28
May
2008
Alzheimer’s Disease is the #1 type of dementia in the elderly – about 60-80% of cases. About 4 million Americans. Occurs between ages 40-90, is progressive, and causes memory loss, global cognitive dysfunction, personality changes, and loss of independence due to poor executive functioning. It comes on slowly, usually starting with short-term memory loss.
drjohnhong 
neurological, senior citizen 
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19
December
2007
Migraines affect 40 million Americans. Painful and a big cause of loss of work
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8
August
2007
Benign Positional Vertigo (BPV) is vertigo that occurs with head positional changes. Vertigo means a spinning sensation, not lightheadedness. The in peripheral BPV, the ear contains the balance center, and it senses gravity and crystals in the balance center causes the spinning sensation. In central BPV, vertigo occurs because of a problem in either the brain’s brainstem or cerebellum. Unlike central BPV in which the vertigo stays as long as the head is in the “right” position, peripheral BPV is transient – so it “burns” out after a while despite being in the same head position.
Clinical: vertigo spells usually less than a minute. BPV affects a person weeks to months without meds or intervention. Then poof! It goes away on its own. It can come back periodically and for some reason vertigo occurs mostly in the spring time.
What triggers a spell: rolling in bed, getting out of bed, looking over the shoulder, looking up.
Nausea and even vomiting can occur because dizziness can make you up-chuck.
Cause: in peripheral BPV the balance center of the inner ears (semicircular canals) have foreign bodies (like calcium crystals). These crystals hit the triggers in the canals and it gives the sense of spinning, like on a roller coaster or merry go round. The calcium crystals come from the utricular sac (where all 3 semicircular canals meet)
35% of the time there is no known reason for BPV. Some causes are head trauma, Meniere’s disease (30% of cases), history of ear surgery, vestibular neuritis, stroke to inner ear, and giant cell arteritis.
For those who have central BPV (the vertigo doesn’t diminish as long as the head stays in that position), MRI probably needs to be done to check for Chiari malformation, cerebellar degeneration, and spinocerebellar ataxia.
Diagnosis: Dix-Hallpike and Barany Maneuvers are easily done in the doctor’s office, unless you have a neck problem like Rheumatoid arthritis. Both maneuvers swing the head around to invoke vertigo. Vertigo is seen by the doctor by something called nystagmus – the eyeball swings around or back and forth very quickly.
Treatment: ENTs are known to reposition the head to get the calcium crystals out if it is peripheral BPV: Epley maneuver. Brandt-Daroff exercises as well.
Medicines are to treat the dizzy feeling and if necessary nausea and vomiting.
For those who have recurrent BPV, it comes on usually 1-3x/year but for most people BPV doesn’t haunt them for life.
Hearing test might be needed to check for Meniere’s Disease.
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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.
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30
May
2007
Parkinson’s Disease
Parkinson’s Disease is a progressive degenerative disease that destroys a part of the brain, in particular the midbrain’s basal ganglia, and it helps to control movement. Millions of people have it now. Rare before the age of 40, 1% over the age of 65, and 2.5% of people over the age of 80. Parkinson’s Disease that causes dementia affects about 0.2- 0.5% of people over the age of 65. Parkinson’s Disease peaks between 70-79 years of age and is twice a common in men compared to women.
Cause of Parkinson’s Disease: we aren’t sure. It might be genetic. Perhaps exposures are associated with Parkinson’s Disease, such as pesticides and heavy metals (mercury, zinc, iron, manganese). The basal ganglia release dopamine, a chemical to help control movement in the body. In Parkinson’s Disease, there is a lack of dopamine release from the basal ganglia to the key movement center of the brain.
Symptoms: Falling down, change in walking, worsening of handwriting, slowing down in movement, resting tremor that goes away with movement. Fatigue, dementia, even psychosis. Drop in blood pressure, incontinence, erective dysfunction, slow GI system can occur with worsening Parkinson’s Disease
Signs: 1) A resting tremor. Pill rolling tremor is seen so the thumb and index finger look like they are rolling a small marble. 2) Rigidity. On exam, while extending the arm it looks like a cogwheel movement – an unsmooth mechanical motion. 3) Akinesia, meaning lack of movement. Even the face is blank, called a masked face. 4) Gait disturbance, so turning around can call a fall. Shuffling the feet occurs.
Other diseases that can be mistaken as Parkinson’s Disease include a stroke to the basal ganglia, progressive supranuclear palsy, and multiple system atropy. Some medicines cause Parkinson-like symptoms. These drugs block dopamine receptors of the brain. Antipsychotics are big ones doing this. Metoclopramide (Reglan) for GI motility can cause this.
Treatment: no cure unfortunately. Medications don’t slow down this progressive disease. But researchers are working on drugs to slow it down.
For symptom treatment, levodopa (such as Sinemet) is used to replete the lack of dopamine in the brain. MAO B inhibitor, such as selegiline, is used – and you hear all the pharmaceutical commercials say, “Don’t use our drug if you take an MAOi.” Dopamine receptor agonists include Mirapex, Requip, Parlodel, and Permax. Also anticholinergics can be helpful in Parkinson’s Disease, such as amantadine and Cogentin. COMT inhibitors (Tasmar, Comtan) are used to assist levodopa drugs, because levodopa tends to “wear off” between dosings and after 5 years usually aren’t as effective as once before. In postmenopausal women, estrogen might be helpful – but then there is increased risk of heart attack, blood clot, and breast cancer.
Unfortunately all these medicines have side effects, like fatigue, nausea, headaches.
Surgical procedures are still being investigated.
It is vital to see a neurologist and discuss all your options with him/her.
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