In this episode of the Sarasota Neurology Podcast, Dr. Kassicieh, a recognized Parkinson’s disease expert, provides an overview of the disease and current techniques for managing it.



Parkinson’s disease is the second most common neurodegenerative disease seen in the United States. Only Alzheimer’s disease is more common. They both share the common fact that they are progressive neurological diseases that result in patients losing functional ability. Alzheimer’s disease affects memory, the ability to remember how to do things and general loss of mental function. Alzheimer’s patients are mostly not aware of the fact that they are neurologically deteriorating. They will make excuses for their memory short comings. Like Parkinson’s disease it is important to recognize Alzheimer’s early so that treatment can be started and outcomes will be improved.

Parkinson’s disease is primarily a progressive loss of the ability to move normally. There is a gradual slowing of movements as well as doing routine tasks such as shaving, dressing and getting ready to go out. Walking is affected and patients tend to shuffle with a forward stoop. Although tremor is common in Parkinson’s patients, not all have this. The converse is true: not everyone with tremor has Parkinson’s disease. There are many treatment available for Parkinson patients to improve their quality of life.

Not everything that shakes is Parkinson’s. If you are concerned that you or someone you love may be suffering from this or another movement disorder, please call (941) 955-5858 or click here to schedule your appointment today. If you’re outside the Sarasota area and unable to travel here, please locate a movement disorder specialist in your area.

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How I Avoided Knee Surgery

Parkinson disease was first described by James Parkinson in 1817 Over the years, various medication therapies have been FDA approved for Parkinson disease. In the 1960s, Sinemet (carbidooa-levodopa) was approved. Sinemet was and still is the gold standard therapy for Parkinson disease. While it is the gold standard, it should not be the first drug used to treat Parkinson disease. It should be the third or fourth drug used. Early use of Sinemet can result in unwanted, irreversible side effects.

Dopamine agonist were FDA approved in the 1990s for first line Parkinson disease therapy. These medications mimic the effect of dopamine in the brain of Parkinson disease patients. Dopamine is the brain chemical that is deficient in these patients. Mirapex (pramipexole) and Requip (ropinirole) are two commonly used dopamine agonists in the treatment of Parkinson patients.

The newest dopamine agonist which was FDA approved for Parkinson treatment is Neupro. Neupro is unique in that it is a dopamine agonist patch medication. This transdermal patch system is applied once daily to clean, dry skin. The benefit is that Parkinson patients get a 24 hour continuous medication dosing. Patch application sites need to be rotated daily, to prevent skin irritation. Neupro comes in several dosage strengths. Like other Parkinson medications, the dose needs to be adjusted for ideal patient functioning, with minimal side effects.

Dopamine agonists can have potential side effects. This class of medication can cause symptoms of hallucinations, confusion, lowered blood pressure, drowsiness, sudden sleep attacks – particularly while driving. Other side effects include stomach upset, nausea and compulsive behaviors – including gambling, eating and hypersexuality.

Parkinson disease does not need to be a disabling condition. With careful neurological management and detail to your specific needs, a Parkinson patient can have an excellent, functional quality of life for many years.

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Huntington’s disease is a neurodegenerative disease that is a genetic, progressive neurological disorder that slowly takes away a persons ability to walk, talk, and reason. It is characterized by the initial subtle symptoms of change in personality and motor skills ability. As the condition progresses, patients develop involuntary movements known as chorea (hence Huntington’s Chorea.)  The word chorea comes from the Greek word choreia, which means “to dance”, which describes the uncoordinated, jerky body movements associated with the condition. Other motor symptoms eventually appear and may include difficulty speaking, walking or writing.  It was reported in detail in 1872 by the American physician, George Huntington (1850-1916).

Symptoms of Huntington’s disease usually appear between the ages of  35-44 years old. Affected individuals can show a general lack of coordination and an unsteady gait.  Other symptoms include  depression, mood swings, forgetfulness, clumsiness, and involuntary twitching. As the disease progresses, concentration and short-term memory decrease and involuntary movements of the head, trunk and limbs increase. Huntington’s dementia eventually occurs. Patients will have memory loss associated with difficulty in abstract thinking, planning and avoiding inappropriate behavior.

In 1993, scientists discovered the gene that causes Huntington’s disease. HD is a genetic mutation stemming from the formation a chain of abnormal DNA sequences. There are four building blocks of DNA. Repeating DNA chains of cytosine-adenine-guanine (CAG) code for the protein glutamine, an amino acid. As a result, these long glutamine chain proteins clump together and are toxic to brain cells (neurons.) The more CAG repeat sequences there are, the more severe the symptoms of HD.  Scientists have also discovered the more severely the gene is mutated, the earlier the onset of the disease.

There is no known cure for Huntington’s disease at this time .  There are, however, treatments which can be employed to reduce the severity of some symptoms.  Tetrabenazine was developed specifically to reduce the severity of chorea in HD. Other drugs that help to reduce chorea include Haldol, Risperdal and other neuroleptic medications. Valium like drugs known as benzodiazepines may also be helpful. Rigidity can be treated with antiparkinsonian drugs, and myoclonic hyperkinesia can be treated with valproic acid. Depression is common in HD and can be managed with medications in the serotonin reuptake inhibitor family, such as Prozac or citolopram.

Huntington’s Disease profoundly affects not only the patient, but the entire family — physically, emotionally, socially and economically.  Since there is no known cure and the prognosis is poor, a plan of action should be developed jointly with a qualified neurologist who specializes in movement disorders so that the patient’s quality of life can be maintained as long as possible. Your neurologist can also help you locate and connect to some of the many support groups, organizations, and resources available to help with both the patient and the family and caregiver(s).

Innovative research is underway and aims to find better treatment options and ultimately hope and a cure for this debilitating condition.  If you suspect that you or someone you love may be suffering from Huntington’s Chorea, contact Sarasota Neurology for an appointment.

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Myasthenia gravis is a rare disorder of muscle weakness, affecting approximately 70,000 individuals in the United States. Many confuse this with multiple sclerosis. Multiple sclerosis is a central nervous system disorder affecting the insulation (myelin) on nerve cells in the brain and spinal cord. In contrast myasthenia gravis is a muscle disease where transmission of electrical impulses to the muscle fail. This results in the muscle not contracting fully, resulting in weakness. This condition can selectively affect the eye muscles, muscles of the head and neck or be generalized affecting all muscle, including the diaphragm. If the diaphragm is involved, patients can have varying degrees of breathing problems, including respiratory failure.

Myasthenia gravis (MG) is the standard model of a neurological autoimmune disorder. It is the the best understood of all autoimmune diseases. In autoimmune diseases, the body’s immune system fails to recognize a particular body system as being part of “itself.” In MG, the immune system does not recognize the transmitter receptors for acetylcholine (the muscle communication transmitter) as being part of the body’s own system. The immune system for antibodies against the receptors and attacks them. With fewer receptors on the muscle membrane, the muscle does not get the full chemical message to contract. This causes affected individuals to have weakness in the muscles affected by MG. These antibodies can be detected by a blood test for acetylcholine receptor antibodies. It is important to note, however, that not all patients with myasthenia will have a positive antibody test, known as a false negative (as high as 25%.) Particularly patients with ocular myasthenia frequently have negative tests. This does not mean that they do not have the condition.

Diagnosis of myasthenia is based on a careful medical history and detailed neurological exam. All patients with MG have some degree of visual symptoms including double vision or eyelid drooping. The presence of variable eyelid drooping, particularly if it shifts from side to side, is virtually diagnostic of myasthenia gravis. Confirmatory tests can include EMG testing and a chemical test known as the Tensilon test. Tensilon (edrophonium) is a chemical that temporarily blocks the enzyme that stops the action of acetylcholine. This has the effect of making the acetylcholine receptors that are “on” stay on longer, thereby combating weakness. Patient’s with suspected myasthenia can be given Tensilon. This short acting drug will temporarily reverse the weakness that myasthenic patients have. Other lab work should be performed to exclude other muscle diseases, thyroid problems or other metabolic problems that could cause muscle weakness.

Once the diagnosis is made, patients can be treated with Mestinon ( pyridostigmine.) Mestinon is a long acting version of Tensilon and works by inhibiting cholinesterase, the chemical that breaks down acetylcholine. If we did not have this enzyme, we could not relax our muscles. When acetylcholine is removed from the muscle receptor the muscle no longer contracts. Mestinon works well for symptomatic relief of the muscle weakness and associated symptoms of MG. Other symptoms associated with weakness can include chewing and swallowing difficulties, weakness of breathing with shortness of breath and generalized weakness. Double vision and drooping eyelids, conditions made worse by being in bright sun light, are frequent complaints.

For patients that have persistent symptoms, despite Mestinon therapy, clinicians will frequently employ the use of immunosuppressant therapy that will dampen the response of the immune system. This has the effect of limiting the destruction of the acetylcholine receptors on the muscle membrane surface. The most commonly used drug for this is Prednisone, a steroid drug, frequently used to treat autoimmune disorders. Although Prednisone works very well, it has its downside. Prednisone side effects can include weight gain, elevated blood sugar, cataracts, accelerated osteoporosis and other serious medical problems. Other immunosuppressants have been used with success. These include Imuran (azathioprine), cyclosporine, Cytoxan (cyclophosphamide) and CellCept (mycophenolate.) While being helpful in treating MG, these powerful immunosuppresants have their own lists of potential side effects. The purpose of immunosuppressant therapy is to cause myasthenia to go into remission. This is not always successful.

For patient’s with a severe worsening of their myasthenia symptoms, hospitalization may be necessary. Higher dosage, intravenous steroids can be given in combination with a blood filtering technique, known as plasmaphersis. The latter is used to filter out the acetylcholine receptor antibodies. A surgical technique, thymectomy, can be used to remove the thymus gland in the chest. This gland is responsible for making the cells that make the acetylcholine receptor antibodies.

Myasthenia gravis is a serious neurological condition and autoimmune disease characterized by muscle weakness that can affect vision, swallowing, breathing and general activities. Serious complications, including respiratory failure, can develop for untreated patients. Affected individuals should seek out care from a board certified neurologist, preferably one specializing in movement disorders or neuromuscular disease.

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One of the most frustrating neurological conditions is restless legs syndrome (RLS.) It is characterized by an intense overwhelming need to move your legs at night or when sitting or resting. This can be so severe that affected individuals have difficulty sitting through a movie or driving in a car for any distance. Occasionally RLS can be associated with abnormal sensation, particularly in the feet and lower legs. The abnormal sensory symptoms are a form of peripheral neuropathy that is associated with RLS. Symptoms can be so severe as to be an impairment to sleep and feeling of well being. RLS is consider to be a form of sleep disorder, even though individuals can have symptoms during the day, while awake. New research findings that were reported in the New England Journal of Medicine indicates that there is a genetic component to RLS. There are many who doubt the actual existence of RLS but those affected with this condition would disagree. As a movement disorder specialist, having seen many patients with this condition, there is no question that it is real. To ignore the medical literature and scientific evidence on the existence of RLS is foolish.

RLS can markedly impair the quality of life of affected individuals. They typically have chronic sleep deficit with a higher incidence of depression. The recent report on the genetic linkage of families with members affected with RLS is fascinating. Another common sleep condition, periodic limb movements of sleep, shows a stronger genetic correlation to run in families due to a specific genetic sequence variant at the 6p chromosome. Many of these individuals have RLS. If one isolates out the patients with RLS only, the genetic linkage becomes less clear. It is perhaps that RLS represents a subset of individuals with some chromosomal variation. This may serve as a marker for potential development of RLS in patients who have a history of RLS or periodic limb movements of sleep. These individuals can also have trouble with elevation in their blood pressure as well as other conditions associated with long standing sleep deprivation. There are several excellent treatment options for RLS including the dopamine agonists, Klonopin, low dose mild narcotics and other medications. If you are affected with this condition, it is important to get medical help as excellent treatment exists to control symptoms.

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Essential tremor is a common disorder than is characterized by involuntary shaking of the head, jaw, hands or legs. It is estimated that there are 5-10 million affected individuals in the United States. Unfortunately, many patients are incorrectly diagnosed as having Parkinson’s disease when they actually have a form of essential tremor (ET). ET tends to run in families and can have onset anywhere from 20-60. Parkinson’s disease most commonly starts after the age of 60 and is generally thought not to be hereditary. The characteristics of essential tremor and Parkinson related tremor are quite different. Typically the tremor seen in Parkinson’s disease occurs in the hands and is seen with the hand at rest. The tremor has a unique “pill-rolling” quality to it. The Parkinson tremor stops when the individual moves or uses their affected hand. Essential tremor is not present when the affected limb is at rest. When an individual moves their arm or tries to grasp or hold an object, then their tremor becomes apparent. This is most readily seen when trying to write, hold a beverage container or use eating utensils. Writing is affected in both conditions. In essential tremor, the writing becomes jerky with a zig-zag appearance to letters whereas with Parkinson patients, their writing becomes progressively smaller, trailing off into a non-legible line. It is uncommon for Parkinson patients to have head, jaw or leg tremor. These are much more commonly seen in the ET population. Patients with Parkinson’s disease have other clinical features that benign tremor patients do not have.

Treatment for patients with essential tremor (benign tremor, familial tremor) is readily available. Many patients have already discovered that small amounts of an alcoholic beverage will temporarily stop their tremor. Medications used to reduce tremor severity may include primidone, clonazepam, propanolol, mirtazepine or Topamax. All of these medications can be helpful but there is a potential for side effects, as with any treatment. For patients with severe, disabling tremor that is not responsive to medical treatment, surgical treatment with deep brain stimulation can be very effective. This procedure is highly effective in minimizing or completely controlling tremor. It has been approved for use since 1997. This procedure can dramatically improve a patient’s quality of life.
In summary, if you or one of your family is affected by obvious tremor, it is in their best interest to see a movement disorder specialist to get the correct diagnosis and treatment. The treatment and prognosis of essential tremor and Parkinson’s disease is quite different. The medications used for one will not help the other. Significant problems with unwanted side effects can develop if each condition is not treated properly.

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Botox (botulinum toxin Type A) has been available in the United States for clinical use since 1989. At that time it was approved by the FDA for treatment of eye and facial muscle spasm disorders, blepharospasm and hemifacial spasm respectively. Then in 2000 the FDA approved Myobloc (botulinum toxin Type B) for treatment of cervical dystonia, a condition of involuntary neck muscle spasm. The dystonias, as a class of muscle spasm disorders, are characterized by involuntary muscle spasms involving the muscles in the neck, face and extremities. The cause of the majority of these conditions is unknown. In some individuals, spasticity (tight muscles which cannot be relaxed, a form of dystonia) can result from stroke, traumatic brain or spinal cord injury or cerebral palsy.

Prior to the use of Botox, it was very difficult to treat muscle spasm disorders. Medications had side effects and surgery had limited benefit associated with the risk of complications. Botox opened an entirely new avenue to treat spasticity. The drug works by causing a chemical relaxation of muscles that are injected. Botox is highly selective in that it remains in the muscles that it is injected into. Patients with cervical dystonia have difficulty with their head pulling to one side of the other. They may also have their head pulling backward or forward. Not only is this condition painful, it also causes patients to have functional difficulty with activities such as driving, playing sports or even eating. In patients with limb dystonia, there is involuntary spasm of an arm, leg or both. This can cause difficulty with dressing, walking or even personal hygiene (if their hand is fisted up.) Botox (or Myobloc) can provide excellent relief of these symptoms thereby improving patients’ quality of life. For patients with severe muscle spasticity from stroke, Botox provides relief of the tight muscles allowing for greater ease in certain activities. It is important to note that Botox (or Myobloc) will not restore function of any limb affected by the stroke. What the treatment will do is provide increased comfort due to reducing pain from spasm and allow for improved ease in doing some daily activities.

Blepharospasm is characterized by involuntary blinking which can result in forced eye closure and functional blindness. Affected individuals may have difficulty driving or watching a movie because of this. Botox has been shown to be the single most effective treatment for this condition. Of all the muscle conditions treated with Botox, none respond as well as those patients affected with hemifacial spasm. This condition affects one side of the face and is characterized by spasm the facial muscles on that side. This can also result in a degree of functional blindness. While most conditions treated with Botox (or Myobloc) have a therapeutic effect for 2-3 months before requiring retreatment, patients with hemifacial spasm may not need retreatment for anywhere from 3-6 months.

For any patient considering receiving Botox or Myobloc, it is important to see a physician familiar with diagnosing and treating these uncommon movement disorders. These individuals are familiar with administration of Botox or Myobloc which will help to obtain optimum results from each treatment

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Botox is a potent neurotoxin that causes muscle paralysis by blocking the release of the neurotransmitter, acetylcholine, from the nerves that control muscles. When given under controlled clinical applications, this medication can have a dramatically beneficial effect in relieving muscle spasm due to certain conditions such as cervical dystonia, blepharospasm, hemifacial spasm and limb dystonia. Over the past several years the media has reported that Botox can relieve migraines. These claims are based on random reports of individuals who may have gotten some benefit. The manufacturer of Botox, Allergan, has conducted several nationwide studies on the use of Botox for headaches, none of which have shown a statistically significant difference over placebo. Sandra Leong writes in Natural Headache Remedies a summary about the use of Botox in the treatment of various headache disorders. She notes that one theory on how Botox works for migraine is by relieving the muscle tension. It should be noted however that physiologic studies have not shown an overall increase in muscle spasm around the head in patients suffering from acute headache attacks. It is also important to note that the placebo effect in headache studies is as high has 35%.

In a summary of the studies done by Allergan for headaches, Medical News Today lists the previous and ongoing studies that the company is conducting to analyze the potential benefits of Botox in the treatment of migraine and other headache disorders. Personally, having participated in several of these Botox trials, I would agree with the study results that there was no distinct clinical benefit from Botox over placebo. It is important to note however that these were randomized, double blind placebo studies where neither I or the patient knew if they were getting Botox or placebo saline injections. I base my conclusions on reading the final study reports. At the Florida Headache & Movement Disorder Center, we carefully screen patients with head and neck pain for the possibility of benefiting from Botox therapy. Only very few patients actually meet my criteria for using Botox for migraine treatment. Even with this careful selection of patients, our results are about 50% success rate, slightly higher that the placebo effect rate. The patients that benefit the most from Botox treatment most commonly have a high degree of muscle spasm in their neck and head, associated with but separate from their actual headaches. There have been reports by other respected headache specialists, in non-controlled trials, that Botox may effective for some patients with migraine.

In conclusion, Botox has not been shown to have a major therapeutic advantage in the treatment of otherwise intractable migraine and headache disorders. The “media hype” is without scientific basis to back up the claims cited in many reports. If you have recurrent headaches, your best bet it to be evaluated and treated by a board certified headache specialist.

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Deep brain stimulation is an innovative way to control severe tremor or some of the motor symptoms of Parkinson’s disease. This medical device was approved by the FDA in 1997 for treatment of patients with severe tremor that was not controlled by medications. A few years later, it was approved for treatment of Parkinson tremor and dyskinesias (involuntary head, arm and leg movements.) The main deep brain stimulation unit, manufactured by Medtronic, is called Activa Soletra. This is a small pacemaker-like device that is placed under the skin, just under the collar bone. The small electrode wire is then run under the skin, behind the ear and through the skull. The electrode tip is placed in a specific area in the brain that is responsible for tremor and dyskinesia control. A patient may need one or both sides done with a stimulator unit, depending on the severity and nature of their movement disorder. The risk of brain stimulator therapy is low other than at the immediate time of surgery. Once healed, patients can expect fewer side effects from deep brain stimulator therapy than from the several medications they may have to take to control their Parkinson symptoms. It should be noted that the best possible result from brain stimulator therapy will not exceed that of a Parkinson patient’s best response to levodopa therapy. Essential tremor patient’s can generally expect to completely stop medications that they are on for tremor control. Brain stimulator therapy is a safe, scientifically proven method for control of disabling tremor or other limb movements. It does not substitute for Parkinson medication but may help in reducing the amount of medication a patient has to take.

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Restless legs syndrome is a movement disorder that affects approximately 10% of the American population. Affected individuals have the uncontrollable urge to move their legs, particularly at night when sleeping. Symptoms can also occur with sitting for prolonged periods of time such as when driving, flying or watching a movie. If the condition worsens, the arms can also be affected. Patients with RLS can have a numbness, burning or tingling sensation in their extremities. RLS causes significant sleep difficulties and over time, chronic sleep deprivation. Patients can find it difficult to fall asleep or are awakened repeatedly at night from their legs moving. This will also disturb their bed partner’s sleep. Another movement disorder called Periodic Limb Movements frequently accompanies RLS, affects patients. PLM occur only when a patient is asleep.
RLS and PLMs can be effectively treated with readily available medications that are effective for most individuals. Requip was approved by the FDA one year ago and Mirapex November 2006 for treatment of RLS. Improved quality of sleep results in lessening of a risk of medical problems. Job security and quality of life are also dramatically improved. Physicians specializing in sleep or movement disorders should be consulted for diagnosis and treatment.

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