical current to the brain while the patient was participating in physical therapy. Guess what? It worked. Patients who were partially paralyzed on one side of their body regained a remarkable amount of movement. But timing is everything and before we could commercialize the device and obtain FDA approval, the stock market ran into a brick wall and there was no way the company could continue without another stock offering, so it went under. Actually, Saint Jude bought the technology but never really did anything with it.

The thing I loved about working at Northstar was all the bright energetic minds. I’m happy to say that many of the engineers and thinkers migrated from Northstar to another start-up company, NeuroVista. What they’re working on is a really cool sensor that is able to predict when a person with epilepsy is going to have a seizure.

There is a genetic line of dogs that have seizures and the company has successfully tried the device on the seizure-prone dogs with good success. Enough so that the company is starting their first clinical trial on humans in Australia. Check them out at http://www.neurovista.com.

If you’re interested, check out a recent interview that was broadcast on Australian TV:

http://www.abc.net.au/7.30/