Saturday, July 26, 2008

Overactive bladders

This posting is not really about twitchy aging bladders that can't hold their own against a simple cup of coffee without whining uncomfortably for attention, but rather about the effect those frequent signals to head for the head have on our already addled brains.

Here's how the bladder connects with brain. That 'gotta' go now' message is sent to Barrington's nucleus, the brain center in charge of bladder contraction and urination. But no simple reflex here; rather than just send back a simple command to let 'er rip or hold on a moment dear, Barrington's nucleus feels compelled to tell the locus ceruleus all about it. This is the area in our noggin in charge of arousal and attention. I guess it makes sense because someone's got get up, find the loo, and transport the bladder there to do its business.

So researchers in Pennsylvania asked a group of rats to participate in an experiment wherein their bladder outlets were surgically narrowed to mimic an obstructed or overactive bladder(1). While Barrington's nucleus showed decreasing activity in the obstructed rodents compared to a control group (which may explain why people with OAB leak without knowing it until it's too late), the obstructed group demonstrated a hyperactive locus ceruleus.

Because the locus ceruleus is connected to the cerebral cortex, an area in charge of thinking, mood, and memory, the Philadelphia investigators conjectured that this hyped up bladder thing ultimately could affect behavior in an adverse sort of way. Indeed, the poor blocked-up rats brain activity consistent with chronic hyperarousal as seen in persons feeling anxious or stressed. And when the rats with obstructed bladders slept, their brain activity showed theta waves associated with restless sleep.

Researchers concluded: "Overactive bladder as a result of partial obstruction is particularly prevalent in the elderly, a population that is also vulnerable to neurobehavioral deficits and sleep disturbances. The present findings suggest that this visceral dysfunction may contribute to neurobehavioral and sleep deficits in this population."

Of course, surgically obstructed male rats are one thing, and aging women with overactive bladders quite another, but OAB may be just another brick in the deteriorating wall of our aging brains.
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(1)Rickenbacher, E. et al. Impact of overactive bladder on the brain: Central sequelae of a visceral pathology. Proc Natl Acad Sci U S A. 2008 Jul 21. [Epub ahead of print]

Monday, July 14, 2008

Diastolic dysfunction

The diagnosis of diastolic heart failure, unfortunately, is often missed by unwary physicians.
---heartdisease.about.com/od/livingwithheartfailure/a/diastolic_HF.htm


Before I say more than a few words about diastolic dysfunction, I want to note that I am mostly not unwary. Who'd want to go to an unwary physician anyway? I will admit, however, that I was a little unwary regarding the consequences of diastolic dysfunction, but I am no longer so. Here's the scoop.

If diastolic dysfunction is a new one to you, I'm here to tell you it was not part of my original medical education. When I learned about heart function gone awry, it was all about a delivery deficiency. In other words, a failing heart is unable to squeeze out sufficient blood with each beat. As a result, tissues receive less oxygenated blood, the lungs receive less blood to oxygenate, blood backs up as it waits for its turn to pass through the stressed-out heart, and the lungs, liver, and legs fill with fluid. All this is now known as systolic heart failure or a failure of the heart to adequately eject blood during contraction aka systole. What a messy fluid build-up and lack of blood flow results from systolic heart failure after heart attacks, viral infections, rhythm disturbances, or alcohol toxicity among other things.

So several years ago, I started seeing 'diastolic dysfunction' showing up on echocardiogram results. "What on earth," I asked my friends the cardiologists, what were they seeing on ultrasound examinations of the heart that qualified as an abnormality of the relaxation phase of the heartbeat.

Whereas systolic dysfunction is a delivery problem as noted above, I learned that diastolic dysfunction is an acceptance problem. Once blood is squeezed out during systole, the heart relaxes to accept a new load of blood in preparation for its next beat. The heart muscle slackens, the mitral valve opens, and blood rushes in to the big chamber known as the ventricle. Just to get that extra kick, the top chamber known as the atria squeezes a bit more in just before the ventricle begins to contract once again. If the ventricle is stiff, however, from years of working out against high blood pressure, diastole does not go so well. The ventricle is unable to accept as much blood.

Early on in diastolic troubles, that last atrial squeeze gets the heart volume up to normal. The patient motors on oblivious to the chaos brewing in his/her overworked heart (Naw, Doc, I don't check my blood pressure. I feel fine.) Then stiff becomes stiffer in a ventricular sense, and the heart no longer fills with enough blood to meet the demands of exercise. Fluid begins to back up in the lungs when the patient tries to mow the lawn or go for a walk. The volume overload in the lungs creates pulmonary hypertension which further accelerates the diastolically failing heart thing.

What brought this all to my mind? One of my patients, younger than me, came in with swollen legs. She's a skinny lady, so her edematous ankles were particularly alarming. She has an unfortunate history of hypertension, high cholesterol, smoking, and an inability to exercise for years due to a back injury. Her echocardiogram showed that her heart was pumping okay but she had serious diastolic dysfunction and severe pulmonary hypertension. As if this was not sufficient trouble, her chest x-ray shows one side of her diaphragm is paralyzed, so we are currently looking for a possible lung cancer high in her lungs squashing her phrenic nerve.

So that is why I: 1) ask my patients not to smoke, and 2) press them to keep after their pressure.

Saturday, July 05, 2008

Family and fiber: Colorectal cancer risk

I'm always recommending a screening colonoscopy to my patients 'of age,' after all, I had one, therefore, so can they. Here's the top two excuses (after 'I'm a chicken' and 'I'm embarrassed') that people give me for not undergoing this important screening test, and here's what I have to say to them:

1) No one in my family has colon cancer. While having a first degree relative (parent or sibling) with a history of colorectal cancer (CRC) increases risk 2-fold, 80% of persons who get CRC have no such family history.

2) I eat a high fiber diet. Boston doctors undertook a prospective study of nearly 89,000 women ages 34-59 in 1980.(1) They found no association between dietary fiber intake and the risk of CRC during 16 years of follow-up.

One might raise the question, as did Dr. Neil Raven(2), as to what really constitutes a high fiber diet. He responded to the above study in a letter to the editor wondering if the flaw in the study's design might not be that Boston women who say they eat high fiber aren't really as fiber-filled as they think. He cited information from Dr. Denis Burkitt, a physician who spent time in West Africa studying lifestyle and disease. Per Dr. Raven:

Burkitt began his lecture with a slide showing a stool of a typical Western, "civilized" person, a sausage-shaped thing, familiar to most of us, in a toilet bowl. His next slide was of a stool of a typical rural West African, which looked like a flat cow pie. Burkitt postulated that the West African's stool moved more quickly through the colon, giving carcinogens contained on its surface less time to be in contact with the mucosa — thus less time to induce carcinogenesis.

During the question-and-answer period, many questions from the audience concerned how one determined whether or not a diet was high in fiber in the sense Burkitt meant. Burkitt shook his head at all the salads, cereals, and breads offered as sources of fiber. He showed a slide of the staple cereal eaten by West Africans, which looked, in its wooden bowl, not too different from the stool that came out the other end. The only thing the study by Fuchs et al. proves is what anyone who heard Burkitt's lecture already knew: the American public has been sold a sugar-coated misconception.

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(1)Fuchs, CS et al. Dietary Fiber and the Risk of Colorectal Cancer and Adenoma in Women. NEJM Volume 340:169-176 January 21, 1999 Number 3.

(2)Raven, ND. Dietary Fiber and Colorectal Cancer. NEJM Volume 340:1924-1926 June 17, 1999 Number 24.

Tuesday, July 01, 2008

"The middle of my foot hurts"


My old arch is falling down (click on image; watch it throb!)

"Have you ever heard of Liz Franks?" the octagnenarian asked me, waving her foot in the air.

"Yeah," I said slowly, "I've heard of it [her?!?]. My voice screamed 'haven't a clue,' but my patient proceeded with her story.

"The middle of my foot hurts sometimes when I walk. The PA at my podiatrist's office says it's a Lisfranc injury and it has something to do with a separation in the bones of the feet. He told me that's why my foot hurts and the top of it swells."

Ah, yes, Lisfranc's as in Lisfranc's fractures. And now I had the entire Lisfranc's file open in my brain and the sum total of its contents revealed in those three words.

I looked it up later on the Internet, and learned that Doc Lisfranc was a field surgeon in Napolean's army, and the joints named after him are in the midfoot where the long bones or metatarsals below the first and second toes meet the various bones under the ankle. Wang, whoever he is, has seriously injured his and won't be playing for the Yankees for awhile. On average, Lisfranc's injuries occur abruptly and dramatically in athletes or in those who've fallen from great heights or been injured in car accidents. Lisfranc joints can be subtly sprained in athletic endeavors.

In no case, per my search, do Lisfranc dislocations or fractures occur in little old ladies who now and again get pain whilst walking. Pain in the midfoot of the aged is either midfoot impingement syndrome or degenerative arthritis of the middle of the foot including, perhaps, the Lisfranc joints.

The midfoot is the highest point of the arch. As we age--and by we, I definitely include me--the arch sags or just plain goes to ground causing the bone ends to crash into each other in a painful, unsupported sort of way. As a result, with each weight-bearing step the bone ends grind together. This daily grind, over time, wears down the joints causing degenerative or osteo- arthritis.

While merely impinging on one another's space, this bone on bone action causes episodic pain with weight-bearing activities. Once arthritic, the pain is more consistent, and the entire top of the foot can be painful and swollen. As with all archless conditions, standing in bare feet aggravates the pain; I advise all my flatfoots--including myself--to immediately slip their aging feet into arch-supported clogs or sandals on rising in the morning. Good Feet has a lightweight orthotic perfect for wearing with open-toed shoes.

And, as you may know, I am also a great fan of YogaToes, the plastic toe separators, which pull the toes and their metatarsal bones out of each other's face and space.