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Tags >> General PD Information



By Ron Smith

I was diagnosed with Parkinson's disease (PD) in late 2006. Since then I have put much thought into what this diagnosis means to me and how to cope MOST effectively while living my life as fully as possible and doing things I enjoy doing, especially enjoying life with my wife, Dorothy. It is my sincere hope that what I think has worked for me may also prove helpful to others in dealing and living with the challenge of PD.

Underlying Basis

The underlying basis of my approach is that I need to have an assertive, action and questioning, pragmatic approach rather than a passive, laid back response to dealing with PD in order to make the best of a complicated, challenging life situation. My somewhat pragmatic approach to this is reflective of my engineering education and work experience. Have an orderly plan, ask questions, seek out the facts, then verify and validate the facts (i.e., get a second professional opinion on your diagnosis-I did and found it helpful, and, I suppose, reassuring in a way). It is important to realize that PD can be overwhelming at first, with a lot of possible symptoms, unique for everyone with some downright depressing complexity. It is different for each of us and a rational plan helps coping, at least for me.

While denial is generally not a very positive response, I believe a certain, healthy denial is helpful insofar as denying the disease control of your life and denying it control of your activities, as much as possible. Give the concept some thought!

Key Elements for an Action Oriented Approach

The key elements for dealing with the PD diagnosis for me seem to be centered around the following fundamental aspects, based on my 3-1/2 years of experience, observation, and involvement in the local PD community:

  • Obtaining and using the many excellent and available resources leading to gaining a solid understanding of the disease and its many implications.

  • Selecting and using a knowledgeable and experienced movement disorder neurologist.

  • Learning about and understanding how the various meds used work, their side effects, and all vital contraindications.

  • Implementing lifestyle changes by including a habitual, aggrressive, consistent, regular, aggresssive aerobic and resistence exercise program. Do this if nothing else!

  • Engagement and active participation with your family in your local MPF support group if available - priceless and worth many times over the cost (0, except for donations!). Dorothy is very active with me. I find this essential.

  • Family involvement including participation with your loved ones and family in the MPF sponsored two hour orientation program and 6 week Living with PD workshop and repeat if it's been awhile. We found these both very helpful.

  • Record keeping, communication, and observation. Develop and maintain an up to date clinical history, med list, emergency procedures (for me with another chronic condition this is critical), and observations for your physician on what's going on.

  • Engagement in volunteer work in the PD community. This is giving back for gifts received in knowledge and interaction with others in the PD community.

  • Maintaining good nutrition and emotional health. Vital but a bit removed from my knowledge base and experience to permit much comment.



Fortunately there is a myriad of excellent resources readily available including books, brochures, and paper booklets, internet sources, handouts from the MPF, and library materials maintained by the support groups. MPF has a card with PD contraindicated meds that you should get. MPF also has an information and referral program providing names of nearby physicians experienced in treating PD patients. The presentation by MPF in the orientation program is great and the six week MPF workshop also provides useful documentation. The MPF has many separate resources including its newsletter, The Messenger, in addition to its website (, and over 55 support groups in Michigan. Get on their mailing list.

Your neurologist and pharmacist can also provide information and existing patients are likewise good sources for doctor referrals.

Useful PD books are The Parkinson's Disease Teatment Book (overall coverage) by Ahlskog and Making The Connnection Betweeen Brain And Behavior (med effects) by Friedman. Both are excellent and I got my used copies at nominal cost from Other must haves are Parkinson's Disease Resources List (a total resource listing) and Web Resources for People with Parkinson's (web resources available), both available at no cost from MPF or the Parkinson's Disease Foundation. Finally, the National Parkinson Foundation publishes a great set of booklets including coverage on medication, nutrition, fitness, caring/coping, understanding PD, practical pointers, mind/mood/memory, and speech/swallowing.
Finally, I subscribe to the Northwest Parkinson's Foundation weekly newsletter and monthly letter ( It is provided at no cost and they cover much of the current research and trial info. It keeps me up to date.


I was more comfortable selecting a neurologist who is a movement disorder specialist who primarily treats PD patients, is knowledgeable and experienced (years) in the field and is suggested by other patients and the MPF. If in doubt, seek an interview and go prepared with a list of questions. Get a second opinion of your diagnosis (I did and was happier for it).


Medications (together with exercise) are the cornerstone of treating PD, and every person requires a different combination of medications. What a person takes this year may be changed next year in order to gain more control over the PD symptoms and side effects that all medications have. Keeping on a schedule of taking medications is essential and you need to learn specifics about the medication: what each drug does, when to take it (hours of the day, with or without food), what is supposed to be the positive effect, what are the side effects, and if there are other medications that you should not take with them. It may take a little time to learn about the different drugs and forms - like learning a new language. You can do it with help from others. Get Friedman's book to help in dealing with the side effects.

Record Keeping and Communication

Maintain an up to date clinical history and a list of your meds and consider an ID alert system such as Medic Alert (which I use). I find it helpful. The med list should contain aspects such as the date, file name, patient name, morning and afternoon protocols, script and over the counter (OTC) medications, med names, dosages, purpose-why being taken, prescribing physician, special precautions and contraindications, any PRN meds and when taken, dates when changes are made, and any other special conditions. Maintain a complete clinical history. Space does not permit a conceptual outline here. Keep it all on flash drive.

Engagement In The PD Community

Say thanks to the MPF, interact with the organization and other patients, and participate. Help to keep the invaluable services provided by MPF to continue.

Two last thoughts: I believe that every one of us needs to take an active role in managing our Parkinson's disease and the only useful generalization about PD is that there are no generalizations! Each of us is unique.

Keep On Moving!

Ron was an avid runner and long distance bike rider for some 20 years and a 3:28 marathoner. He was diagnosed with myasthenia gravis in 1997 (a rare neurological disease with some similar symptoms to PD including fatigue) and subsequently spent six years trekking in the Alps on summer vacations. He is a double cancer survivor (thyroid & prostate). He completed the megatransect ( in Lock Haven Pa. in 2005 (not last) and 2007 (last this time), a 25 mile trail walk/run in the Pennsylvania mountains with over 5,000 feet of ascent and descent and big, bad boulder fields to cross. He finished standing in both cases. He welcomes your thoughts and comments on these suggestions (c/o MPF at



Richard Trosch, M.D, Movement Disorder Specialist, Director, Parkinson's and Movement Disorders Center, Southfield, MI, Member, Michigan Parkinson Foundation Professional Advisory Board.

In January, the US Food and Drug Administration approved the use of ioflupane iodine-123 injection or DaTscan,developed by GE healthcare, as an aide in the differentiation of Parkinsonian syndromes from essential tremor. DaTscan is a radionucleotide agent with a high affinity for the dopamine transporter (DaT), a protein found on dopamine neurons. A specific marker for DaT, DaTscan produces images that provide visual evidence based on the density of dopamine transporters. Once injected, DaTscan will bind to or "tag" healthy dopamine neurons in the striatal region of the brain. The radioactivity from this drug may then be visualized by single photon emission computed tomography or SPECT, an imaging technology that is relatively inexpensive and widely available.

DaTscan is now approved in the U.S. for the diagnostic differentiation between Parkinsonism vs. essential tremor. In the European Union, where DaTscan has been available since 2000, it is also indicated for the diagnosis of Lewy Body dementia versus Alzheimer's disease. The projected cost for a DaTscan will be about $1500 to $2000 for the compound, with additional charges of the procedure fee and diagnostic interpretation. Insurance coverage has been established for Medicare and Blue Cross Blue Shield and it is anticipated that coverage by other medical insurers will follow.

How is it administered?

Prior to the DaTscan injection, an oral administration of 120 mg potassium iodine is recommended to minimize unnecessary thyroid uptake of radioiodine. The DaTscan agent is delivered as an injection via an intravenous catheter. After three to six hours, the patient is placed in the SPECT scanner and a detector, called a gamma camera, is used to visualize the distribution and quantity of the DaTscan compound within the brain. This procedure will take about 30 minutes to complete.

The DaTscan agent works by binding to or "tagging" the DaT protein, located on dopamine brain cells. This is used to visualize the location and density of dopamine brain cells, which "light up" on the image. If the parts of the brain where dopamine cells should be remain dark on the scan, an expert reader may diagnose early Parkinson's disease or Parkinsonism. DaTscan has been shown to have a 97.5% diagnostic sensitivity, meaning that it will be abnormal in 97.5% of patients with Parkinson's disease. Because other Parkinsonian syndromes, including Progressive Supranuclear Palsy (PSP), Multiple Systems Atrophy (MSA) and Corticobasal Degeneration (CBD) also have a dopaminergic loss, similar to Parkinson's disease, DaTscan will not be able to discriminate between these disorders.

Reported adverse effects from the DaTscan agent include headache, dizziness, nausea, vertigo, dry mouth, and injection site pain and hypersensitivity reactions. In the European experience, with over 300,000 doses dispensed, no serious adverse effects have been reported. DaTscan in contraindicated in patients with a know sensitivity to iodine, in women who are pregnant or breastfeeding, and in patients with impaired kidney or liver function. Also, certain prescription medications will need to be stopped prior to this study. Although this agent is a radiopharmaceutical, the minimal amount of radiation exposure is considered clinically insignificant.

How will DaTscan be used?

Currently, there is no definitive test for PD. Establishing a diagnosis of Parkinson's disease remains a clinical process, hinging on the patient's description of their symptoms and the physician's findings on neurological examination. The accuracy of a diagnosis of PD is dependent upon the skill and experience of the examining physician and remains a "best guess". Studies examining the accuracy of this guess have found an error rate of about 25 to 30%. Improved diagnostic accuracy can be achieved by following a patient's clinical course over time and by demonstrating an improvement with levodopa treatment. A diagnosis of "definite" Parkinson's disease, however, requires pathologic confirmation. During life, if the classic Parkinson's disease symptoms, signs and response to levodopa are present, a diagnosis of "probable PD" may be made. Clearly, objective measures to aide in the diagnosis of PD are needed and much work is being done to discover biomarkers for this illness.

DaTscan will serve as a diagnostic adjunct, meaning it can provide additional information about a patient's condition. It cannot be used to establish a diagnosis of PD, however, it may provide additional information to help establish or refute a particular diagnosis. The utility of DaTscan in the diagnosis of PD will be limited to special circumstances. If you have already received a diagnosis from an expert and are responding well to dopaminergic therapy, PET and SPECT scans would not add any new information and therefore likely to be unnecessary. Several experts have suggested that approximately 5% of Parkinsonism/PD cases may be DaTscan candidates, with the majority of Parkinson's disease patients not requiring this test. Instead, DaTscan will be reserved for cases where there is diagnostic uncertainty, for atypical cases of tremor, when the distinction between PD and essential tremor is unclear, in psychogenic Parkinsonism, and for patients who have a difficult time accepting the diagnosis of Parkinson's disease.

Within the neurologic community, skeptics have voiced concerns about the potential for inappropriate testing, overuse and/or misinterpreted testing. Whether an internist or general neurologist should ever order a DaTscan has been the subject of considerable debate. Clearly, most Parkinson's disease patients will not benefit from a DaTscan and the non-specialist may not be trained to recognize when this test is required. A less expensive alternative, a consult with a movement disorders specialist, provides greater diagnostic accuracy and will prevent unneeded testing.



Roger L. Albin, MD, Anne B. Young Collegiate Professor of Neurology, University of Michigan Medical School, Past MPF Advisory Board Member

The evaluation and diagnosis of Parkinson's disease (PD) and related conditions is based almost completely on a careful history and physical examination. There are no radiological or laboratory measures that contribute significantly to the evaluation of PD and related disorders. The point of departure for establishing a specific diagnosis is identification of the syndrome of parkinsonism.

A syndrome is a constellation of related symptoms and examination findings that point to dysfunction of a specific organ or part of an organ. Syndromes usually have several causes. In the case of parkinsonism, all the key features stem from impaired production or action of the brain chemical dopamine. Parkinsonism can result from degeneration of dopamine producing nerve cells, blockade of dopamine action by certain types of drugs, or loss of the nerve cells that are the targets of dopamine action.

The key clinical features of parkinsonism are bradykinesia (slow movement), rigidity (an increase in the resistance of an affected body part to passive movement of that body part by an examiner), resting tremor (rhythmic involuntary movements when the affected body part is relaxed), and loss of postural reflexes (impairment of the body's ability to maintain an erect posture when displaced rapidly by an examiner) (Table 1). Discovery of two or more of these findings by a competent examiner indicates an abnormality of dopamine mediated signaling within the brain. If these features are not present, then PD and related disorders are excluded. An important corollary point is that these clinical features and symptoms should exhibit insidious onset and slow worsening. Sudden onset of these features would be very unusual for PD or any related disorder.

Difficulties with diagnosis of PD arise in two specific contexts; (1) initial diagnosis, and (2) individuals thought to have PD whose clinical course is atypical. When an individual is initially found to have parkinsonism, there are 3 major possible explanations.

  • The first is PD itself.

  • The second is drug-induced parkinsonism, a situation in which a prescribed drug impairs the action of dopamine and results in parkinsonism. Many drugs used in psychiatric practice have this side effect. Some drugs used for treatment of nausea can also have this side effect. These side effects do not usually occur after short-term use of these drugs but generally follow weeks to months of administration.

  • The third possible explanation is one of the PD related disorders (see below).

A fourth possibility that should be mentioned is Benign Essential Tremor (ET), even though this disorder does not exhibit parkinsonism. ET is a very common entity among older Americans. It is distinct from parkinsonism in that the tremor is not present at rest but occurs with use of the arms and there is no bradykinesia, rigidity, or loss of postural reflexes. Inexperienced physicians sometimes confuse these entities.

A definite diagnosis of PD is possible only after death with pathologic examination of the brain and detection of characteristic abnormalities. Clinical diagnosis of PD is based on the presence of two or more features of parkinsonism, the exclusion of other causes of parkinsonism (such as drug-induced parkinsonism), and the presence of significant improvement with a dopamine-like drug, either in the form of an L-dopa preparation or a dopamine agonist. PD responds well to treatment with these agents while the other neurologic diseases causing parkinsonism do not. Despite the apparent imprecision of this approach, it is actually very successful and studies comparing clinical diagnosis by expert clinicians with pathological diagnosis have shown clinical diagnosis to be quite accurate.

If these conditions are satisfied, the diagnosis is almost certainly PD. Difficulties occur in diagnosis when one of the other neurologic disorders causing parkinsonism is present.

Table 1: Parkinsonism: The Dopamine Deficiency Syndrome

Resting Tremor
Loss of Postural Reflexes

Table 2: Differential Diagnosis of Parkinsonism

Drug Induced
Dopamine Antagonists; Anti-Psychotics, Anti-Emetics
Catecholamine Depleters; Reserpine, Tetrabenazine
False Transmitters; a-Methyl-Tyrosine
Essential Tremor - Not Really a Mimic
Other Neurodegenerations Affecting the Basal Ganglia
Progressive Supranuclear Palsy
Multiple Systems Atrophy
Corticobasal Degeneration
Idiopathic Parkinson's Disease

Table 3: Discordant Features

Atypical Presenting Features
- Lack of Tremor
- Symmetrical Onset
- Early Autonomic Dysfunction
- Early Cognitive Dysfunction
- Unusual Eye Movement Findings on Examination
- Atypical Movement Control Problems of Affected Limbs
Rapid Progression
Lack of Response to Dopamine Replacement

Table 4: PD-Like Syndromes

Progressive Supranuclear Palsy (PSP)
Multiple System Atrophy (MSA)
Corticobasal Degeneration (CBD)
Lewy Body Dementia (LBD, DLB)


Clues indicating the symptoms are not PD

The most important clue that another neurologic disorder is present is lack of significant response to a dopaminelike drug. These drugs must, however, be tried at adequate doses and for proper lengths of time. A short trial at a low dose may simply not be adequate to assess response.

Some other clinical features may point away from PD. Most, but not all PD patients, have resting tremor. The PD-like disorders usually lack tremor. PD typically begins on one side of the body where most of the PD-like disorders have symmetric onset (for an important exception, see below). Rapid progression of parkinsonism is another important clue. We expect PD patients (with appropriate treatment) to do well and progress slowly for at least 3-5 years after diagnosis. Finally, each of the PD-like disorders has characteristic features that assist in the diagnosis.

Other Disorders

The four major disorders that can mimic PD are Progressive Supranuclear Palsy (PSP), Multiple System Atrophy (MSA), Corticobasal Degeneration (CBD), and Lewy Body Dementia (LBD).

PSP is characterized by certain types of eye movement abnormalities, particularly difficulty with voluntary movements of the eyes in the vertical plane.

MSA is distinguished by difficulties with the autonomic system, the part of the nervous system responsible for maintaining blood pressure and similar functions. MSA patients frequently have difficulties with maintaining an appropriate blood pressure when standing, have problems with control of their bladders, may have sweating changes, and in men, impotence is common.

CBD is a rare disorder which typically presents with asymmetric abnormalities of limb function. There may be a combination of clinical findings suggesting parkinsonism and abnormalities of limb use reflecting dysfunction of the cortex; the so called thinking part of the brain.

LBD is quite common but does not usually present with parkinsonism, but rather with dementia. Dementia is uncommon in patients with early PD but when dementia occurs prior to or approximately coincident with the development of parkinsonism, LBD is the likely diagnosis.

These PD-like disorders are individually rare but their aggregate prevalence is significant. Perhaps as many as 15% of patients presenting to Movement Disorder Clinics for evaluation of parkinsonism turn out to have one of these PD-like disorders. Making a specific diagnosis of one of these disorders is often quite difficult. The characteristic clinical features may not appear until months to years after the emergence of parkinsonism and prolonged clinical follow-up is necessary often to confirm a specific diagnosis. There is no effective primary medical or surgical therapy for any of these disorders. The emphasis is on assistive care with physical therapy, occupational therapy and interventions that palliate some of the symptoms. Making a specific diagnosis as early as possible is important to improve patient and family comprehension, reduce unnecessary medication trials and diagnostic studies, and to focus attention of appropriate assistive interventions.



by Ray Buch (from Lansing Area Parkinson Support Group Newsletter, June 2011). Ray has been a clinical social worker, flat-water paddler and kite flyer through his entire adult life. He delights in his wife and lifelong companion, Lindy, his two adult offspring, his 93 year old dad and an insatiable curiosity.

What does it take to stay upbeat in the face of a siege on one's health (or on one's self). When every day is a battle and no matter how many battles are won, the chances of winning the war are nil. Under these circumstances, we should find that nearly everyone is depressed or despondent. The fact that everyone is not depressed or despondent is worth understanding.  

We often begin to understand something difficult by studying an extreme example of the issue. One of the most difficult chronic situations to "get through" is being a prisoner. In 1946, Viktor Frankl wrote Man's Search for Meaning. A survey by the Library of Congress and the Book of the Month Club in 1991 deemed it "one of the ten most influential books in the United States." Frankl searches for the reasons some survived the German concentration camps and some did not. He learned that aside from the harshness of the situation, if a person retained the belief that he had freedom to choose (whether to be sad, despondent, angry or not), his chances of survival went up remarkably. Sometimes it was the belief that others were worse off, or a moment of camaraderie; at other times it was an imagined image of a beloved person (wife, lover, parent even God).

I've talked with some of the individuals who have had PD or other chronic conditions over a longer period of time. They indicate that the essential element for managing one's self is to choose to "stay in the present," "be occupied with what can be rather than what might be," and "prepare for tomorrow, but live in today."  The guidance is to maintain one's mind in the present. Some psychologists believe that increased levels of anxiety come from trying to solve the future problems of one's life without having enough information. The idea is that the mind continues to cycle back over the same unresolved questions because no new information has been acquired to help resolve the problem. The obvious answer is to provide new information, which is why many people with PD spend a great deal of time reading about
every aspect of the disease. However, there is little possibility of getting much information about how things end up for them.

A.J. Heschel, one of the most prominent religious thinkers of the 20th century, used the term radical amazement to denote being constantly aware of the large and small things, processes and events as a means to being aware of and in contact with God. This is very close to many of the meditative aspects of yoga:  constantly being in the present. The many forms of yoga and the preoccupation with practice attest to both the difficulty and reward that comes from "staying in the present."

Perhaps a less ethereal and more common example of "staying in the present" might be useful to many of us. Consider for a moment the idea of celebration. The dictionary has two common definitions.

• To celebrate a holiday or commemorate a special day like Christmas, Independence Day  or Thanksgiving where we spend some time thinking about the special issue being commemorated and enjoy a certain amount of revelry.

• To proclaim, publish, praise or make a ceremony to acknowledge.

It is this second type of celebrating with which we are familiar that is similar to radical amazement. Imagine if we were able to maintain the awareness of not just one idea or situation or beautiful thing every day, but maintain that same level of delight, joy and awareness of many, many things every day. We certainly wouldn't have much "brain time" to be over-concerned about what might happen five or ten years in the future.



Akinetic-rigid syndrome: A syndrome, or collection of systems, consisting of lack of movement (akinesia) or reduced movements (hypokinesia), slow movements (bradykinesia), and stiffness or rigidity (involuntary resistance to movement). The rigidity is of a type called cogwheel rigidity.

Basal ganglia: A group of nuclei, or clusters of nerve cells, near the base of the brain that is important in regulating both movements and emotions.

Bradykinesia, hypokinesia & akinesia: Bradykinesia means slow movements. Hypokinesia means reduced movements and generally refers to making smaller movements than intended, such as the small steps seen when a Parkinsons patient walks, or the small size of a Parkinsons patient's handwriting (called micrographia). Akinesia means lack of movement.

Cogwheel rigidity: " A type of rigidity in which, when a patient's limb is moved by the examiner, it resists and gives way in small, step-like movements as if it was being controlled by a cog-wheel.

Dopamine: One of a number of chemicals used by nerve cells as neurotranmitters. Messages are carried electrically along individual nerve cells but signalling from one nerve cell to another is usually accomplished by releasing a neurotransmitter chemical. Dopamine is the main neurotransmitter of the nerve cells which die off in Parkinson's disease.

Dysarthria:  soft voice or inarticulate speech.

Dyskinesia:  Abnormal writhing movement of voluntary muscles.

Dystonia:  Involuntary spasms of muscle contraction that cause abnormal movement and posture.

Epidemiological studies: Statistical studies of the occurence of diseases in populations and environments.

Familial Parkinsons: Some unusual forms of Parkinson's disease run in a few families. Abnormal genes have been identified in some of these families, but abnormalities in these genes are NOT found in most patients with Parkinson's disease. Alpha-synuclein and parkin are the proteins coded for by genes identified as being abnormal in some familial forms of atypical Parkinson's disease. Normal alpha-synuclein is also the major protein in Lewy bodies, the pathologic inclusions found in typical Parkinson's disease. The normal functions of alpha-synuclein and parkin are not yet clearly established.

Freezing:  Temporary inability to move.

Levodopa:  Levodopa was the first major breakthrough in the treatment of Parkinson's disease.  Levodopa is used by the brain to produce the chemical dopamine, which is deficient in persons with PD. The neurotransmitter is converted by the neurons in the brain into dopamine, which is stored within the cells until needed by the body.

Neurodegenerative Disease: A disease in which nerve cells in the brain or spinal cord (central nervous system, CNS) progressively die or degenerate.

Neuron:  a cell that generates or conducts electrical impulses to carry information from one part of the brain to another.

On-off phenomena:  sudden, unpredictable changes in motor performance by people on levodopa therapy.

Parkinson's Plus diseases: These are neurodegenerative diseases which cause the akinetic-rigid syndrome or parkinsonism PLUS additional symptoms not usually seen in Parkinson's disease. These diseases are progressive supranuclear palsy or PSP, corticobasilar ganglionic degeneration or CBGD, and multiple system atrophy or MSA, which includes Shy-Drager Syndrome, olivopontocerebellar atrophy or OPCA, and striato-nigral degeneration.

Pathology of Parkinson's disease: Examination of brain tissue from Parkinson's disease patients under the microscope shows loss of the dark-colored dopamine-producing nerve cells in the substantia nigra pars compacta and appearance of Lewy bodies, abnormal small round clumps of protein and other materials which are rarely seen except in Parkinson's disease.

Postural reflexes: Postural reflexes are the involuntary movements people automatically make to maintain their balance when standing and walking. Impairment of the postural reflexes causes poor balance and a tendency to fall.

Resting tremor: Tremor is a rythmic movement or shaking of any part of the body. The tremor of Parkinson's disease is called a "resting tremor" because it is present when a limb is at rest and may be reduced or go away when the limb is held up or otherwise used by the patient. Most other types of tremor are reduced or absent when the limb is at rest and relaxed.

Striatum: A region of the brain made up of two nuclei, or clusters of nerve cells, the globus pallidus (which means "white ball") and caudate (which means "tailed"). These two nuclei are part of a group of nuclei called the basal ganglia, which is important in regulating both movements and emotions.

Substantia nigra: This literally means "the black substance" and is a region in the brainstem (where the spinal cord joins the brain) where there is a group of dopamine-producing nerve cells, which appear darker than the surrounding tissue. The dopamine-producing nerve cells are in the pars compacta (meaning "compact or dense part"). There is another part called the pars reticulata ("speckled part").

Edwin B. George, MD, PhD., Wayne State University School of Medicine, 2003



When you visit your neurologist, there are several things that regularly occur: forms to fill out, lots of questions and, usually, a neurologic examination.

Do you ever wonder what neurologists are really doing to you during your physical exams and what they are looking for?

In general, the neurologic exam concentrates on several specific areas: mental status, cranial nerves, motor function, sensation and reflexes.

Depending on whether it is your first visit or a routine follow-up visit, the exam's length and complexity may vary. It actually begins before you realize it!! The neurologist checks the forms you filled out to see if the handwriting is small or shaky, then closely observes you during the initial interview - is there a lack of facial expression, a lack of movement of one arm or leg, a tremor and is the voice loud or indistinct? Often the diagnosis of Parkinson's disease is reached within the first minute or two the neurologist is in the room.

Then the neurologic examination begins. Although the exams performed by different neurologists vary widely, and also from one visit to the next, there are certain things a neurologist checks to determine the diagnosis (is it Parkinson's disease?) or to see how well you are responding to medication.

Mental Status: During the interview, and often with additional questioning, us¬ing standardized tests of cognitive function, the neurologist assesses your memory, concentration skills, language skills and orientation.

Gait: Usually you are asked to walk back and forth, on your toes and heels, then in a straight line. Observing whether you swing your arms normally or not may provide an early tip-off to the diagnosis of Parkinson's disease. You may be pushed or pulled to see how well you can maintain your balance (postural stability). You also watched to see if you have trouble rising from a chair and whether you stand straight or stooped.

Cranial Nerves: The cranial nerves are those that supply the eyes, face, ears, mouth/tongue and neck. A lack of facial expression (masked facies) may be noted, but there can be certain abnormalities that indicate a diagnosis of something other than typical Parkinson's disease (an inability to normally move the eyes, for example).

Motor Function: During this portion of the examination, your doctor checks your strength, pulling or pushing your arms and legs, comparing one side of the body to the other, and seeing if there is a difference between the upper and lower limbs. Your doctor will also move your arms and legs while you relax, to decide if there is increased tone or stiffness. (In Parkinson's disease we are looking for "cogwheeling," which is a type of stiffness with a "ratchety" feeling.) The speed of your movements is also examined: you are often asked to hold your arms in front of you and rapidly move them from "palm up" to "palm down," something called "rapid alternating movements." Additional maneuvers may be performed, such as finger tapping and repetitive "hand opening-closing," looking for bradykinesia (slowness of movement). The speed of these rapid movements often helps in making the diagnosis. It is important to note whether the abnormalities are worse on one side or the other.

The search for tremor actually continues throughout the entire time with your doctor. A tremor observed while a person is sitting quietly is known as a resting trem¬or and is the most typical type seen in PD. Often, this tremor is visible while you are walking, and is also called a "pill-rolling" tremor, named after the movement that an old-time pharmacist would make as he created a pill between his fingers. Tremor can also be seen with certain activities (holding objects, writing, etc.), and may or may not be seen in PD. Often you are asked to hold your arms outstretched, or to touch your finger to your nose.

Sensation: The sensory exam consists of being poked with a pin, lightly brushed with cotton/tissue, or asked whether you feel a vibrating tuning fork, or if a finger or toe is moved upward or downward. Again, the physician wants to know whether you feel these sensations equally on both sides of the body and whether it differs between how it feels in your feet/hands (distal sensation) or closer portions of the limbs (proximal sensation). This portion of the exam is probably the least important in the diagnosis of PD. However, certain abnormalities might be clues to a different neurologic disorder.

Reflexes: Here the doctor observes how your limbs react to being tapped with a reflex hammer (deep tendon reflexes). In particular, are the responses equal on both sides and are they increased or decreased in a particular pattern? Another very important reflex commonly tested is the plantar reflex, when the bottom of your foot is stroked unpleasantly to see what direction your toes move. This is one of the most important tests in neurology. If the toes move upward in a specific way, it is known as a "Babinski sign." This is not usually seen with PD, but may indicate another disorder.

The neurologic examination remains the most accurate way to diagnose Parkinson's disease, coupled with the history that you give. Testing is generally not required to make a diagnosis, but is occasionally ordered to rule out a different diagnosis, if there are unusual features noted during the exam. Remember: the length of the neurologoc exam may vary from visit to visit, with the initial consultation generally being the most extensive examination, and follow-up visits being shorter. When it is only a brief office visit, only a few things may be tested to decide if medication is helping, or if changes are required. While the examination is very informative and can usually result in a definite "yes" or "no" to the question of whether you have PD, some of you may have experienced exams where the neurologist is not certain and asks you to return in a few months or a year to see if your physical exam changes.

Despite all the advances that have been made in the field of neurology, the examination remains essential.

Neurologist Dr. Glen Ackerman, M.D., is a past Chairman of the Michigan Parkinson Foundation Professional Advisory Board and is a cur¬rent Member. He is Assistant Professor of Neurology, Michigan State University School of Human Medicine and School of Osteopathic Medicine, and is Head of its Movement Disorders Clinic.