Do I have parkinson’s quiz

10 Early Signs of Parkinson’s Disease

It can be hard to tell if you or a loved one has Parkinson’s disease (PD).

Below are 10 signs that you might have the disease. No single one of these signs means that you should worry, but if you have more than one sign you should consider making an appointment to talk to your doctor.

Tremor

Have you noticed a slight shaking or tremor in your finger, thumb, hand or chin? A tremor while at rest is a common early sign of Parkinson’s disease.

What is normal?
Shaking can be normal after lots of exercise, if you are stressed or if you have been injured. Shaking could also be caused by a medicine you take.

Small Handwriting

Has your handwriting gotten much smaller than it was in the past? You may notice the way you write words on a page has changed, such as letter sizes are smaller and the words are crowded together. A change in handwriting may be a sign of Parkinson’s disease called micrographia.

What is normal?
Sometimes writing can change as you get older, if you have stiff hands or fingers or poor vision.

Loss of Smell

Have you noticed you no longer smell certain foods very well? If you seem to have more trouble smelling foods like bananas, dill pickles or licorice, you should ask your doctor about Parkinson’s.

What is normal?
Your sense of smell can be changed by a cold, flu or a stuffy nose, but it should come back when you are better.

Trouble Sleeping

Do you thrash around in bed or act out dreams when you are deeply asleep? Sometimes, your spouse will notice or will want to move to another bed. Sudden movements during sleep may be a sign of Parkinson’s disease.

What is normal?
It is normal for everyone to have a night when they ‘toss and turn’ instead of sleeping. Similarly, quick jerks of the body when initiation sleep or when in lighter sleep are common and often normal.

Trouble Moving or Walking

Do you feel stiff in your body, arms or legs? Have others noticed that your arms don’t swing like they used to when you walk? Sometimes stiffness goes away as you move. If it does not, it can be a sign of Parkinson’s disease. An early sign might be stiffness or pain in your shoulder or hips. People sometimes say their feet seem “stuck to the floor.”

What is normal?
If you have injured your arm or shoulder, you may not be able to use it as well until it is healed, or another illness like arthritis might cause the same symptom.

Constipation

Do you have trouble moving your bowels without straining every day? Straining to move your bowels can be an early sign of Parkinson’s disease and you should talk to your doctor.

What is normal?
If you do not have enough water or fiber in your diet, it can cause problems in the bathroom. Also, some medicines, especially those used for pain, will cause constipation. If there is no other reason such as diet or medicine that would cause you to have trouble moving your bowels, you should speak with your doctor.

A Soft or Low Voice

Have other people told you that your voice is very soft or that you sound hoarse? If there has been a change in your voice you should see your doctor about whether it could be Parkinson’s disease. Sometimes you might think other people are losing their hearing, when really you are speaking more softly.

What is normal?
A chest cold or other virus can cause your voice to sound different, but you should go back to sounding the same when you get over your cough or cold.

Masked Face

Have you been told that you have a serious, depressed or mad look on your face, even when you are not in a bad mood? This is often called facial masking. If so, you should ask your doctor about Parkinson’s disease.

What is normal?
Some medicines can cause you to have the same type of serious or staring look, but you would go back to the way you were after you stopped the medication.

Dizziness or Fainting

Do you notice that you often feel dizzy when you stand up out of a chair? Feeling dizzy or fainting can be a sign of low blood pressure and can be linked to Parkinson’s disease (PD).

What is normal?
Everyone has had a time when they stood up and felt dizzy, but if it happens on a regular basis you should see your doctor.

Stooping or Hunching Over

Are you not standing up as straight as you used to? If you or your family or friends notice that you seem to be stooping, leaning or slouching when you stand, it could be a sign of Parkinson’s disease (PD).

What is normal?
If you have pain from an injury or if you are sick, it might cause you to stand crookedly. Also, a problem with your bones can make you hunch over.

What can you do if you have PD?

  • Work with your doctor to create a plan to stay healthy. This might include the following:
    • A referral to a neurologist, a doctor who specializes in the brain
    • Care from an occupational therapist, physical therapist or speech therapist
    • Meeting with a medical social worker to talk about how Parkinson’s will affect your life
  • Start a regular exercise program to delay further symptoms.
  • Talk with family and friends who can provide you with the support you need.

For more information, visit our Treatment page.

Because Parkinson’s disease is a progressive condition, it can be difficult to spot the early warning signs. However, we’ve put together a list of 10 of the most common early signs and symptoms of the disease, according to the National Parkinson Foundation.

1. Tremors and Shaking
This is one of the most recognized symptoms. Although there could be many other reasons for tremors, facial-twitching or limb-shaking is a common early warning sign of Parkinson’s disease.

2. Small Handwriting
Many Parkinson’s disease patients find that their handwriting suddenly becomes very small. The way you write may also have changed if you are in the early stages of the condition.

Want to learn more about the latest research in Parkinson’s Disease? Ask your questions in our research forum.

3. Loss of Smell
Many people temporarily lose their sense of smell due to colds or the flu, but if the loss is sustained over a length of time without any noticeable congestion, then it could be an early sign of Parkinson’s disease.

4. Sleeping Disorders
Trouble sleeping can be attributed to many illnesses and Parkinson’s disease is one of them. Waking due to sudden body movements, or thrashing your legs in your sleep could be a warning sign of the condition.

5. Stiffness in Walking and Moving
General stiffness that can’t be attributed to exercise aches and pains and doesn’t ease up when moving around could be an early warning sign of Parkinson’s disease. Many patients complain that it feels like their feet are literally stuck to the floor.

MORE: Did you know that Parkinson’s disease patients may benefit from dancing?

6. Constipation
Unable to move your bowels is also a common early sign of Parkinson’s disease. Although this is a common enough problem in healthy people, Parkinson’s patients are more susceptible to constipation. If you suddenly find you’re constipated and consider your diet normal then you should have a doctor check you out.

7. Low or Soft Voice
A sore throat or a cold can change the way you speak, but if you have been experiencing a sudden softness to the tone of your voice and are now speaking in a quieter or hoarser tone, this could be an early symptom of Parkinson’s disease.

8. Masked Face
A face set into what others may perceive as a bad mood or being angry or depressed is a common early sign of Parkinson’s disease. Also, an expressionless face with unblinking eyes could be a warning sign.

MORE: Check some seated exercises for patients with Parkinson’s disease

9. Dizziness or Fainting
Feeling faint or dizzy is an indication of low blood pressure, which is an early warning sign of Parkinson’s disease. If you are regularly feeling dizzy when you stand up then you should see your doctor.

10. Stooped
If you suddenly become stooped or your back hunches over then this could be an early warning sign of Parkinson’s disease. A slouch or hunch could be attributed to other conditions, such as arthritis or other bone diseases, but you would need to see your doctor to determine the cause.

MORE: Did you know that there’s an eye test that can help detect Parkinson’s before first symptoms show up?

Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.

CASE

In July 1996, a previously healthy 37-year-old female patient presented pain in her left leg, located on the groin, radiating up to lumbar region and down to the thigh. The pain was constant, but would get much worse when she walked, halting her from ambulating normally. From July 1996 to December 1996, she sought four orthopedists, performed lumbar spine X-ray and bone scintigraphy, and received two diagnoses, lumbar pain and coxofemoral joint affection, and anti-inflammatories were prescribed, with no relief of the symptoms. A lumbar root anesthetic block with lidocaine was tried, without improvement. For the coxofemoral joint disease, a surgical intervention with placement of coxofemoral prosthesis was advised, which was prompted refused by the patient. Besides the pain, in October 1996, she had started to feel numbness in the left leg. The patient continued to complain of walking difficulties, ultimately needing a cane to ambulate. In December 1996, due to lack of therapeutic response, she was advised by the last orthopedist to seek for acupuncture and psychiatric treatment. Acupuncture was not of any help, as well as the use of anxyolitics.

In June 1998, the patient looked for the fifth orthopedist who ordered a four-member electromyogram that was normal. The orthopedist ruled out organic disorders, and advised her to seek for a second psychiatrist, which the patient refused, returning to the prior orthopedist. The pain started to abate slowly, allowing the patient to walk without the aid of the cane, but the “numb leg” feeling was getting worse, leading her to drag the left lower limb. In November 1998, she sought for the sixth orthopedist who suspected of an inguinal hernia, referring her to a gastroenterologist. An abdomen ultrasound exam was ordered, which ruled out this diagnosis. She was advised to seek for an orthopedist or a neurologist. At that time, she was starting to complain of an ill-defined sensation in the left arm. She looked for the seventh orthopedist, which referred her to a neurologist.

The patient underwent the first neurological evaluation in February 1999. An electroencephalogram (EEG) and a head computed tomography (CT) were ordered, which were normal, and with these results the neurologist ruled out any neurological abnormalities. Two months later she consulted the second neurologist who ordered a new head CT and EEG, which were normal. A cerebral arteriography was indicated to investigate for stroke, which was refused by the patient. In the months that followed, the motor problems continued to get worse, interfering even more with gait and activities of daily living (ADL). There was almost no pain. In October 1999, she consulted a neurosurgeon who examined her, revised all the procedures performed, but did not get to a definitive diagnosis.

From December 1999 to April 2000, a general practioner and a physician expert in psychosomatic disorders evaluated her. The latter ordered a new bone scintigraphy, which was normal, and referred her to a second neurosurgeon, who diagnosed fibromyalgia. In September 2000, as the patient would not improve with the current treatment, she sought for the third neurologist, who ordered a magnetic resonance of the brain which was normal. In October 2000 the patient was evaluated by the eighth orthopedist, who ordered a coxofemoral joint ultrasound, which was also normal, and an orthopedic illness was definitely ruled out.

In November 2000, the patient was seen at the Movement Disorders Outpatient Clinic Division of Neurology of the Hospital das Clínicas de São Paulo. Besides the previous data, there was no noteworthy medical or family history. A rigid-akinetic syndrome affecting the left hemibody was noticed, leading to writing and gait difficulties, with a tendency to the patient walk on her toes on the left side. There were no other neurological or cognitive abnormalities. Based on the clinical picture, lack of abnormalities on neuroimaging and copper metabolism tests, a diagnosis of early-onset Parkinson’s disease was made. The patient underwent a treatment challenge with levodopa/benserazide 200 mg/50 mg in an initial dose of 1/2 tablet three times daily. As there was no improvement after the first week of treatment, the dose was titrated up to 1 tablet three times daily. After ten days, a clear improvement in motor performance was observed, as reflected by gait, ADL and professional activities, especially with improvement in her typing skills. Afterwards, as a treatment maintenance strategy, a reduction in levodopa total dose was possible with association of the dopaminergic agonist pramipexol. This therapeutic regimen was kept with good control of motor difficulties. Posteriorly, amantadine was added to the treatment scheme to better control the parkinsonian symptoms.

In the following months, the parkinsonian syndrome started to affect the right hemibody. After three years of treatment, the patient started to experience dose-peak dyskinesias, more on the left side. Dyskinesias progressively increased in severity, demanding reduction of the dose of dopaminergic agents, leading to subsequent worsening of parkinsonian symptoms. This problem was overcome by performance of right postero-ventral pallidotomy, to obtain a better control of dyskinesias and of the parkinsonism, even with lower doses of dopaminergic drugs.

The Ethics Committee of our institution approved this article and the patient gave full informed consent.

DISCUSSION

The diagnosis of PD in this patient was difficult to make because of the several atypical features presented, such as age at onset below the usually seen, pain as the first clinical manifestation, absence of rest tremor, and beginning of the illness in the lower limbs. PD usually starts in middle-aged individuals, with a prevalence of about 2% after 65 years of age2, but 4 to 12% of PD cases start before 40 years of age, characterizing early-onset PD3. In these cases, differential diagnosis is rather broad, and one should consider genetic forms of the illness, such as PARK 2 (parkin), PARK 6 (PINK1), and PARK 7 (DJ-1). However, the detection of these mutations is not yet available in clinical practice, and its diagnosis would not alter treatment4,5.

Other diseases that may have parkinsonian features as their initial manifestations should be considered in the differential diagnosis of early-onset PD, such as dopa-responsive dystonia (DYT5), Wilson’s disease (ruled out in this patient with the appropriate laboratory tests), juvenile form of Huntington’s disease, type 2 and 3 spinocerebellar ataxias, rapid-onset dystonia-parkinsonism (DYT12), and neuroacanthocitosis, besides toxic and metabolic cause of parkinsonism6. In this patient, the slow disease progress, the normal imaging procedures, the good response to levodopa and the absence of any personal and family medical history allowed us to rule out all these possibilities.

Regarding to the phenomenon of pain in PD, it can at times occur in the early years of the illness. This symptom, when the disease is not yet full-blown, usually leads the patients to seek other medical specialties, in which the degree of suspicion for PD is not as high as in neurology, often leading to a delay in the diagnosis, as happened in our case. Gilbert7 reports a 65-year-old patient who sought for medical advise due to a 2-year-long pain in her arms that, following extensive orthopedic evaluation, was discovered to be caused by PD after a tremor in her right leg appeared.

Pain may be related to the akinetic-rigid syndrome even when it is slight enough to be clinically recognizable. However, there are other mechanisms involved. Pain in PD was initially considered to be an analogous of post-stroke central pain syndromes8 but, different from these, there is increased evoked pain sensitivity to thermal stimuli, whereas in central pain disorders there was a decrease in these responses9.

The neurodegenerative process in PD may lead to interruption of pain-inhibitor dopaminergic and nigral descendent pathways from the mesencephalon, thus liberating nociceptive activity in the fist neuron of the dorsal root. This neurodegeneration process may also initiate a cascade of hypersensitivity to painful stimuli in basal ganglia and other rostral areas8,9. However, levodopa does not appear to improve spontaneous pain8. In PD, there is not only loss of dopaminergic neurons, but also other neurotransmitter systems are involved, such as serotoninergic, cholinergic, noradrenergic, and peptidergic neurons1. It is likely that loss of cell in other brain regions such as locus coeruleus, pontine tegmental area, anterior cingulate gyrus, insula, medial thalamic nucleus, amygdala, and hypothalamus, have a role in the generation of pain in PD. These regions modulate ascendant nociceptive pathways through noradrenergic afferents8.

The form of PD that begin with an akinetic-rigid syndrome is more difficult to diagnose than when the classic resting tremor is present. This type of presentation occurs in about 20% of PD cases1, and the time lag between the initial manifestations and its diagnosis is always greater than the one observed in the tremor-dominant syndromes. The cases of PD that start with an akinetic-rigid syndrome usually evolve faster, and gait and stance disturbances occur more frequently. Occasionally, cognitive abnormalities in the form of a dysexecutive syndrome may occur in this group of individuals10. Some studies demonstrate that early-onset PD patients most often present the tremor-dominant type of disease6,11,12. Lewis et al.10, however, argue against this information.

Our patient presented her initial manifestations in her lower extremities, a quite rare atypical feature in PD. Most often, PD starts in the upper limbs13, but in about 20% of cases it can begin in the legs14.

SN is a quite heterogeneous nucleus, with regional variations in its striatal projections and in the distribution of its biochemical markers. SN pars compacta is divided into a ventral and dorsal tiers. The lateral and ventral regions send efferents to the dorsal putamen, whereas neurons dorsally located in the SN project to the ventral regions of the caudate nucleus. The lateral and posterior parts of the SN are related to the dorsal and lateral regions of the putamen15. There are no data concerning somatotopic organization of the SN pars compacta, but there is clear somatotopic correlation between motor cortical areas and the putamen16,17.

Fearnley and Lees16 in a pathologic study of 50 PD cases, and Damier et al.18 in a immunohistochemistry study of five cases of PD, demonstrated that the degenerative process in the SN pars compacta starts in its ventral tier, specially in the lateral region, extending further to the medial region. One would expect the symptoms to begin in the lower limbs. Fearnley and Lees16 suggest that the small deficits in the hands are soon perceived, and that these same clinical abnormalities in the feet and legs can be missed in the early years of disease, what could explain this paradox. The authors argue that dystonia in young-onset PD usually starts in the legs, not involving the arms. Lewis et al.10 argue against this theory, stating that it does not explain all the PD cases that begin in the lower limbs. This issue needs to be further elucidated.

Vidailhet et al.17 in a prospective study of 20 PD patients observed the symptoms to begin in the lower limbs in a third of the cases, or preceding or evolving along with the symptoms in the upper limbs. The authors state that doctors pay less attention to the legs when evaluating early-onset PD patients. Besides, according to the authors and to Fearnley e Lees16, parkinsonian symptoms in the arms are easier to be detected, as far as minimal functional abnormalities may alter hands fine movements, whereas the movements of the legs and feet are simpler, and minimal deficits may go unnoticed. However, Schelosky and Poewe13 in a study of 250 PD cases demonstrated that the disease predominantly affects upper limbs in the beginning.

In the cases starting in the lower limbs, the first symptoms may be rest tremor, or a hypokinetic-rigid syndrome, as in the case described here.

For all those reasons presented, one can understand why PD in this patient was diagnosed only after 4 years from the onset, during which period the patient looked for 8 orthopedists, 3 neurologists, 2 neurosurgeons, 2 psychiatrists, and one gastroenterologist, summing 16 doctors. It must be emphasized that the good response to levodopa along with the development of levodopa-induced dyskinesias was a valuable proof to make the diagnosis.

1. Tolosa E, Wenning G, Poewe W. The diagnosis of Parkinson’s disease. Lancet Neurology 2006;5:75-86.

2. Periquet M, Latouche M, Lohmann E, et al. Parkin mutations are frequent in patients with isolated early-onset parkinsonism. Brain 2003;126:1271-1278.

7. Gilbert GJ. Biceps pain as the presenting symptom of Parkinson disease: effective treatment with l-dopa. South Med J 2004;97:776-777.

8. Buzas B, Max MB. Pain in Parkinson disease. Neurology 2004;62:2156-2157.

9. Djaldetti R, Shifrin A, Rogowski Z, et al. Quantitative measurements of pain sensation in patients with Parkinson disease. Neurology 2004; 62:2171-2175.

10. Lewis SJG, Foltynie T, Blackwell AD, et al. Heterogeneity of Parkinson’s disease in the early clinical stages using a data driven approach. J Nerurol Neurosurg Psychiatry 2005;76:343-348.

13. Schelosky L, Poewe W. Topographical onset and progression of motor symptoms in idiopathic Parkinson’s disease. Mov Disord 1990;5 (Suppl 1):S13.

14. Dickson JM, Grünewald RA. Somatic symptom progression in idiopathic Parkinson’s disease. Parkinsonism Relat Disord 2004;10:487-492.

15. Parent A. Carpenter’s human neuroanatomy. 9.Ed. Philadelphia: Williams & Wilkins, 1996:557-582.

17. Vidailhet M, Bonnet AM, Marconi R, Gouider-Khouja N, Agid Y. Do parkinsonian symptoms and levodopa-induced dyskinesias start in the foot? Neurology 1994;44:1613-1616.

18. Damier P, Hirsch EC, Agid Y, Graybiel AM. The substantia nigra of the human brain II. Patterns of loss of dopamine-containing neurons in Parkinson’s disease. Brain 1999;122:1437-1448.

Received 1 August 2006, received in final form 23 October 2006. Accepted 9 December 2006.

Dr. Flávio Augusto Sekeff Sallem – Rua Dr. Diogo de Faria 1226 / 24 – 04037-004 São Paulo SP – Brasil. E-mail: [email protected]

Parkinson’s Disease: Symptoms

How do early symptoms of Parkinson’s disease (PD) come on?

Early symptoms of Parkinson’s disease (PD) are usually mild and generally occur gradually. You may have fatigue or a general sense of uneasiness. You may feel a slight tremor or have difficulty standing. Some may notice that their speech has become softer or that their handwriting has changed (written letters/words are smaller). You may forget a word or thought and have feelings of depression or anxiety. Generally, friends and family may begin to notice the changes before you do. They often notice the stiffening or lack of movement in the body (no arm swing when walking) or the absence of facial expression (“masked face”).

As the disease goes on, it begins to interrupt daily activities. It is important to note that not all patients experience the full range of symptoms. In fact, most patients have mild, non-intrusive symptoms.

What are the symptoms of Parkinson’s disease?

Muscle rigidity. Rigidity is the inability for the muscles to relax normally. Most patients with PD develop some degree of rigidity, or stiffness of limbs. This rigidity is caused by uncontrolled tensing of muscles and results in the patient being unable to move freely. Also, patients may experience aches or pains in the affected muscles.

Tremor. In general, tremor (shaking) begins in the hands and arms. It can also occur in the jaw or foot. Tremor usually involves the rubbing of the thumb against the forefinger. It is more apparent when the hand is at rest or the patient is under stress. In the early stages of the disease, usually only one side of the body or one limb is affected. As PD progresses, tremor may become more generalized. Tremor usually worsens with stress. Tremor rarely disables a patient and often disappears during sleep and when the arm or leg is being moved. Not every patient with PD has tremor.

Bradykinesia. Bradykinesia is the slowing down of movement and the gradual loss of spontaneous activity. It is caused by the brain’s slowness in transmitting the necessary instructions to the appropriate parts of the body. This symptom is especially stressful for PD patients, given that it is unpredictable and can be quickly disabling. One moment a patient is moving easily, the next they need help moving at all. This makes accomplishing simple tasks and participating in daily routines extremely difficult. Bradykinesia affecting the facial muscles may cause a mask-like appearance.

Changes in walking pattern (gait). This commonly includes the inability of a patient to swing their arms naturally while walking, taking short shuffling steps, “freezing spells” (difficulty starting to walk and difficulty stopping), bend forward (stooped posture), and difficulty in maneuvering turns and corners.

Other symptoms of PD

  • Loss of balance and falls
  • Forward or backward lean that makes them more likely to fall
  • Stooped posture (when the head is bowed and the shoulders are slumped)
  • Shaking of the head
  • Voice and speech changes; voice will become softer, with poor enunciation
  • Loss of motor skills
  • Memory problems
  • Constipation
  • Depression
  • Feelings of fear and anxiety
  • Confusion
  • Dementia
  • Fatigue
  • Drooling
  • Skin problems, such as dandruff
  • Difficulty swallowing and chewing
  • Stress and tension
  • Sleep disturbance
  • Urinary problems
  • Sexual dysfunction

It is important for you to visit your doctor if you are experiencing any of these symptoms so you can receive the proper evaluation and diagnosis. There are other conditions that appear similar to PD, including:

  • Parkinson’s plus, like progressive supranuclear plasy (PSP), corticobasal degeneration (CBD), multiple system atrophy (MSA), and vascular Parkinson’s.
  • Depression
  • Aging
  • Use of anti-psychotic drugs
  • Other degenerative disorders of the brain

If you have questions about the possibility of PD with you or someone close to you, talk with your doctor as soon as possible.

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This is not an attempt to give a comprehensive description of Parkinson’s disease, but rather to present some basic facts and then give a few examples in the form of films and stories. Please report any errors you can find by commenting on this post. Illustration of Parkinson’s disease by William Richard Gowers, which was first published in A Manual of Diseases of the Nervous System (1886) (Source: Wikipedia)

Parkinson’s disease

Parkinson’s disease, or PD for short, is an incurable, neurodegenerative and neuropsychiatric disease caused by a lack of the neurotransmitter dopamine in the brain. It affects about 2% of the elderly in the US and the older you get, the bigger the chances are that you will get PD. The drawing to the left was made in 1886 but is probably still a very accurate picture of how most people see PD.

The first person in the Western world to describe this condition was a doctor in London called James Parkinson. He described the disease that would be named after him based on cases he saw in his medical practise or observed in the streets of London like this:

“Involuntary tremulous motion, with lessened muscular power, in parts not in action and even when supported; with a proprensity to bend the trunk forwards, and to pass from a walking to a running pace: the senses and intellects being uninjured.” James Parkinson, An Essay on the Shaking Palsy, 1817.

PD is diagnosed on the basis of four cardinal symptoms: tremor, bradykinesia (slowness of movement), rigidity (stiffness), and problems with posture and gait. There are also a large number of non-motor symptoms that a person with PD may experience, where the most common probably are depression and other mood disorders, pain, cognitive problems, sleep issues, and problems with digestion and other autonomic functions. In addition, the available treatments for PD often causes different side effects of varying severity, mainly of a motor function or behavioural nature. Luckily, most persons with PD will not exhibit all of these symptoms or side effects.

The condition can be difficult to diagnose and it is unfortunately not uncommon to have to go a long time without a correct diagnosis. There are a number of conditions that can be mistaken for PD and vice versa, some of which are: essential tremor, dystonia (esp Dopa-responsive dystonia, DRD), and normal pressure hydrocephalus. (Thank you Peggy Willocks, for pointing out that this topic was lacking.)

PD is mostly managed with medication, and persons with PD often take several drugs multiple times a day, 4-6 different prescription drugs up to 6-8 times per day in different combinations is not an unusual regimen.

Here is an excellent introduction to PD:

If you want to know more about the motor aspects of PD, check this film:

And if you want to know more about the non-motor symptoms of PD, check this film:

For a great introduction to how PD can be managed with medication, see this film:

In conclusion, these are what I consider the most important things to be aware of when it comes to PD:

  1. Not only old people can get PD. Sure, most people are old-ish when they are diagnosed with PD, but somewhere between 5 and 10% actually get PD before the age of 50. The condition is then called “Young Onset PD” (YOPD). In some cases, such as my own (see under “personal stories” below), the disease starts under the age of 18 and is then called “Juvenile Onset PD”.
  2. Everybody with PD does not have a tremor. About 25% of cases do not have the classical PD tremor.
  3. PD is a very individual disease. I have personally met over 1,000 individuals with PD and none of them have probably had the exact same sets of symptoms and treatment as another.
  4. PD is an extremely variable condition. Symptoms and signs can come and go literally from one minute to the next, something that of course severely affects the person with the disease.
  5. PD is not easy to live with but there is a lot you can do to help yourself if you have it. Knowledge is absolutely essential to manage any chronic disease and especially PD.
  6. Medication timing is key in PD. Our medications are what makes us go round, literally. They are like our gasoline AND our transmission fluid combined and I find that being almost religious when it comes to medication timings, really helps me stay as well as I can with this difficult disease.
  7. Stay active! Stay active! STAY ACTIVE! The only thing that slows down the progression of PD is physical activity, which is why I try to walk at least 7,000 steps per day and also make sure to challenge myself mentally as often as I can.

The World Parkinson Coalition organises the World Parkinson Congress (WPC), which combines scientific content with patients’ interests, making it the best meeting in the world for persons with PD. The next congress will take place in Portland, Oregon, in September 2016. Don’t miss it, I know I won’t!

I made a film for the video competition of the World Parkinson Congress 2013, where I give my view of medications in PD, watch it here:

Personal stories

Here are a few personal stories from persons with PD. If you want me to link to your story of PD, comment below or use the contacts page.

Sara Riggare (me): “The Patient Perspective” from The Journal of Parkinson’s Disease 20th March 2014

Jean Burns:

Parkinson’s disease

  • Overview
  • Discovery
    • Early symptoms of Parkinson’s disease
    • Path to diagnosis of Parkinson’s disease
    • Getting the diagnosis of Parkinson’s disease
    • Telling others
    • Information about Parkinson’s disease
    • Causes of Parkinson’s disease
  • Treatment
    • Levodopa: medication for Parkinson’s disease
    • Dopamine receptor agonists: medication for Parkinson’s disease
    • Other medications for Parkinson’s disease and how to manage medication
    • Surgery for Parkinson’s disease: Deep Brain Stimulation and lesioning
    • Professional help for Parkinson’s disease
    • Self help for Parkinson’s disease
  • Parkinson’s symptoms
    • Tremor and loss of physical control in Parkinson’s disease
    • Parkinson’s disease and problems with movement
    • Embarrassing symptoms of Parkinson’s disease
    • Mental disturbances with Parkinson’s disease: depression, hallucinations and compulsive behaviour
  • Living with Parkinson’s disease
    • Redefining yourself
    • Keeping going
    • Work, career, benefits
    • Driving and journeys
    • Support and support groups
    • Parkinson’s UK and Parkinson’s disease nurses
    • Now and the future
    • Caring, care and carers
    • Advice to others
  • People’s Profiles
    • 2 years or under
    • 3-4 years
    • 5-7 years
    • 8-12 years
    • Over 12 years
    • DBS
    • Carers
  • Resources and Information
  • Credits
  • Magnesium, muscles and Parkinson’s

    Recipes & Nutrition

    Author: Kathrynne HoldenPublished: 26 September 2018

    Prep: Cook: Serves:

    A lack of magnesium can cause leg cramps, insomnia and fatigue – and is often found in those living with Parkinson’s. Our guest dietician Kathrynne Holden, author of “Eat Well, Stay Well with Parkinson’s Disease”, assesses the importance of the mineral, and offers advice on how to make sure you are getting enough

    Do you often have nighttime leg cramps, or restless legs syndrome? If so, you might be deficient in a very important mineral – magnesium.

    Recent research has suggested that people living with Parkinson’s are often deficient in magnesium, which may have a protective role to play in regard to neurological diseases in general.

    Magnesium is a mineral involved in hundreds of processes throughout our bodies. It belongs to the electrolytes family, which affects functions such as muscle movement. It can be difficult to pin down magnesium deficiency and – as blood tests aren’t always reliable – it’s important to be aware of symptoms, as they may be the best indicators of deficiency.

    The symptoms of magnesium deficiency include insomnia, fatigue and weakness; muscle cramps, spasms and twitches; restless legs syndrome; confusion, irritability, anxiety and depression; a loss of appetite; and difficulty breathing.

    Confusingly, these symptoms can be caused by a range of other factors that are not to do with magnesium. However, since magnesium deficiency is widespread in Parkinson’s, you should talk to your doctor if you experience some of these.

    What does magnesium do?

    Magnesium is needed for energy production, to convert vitamin D to its active form, to control blood glucose, and to regulate blood pressure, among hundreds of other important tasks. Perhaps most importantly for people living with Parkinson’s, it plays an especially important role in muscle function. When there is a magnesium deficiency, the muscle isn’t able to relax as easily, causing cramping or spasms. In extreme cases it can lead to tetany – a severe contraction of the muscles, usually in the hands or feet but sometimes in the esophagus or larynx (voice box). It can even affect lung function, making it more difficult to breathe.

    The best insurance is to eat foods rich in magnesium – it is usually better absorbed from food than from supplements. These include nuts such as almonds, cashews and peanuts, fruit and vegetables like spinach, avocado, potatoes and bananas, as well as cereals and pulses.

    If you think you might need supplements of magnesium, you should discuss this with your doctor, as there are some conditions that need care when it comes to magnesium supplements. Kidney disease, diabetes, slow heart rate, bowel obstruction, myasthenia gravis are examples. Also, magnesium supplements can interact unfavourably with some medications.

    If your doctor agrees that magnesium supplements are a good idea, they will indicate how much you should be taking.

    Magnesium is among the minerals most vital to human health, but it’s also one of the most neglected. Take a few moments to consider whether you’re getting enough of this important nutrient, or whether it might be a good idea to talk with your doctor about supplements.

    For more information on nutrition and Parkinson’s please visit the EPDA website.

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    Dietary Supplements for Parkinson’s Disease

    Dietary supplements are products that contain a dietary ingredient, such as a vitamin, mineral, amino acid, or herb. Also called nutritional supplements, they are taken by mouth and are intended to add nutritional value to the diet. Many people use dietary supplements for general health and well-being, and people with PD also look to supplements to improve their health.1,2

    There are no dietary supplements that have been proven to slow the progression of PD; however, scientists are researching several supplements to understand the role they may play in PD. All supplements should be discussed with a doctor before taking them as they may interfere with PD medications or potentially cause serious side effects.1,2

    Coenzyme Q10

    Coenzyme Q10 (CoQ10) is an antioxidant (substance that helps clear toxins) that helps the cells obtain energy from oxygen. A recent, large multi-center clinical trial that looked at people with PD taking CoQ10 compared to those taking a placebo showed no benefit of CoQ10, causing the study to be terminated. However, scientists are using the results of this trial to determine if other forms of CoQ10 could be effective or if taking CoQ10 at the early stages of the disease may be helpful.2,3

    Creatine

    Creatine is an amino acid that increases levels of phosphocreatine, an energy source for the muscles and the brain. In experimental studies, creatine has shown to protect against nerve cell injury. Some studies have shown creatine may help slow the progression of PD among people in the early stages of the disease. Other studies have not found a benefit of taking creatine for people with advanced stages of PD. One long-term study conducted in multiple centers in the U.S. and Canada evaluated creatine compared with a placebo. Study participants were given either creatine or a placebo for at least five years, and there was no evidence to support the use of creatine.2,3,4

    Vitamin C and Vitamin E

    Vitamin C and vitamin E are both antioxidants. One study that evaluated these vitamins found that they helped delay the need for PD medications. Taking vitamin E alone did not seem to have the same benefit, and vitamin E supplements can increase the risk of bleeding, especially in those who take blood thinners, like Coumadin, Plavix, or aspirin. Vitamin E has also been studied for its potential to reduce the risk of developing PD; however, dietary intake of vitamin E did not show any reduction in the risk of developing PD.3,5

    Glutathione

    Glutathione is a compound that has several effects on nerve cell metabolism and is a powerful antioxidant. Studies have shown that glutathione is depleted in the substantia nigra (one part of the brain that is damaged by Parkinson’s) in people with PD. A recent placebo controlled study did not show that glutathione improves in motor symptoms compared to the control group. Current research is investigating if glutathione may prevent the progression of the disease.2,6

    Curcumin

    Curcumin is the spice in turmeric, often used in Indian cuisine and medicine. Curcumin has antioxidant, anti-inflammatory, and anti-cancer properties, and it seems to provide protection against nerve cell injury. In research studies, curcumin has shown that it can prevent the clumping of the protein alpha-synuclein. Clumps of alpha-synuclein, also called Lewy bodies, are one of the hallmarks of PD. Preventing Lewy bodies from forming could potentially reduce symptoms or slow the progression of the disease, although research is still in its early stages.7,8

    Herbal remedies

    Some people with PD take St. John’s Wort (Hypericum perforatum) to ease depression, which is a common non-motor symptom of PD. Since St. John’s Wort has been shown to have similar properties to antidepressants, it should not be taken along with antidepressants.2

    Other people with PD use herbal remedies for insomnia, to calm anxiety, or improve overall well-being. There are no scientific studies that prove the effectiveness of herbal remedies for people with PD, and anyone using them should speak with their doctor to ensure they don’t interfere with other medications.2

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    Most people recognize the later stages of Parkinson’s disease — tremors and a shuffling walk are the most common signs. But the condition is difficult to diagnose early on; doctors don’t pinpoint most cases until they’re well past the initial stages. So is there a way to spot signs and seek treatment earlier?

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    Yes, but you need to know what to look for.

    The vague symptoms of Parkinson’s could point to many problems. That’s what makes early specific diagnosis difficult. And that’s what frustrates those who search for reasons behind your movement problems.

    But, there are recognizable signs that could at least put you and your doctor on alert, says neurologist Hubert Fernandez, MD, Director of Cleveland Clinic’s Center for Neurological Restoration. And getting a neurologist involved earlier is the key, he says.

    “It’s not uncommon for patients to see a rheumatologist or orthopedist for six months to a year for pain in the right shoulder or dragging the right leg. They might even get steroid injections that don’t work,” he says. “But, only a neurologist can diagnose Parkinson’s.”

    Symptoms follow stages of the disease

    Parkinson’s motor problems are quickly recognizable, Dr. Fernandez says. The tremors — rhythmic movement of lips, chin, hands and legs; rigidity; stiffness and slowness are hallmark signs. Balance and gait problems are also common.

    But, Parkinson’s symptoms start long before these problems emerge. As a progressive disease, Parkinson’s destroys the brain’s nerves from the bottom up, he says.

    Stage 1: Parkinson’s attacks the base of the brain stem — the medulla — initially. This may cause constipation and can cause people to lose their sense of smell. These symptoms could strike decades before you see your first tell-tale tremor, Dr. Fernandez says.

    Stage 2: Nerve deterioration in the pons (the brain’s message center) is next. Damage at this stage may lead to depression and REM sleep disorder. A person may “act out” their dreams while they sleep, potentially hurting themselves or others.

    Stage 3: The tremor and shuffle appear here because the disease is attacking the part of the brain largely responsible for movement.

    Stage 4 and 5: These are the most advanced Parkinson’s stages. Dementia and hallucinations often occur at this point.

    When should you consult a neurologist?

    Of course, not everyone who experiences constipation or depression, or who loses the sense of smell is at risk for developing Parkinson’s disease, Dr. Fernandez says. But, if you have those problems along with any of these factors, make an appointment with a neurologist:

    • First-degree relative with Parkinson’s with onset before age 60
    • One of the four motor features: resting tremor, stiffness, slowness, gait/balance problems
    • Repeated head trauma
    • REM sleep disorder

    4 things you should know about Parkinson’s

    In addition to learning what symptoms to watch for, there are four things you should know, Dr. Fernandez says:

    1. It’s a progressive disease. Parkinson’s disease worsens over time, but each patient progresses differently. Doctors will treat the symptoms to limit how much they impact your daily life.

    2. The cause is largely unknown. In 95 percent of cases, doctors don’t know why patients develop Parkinson’s. Often, a combination of factors are involved, including genetic susceptibility and environmental factors (such as having multiple head injuries). Research shows that genetic mutations are responsible for the rest of cases.

    “We don’t know what factors contribute to Parkinson’s,” he says. “And, we’re just beginning to uncover the susceptibility genes.”

    3. Treatment is symptom-dependent. How bothersome your symptoms are will determine how aggressively your doctor treats your disease. If your symptoms don’t disrupt your daily functioning, he or she likely will postpone prescribing medication.

    Dopamine, a chemical found naturally in the brain, is lacking or not produced in high enough quantities in people with Parkinson’s disease. Patients may take levodopa, a pill that is converted to dopamine when it reaches the brain. This helps manage Parkinson’s symptoms.

    It is often prescribed with a second drug called carbidopa, which prevents the nausea that can be caused by levodopa alone.

    Doctors also may use deep brain stimulation to treat you if you don’t get relief with levodopa, Dr. Fernandez says.

    4. Stroke, infection or other neurological conditions can mimic Parkinson’s. Don’t make any assumptions about your condition before you see a neurologist or Parkinson’s expert for a proper diagnosis.

    Ultimately, remember that your journey with Parkinson’s is unique — so work closely with your doctor, Dr. Fernandez says.

    “It’s important to remember that everyone’s experience with Parkinson’s is different, and treating it is about targeting the symptoms,” he says. “The most important thing is getting a good evaluation by a neurologist or Parkinson’s expert to make sure you’re on the right path.”

    End-Stage Parkinson’s: What to Expect

    Parkinson’s disease is a progressive neurodegenerative disorder that causes dopamine levels to drop. When most people think about the symptoms of Parkinson’s disease, they picture tremors, muscle stiffness, slow movement, and loss of balance. These symptoms are present in the early stages of Parkinson’s disease.

    Parkinson’s disease affects each individual differently. Some people are diagnosed with Parkinson’s disease early in life and remain in the early stages for many years. Others will skip stages or rapidly progress to end-stage Parkinson’s disease.

    What is End-Stage Parkinson’s Disease?

    Regardless of how long it takes to get there, when patients reach stage four of Parkinson’s disease, their symptoms become debilitating. Patients with stage four Parkinson’s disease have visible bradykinesia and rigidity. In most cases, stage four patients need assistance to walk, stand, and move.

    When patients reach stage five – the final stage of Parkinson’s disease – they will have severe posture issues in their back, neck, and hips. They will require a wheelchair and may be bedridden.

    In end-stage of Parkinson’s disease, patients will also often experience non-motor symptoms. These can include incontinence, insomnia, and dementia. Some medications used to treat Parkinson’s disease can cause hallucinations. This is seen more frequently if the patient also has dementia.

    Hospice Eligibility for Parkinson’s Disease

    Due to the progressive nature of Parkinson’s disease, it can be challenging for families to know when their loved one is eligible for the support of hospice care. If a loved one has been diagnosed with six months or less to live or if they have experienced a decline in their ability to move, speak, or participate in the activities of daily living without caregiver assistance, it is time to speak with a hospice professional about next steps.

    Some of the things that that determine hospice eligibility for Parkinson’s disease include:

    • Difficulty breathing including dyspnea at rest or the need for supplemental oxygen at rest
    • Rapid progression to wheelchair or bed bound
    • Unintelligible speech
    • Inability to perform Activities of Daily Living (ADLs) without assistance
    • Inability to eat or drink sufficiently
    • Complications including pneumonia, sepsis, pyelonephritis, decubitus ulcers
    • Additional comorbidities

    Hospice care is covered by Medicare, Medicaid, and most traditional insurance plans at no cost to the family. All medications, medical equipment, and medical supplies related to the patient’s terminal illness will be provided at no cost. In addition, Crossroads Hospice & Palliative Care will coordinate a plan of care with the patient’s physician and family to ensure all of their physical, emotional, and spiritual needs are met.

    If an individual with end-stage Parkinson’s disease is not yet eligible for hospice care, they may benefit from Crossroads’ palliative care program which partners with the patient’s physician to provide home visits from a nurse practitioner and social worker. These visits can be especially helpful if the patient is no longer able to walk on their own, making visits to the doctor’s office more challenging.

    Plan Ahead

    It can be empowering for patients who have been diagnosed with Parkinson’s disease to make their end-of-life wishes known early in the disease progression by creating an advance directive and establishing a durable power of attorney to ensure their healthcare wishes are followed.

    Hospice care can provide invaluable support to families as their loved one’s condition declines. To learn more about the care we offer to patients with Parkinson’s disease, please call 1-888-564-3405.

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