Parkinson’s disease: Management-a quick one on one

In this blog post let us dwell on the management of Parkinson’s disease (PD). As stated earlier PD is a progressive neurodegenerative disease. This means that as of now PD CANNOT be cured. Once the disease begins it slowly but surely progresses. The rate of progression varies from patient to patient. While PD cannot be cured, there are a number of medications available which can control the symptoms of PD. At times the response with these medications is dramatic and very gratifying. A few salient points:

NOT every patient of PD needs to be treated. When PD initially begins the symptoms are usually mild and may cause minimal interference to the patient’s lifestyle. The mild tremor of PD might be dismissed by the patient as a mere nuisance. At this stage of the disease, the patient does not exhibit problems with his/her gait or balance. The rigidity, bradykinesia is not disabling. At this stage of the disease, the neurologist may opt to simply keep the patient under observation. The patient and the family are educated about the disease and instructed to remain in follow up (come for follow up appointments after very 3-4 months).

The most effective medication for the treatment of PD is LEVODOPA. Since PD is caused by deficiency of dopamine in the brain, the most effective way to treat it is to give dopamine from outside. So levodopa is administered in tablet form usually 3 times a day. Levodopa is combined with another chemical called carbidopa which helps to prevent the breakdown of levodopa in the stomach and thus ensures that high level of levodopa is absorbed and reaches the brain. This combination of LEVODOPA+CARBIDOPA is the main medication used to treat PD. LEVODOPA+CARBIDOPA combination tab is marketed by many different pharmaceutical companies under different names (Please check the common brand name of this combination in your country). The tablet is usually started at low dose three times a day. The neurologist then titrates the dose up based on clinical response and side-effects. The medication is usually well tolerated by most patients and the effect is gratifying. It is important to emphasize that this medication still remains the MOST effective medication for PD. LEVODOPA comes in many different formulations including now in an inhaled form. These formulations are prescribed as the disease advances. Please discuss the same with your neurologist.

DOPAMINE AGONISTS: is another class of medication commonly used to treat PD. As the name suggests medications in this class act by stimulating dopamine receptors in the brain. While not as effective as LEVODOPA+CARBIDOPA, dopamine agonists are commonly prescribed. Commonly used dopamine agonists include pramipexole (Mirapex), rotigotine (Neupro), and ropinirole (Requip). Some neurologists prefer to use a medication in this class as first line treatment and use LEVODOPA+CARBIDOPA when PD symptoms are more bothersome (PD is more advanced).

Amantadine is another medication used to treat PD. It is usually used in combination with either LEVODOPA+CARBIDOPA or DOPAMINE AGONISTS.

Anticholinergic drugs such as benztropine and trihexyphenidyl are also commonly used. These drugs are helpful in controlling symptoms such as tremor and muscle stiffness.

Drugs referred to as selective MAO B inhibitors such as selegiline are used by neurologists usually early in the disease course. There is limited evidence to suggest that medications in this class may be “neuroprotective”.

COMT inhibitors: another class of medications used in the treatment of PD.

Neurostimulator such as DEEP BRAIN STIMULATOR (DBS): A neurostimulator called DBS is sometimes implanted in PD patients. DBS is usually implanted in the brain of PD patients with advanced disease who are experiencing motor fluctuations, medication side-effects called dyskinesias and medication refractory tremor. Please discuss this further with your neurologist.

While medications form the cornerstone of treatment of PD, there are a number of other simple interventions which are very effective. It is important to remember that PD affects the motor system causing problems with gait and balance. Hence I make it a point to emphasize the importance of exercise to my patients and their family. Exercises which improve gait and balance are the most helpful.

dance is a good exercise for patients with PD. (USEFUL RESOURCE:

–many are surprised to find out that boxing is a good exercise for patients with PD (USEFUL RESOURCES: and

–yoga is also a good form of exercise-it improves balance and helps reduce the stiffness in PD patients)

Parkinson’s disease patients are prone to falling. Hence falls are an important cause of morbidity in patients with PD. So simple interventions designed to reduce the risk of falling are helpful. (USEFUL RESOURCE: NATIONAL INSTITUTE ON AGING: Fall proofing your home,your%20way%20when%20you%20walk.)

Nitin K Sethi, MD, MBBS, FAAN

Director and Chief Coordinator Brain Care Foundation (

Please support ongoing research in PD and more importantly PD patients and their families. Source of image is

Parkinson’s disease: a quick one on one

Parkinson’s disease (PD) is a common neurological disease. This disorder of the brain is seen in people of all races and both sexes. PD is caused by the deficiency of a neurochemical called DOPAMINE in the brain. In this blog post I shall discuss the clinical presentation and diagnosis of PD.

Parkinson’s disease is included under the category of neurodegenerative brain disorders. What that means is that the disease is progressive. Once the disease starts, it slowly progresses. The rate of progression though varies from patient to patient. The disease onset is usually insidious. Most people first exhibit signs of the disease after age 60 (in some people the disease may start in the late 40’s or in their 50’s-this is then referred to as Early Onset Parkinson’s).

Disease onset-onset of PD is usually insidious and at times may not be noticed by the patient or the family. Typical first symptom may be a slight tremor (shaking) in the thumb of one hand/finger of one hand, the hand itself or the chin. The tremor is not disabling at onset and hence ignored by the patient/family. It is important to emphasize here that NOT ALL TREMORS ARE PD. There are numerous causes of tremor, many which are benign (do not signify any serious disease). PD tremor has some special characteristics (features) which helps to distinguish it from other types of tremors.


  1. The tremor is usually insidious in onset and of low amplitude.
  2. The tremor is usually asymmetrical at onset (one thumb/one hand). As the disease progresses the tremor becomes more prominent and may involve both the sides of the body.
  3. PD tremor is typically what is referred to as a RESTING TREMOR. What this means is that the tremor is most prominent when the hands are completely at rest (example-the tremor is noted when the patient’s hands are resting on his/her lap, resting on the driving wheel). This is an IMPORTANT distinguishing feature of PD tremor. Tremors which are more prominent when the hands are extended in front (POSTURAL TREMOR) or while in motion are usually not due to PD.


PD initially presents with motor symptoms. Patients do not have sensory symptoms such as pain, numbness, tingling. The common motor symptoms of PD are the following:

  1. Tremor: tremor of PD is a resting tremor (see above).
  2. Bradykinesia: the word bradykinesia means “slowness of movement” and is one of the main symptoms of PD. The patient is slow to walk, slow to initiate movement. As PD progresses, the patient becomes more and more bradykinetic (slow). There is loss of spontaneous movements such as facial expressions, gesturing, eye blinks.
  3. Rigidity: rigidity is another cardinal symptom of PD and refers to the stiffness which PD patients feel in their muscles. Rigidity can be detected by the neurologist on clinical examination.
  4. Disturbance of gait and posture: patients with PD experience a disturbance in their gait (how a person walks) and posture. A patient with PD is usually stooped (bent) forwards and walks with short quick steps. This is referred to as the SHUFFLING GAIT OF PD. This disturbance of gait and posture makes PD patients more prone to falls. It is important to emphasize here that FALLS ARE AN INPORTANT CAUSE OF MORBIDITY IN PD PATIENTS.

Photo source: *photo: (the above image has been edited)


The diagnosis of PD is predominantly clinical and has not changed much since the disease was first described by James Parkinson, an English surgeon in his now famous 1817 work AN ESSAY ON THE SHAKING PALSY.

PD is diagnosed in the following way:

  1. Clinical examination by a neurologist: neurologists are able to diagnose PD after taking a history and doing a neurological examination in which they assess for tremor, bradykinesia, rigidity and gait/posture.
  2. Neuroimaging: it is important to emphasize that neuroimaging studies such as CT scan head and MRI brain are usually reported normal in patients with PD.
  3. New imaging modalities: DaT scan is a new imaging test which uses a small amount of a radioactive tracer drug to determine how much dopamine is available in a patient’s brain. It is important to emphasize that DaT scan is neither needed nor a definitive test for PD diagnosis. It is primarily helpful in differentiating Parkinson like diseases (Parkinsonian syndromes) from a more benign condition called essential tremor (ET).

DISCLAIMER: The information in this blog is for educational and informational purposes only. It does not constitute medical advice. Use of the site content does not establish any patient-doctor relationship. If you choose to write to me or post a comment on this blog, please do not divulge any personal medical information.

Nitin K Sethi, MD, MBBS, FAAN

Not all tremors represent Parkinson’s disease

Patients frequently come to see me for evaluation of their tremor.  Invariably the history is that the tremor was first brought to their attention by a close friend or a family member. The patient is worried that he/she has Parkinson’s disease and hence seek a neurologist’ s attention. Rarely are they bothered by the tremor per-se. By that I mean the tremor is usually not disabling and does not impair their quality of life at least initially. So do all tremors represent Parkinson’s disease? Are there any benign tremors? Which tremors warrant medical attention? These are some of the issues I plan to dwell on in this blog post. I hope some of my readers shall find the information useful.

So what exactly is a tremor. Well neurologically a tremor is characterized by rhythmic oscillatory and involuntary movement across a joint. I used the work involuntary because tremors at times can be voluntary. Voluntary tremor is usually psychogenic (meaning it has a psychological basis to it). We shall not discuss psychogenic/voluntary tremors in this post though. Suffice to say that a doctor shall be able to identify psychogenic tremor based on the history and examination findings alone.

So what do I look for when a patient with tremor comes to me seeking an explanation. Well the age of the patient is the first clue to the etiology of the tremor. Idiopathic Parkinson’s disease usually starts off in the sixth to seventh decade of life. Familial Parkinson’s disease can start at a younger age but usually the tremor is not so prominent nor is it the initial manifestation. There can be many causes of tremor in the “young”.  Various medical conditions some more common such as hyperthyroidism, hepatic and renal diseases and some more exotic such as Wilson’s disease (due to a problem with copper metabolism in the body)come to mind.  At times the answer is more innocuous and the tremor is either due to stress or excessive intake of coffee and other caffeine containing drinks. In that case all that is needed is reassurance. One other disease that needs to be kept in mind is multiple sclerosis though usually more findings are documented in exam (meaning that the tremor is not see in isolation). One should never forget to ask patients about the use of prescription, over the counter and illicit drugs. Many drugs such as sodium valproate (commonly used to treat seizures and at times bipolar disorder), bronchodilators (drugs used to treat asthma, reactive airway disease and chronic obstructive airway disease) cause a coarse postural and kinetic tremor as a side-effect. Once the drug is stopped the tremor abates.

Another common entity frequently confused with Parkinson’s disease is what is called essential tremor or also sometimes referred to as benign essential tremor. Patients who have essential tremor are usually in the same age group as patients with idiopathic Parkinson’s disease and hence the confusion and concern arises. Essential tremor has the following characteristics: it is usually a postural tremor (meaning that the tremor is most prominent when the hands are kept out and maintained at a posture such as having them stretched out in front of you. Remember the classical tremor of Parkinson’s disease is a resting tremor. Meaning the tremor is most prominent when the hands are at rest like for example resting on the patient’s lap and the patient’s attention is diverted). Essential tremor is a faster and finer tremor as compared to the tremor of Parkinson’s disease which is a slower (2-5 Hz) and of higher amplitude. A point to note here is that tremors are frequently classified based on their frequency, amplitude and position (rest Vs postural Vs kinetic).  Patients who have essential tremor frequently in addition to the hand tremor also may have a head tremor (the head shakes either from side to side [no-no tremor] or up and down [yes-yes tremor]). They may also have a tremor in their speech (voice tremor). On further questioning some of them may admit to having the tremor run in their family (meaning their father and grandfather also had a similar tremor). They may have also noted that when they drink alcohol the tremor becomes less prominent.  Infact some patients start drinking excessively for this very reason! Essential tremor usually progresses very very slowly (if at all) and may never become problematic and disabling in the patient’s lifetime.  Hence it does not need to be treated unless it is socially disabling (“Doctor Sethi I cannot drink a glass of wine without spilling it over my dress!” “Dr Sethi  I am so embrassed when my hands shake in a business meeting!”). Essential tremor is not accompanied by the other signs and symptoms which accompany Parkinson’s disease such as gait problems, freezing, stiffness, rigidity and mask like facies.

So not all tremors represent Parkinson’s disease. A quick visit to your “local” neurologist shall give you an answer to what kind of tremor you have.

Early signs of Parkinson’s disease: making the diagnosis

Early signs of  Parkinson’s  disease: making the diagnosis

Nitin K Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian Hospital

Weill Cornell Medical Center

New York, NY 10065


Well it is the start of a new year and a new decade. Welcome twenty ten. I wish all the readers of my blog a very happy new year. Recently I saw a patient in my office and he shall be the subject of my post. He came to see because of his tremor. Actually I should not say he came to see me, the patient infact felt there was nothing wrong with him.

Dr. Sethi, I have noticed a tremor in my right hand for the past 3 months. It does not bother me. I feel fine. It is my wife who wants me to come and get this checked out” he said.

As I examined him I realised his ” hand shakes” problem was something more sinister as I found tell tale signs suggestive of Parkinson’s disease. That is what I shall discuss here, how does one go about making the diagnosis of Parkinson’s disease ? What are the points in the history and examination that make me as a doctor consider this diagnosis?

Parkinson’s disease may start off very innocuously. All my patient had noticed was that for the past3 months he had a tremor in his right hand. The tremor did not bother him and did not interfere with any activity of daily living such as writing, getting dressed, eating and so forth.  He in fact would not have sought a neurological consultation if his wife had not insisted.  That said and done, there are certain characteristics of the tremor which can aid in the diagnosis. The classical tremor described with Parkinson’s disease is what is called a resting tremor. Now pray what does that mean? Simple the tremor is most prominent when the hands are rest. Let me explain with the aid of an example. While I was talking to my patient and eliciting his medical history, my visual attention was focussed at his hands which were at rest on his lap. I noticed his right hand to have a tremor, the tremor became more prominent when he was distracted. If I asked him to look at his right hand, he could stop the tremor for a few seconds but then the tremor came back. He did not have  a tremor in his left hand or in his legs. When the arms were extended (held up in front of him), the tremor  abated.

So point number 1:  Sporadic Parkinson’s disease usually starts of in the sixth to seventh decade of life. The initial presentation may be quite subtle with only a mild tremor. The tremor initially is asymmetrical (that is it may only be in one hand) and classically it is a resting tremor (most prominent when the hands are completely at rest). The tremor becomes less prominent when the hands are doing something (in motion) and completely abates when the patient falls asleep. Remember the tremor at least initially during the disease course may not be bothersome for the patient and may not impair his quality of life. Hence the patient may not seek attention and the diagnosis may be delayed.

There are some other early signs of Parkinson’s disease. On close inspection I was able to document them in my patient too. When he spoke to me, his face lacked the usual emotions. What do I mean by that. Well when we speak our face show a variety of emotions, we frown, we roll our eyes, sometimes our eyes smile and so forth. A Parkinson’s disease patient has what is called a “mask-like” face-there is a paucity of normal facial expressions.

So point number 2.  Mask like face

Parkinson’s disease patients have a characteristic gait. For want of better words, they walk stiffly. The classical gait is described as bent forward, walking with short quick steps (as if they are going to topple over) and the arms are held by the side (they do not have the usual arm swing).

So point number 3. Gait (They walk funny!!!)

So if you or any of your loved ones show these signs, make sure you get a neurological opinion. Your doctor shall be able to elicit further points in the history and examination which shall help secure the diagnosis of sporadic Parkinson’s disease. Remember the diagnosis of Parkinson’s disease remains a clinical diagnosis (one made by a doctor after history and examination). There are no confirmatory tests (at least none that are used in the office setting).




Tremor: a question and an answer

Another of my readers emailed me this question. My response to it follows:

Jeff Street
on October 16, 2008 said:

I’ve been having tremors over the past 4 months in my hands, feet and legs, and lips. They are more prominent (especially in my hands) after exercise. My physician did blood work and it indicated I was “mildly” hyperthyroid (slightly low TSH, normal T3/T4). He blames the tremors on this condition. He has prescribed propranolol 20mg BID for the tremors, but wants to wait and see if the thyroid might correct itself before putting me on Methimazole (due to its side effects). My symptoms seem rather profound for a “mild” case of hyperthyroidism. Do you have any further suggestions or input?

Dear Jeff,
thank you writing in. As I stated in my earlier post on tremors (you can read my post at my website ) tremors can be of various kinds. The kind of tremors you are describing when your hands are outstretched (but you also have them in your feet and lips) are likely not due to a neurological condition per-se. We all have a subtle tremor in our hands, this is called physiological tremor. If you make people hold their hands out in front of you, you shall be able to notice it is you pay close attention. Now suppose this person goes and drinks 6 cups of large Starbucks coffee and you again make him or her stretch their arms in front of you, the tremor shall be more prominent. This is called enchanced physiological tremor. As the name says, these tremors are physiological and not pathological (we all have them, some more prominently than others).
There are certain medical conditions which may cause tremors or make the physiological tremor more prominent. One such condition is hyperthyroidism. Patients who have hyperthyroidism do have tremors of their hands and also of their tongue (if you make them stick their tongue out, you shall be able to notice the tremor). Some medicines and drugs of abuse also cause tremors. Patients who drink alcohol heavily are tremulous, especially if they stop drinking suddenly.

Not all tremors need to be treated. We only treat a tremor if it becomes disabling for a patient or causes social embrassement. Propanolol (a beta blocker drug used as an anti-hypertensive medication) does have a role in treating postural tremors. Your doctor may like to slowly taper the dose up and see if it gives you any relief. I cannot comment if hyperthyroidism indeed is the cause of your tremor. As you can see from what I wrote above there can be protean causes of tremor some neurological (neurodegenerative in etiology like Parkinsos’s disease), other more benign (Benign Essential Tremor) and toxic/ metabolic causes of tremors (hyperthyroidism, drug induced tremors etc).
My advise to you would be to follow your doctors instructions and see if the propanolol gives you benefit. As I stated earlier, he has started you on a low dose and may taper it up over a period of time. If this tremor does not subside, then you may need a neurological work-up to try to determine the etiology of the tremor.
Please feel free to write in again.

Personal Regards,
Nitin Sethi, MD

The tremor of Parkinson’s disease

                                                     The tremor of Parkinson’s disease

Nitin. K. Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian

Weill Cornell Medical Center

New York, NY 10065

Since many of the readers of my blog and website ( have written in asking about tremor, I thought in this post I shall describe the tremor seen in Parkinson’s disease in detail. The classical tremor described in Parkinson’s disease is a resting tremor which has a frequency of about 2-5 Hz. Let me explain in more simple terms what I mean by that.

The tremor in Parkinson’s disease is present at rest and not when the hands/ limbs are in motion (when the patient’s hands are placed on a table and are completely at rest, the tremor comes out. Now if you ask the patient to hold the hands in front of themselves or to perform some action like picking up a glass of water and bring it to their lips, the tremor becomes less prominent and may not be noticable. Hence it is called a RESTING TREMOR). Another way to observe the resting tremor is to see the patient walk. When we walk, our arms are held by the side of the body and are completely at rest, if a person has a resting tremor it is clearly visible.

The tremor in Parkinson’s disease has a frequency of about 2-5Hz ( meaning that the tremor is not very fast). It also has a large amplitude (meaning that it is not fine rather it is a gross tremor and can be well appreciated by the naked eye from a distance).

The tremor of Parkinson’s disease disappears/ stops when the patient falls asleep (most of the tremors abate on sleeping and hence this quality does not aid in differentiating the tremor of Parkinson’s disease from other tremors).

The classical tremor of Parkinson’s disease is a pill-rolling tremor (meaning the tremor consists of flexion and extension of the fingers in connection with adduction and abduction of the thumb. Imagine yourself rolling a pill, that is how the tremor looks like!!!)

Most importantly the tremor in Parkinson’s disease is accompanied by other signs of Parkinson’s disease such as rigidity (the tone of the muscles of the limbs is increased), bradykinesia (slowness in the execution of movement) and a disturbance of gait and posture (the gait is slow, stooped forward-we call this a festinating gait and their posture is off so patients are more prone to falls). That said and done signs of Parkinson’s disease may appear at different times and not all at once. At times the first/ earliest manifestation of Parkinson’s disease is the presence of an asymmetrical resting tremor (meaning the tremor usually appears asymmetrically/ only in one hand).


Parkinson’s disease: when to treat and how?

Recently I was asked by someone when should we treat a patient with Parkinson’s disease, early on in the disease course or later when the clinical symptoms are more florid? As you know Parkinson’s disease is a progressive neurodegenerative condition characterized by tremor (resting tremor of the limbs, see my post on tremors, rigidity (stiffness), bradykinesia (patients have less spontaneous movements) and a characteristic disturbance of gait and posture (patients walk stooped forward and their balance is off, making them more prone to falls).

As you can well imagine all these symptoms do not start off all at once. Infact the onset of Parkinson’s disease is quite insidious and generally asymmetrical. In its earliest stages, all the patient may have is a unilateral (one hand) tremor. Later as time goes by and the disease progresses the symptoms become more florid and the bardykinesia and disturbance of gait and posture appear.

So that brings us to the question of my post, just when do we start treating these patients? Should we treat them early or should we treat them in the later stages?

There is no good answer to this question. One concern which has been raised is that if you treat patients with Parkinson’s disease with levodopa/ syndopa (the combination is called Sinemet in The United States), early on in the disease course, the drug itself may hasten the progression of the disease (the thinking behind this is the concern that levodopa may increase the breakdown of dopamine secreting cells in the basal ganglia).

On the other hand, there is some evidence to suggest that early treatment is better because it prevents the compensatory change in hardwiring which occur in the brain in the face of decreasing dopamine (some of the neurons such as that of the subthalamic nucleus become overactive in the face of decreasing dopamine secretion and this later on leads to more problems such as the on-off phenomena).

So what is the answer? I think a patient should be treated when he devlops symptoms that start bothering him or interfere with his functioning and activities of daily living. If that occurs early in the disease course, so be it, he warrants treatment. Nowdays apart from levodopa/syndopa (Sinemet) there are many other drugs which can be used to treat the disease especially in the early phases. These drugs ( dopamine agonists like Requip (Ropinirole) and Mirapex (Pramipexole) and selegine) are less stronger than levodopa/syndopa combination but are thought to have less “neurotoxicity” and hence are preferred to be used in the early stages of the disease.

Your doctor shall help you navigate these questions. Have a good weekend everyone. It is Saturday morning here in NYC as I pen this, I think I shall go for a run.

Personal Regards,

Nitin Sethi, MD

Parkinson’s disease

Parkinson’s disease is a relatively common neurodegenerative disease. It was first described by James Parkinson in his now classical essay titled ” The Shaking Palsy”. James Parkinson was an astute observer and his longitudinal description of the disease which now bears his name was on the basis of just a single patient.

Like other neurodegenerative diseases, Parkinson’s disease starts in the later age groups (60’s and onwards). Sometimes it may start in the younger age groups especially if there is a family history of the disease. This is referred to as Familial Parkinson’s Disease.

Typical Parkinson’s disease has a clinical triad consisting of:

a) rigidity (patient’s are rigid–when you passively move their limbs you experience increased resistance. Rigidity is a condition in which the tone of the body is increased. Tone refers to the resistance offered to passive movement of a limb across the joint)

b) bradykinesia or akinesia: as the name suggests, this means that the patient’s are bradykinetic. They have paucity of spontaneous movements, when they walk they do not have the characteristic arm swing which describes the human walk.

c) resting tremor: Parkinson’s disease (PD) patient’s have a characteristic tremor in their hands and feet. The tremor is a resting tremor meaning that it is most prominent when they are relaxed and their arms are at complete rest (when you walk, your arms are at rest by the side of your body and the tremor can be clearly seen).


Other features of Parkinson’s disease (PD):

d) PD patient’s have a typical disturbance of gait and posture. They seem off balance and are prone to falls. They walk bend forward in short quick steps (as if chasing something). This characteristic gait of PD patient’s has been referred to as festinating gait. If you accidently push a PD patient to the side or backward or forward, they are unable to compensate and may fall down. Falls and the disturbance in gait and posture is an important cause of morbidity in PD patient’s. When PD patient’s turn they do not turn in one smooth motion rather thay turn with small steps.

e) PD patient’s have a mask like face. They do not have the characteristic facial expressions which so define when humans talk. They may not blink while speaking ( sort of staring look), do not smile or frown.

f) PD patient’s may notice a change in their writing. Typically the hand writing becomes smaller and smaller and more illegible. This is referred to as micrographia.

g) The voice of PD patient’s is monotonous and lacks the variations in the pitch and tone which defines human speech.


A point to note here is that unlike Alzheimer’s disease, PD patient’s usually have no impairment in memory at least in the early to middle stages of the disease. Later on in the disease course, they may develop cognitive impairments, this condition is referred to as Parkinson’s disease dementia (PDD) or dementia associated with Parkinson’s disease.