Alaska

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About five years ago she noticed the tremor in her right hand. Now as she sits in the examination room, her slightly swollen hand vacillates steadily as she rests it on the arm of the chair. She feels the muscles cramping and shortening and uses her other hand to straighten the fingers. Gradually she has lost most of the strength, dexterity and the ability to write legibly. She states she has taken Azilect for two years and sees little improvement.

Ah, but that’s good, the doctor states. It means progression of your illness is slow; the other side of the body may be affected with disease, within that time. The comment buoys the patient’s sentiments, somewhat. The specialist in movement disorders asks about her prior medical history and learns the patient underwent heart surgery to amend a leaking heart valve, seven months prior. Surgeons removed her thyroid two years ago and she suffers from high blood pressure, and high cholesterol. She states she is healthy, otherwise; comments from an optimist.

As the specialist dives into a description of how and who implicated dopamine as the neurotransmitter depleted in Parkinson’s disease, the steady murmur of his voice and the quality of the fluorescent overhead lights lulls the listeners into a stupor. The patient has brought a cup of coffee with her, remarking it’s decaffeinated, and the doctor remarks smoking and drinking coffee are two habits that are negatively correlated with illness and PD; the more one smokes and drinks coffee, the smaller the likelihood one will acquire PD.

On physical examination of the patient, the specialist discovers brisk reflexes; probably a byproduct of high blood pressure he comments. He inquires whether she has had an MRI of the brain, as people with long-standing high blood pressure commonly have a multitude of small white spots scattered just under the cortex of the brain. The neurologist feels the fluidity of movement from the left elbow and wrist and senses some rigidity in the muscles of the biceps. When he asks her to walk in the hallway, her gait is regular, with wide steps though she tends to hold the right arm and hand at her side, while she swings the left.

Sitting again in the examination room the patient asks about exercise. The doctor encourages the patient to discover when her cardiologist feels it safe to increase her heart rate, and then describes a clinical experiment in which researchers trained monkeys to jog on a tread mill six hours a day. Those mokeys that underwent an experimental unilateral injection of a toxin that destroys dopamine neurons to one side of the brain, recuperated much faster, while those that did no exercise remained disabled. He states exercise, especially aerobic activity, enhances repair in the brain and provides a neuroprotective benefit. The patient confides she had to end her membership to the gym, as the temptation to get on the aerobic machines was overwhelming. She states she has always been an active person, and not allowing her heart rate to climb has been difficult. Yoga and Tai Chi are also helpful for those with PD, the physician states.

The doctor creates a chart for the patient, detailing how to increase the dosage of Sinemet. She should aim for the smallest dose that eliminates the stiffness and rigidity in her hand. He also encourages her to seek physical therapy for her hand, to regain strength and extensibility in the muscles. The doctor states he would like to see her again in three months time to see whether the transition to Sinemet has gone smoothly.

Before leaving, the patient reveals she lived in Alaska for sixteen years raising four children. The darkness of the winters never bothered her, or made her feel blue; an unusual blessing for a person with PD, where depression affects 70% of the patient population.

Mute and Temulous

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Entering the examination room the male patient sits in a chair with a large board for writing. Perhaps he has had a stroke and can’t speak. The patient writes his wife will return soon and the physician begins speaking with him, as he sits down. This clinic, Tuesday morning clinic is a Parkinson’s disease clinic, he explains to the patient, who nods in reply. In front of the doctor is a list of symptoms the patient deals with. Tremor is high on the list. The specialist continues speaking, reading the list of medications the patient relies on, and the three pages of medical history patients are asked to fill out.

The wife enters wearing a purple summer dress. The doctor asks when the tremor in the hands first began, and the spouse replies he has had tremor for a long time, and being a mechanic and depending on his hands, he has not worked in some time. The patient writes well, when he chooses to report something, with no indication of tremor in the handwriting. The wife clarifies the story by noting the patient required hospitalization in February after going on a drinking spree of four days. He became psychotic and lost touch with reality. In the care of a community hospital, the patient received an IV drip of saline, and nothing more. The nursing staff did not give the patient thiamine with the IV? The physician asks,and the wife, once a surgical nurse, reported never having seen anything more than saline.

Much earlier in his life, the patient was in a car accident that trapped his hands between his Thunderbird T- back and the asphalt road. Surgery attempted to reconstruct his fingers, but several digits remain stuck in a claw- like position. Another accident; the hammock he slept in collapsed during the night, resulting in fractures to vertebra in his neck and damage to nerves in the left arm, leaving the hand numb, and the left arm useless.

More recently, the wife having taken a position requiring traveling from Monday through Friday, saw little of her spouse and he began drinking heavilyHence the hospitalization for psychosis, in February. Four days after having returned home, the patient again became delirious, hallucinated and lost the ability to walk. The doctor states the scenario sounds reminiscent of Wernicke Korsakoff Syndrome, where drinkers undergo debilitating alcohol withdrawal. The wife took her spouse back to the hospital, where she claims hospital staff related they could do nothing for him. The cause of the syndrome is due to severe deficiency of thiamine, and if not treated the drinker undergoes damage to the brainstem; memory, gait and voluntary gaze are all affected.

On physical examination, the patient is weaker on the left, probably resulting from the old injury to the neck and damage to the nerves that innervate the arm. Muscle tone is supple, and the specialist feels no rigidity, and sees no slowness in movements. Resting tremor is slight.
The doctor views the MRI conducted in the community hospital and notes the poor test quality. Though judged normal, the physician notes some shrinkage of the midline cerebellum on the MRI, typical of those who drink heavily. He comments it’s worth having the test repeated at the institution, as their current technology may be capable of catching something unremarkable on the poor quality image of the brain. He admits he does not know the cause of the patient’s inability to speak. He asserts the problem may be a psychiatric one, though all psychiatric illness has a physical disturbance that can be explained, biochemically. The wife interjects the psychiatrist told her yesterday it is not a psychiatric problem. The doctor counsels the patient to care for himself, by eating a healthy diet, taking a multivitamin and exercising daily, and the brain will repair itself, and not to seek too many doctors as they’re likely to mess things up.

There is no Parkinson’s here, the doctor concludes. Sent by another neurologist who noted the tremor of his hands, the patient came to rule out a movement disorder. The effects of medications cause many movement disorders, the doctor concedes, and at least one of the drugs the patient uses, lists tremor as a side effect. The psychiatric medications the patient depends on have stabilized his bipolar disorder, and the neurologist feels reluctant to change any of them, though he feels the patient would benefit from physical and speech therapy, and a new MRI.

Seventy-six years

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Alot can happen in seventy-six years; twenty years of hypertension, seven years of diabetes, a quadruple bypass for the heart, three transient ischemic attacks, two strokes, thyroid imbalance, and Parkinson’s disease brings the patient in to see the specialist in movement disorders. The patient was diagnosed only three months prior, and yet he is in stage three of the illness (according to the H&Y scale), evident with bilateral symptoms and impairment of balance and equilibrium. His dose of Sinemet is high, 25/250 three times per day, and yet he experienced no nausea when he began the medication.

The patient wears a freshly starched short sleeve linen shirt. He is balding and he wears glasses, yet he takes them off when the doctor examines his eye movements. The spouse comments the way her husband holds his lips and jaw have changed. He admits he grinds his teeth now, the doctor comments some of the jaw clenching may be an involuntary movement caused by relatively high doses of Sinemet.

The patient has several atypical symptoms that may be reason to consider whether he suffers from Shy Dragers Syndrome, currently called multiple system atrophy.

Doctors classify the disorder into 3 types:
the Parkinsonian-type: symptoms of Parkinson’s disease- slow movement, stiff muscles, and tremor
the cerebellar-type: causes problems with coordination and speech
the combined-type: symptoms of both parkinsonism and cerebellar failure. Problems with urinary incontinence, constipation, and sexual impotence in men happen early in the course of the disease. Other symptoms include generalized weakness, double vision or other vision disturbances, difficulty breathing and swallowing, sleep disturbances, and decreased sweating.1

Patients with the disease respond less favorably to medications aimed to treat PD symptoms, though they may derive a general feeling of well- being. The wife of the patient reports he has dramatically improved with the medication. He lacked any facial expression, his arm failed to swing when he walked, and the tremor in his hands and feet was nearly constant. All of these symptoms have changed for the better with medication.

The loose ends hang about, unresolved. For example, when he is not speaking the patient lapses easily into a pattern of hyperventilation. Could this quirky behavior be the result of ischemia, or a lack of oxygen, to the vessels in the brainstem that govern the rate of breathing? What can account for a sudden fainting spell, besides a sudden drop in blood pressure, which commonly occurs in Shy Dragers? What can be said for the need to urinate every two hours?

The doctor recommends the patient stay on the current level of medication, though it may behoove him to add coenzyme Q10 to his daily intake, at levels between 300 and 900 mg per day. The specialist advocates aerobic exercise, beginning at thirty minutes, three times per week, and notes he would like to see them again in four months, to check on him.

PD, levodopa, hallucinations and sleep

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Difficulty writing was the first symptom of his illness. Then his wife noted his walking was slower, and his face more fixed and rigid. Since diagnosis in 2001, he has taken a very light dose of medications: three doses of 25/100 daily and Mirapex. The doctor comments he has had a long honeymoon period; fortunate man. He sits without expression in the office chair, yet he asks questions. He wonders about the frequent hallucinations his is having. The doctor tells him that hallucinations are very common in PD patients. He relates a story of an older man who sees a young naked woman get into bed between him and his dozing wife. The physician asks the patient whether he reached out to see whether the woman was a hallucination, and he replied he didn’t dare move, for fear he would wake his sleeping spouse. That dream the patient comments, is one he would like to have. Instead, the dog hallucination visits him nightly.

When the honeymoon period runs out, patients begin to experience lapses in the effectiveness of medication. These periods, commonly known as “off” periods become more pronounced as illness progresses. The doctor notes the dopamine- rich cells in the brain lose their ability to store excess dopamine, their buffering capacity wanes and patients begin to vary in their levels of function according to the level of medication that reaches the brain. Here, the physician begins speaking about the importance of avoiding proteins, especially milk proteins in the morning meal. Milk proteins compete strongly with the morning levodopa (Sinemt) for passage into the brain; their presence in the diet inhibits the ability of levodopa to get through the blood- brain barrier. This is the reason for having a non-dairy creamer like Cremora instead of milk in coffee and cereal. Dopamine agonists, like Mirapex do not have this problem.

The physician dips into a discussion of sleep and PD, noting the disease ruins normal sleep architecture, causing sleep to fragment. Patients may doze during the day. Excessive daytime napping impedes sleeping ability during night hours, and works to further weaken normal sleep cycles. The body requires a certain amount of rapid eye movement sleep, when not acquired at night, the person with PD becomes susceptible to hallucinations, which are essentially waking dreams. In a study the physician conducted, he found 26% of patients with PD hallucinated; all 26% had fragmented sleep. Novel tranquilizers, such as Seroquel and Clozaril, when given in small doses in the evening counteract fragmented sleep patterns and encourage slumber. The physician prefers patients have a solid length of time given to sleep, as it is more likely they will acquire the needed amount of dreamtime. With a fixed sleep schedule, patients are less likely to hallucinate.

The practitioner- researcher informs the patient and family about a clinical research study he’s involved in, asking whether the patient would be willing to provide a sample of blood. The aim is to find out whether an agent or biomarker exists in the blood that changes with progression of illness. By identifying such an entity, it would be possible to gauge whether medications can truly inhibit the progression of disease.

Yenta

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Yenta, was the word she used to describe her brother in law. He has a lot wrong with him; the high blood pressure was discovered when he was in his thirties. Diabetes; he uses an insulin pump, and has a neuropathy in the left leg and foot, as a consequence of the illness. He underwent cardiac ablation, had a triple by pass surgery to his heart, and wears a pacemaker. The pacemaker for his heart makes an MRI of the brain impossible. He is sometimes incontinent, has difficulty rising from a chair, and has fallen and injured his right shoulder; doctors think he has a torn labrum and will need surgery. The toes of his left foot curl up in dystonic spasms he cannot control. Some time ago, he worked as an architect, and he retains the ability to draw well, though his handwriting has succumbed to illness.
They come for another opinion of what they can do for their family member. The patient has had speech and physical therapy. The specialist reads the notes from other physicians and the differential diagnosis; the list of possible diagnoses the patient may suffer from. Over the course of several months, the wife has seen her spouse decline in function. She contends he has lost a lot of drive. He was a Type- A personality and now lacks the motivation for common things. His personality has become more emotional, and he admits he cries easily. The physician listening comments to the medical student sitting next to him that it sounds as though the frontal lobes are affected, as the area on both sides of the brain, dampens emotional expression.
The specialist performs the physical examination and notes the patient’s eye movements are full. The women mention the patient usually has his eyes closed, and frequently walks into objects when using his walker. This makes some sense to the specialist, as other neurologists have noted he may suffer from Supranuclear Palsy, which usually results in the patient having difficulty looking downwards, though this is not his problem right now. Botox injections to the muscles of the foot helped relieve the uncontrollable spasms on the right. When given to the muscles around the orbit of the eyes, they have been less effective.
The specialist is concerned the patient may suffer from normal pressure hydrocephalus, which can mimic vascular, or lower body parkinsonism. He requests a CT of the brain, which will show whether the ventricles are enlarged. If so, a neurosurgeon can place a shunt in the brain, allowing the excess cerebral spinal fluid to drain out of the brain and into the body.
The doctor recommends the family have a consultation with a fellow neurologist trying to assemble a group of patients for a study on progressive supranuclear palsy. The colleague intends to do a drug study to discover whether a certain medication is useful in that population. At the very least, they will get another opinion from a movement disorder specialist, who will have the results of the CT of the brain to possibly to rule out normal pressure hydrocephalus.

White-haired Sisters

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Tuesday morning hours are allocated for new Parkinson’s patients, but secretarial staff performs scheduling and their understanding of the illness is basic, tremors. For hints, the doctor peruses the patient’s history. Sometimes the nursing staff scans the paperwork the previous day; in this case, the history is online shortly before the patient enters the room. The physician has several moments to form an opinion about what he might see. He knows the patient’s history is atypical for someone with a diagnosis of Parkinson’s disease, and when he meets the patient and her sister, he has further doubts. The woman who has come for a second opinion speaks, emphasizing certain words with hand gestures. At times, she pulls her body to the front of her chair and speaks as she sits on the edge of her seat. Her face is animated and worried. She explains her sister is present because she frequently forgets things.

In efforts to find out what the true cause of her discomfort is, she has sought the help of an alternative type of doctor. He has told her that she suffers from Candida, a fungal infection. He has restricted her diet eliminating sugars, fruit and white bread. She has lost weight on the diet, and some strength.

At the moment, she feels fine though there may be hours in her day when her body aches. The doctor asks whether the pain she feels is worse on one side of her body. Some people with PD experience deep aching pain, akin to what one would experience after having performed a grueling workout on untrained muscles. The pain stems from having muscles in contraction for prolonged spans of time. The patient’s painful episodes engulf all of her body. She mentions the burning sensation she feels in her feet, her precarious sense of balance, double vision and that she has always been a nervous type of person. She has suffered with depression for years, and sees a psychiatrist regularly to adjust her medications.

The doctor scans the past blood test results and notes her rheumatoid factor was within normal limits. On physical examination of the patient, he notes her neck is supple, as is her right side. On the left side, she has the slightest hint of rigidity in the muscles surrounding her arm joint. Her eye movements to the left are difficult due to a weak lateral rectus in the left eye; the muscle pulls the left eye away from the nose and towards the temple, and accounts for her double vision and lack of depth perception. Brisk reflexes of her arms and legs hint her nerve roots may be compressed in her neck. Yet, having reflexes indicates she lacks a neuropathy, and having sensation to vibration and pinprick means her peripheral nerve fibers are also working adequately, so she should have position sense. The patient admits she has had problems with her neck, in the past.

She asks, what will account for her decreased sense of balance? Her troubles with vision? She knows the answer to her own question. Three things give us our location in space: the vestibular system, feedback from muscles, and our eyes. Summarizing his findings the doctor feels she might have some subtle signs of PD, but she lacks sufficient evidence to suggest she needs dopamine replacement. He feels she may suffer from a parkinsonian syndrome, such as lower body PD, caused by microvascular disease; a condition commonly caused by diabetes, high cholesterol and high blood pressure. An MRI of the brain will confirm whether there is evidence for this diagnosis. Meanwhile, he suggests she gradually discontinue taking the Stalevo, eat a balanced diet rich in vegetables and fruits to provide food-based antioxidants and fiber, exercise daily to increase circulation to the brain, and take 300mg of coenzyme Q10 to keep her mitochondria happy.

Second Opinion

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The dark glasses he wears lie on the physician’s desk in front of him; he had cataracts removed from both eyes, but he still suffers from macular degeneration- a condition where retina gradually thins and results in blindness. He carries a large magnificying glass which he holds close to his nose as he peers at his list of medications. The purpose of the visit is to seek another opinion regarding the tentative diagnosis of Parkinsonism. He has already seen several physicians who have conflicting opinions about his tremor.

Losing his hearing, the patient asks the doctor to speak up, interrupting him, as he speaks. The doctor repeats himself, with abbreviated thoughts. The patient holds his palm up towards the doctor, interrupting, telling him to let him speak. His hands are big, his finger long. Several of the fingernails on his left hand are cropped off, midway through the nail. He is 88 years old and states with a serious expression that he expects to live to 120. An American chess champion in the over 75-year division, he visits Florida once a year to compete. He claims in his youth he could play ten games blindfolded, now he can play only one game this way; his short term memory is not what it was. But it is the tremor in his hands that bothers him, especially when eating soup. Three years ago, he noticed his handwriting became larger and shakier. He comments also he has lost the bounce in his step; he no longer rises up onto his forefoot when he walks. Balancing is tricky.

The doctor stands and takes the man’s hand, and folds it inward towards his shoulder and out. He tells the patient his upper body is supple, without rigidity. The patient concedes he was a magician, and takes a packet of cards from a small leather case in his trouser pocket. He describes a trick he was able to do with one hand, holding the deck of cards divided into two bundles, he was able to shuffle them with one hand. Standing, he positions the cards in his left hand, and then nothing happens. The doctor follows his actions, and nods, understanding dexterity is gone from his hands. With a tuning fork, the doctor assesses the patient’s reflexes and notes whether the patient can sense the vibration of the fork, when applied to the bony prominences of his feet and legs. Noteworthy, the patient fails to feel vibration applied to the right leg. The physician explains it is a cheap way of assessing the integrity of the long nerves in the body, and states the lack of sensation explains some of the change in his walking style, as he appears to have a mild sensory neuropathy. The cause, the physician guesses is from compression of the nerve roots in the spine. The doctor explains we rely on three mechanisms to keep us upright in space; position sense derived from the sensory nerves in our limbs that pick up vibration, fine touch and temperature; our vestibular system and our vision.

When the physician summarizes his findings, he notes the patient has a mild action tremor, and a mild sensory abnormality in the right leg and foot. He would like an MRI to look at the blood vessels of the brain. However, the patient leaves on Thursday to his home state, he’d prefer to have the testing performed there. The doctor agrees to send notes to the physicians involved in his care and the conversation shifts to what sort of cutting edge therapies exist in the field of Parkinson’s and Alzheimer’s disease. Sitting behind the desk, the physician explains a study in which people with Alzheimer’s are getting GCSF(granulocyte- colony stimulating factor) to remove the amyloid plaques from the brain and improve cognition. The patient voices some interest in undergoing the same treatment, and the doctor wonders whether that would be ethical, or even practical, as the patient lacks the symptoms of those with the illness. He also notes when the amyloid is removed it can get stuck in small blood vessels, and result in micro-hemorrhages. He is unsure of the consequences of such trauma in the brain of a healthy, yet older individual. The man, wearing a woolen red sweater over a collared shirt, reaches into a file and withdraws the list of therapies he receives regularly from a physician whose specialty is aging. In the second or third line is a product called Neupogen, the same substance used in the research study for patients with Alzheimer’s.

Internal Tremors—-felt by the patient but not seen by others

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Fifty years of age, with a multitude of health problems, he appears at the clinic to rule out parkinsonism as the cause of his tremor. Since he began using the CPAP machine to sleep, he has noticed feeling tremulous in the morning. Sometimes the symptom lasts only an hour, but occasionally the feeling stretches out to encompass the entire day. The movement disorder specialist asks what part of the body is affected. With his hand to his chest, the patient indicates he feels the vibrations occurring in his torso, and the movements feel similar to the heart palpitations he’s experienced, though he has asked his wife to touch his shoulder and see whether she can detect the quivering motion, and she feels nothing.
The doctor considers this then gazes at the patient’s medical history. Various practitioners have diagnosed the patient with lupus, myasthenia gravis, and multiple sclerosis- all neurological conditions. The doctor states that lupus can produce a wide range of neurological conditions, and possibly tremor. Diabetics may also experience tremor in an episode of low blood sugar or hypoglycemia, occurring due to an imbalance between insulin or diabetic medication, food consumption and level of exercise and activity. The patient is unable to exercise due to failed spinal surgery. He recounts he has put on eighty pounds because of his immobility. Diabetes as a cause of the trembling doesn’t seem to fit the patient’s description of the action continuing throughout the day.
The specialist relates in a study he is familiar with, people with Parkinson’s disease were asked whether they experienced an internal tremor. Those that reported such a sensation all had depression in common. For people diagnosed with PD, there appears to be a correlation of that symptom and clinical depression. Though the patient lacks slowness, rigidity, and a resting tremor, a course of an antidepressant may alleviate his symptom. The medication the physician has in mind is an old-fashioned antidepressant, Doxepine. However, the medication can’t be given to people with cardiac arrhythmias, which he experiences. Inderal or the generic propanalol is helpful in blocking tremor, though the medication also veils the symptoms that come as a consequence of hypoglycemia; dangerous for a diabetic who may pass out or experience a seizure when blood sugars drop too fast. Depending upon how uncomfortable the tremor is, the physician concedes the whole class of SSRI’s that include Zoloft, Paxil and Prozac are possibilities, if he would like to see whether they calm the symptom. The physician concedes the good news is the patient does not have evidence to suggest he suffers from parkinsonism.

He is young

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He’s young, wearing blue jeans, a polo shirt and sporty shoes. Told that he has the symptoms of Parkinson’s disease, he wants another opinion, before he can stare the future in the face. Online, he’s read about the drugs given regularly to control the symptoms and learned they eventually lose their efficacy. The movement disorder specialist interrupts him, and clarifies the facts about the disease, and the changes that proceed as illness evolves. He explains levodopa does not lose its usefulness; rather that other neurotransmitter systems (like noradrenaline) become involved, and dopamine replacement cannot affect those systems. For example, sudden freezing episodes and loss of balance which gradually appear as the disease advances typically don’t respond well to dopamine replacement and we do not have medicatons that will directly improve those symptoms. Attempts to replace noradrenaline with a precursor have not been helpful in ameliorating freezing episodes. In addition, repeated dosing with levodopa/carbidopa affects the neurons downstream of the dopamine system resulting in development of what appears to be an excessive and/or erratic response to levodopa. Whether this is a function of the way the drug is given- intermittently, so the body contends with repeated wave- like influxes, or if the change is due to the neurotransmitter itself, is still unclear. Note that levodopa gets converted into dopamine in the brain. The neurons which are originally able to store an excess of dopamine in neurotransmitter terminals are lost and so the response to medicine parallels the circulating blood levels of levodopa. The combination of loss of dopamine terminals and the development of supersentivity of the dopamine receptors in the striatum becomes evident when people with PD begin experiencing motor fluctuations, wearing off, freezing and excessive involuntary movements known as dyskinesias. The doctor reassures the young patient this is one of the reasons why people under the age of sixty rarely get initial treatment with Sinemet and are started with dopamine agonists (“synthetic” medications which act like dopamine), which are less likely to produce dyskinesias than levodopa/carbidopa.
Physical examination includes determining the level of rigidity in his left side, the dexterity of his movements, the attributes of his gait and the fullness of his eye movements and other subtle symptoms. The doctor agrees with the previous diagnosis, the patient has the signs of a parkinson syndrome, only when he takes levodopa, will they be able to determine whether he suffers from a deficiency of dopamine; a positive response to the drug, as in easing of symptoms means he suffers from Parkinson’s disease. At the moment he recommends Azilect or the generic rasagiline, an MAO inhibitor, which has been shown to slow the progression of illness as well as ropinirole, a dopamine agonist that acts directly on dopamine receptors. The doctor scans the MRI of the brain, looking for evidence of a stroke, which might also account for some of the weakness on the left side of the body, but finds nothing.
When the patient has the two prescriptions in hand, he confides he has had a hard time falling asleep and received a small prescription for Xanax from his general physician. He asks whether the physician has an opinion on the medication. The specialist responds he dislikes the medication for treatment of depression, if that is the cause of the sleeplessness. Xanax is a depressant, and habit forming. It can be used in the short term, but he adds he would like to see the patient in six months, to see how he is faring on the two medications. At that time, they can speak again about whether there might be a need for a medication for depression. He adds the vast majority of patients with PD have need of an antidepressant, and it can be a helpful tool in maintaining a positive outlook and a high quality of life.

Latin and Handsome

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He’s Latin, the kind of patient that when I learn he is sixty- one, I am surprised, he could be forty- seven. His hair is still mostly dark and his daughter- in- law accompanies him, when he comes in for a second opinion on his diagnosis. Shuffling gait and increased muscle stiffness are the two symptoms that initially warranted a physician’s visit. When the first neurologist gave him a scant ten minutes of his time, he sought a second opinion.
The disease is apparent in the lack of expression in his face. An attractive man with dark features, his face lacks the spontaneous motion typical of healthy people; even the fixed way he holds his head indicates some level of rigidity. He has had three surgeries on his back and neck due to collapsed and herniated disks and his brisk and spreading reflexes indicate the long cortico-spinal tracts running through the spinal cord were injured at a previous time. His gait also is peculiarly parkinsonian. Though he lifts his feet adequately, his torso and in particular his arms, fail to oscillate with the motion of his legs and feet. When he gets to the wall and needs to turn around, he takes several steps, rather than turning on his heel and swiveling his trunk.
The previous neurologist gave him a prescription for Stalevo. The dose was either too low to see any improvement in symptoms, or the proteins in his diet blocked the conversion of levodopa to dopamine in the brain. The specialist in movement disorders cautions the patient, telling him dietary proteins; especially those in milk interfere with the way medicine gets transported to the brain. If he is unable or unwilling to reduce the morning and lunchtime proteins, he will need to take a larger dose of the medication to see its effect upon his muscles. With this in mind, the physician writes out a chart of how to increase the dosage of medication. Every three days the patient is to increase the dose by half a tablet, at one meal. When he sees the medication is enabling him to move more freely throughout entire day, he is to cease increasing the dose, and stay at that level of medication. The doctor indicates, this is a stairway in which you can go forward and go backward, to attain the appropriate dose.
In addition to regular medications, the physician recommends the patient also use an over the counter supplement, enzyme CoQ10. Laboratory studies indicated the antioxidant at doses of 1200 mg/per day, were capable of slowing the process of disease. Though few patients can afford to buy such high levels of the supplement, they may receive some health benefits from a lower dose; the doctor indicates 300mg/day.
Other issues concern the patient. He worries about his constipation. The physician recommends changing the diet to include a large amount of fiber and copious water, as well as a stool softener. A previous MRI indicated the patient has decreased blood flow to the brain. For this, he received a prescription for persantine, which decreases the stickiness of platelets, thereby increasing blood flow. The specialist also notes that with time Parkinson’s disease affects the autonomic nervous system, which includes bowel, bladder and sexual function. He states many of his patients ask for a prescription for Viagra, and he has no problem prescribing it, as it doesn’t interfere with any of the medications and he is not taking medications to prevent angina. The specialist asks the patient to make another appointment in four months, so he can see how he is faring.

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