25
July
2007
Multiple Sclerosis (MS) is a disease of the central nervous system of unknown cause. The nerves are damaged through inflammation, probably the immune system attacking the sheaths of the nerves. It is #1 nontraumatic cause of disability in young adults. On average it afflicts people aged 15-50years old. Women are 2x more affected then men. 350,000 American have it, in particular those of Northern European descent. On the other hand 11% of MS patients at Johns Hopkins in Baltimore are African American.
Autoimmune? It is thought the immune system attacks an infection, say a virus such as human herpesvirus 6 or EBV, but then mistakenly attacks the coating of the nerves (myelin) as well. After enough nerves are damaged, the symptoms of MS appear and as well are detected on MRI. When the nerves can transmit signals to the body, muscles and organs are affected. And the brain lesions that form lead to fatigue, depression, and poor memory. After enough inflammatory attacks of the nerves, the nerves can eventually be permanently damaged.
Symptoms include fatigue and depression which often occur early. Because MS destroys the function of nerves, so numbness, tingling (parathesias), and weakness can result. Loss of vision in one eye or double vision, heat sensitivity, Lhermitte’s sign (feeling electricity shoot down the spine when flexing the neck), tremor, imbalance, poor movement & coordination, vertigo are more symptoms of MS. Bladder problems are common – either losing control to have incontinence or the opposite – retention. Also sexual problems can develop. A person with MS might only have a few symptoms which makes diagnosis difficult.
There are a lot of diseases that have similar symptoms as mentioned above, so making the diagnosis of MS can be a challenge. And on the flip side, people who don’t have MS often freak out thinking they have MS when really it is a different problem, such as B12 deficiency, Lyme disease, diabetes complications, etc.
Types of MS: 4 types are described: Relapsing-Remitting MS (RRMS), Secondary-Progressive MS (SPMS), Primary-Progressive MS (PPMS), and Progressive-Relapsing MS (PPMS).
RRMS: #1 type of the 4 – 80% of all MS patients at onset of MS flair. 55% of all MS patients at any given time (prevalence). The course of RRMS will be frequent attacks followed by remyelination (recovery of the damaged nerves) though permanent damage occurs over a matter of time. So disability occurs in a stepwise fashion gradually going downhill.
SPMS is the end result of RRMS due to long-term damage to the nervous system. With or without MS flairs, the nerves slowly die off leading the person with MS down a hard road of disability. 30% of all MS patients are in SPMS stage
PPMS means MS symptoms progress without any obvious relapses. No acute flairs but a gradual decline in function.
PRMS is rare, only 5% in which MS progresses without flairs, but even more so with flairs. No remitting.
Diagnosis: MRI of the brain is the best way in light of clinical symptoms. White plaques are seen in the white matter of the brain and in the spinal cord. Unfortunately, there are over a dozen infections that can mimic MS on the MRI.
In my experience, neurologists often don’t have a clear cut diagnosis of MS. In 2000, two MS societies convened to re-define the criteria to diagnose MS. In their meeting they said 1 clinical episode of an MS flair followed by detection of new lesions on MRI 3 months later is considered MS. This criteria is more stringent than before.
Lumbar puncture to evaluate the CSF (cerebral spinal fluid) can aide in diagnosis MS, in particular oligoclonal bands. But the sensitivity is pretty low early in the course of MS.
Evoked potential tests are also used to aide in diagnosis.
Treatment: the mainstay class of drugs is IFNb (interferon beta) and glatiramer acetate for RRMS. Avonex is IFNb-1a. IFNb-1a and 1b and glatiramer acetate are FDA approved for RRMS and has been clinically proven to reduce the frequency & severity of relapses. Will it prevent disability in the future? Probably but not for sure.
Mitoxantrone is chemotherapeutic in SPMS, PRMS, or worsening RRMS. But because it is toxic to the heart, it can only be used 2-3 years. Also leukemia can develop
Natalizumab is a monoclonal antibody that is being studied
Management: for me as PCP, persons with MS do tend to ignore their overall health, such as PAP smears, cholesterol, exercise, diet. Also with disability, osteoporosis can develop as well as bed sores. So I look out for all these things. Also depression and fatigue greatly affect the quality of life so antidepressants for mood and stimulants for energy can be used.
drjohnhong 
Uncategorized, neurological 
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18
July
2007
Rocky Mountain Spotted Fever (RMSF) is a tick-borne disease by a bacterium called Rickettsia rickettsii. Even though RMSF sounds like it is only in the Rocky Mountains (where it was first described), it occurs throughout all the Americas. It is most prevalent in the Southeastern and South Central states. North Carolina has a larger percentage of cases, though there aren’t that many cases overall. In 2004, 1,454 cases of RMSF were reported to the CDC.
I’m writing about this because a viewer/reader in Charlottesville, VA asked me to talk about it because her husband was severely affected by RMSF this year (2007). Rural and suburban regions have the most cases of RMSF though some cases from parks in NYC have been reported!
Spring and early summer is when RMSF appears the most, as most tick-borne illnesses are. Outdoors people are obviously most at risk – so, white men. Most cases are in people aged 40-64. Dog can carry the infected ticks and pass them on to their owners.
The common brown dog tick (Rhipicephalus sanguineus – wow say that 3 times fast, or at all) may be a vector (carrier) for RMSF. Possibly infection can occur without a tick bite, in which contamination might be due to contact or inhalation with tick poop or tick tissue.
Clinical: Incubation period is 2-14 days, but most occur a week after infection. Flu like symptoms occur first – in particular a fever, as in the name for RMSF. So there are headache, body aches, nausea. Belly pains occur usually in children.
The RASH! That is why RMSF has its name. But it takes 3-5 days for the rash to develop after the flu symptoms occur. So that makes it difficult to diagnose RMSF initially. The rash starts on the ankles and wrists, spreading out from there including to the soles and the palms. It is red and very evident because they aren’t tiny – they are like large constituency of small dots to form polka dots. It isn’t an itchy rash nor like hives.
However, 10% of cases don’t get the rash. Or in darker skinned folks, it might be missed. “Spotless RMSF” can be fatal because without seeing the rash, treatment is more likely to be started too late – and with RMSF, starting treatment soon is vital. After 5d of RMSF symptoms, the mortality rate increases with delayed treatment. One study showed those treated in the first 5 days vs. after the 5th day, the mortality rate was 6.5% vs 22.9% respectively. Though it is estimated the overall mortality rate is less at 3.3%.
RMSF can cause bleeding, swelling, coughing, confusion, neurological problems including seizures. Gangrene can develop in the fingers, toes, ears, and in men the scrotum. Eventually all the internal organs can fail.
Diagnosis: blood tests can be falsely negative in the early stages of RMSF. So treatment is often initiated upon clinic history and physical exam. The blood test usually doesn’t pop up positive until 7-10 days after symptoms started. This IFA test is 95% sensitive 14-21d after the onset of illness. There is not a test for the tick itself should a patient bring it in.
Treatment: the antibiotic of choice is tetracycline. But in kids with growing bones (or a fetus in a pregnant woman), it can cause tooth and bone problems. Chloramphenicol is an alternative antibiotic. 1 week of antibiotics is usually curative.
Prevention: avoid tick bites. DEET so far is the only proven bug repellent against tick bites. Make sure you check your dog everyday for ticks. Check for ticks on the body everyday. It is estimated it takes about 24 hours for a tick to transmit disease to a person. Prophylactic antibiotics are not recommended. There is no vaccine.
drjohnhong Uncategorized, infections 2 Comments » |
12
July
2007
Osteoporosis occurs in more than 2 million American men. By 2025 it is predicted the increase in bone fractures in men will be a greater rate than women. Osteoporosis is a bone disorder of decreased bone strength which increases the risk of fractures. The bone density and quality go decrease leading to demineralization, poor architecture, increased bone turnover, and damaged accumulation. On DEXA (bone mineral density test), osteoporosis is defined as more than a 2.5% standard deviation under the mean (a.k.a T score)
So you probably think osteoporosis is only a problem for women. Overall it has been true because boys probably develop stronger bones during adolescence and puberty compared to girls. Androgens (like testosterone) are known to increase periosteal bone formation (the covering of the bone) while estrogen inhibits this. Also male muscles and weight bearing exercising might contribute to stronger bones. But as we all get older, we all lose bone mass and architecture, women more than men.
The main fractures due to osteoporosis are the vertebrae (spine), hip, and wrist. Less common are upper arm, ribs, collar bone, shoulder gone, sternum, and pelvis. After the age of 50, lower BMD (bone mineral density) is associated with increased fractures. Boys being boys, fractures are more common in boys and young men, but then dips below that of women by age 50.
Fractures lag 10 years behind that of women after age of 50. It is estimated 1/7 men after 50 years age will have an osteoporotic fracture. Unlike women, men are 50% less likely to have a vertebral fracture on x-ray or a hip fracture; and 33% less likely to have a clinical vertebral fracture (that means pain). So 2/3 of men with vertebral fracture don’t know it until diagnosed by a physician.
50% of reasons for male osteoporosis are: lack of testosterone, steroids, and alcohol abuse. In Otherwise other causes include high thyroid, high parathyroid, multiple myeloma, high urine excretion of calcium, low vitamin D – such as in malabsorption syndromes, smoking, anticonvulsants, COPD, kidney stones.
Even though estrogen mentioned above inhibits the “coating” of bones, it is vital in bone resorption – meaning reforming the matrix of the bone which occurs all the time to keep the bone fresh and strong. So young men who have CYP12 aromatase gene or estrogen receptor defects, they might be more prone to osteoporosis. Kyphosis and losing height can be a sign of osteoporosis because the vertebral bodies shrink.
Elder men can develop problems with calcium and vitamin D in the GI system and kidney processing. Also elder men who experience a hip or vertebral fracture have a high mortality rate than women. Why? Not sure. But at 6mo after a hip fracture for a man, there is a 9x increased risk of death compared to someone without a fracture. The cost of male osteoporotic fractures was $2.5 billion in 1995 in the US. It is expected to be 310% more in 2025.
Sign of kyphosis: can’t stand straight and put the occiput against the wall. Also the lowest of the ribs to the upper part of the hip in the line of the armpit is less than 2 fingerbreadths in width.
Treatment includes calcium 500mg three times a day (which can also be taken in by dairy products), 1000IU of Vitamin D a day. But if someone has calcium kidney stones that might not be possible. If man has andropause, testosterone replacement can be considered. Alendronate and Risedronate are bisphosphonates to help the bone density increase. Weight bearing exercises including walking. Also life style modifications like alcohol moderation (<25g a day) and not smoking.
drjohnhong Men issues, Bones & Muscles Comments (0) » |
4
July
2007
Heat exhaustion is when the body becomes dehydrated, mostly from sweat due to the dog-gone heat! Heat stroke is when the body’s core temperature rises to above 105 degrees Fahrenheit. After about 30minutes basically the brain and other internal organs get fried from this elevation in temperature.
Sweating is the #1 way to cool the body down. However, when the relative humidity outside is great than 75%, sweating doesn’t work well. And when the temperature outside is greater than 90 degrees Fahrenheit, the body doesn’t cool off well. So these factors can lead to overheating of the body.
Heat exhaustion symptoms include: lowered blood pressure, lightheadedness, irritability, headache, nausea, fatigue, muscle aches, and hyperventilation.
Heat stroke symptoms include: delirium, losing consciousness, shortness of breath, and excessive bleeding. Heat stroke tends to occur in young healthy people who don’t sweat during exercise on a hot, humid day.
Treatment of heat exhaustion and heat stroke include: get out of the sun, get out of the heat, drink cool fluids, and even ice but don’t induce shivering will increase body temperature. CPR might be needed. Call 911.
Sweaty, sweaty, sweaty. Ooh, it is summertime and it is hot. But all this sweating and heat can cause heat exhaustion, or worse yet heat stroke. So this morning I got up to do the news, not realizing it was the 4th of July — I could have slept in. Such is life. So I hope you watch the video to see ALL MY HARD EFFORTS this holiday morning. Now it is time to baste the ribs on the grill. We are grilling for 8 hours to get it smoky and just right.
drjohnhong Uncategorized, cardiovascular Comments (0) » |
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