Parkinsonisms – Standing up to Parkinson's

Mindset

I am excited about some research news that was shared at a BYU Forum yesterday. Please take time to listen to this facinating discussion about the scientific discoveries of some substances that are now going to human testing, looking very promissing for reversing the protein folding in the brains of Patients with ALS, Parkinsons and alzymers and other neurological imparements.

https://www.youtube.com/watch?app=desktop&v=JkfuvwqcEcw

My researching Dr. Paul Alan Cox brought me to a Ted presentation at:

https://brainchemistrylabs.org on the ‘about’ page. Here is a quote from the page.: “We have only one wish at the Institute for Ethnomedicine: to discover new treatments for serious illnesses. This focus has led to the discovery of two promising new drugs for ALS, Alzheimer’s, Parkinson’s and other tangle diseases.”

I am excited because of the inclusion of some of the same ingredients in our LuminAloe formula as mentioned in the Forum titled “Exploring Nature’s Curiosity Cabinet”

From the website..https://ascendsciences.net Organic Yam Powder

(Dioscorea Villosa) powder – is naturally high in the chemical diosgenin; which in a laboratory can be converted into estrogen. Wild Yam is considered a phytoestrogen food, meaning it comes from plants used to produce estrogen therapy and relief of menstrual-related conditions.

The diosgenin in Wild Yam has been studied extensively and research suggests it supports healthy blood sugar levels. Other respected studies further suggest it is also antiproliferative – which means it may help keep unhealthy or DNA-damaged cells in check. Yet another study suggests diosgenin may support healthy HDL production and help stifle unhealthy LDL production.

Traditionally, Wild Yam was used as an antispasmodic for colic in babies and some people actually call it colic root. However, most people use it due to the DHEA (dehydroepiandrosterone) it contains.”

Conversation on ideation

Please read this discussion and offer your own thoughts. @mckchart said :

I asked the same question (why me ) but get one thing straight it’s not a death sentence so be very positive and make sure you don’t let it get you down ,many a famous person has thrown in the towel and done the unthinkable ,just make sure you have someone to talk to when things get on top of you …….Parkinson’s educator ( feel free to contact me )

……………………………… Here is @pdpatient’s response :

@mckchart, the “unthinkable” was excellently phrased by you and I couldn’t have said it better. However, you have inadvertently opened the proverbial pandoras box for some PwP’s such as me.

I was formally diagnosed in the early summer of 2014 by an MDS af the University of Columbia, NYC. I fell into a rut and things went ft bad to worse and I was contemplating the “unthinkable,” which I really hadn’t thought through. My son was 14 and my daughter was 9 and I was the only breadwinner of the family. My only concern for my family was that I would need to die in such a way that it could not be labeled as a suicide. I had my policy long enough, but I could not trust in the system to honor the payout for a suicide.

Around that time, my most favorite movie actor – Robin Williams had also received a bed diagnosis . I was devastated. Next thing I heard, he had committed suicide. Oops. I have said the “unthinkable,” but it is time for us to face the monster head on and find a way to make this widely known to PwP’s, newly diagnosed PwP’s and their families.

Thankfully, my family came to my rescue and I agreed to take powerful medications that brought me back from the brink. I survived and my family is doing well still. I am grateful to God and the Universe for everything that I have been fortunate to receive despite my perception that others are more deserving than I. After all there are almost 8 billion people on this planet and I am only one of the lucky ones that is still alive

I learned along the way that life doesn’t end with a Parkinson’s diagnosis. Every doctor that I have met has told me that I was not facing a death sentence. True. However, what they don’t say is that the possibility of suicide in newly diagnosed PwP’s is extremely high. This is an existential problem that is overwhelming in its impact and understated in its awareness.

Unfortunately, I am still haunted by the ghosts of this seemingly “easy way out” or so as it seems. It is a path chosen by many and it rears its ugly head once in a while when the symptoms get worse.

This is a topic that is ripe for involved and in depth discussion.

…………………………… P Bear’s response

I do not expect to do myself in over Parkinson’s. However, at one time I had an uncontrolled chronic pain condition that did cause suicidal ideation.

Each person’s circumstances are unique. It is important to tend to our responsibilities. That said, if someone’s health situation is such that they deem it fitting and proper to leave, it is not my place pass judgment on that decision.

I get that your mention of income is in the context of why it was appropriate for you to stay. However, income is not a measure of worthiness, and a more modest description would be preferable in my opinion.

……………………………. Sharon provided “

You might want to refer to this Korean study found in science direct.

sciencedirect.com/science/a…

“Suicide risk in PD patients is approximately 2 times higher than that in the general population. Psychiatric disorders, and also L-dopa medication need further attention with respect to suicide.”

Another good overview can be found in Neuropsychiatry Review

jnnp.bmj.com/content/90/7/822

“Suicide is consistently listed among the top 10 causes of death in the USA, with rates steadily climbing throughout the 21st century and reaching an annual rate of 13.4 deaths per 100 000 in 2016.6 7 It is a dominant cause of mortality among the elderly and persons with neurological diseases including stroke,9 Huntington’s disease10 and epilepsy.”

” Depression in particular is common in PD, with one meta-analysis suggesting that 17% of PwP suffer from major depressive disorder and 35% suffer from clinically significant depressive symptoms.”

In contrast, suicide is not a major cause of PD death (which are falls and pneumonia.)

Atypical

Atypical parkinsonisms are conditions in which an individual experiences some of the signs and symptoms of Parkinson’s disease (PD) — tremor, slowness, rigidity (stiffness), and/or walking and balance problems — but does not have PD. Atypical parkinsonism can be due to certain medications (some anti-nausea and antipsychotic drugs), other brain disorders (repeated head injury or multiple small strokes) or neurodegenerative diseases.

Parkinson’s Plus

The neurodegenerative diseases, which cause damage or death of brain cells, include corticobasal degeneration, Lewy body dementia, multiple system atrophy and progressive supranuclear palsy. These conditions are often referred to as “Parkinson’s plus” because they mimic PD but have extra associated symptoms (the “plus”). They can be misdiagnosed as Parkinson’s disease because no blood or imaging test can, on its own, make a definitive diagnosis. (As with PD, the diagnosis is based on a person’s medical history and physical examination.) Early in the course, people with Parkinson’s plus syndromes also may get some benefit from levodopa, the drug most commonly used to treat PD. A poor response to levodopa, development of additional symptoms and more rapid progression of disease may eventually differentiate Parkinson’s plus from PD, although it can take years for these differences to emerge. As with PD, no disease-modifying therapy has been discovered for any of the neurodegenerative atypical parkinsonisms so treatment is symptomatic and supportive.Corticobasal Degeneration (CBD)Lewy Body Dementia (LBD)Multiple System Atrophy (MSA)Progressive Supranuclear Palsy (PSP)

Management of Parkinson’s Plus

These diseases are complex conditions that progress over time. As ongoing symptoms worsen and new symptoms arise, a person’s needs will change and caregivers’ roles and responsibilities will evolve. A team approach involving the person with disease, caregivers, family members and multiple medical professionals, is necessary to address the multitude of symptoms. As with PD, no disease-modifying therapy has been discovered for the neurodegenerative atypical parkinsonisms. Treatment relies on medications to lessen symptoms, allied health care services, assistive devices (canes or walkers) when necessary and caregiver support. Palliative care specialists can be especially helpful consultants for managing symptoms and coordinating goals of care.

Levodopa is usually the initial therapy for motor symptoms, although most people do not get a significant or long-term response. Other Parkinson’s medications are sometimes used in conjunction with or instead of levodopa, but in general these are not very effective either. For dystonia, Botox injections can be helpful, and for associated non-motor symptoms (such as memory, behavioral or sleep disturbances), doctors may prescribe a variety of other medications.

Physical and occupational therapy are beneficial, specifically for dystonia, gait and balance problems, and falls. In earlier stages of disease, therapists can develop programs aimed at maintaining mobility, preventing falls or falling in ways to minimize injury. They can also assess the need for a cane or walker. In advancing disease, therapists can teach exercises to maintain joint range of motion, evaluate the home for safety and suggest modifications or adaptive equipment (such as shower grab bars or a raised toilet seat), and determine the appropriate type of wheelchair if one is necessary.

Speech therapists can recommend language exercises for speech disturbances and dietary and/or mealtime adjustments for swallowing problems. If swallowing problems are particularly severe (leading to weight loss, choking or pneumonia), your therapist or doctor may discuss starting a feeding tube. While not always required, it’s worth thinking about this possibility early on so that a person (and their caregiver’s) thoughts can be taken into full consideration.

Throughout the course, social workers can provide educational resources, link to support groups and assist with finding in-home care services or alternative living situations. Palliative care providers can be consulted at any point for help with managing symptoms and determining goals of current and future care. In conjunction with a person’s movement disorder specialist, palliative care experts can aid in optimizing medical therapy while lending extra emotional and spiritual support, and c

https://www.michaeljfox.org/understanding-parkinsons/living-with-pd/topic.php?atypical-parkinsonism

It is a process

It took me a while, but I think I figured out why I was having so many stutter steps and near falls. You may recall I said that I can no longer skip. I have been doing little jumps on the WBV machine since I went to therapy. But until this week, I was jumping with both feet at the same time. When I decided to jump one foot at a time, I discovered it has been my left foot doing all the work. I still can’t get my right foot off of the ground as I attempt to hop on the one foot.

This revelation led me to the conclusion, that is why I have been experiencing so many stumbles. I out of habit, always attempted to start out with my right foot! Yesterday, I made a concentrated effort to step out with my left foot first. To my delight, I found that by applying this strategy, I did not stutter step or stumble at all.

I celebrate each little victory. 🙂

Knock on Wood

Written: Feb 2020 Posted:3/17

I experience two totally unrelated conditions which cause me consternation.

* One is a Parkinsonism: I gasp. That is to say I suddenly (without any warning) intake a large gasp of air very quickly filling my lungs…and then sigh it out. Typically it goes unnoticed or John asks me, ‘Are you okay?’ But once in a while it happens while I have liquid to my lips or near, as happened when I was rinsing my hair and accidentally sucked in shampoo. Most recently I gasp/choked on apple cider vinegar, lemon juice and water…after which I coughed for probably the next five hours.

* The second has no link to Parkinson’s as a cause: I think they are esophageal spasms. My father and my twin sister both needed to be cautious with the size of bites they took and frequently had to wait for the muscles controlling the esophagus to relax so the blockage could pass. They each had their throats stretched by medical professionals multiple times. They reported the procedure was very helpful, but the benefits wore off over time. I have a referral for a Gastroenterology specialist on March 25th to discuss these and other issues. (If the virus hasn’t closed them down… before my appoint.)

The doctor was wrong when he predicted to my father, “You’ll most likely die with a piece of meat in your throat.” My Father died at age 94 from a condition totally unrelated to his choking problems. I eat slowly enough that my food rarely causes a problem. When I have gotten in trouble, it has been as I attempt to swallow my prescribed medications and supplements. I have made adaptions to my protocol… I put a single capsule in applesauce, or yogurt or in a spoonful of a Metamucil fiber preparation. Then after a capsule has slid down, I take a drink of water. But as I relate what happened a past Tuesday, I question what other precaution might I take? Perhaps sleep with my head slightly elevated?

Tuesday morning: I had swallowed my very first capsule bathed in a teaspoon full of yummy… and as I picked up the glass for a drink to flush it, I noticed a tightening of my esophagus… probably 3 inches lower than the collar bone… so I hastily took my sip of water, but I was too late, and the water remained above the spasm. It nearly did me in! Besides the pain caused by the spasm, I had to sit really tall, trying to keep the fluid from back flowing into my wind pipe. As the body tries to clear the blockage, little spurts of air bubble up, raising the level of liquid, causing me to feel panic.

As the body strives to clear the blockage, and reflexes attempting to purge the digestive track push: involuntarily pushing in both directions. I’ve heard; a person in the throes of death frequently soil their clothing. Been there, done that. I don’t need that one on my bucket list.

I was shocked by the comment elicited from the very first person (outside of our immediate family) that I confided the doctor had given me the diagnosis of PD: She said, “My father had Parkinson’s… and he died from choking while my mother was feeding him!” Shortly after her comment, a search on the internet revealed the number one contributor to mortality for PwP is aspiration pneumonia: a lung infection that develops after you aspirate (inhale) food, liquid, or vomit into your lungs. You can also aspirate food or liquid from your stomach that backs up into your esophagus.

In many cultures, it’s a common superstition for people to knock their knuckles. It is a tradition of literally touching, tapping, or knocking on wood, or merely stating that one is doing or intending to do so, in order to avoid “tempting fate” after making a favorable or unfavorable prediction or boast.

Rather than knocking, I chose to be proactive. I took my physician’s advice and got a pneumococcal vaccination that reportedly can help protect against infection by 23 types of pneumococcal bacteria, which are common and often cause serious illnesses.

Addendum… March 11 ………… “Worry is like a rocking chair___goes nowhere.”

Two more esophageal spasms this month… have left my chest (and airway sore) and me feeling slightly panicked.

The first one happened in the night during an attack of dystonia in my feet and calves which had wakened me from, a deep sleep. Dystonia, for me, is severe cramping which twists my toes and runs up my legs. Anyway, while I was awake, i also experienced the distress of an esophageal spasm. Although very painful, no fluid was involved.

The next morning, I had finished my breakfast and didn’t have anything in my mouth when another spasm began. As the spasm continued, I was having trouble with moisture blocking my airway. I figured out that to solve the distress, I needed to spit out the saliva as it accumulated, in order to keep breathing.

I have been looking at AND DOING …breathing techniques and exercises to improve lung capacity. I recommend everyone do the same, during the threat of perilous times.

Types (Atypical Parkinsonisms)

Continued from article: (Posted on August 13, 2018 by MyParkinsonsTeam)

Some types of parkinsonian movement disorders have similar motor symptoms as Parkinson’s disease and are also caused by progressive damage to the brain, but do not improve when treated with medications that are effective in Parkinson’s disease. These conditions are known as atypical parkinsonisms or “Parkinson’s plus.” Atypical parkinsonisms may show slight differences in motor symptoms from Parkinson’s disease. For instance, motor symptoms may start on both sides of the body instead of one side, or problems with thinking, memory, and mood may occur first, before motor symptoms.

Multiple system atrophy (MSA)

MSA is a rare condition with about 1,900 new cases diagnosed each year in the U.S. MSA is also known as Shy-Drager syndrome (SDS). MSA seems to affect men and women at equal rates. MSA has motor features in common with other types of Parkinson’s but is more likely to present with symptoms related to the autonomic nervous system. The autonomic nervous system regulates blood pressure, digestion, and temperature, and people with MSA are more likely than those with Parkinson’s disease to experience bladder or bowel problems, excess sweating, and orthostatic hypotension (fainting or dizziness after standing).

In MSA, an abnormal protein called alpha synuclein builds up in regions of the brain including the basal ganglia, the cerebellum, and the brain stem. Alpha synuclein buildup also occurs in Parkinson’s disease, but is usually seen later in the course of the condition, and mostly confined to the substantia nigra region of the brain. MSA affects different types of brain cells than those affected by Parkinson’s.

There are two subtypes of MSA:

MSA-P
MSA-P more closely resembles Parkinson’s, but it progresses more quickly and stops responding to Parkinson’s drugs sooner.

MSA-C
In MSA-C, progressive loss of coordination and balance are prominent. People with MSA-C may show an “action tremor,” or tremor that happens when they reach for an object. Muscle weakness can cause slurring and trouble swallowing. MSA-C can develop as early as a person’s 40s.

Progressive supranuclear palsy (PSP)

Also known as Steele–Richardson–Olszewski syndrome, PSP causes motor symptoms very similar to those seen in Parkinson’s, but they tend to be much more severe and progress much more quickly. Most people develop severe disabilities within three to five years of a PSP diagnosis.

In addition to motor symptoms, people with PSP are likely to have mood and personality changes and cognitive difficulties. Tremors are rare in PSP. In progressive supranuclear palsy, people are more likely to tilt and fall backward, while people with Parkinson’s lean and fall forward.

PSP is also considered a type of frontotemporal dementia (FTD), a collection of conditions that cause progressive damage to the frontal and temporal lobes of the brain. In healthy brains, there is a normal protein called tau that helps form the structure of cells. In PSP, tau protein tangles together in abnormal clumps, and brain cells are destabilized.

Unlike other forms of parkinsonism, PSP can significantly reduce life expectancy. With treatment, a person with PSP may live 10 years after diagnosis.

Dementia with Lewy bodies (DLB)

DLB is characterized by the early development of cognitive symptoms (related to memory, attention, and thinking) and psychotic symptoms such as hallucinations. Parkinsonian motor symptoms occur later in the progression of the disease. After Alzheimer’s, DLB is the leading cause of dementia. DLB typically does not occur before the age of 65. In DLB, alpha synuclein protein builds up throughout the cerebral cortex of the brain, forming collections called Lewy bodies.

DLB is often misdiagnosed as Alzheimer’s. Symptoms of DLB may respond to medications for Parkinson’s or Alzheimer’s, but certain Alzheimer’s medications carry high risk for dangerous side effects if given to those with DLB. DLB and Parkinson’s disease dementia have many features in common, and together they are known as the Lewy body dementias.

Corticobasal degeneration (CBD)

CBD, also called corticobasal syndrome, is a rare type of parkinsonism that usually progresses more quickly than Parkinson’s disease. In CBD, brain cells in the cerebral cortex and the basal ganglia shrink and die. CBD affects men and women approximately equally. Symptoms usually begin between the ages of 50 and 70. Corticobasal degeneration may be considered a type of frontotemporal dementia (FTD).

Motor symptoms in CBD are nearly always asymmetrical – occurring on one side of the body. CBD may also cause cognitive and behavioral symptoms. People with CBD may also have Parkinson’s disease, dementia with Lewy bodies, progressive supranuclear palsy, frontotemporal dementia, and Alzheimer’s-like dementia

Types (Secondary Parkinsonisms)

Continued from article: (Posted on August 13, 2018 by MyParkinsonsTeam)

In some cases, Parkinson’s symptoms are not a disease in themselves, but are caused by certain medications or by other conditions. These types of parkinsonism are referred to as secondary parkinsonism. Unlike Parkinson’s disease, secondary parkinsonisms are usually not progressive and do not respond to the same drugs. Secondary parkinsonisms include drug-induced and vascular parkinsonism.

Drug-induced parkinsonism

Certain medications can cause parkinsonian symptoms as a side effect. Drug-induced parkinsonism is the second-leading cause of parkinsonism after Parkinson’s disease.

Drug-induced parkinsonism may be caused by a range of medications, including:

Antipsychotics such as Haldol (Haloperidol) and Thorazine (Chlorpromazine)
Anti-nausea medications such as Reglan (Metoclopramide)
Antidepressants in the serotonin specific reuptake inhibitors (SSRI) class such as Prozac (Fluoxetine) and Zoloft (Sertraline)
Calcium channel blockers such as Flunarizine and Cinnarizine (not approved for use in the U.S.)
Reserpine
Xenazine (Tetrabenazine)

These drugs do not cause parkinsonism in every person who takes them.

The symptoms of drug-induced Parkinson’s are usually temporary. Symptoms typically fade and disappear within a year of stopping the medication that caused the condition, sometimes within weeks. In some cases, the symptoms of drug-induced parkinsonism are permanent, but they are usually not progressive like other forms of parkinsonism.

Vascular parkinsonism

Vascular parkinsonism is caused by small strokes in the brain where blood vessels have become blocked. Also known as arteriosclerotic or multi-infarct parkinsonism, vascular parkinsonism is usually limited to the legs. Unlike other forms of parkinsonism, vascular parkinsonism appears suddenly rather than gradually and is not usually progressive. Hypertension (high blood pressure), high blood cholesterol, diabetes, and heart disease can contribute to the development of vascular parkinsonism. Unlike most other types of Parkinson’s, vascular parkinsonism can often be seen in computerized tomography (CT) or magnetic resonance imaging (MRI) scans of the brain.

Typical Parkinson’s medications do not improve symptoms of vascular parkinsonism. Treatments are aimed at preventing additional strokes and may include Aspirin or blood thinners and recommendations to stop smoking, eat a diet low in salt and saturated fat, and get more exercise.

Types (Parkinsonism Syndrome)

Lowrey… stated about this article: ( Posted on August 13, 2018 by MyParkinsonsTeam) Volumes of objective, clear and succinct info about PD, with out the border line hysteria often associated with cognitive impairment. Most refreshing! Many thanks for sharing this.

I agree! But, knowing my readers, I have broken the article into three days, to hopefully avoid overload and ‘shut down’ without reading… day 2 will be “Secondary Parkinsonism” Day 3 outlines five “Atypical Parkinsonisms.”

Parkinsonism is a syndrome, or collection of symptoms, characterized by motor issues – bradykinesia (slowed movements), tremors, loss of balance, and stiffness. There are many types of parkinsonism classified by their cause and how they progress. Knowing which type of Parkinson’s someone has helps neurologists prescribe effective treatments and better predict how the disease will progress.

Parkinson’s types

There is no conclusive test to identify what type of parkinsonism someone has. For some people, years may elapse between experiencing the first symptoms and receiving a definitive diagnosis of a specific type. Since all parkinsonisms share similar motor symptoms, Parkinson’s diagnosis can be very difficult. A correct diagnosis is more likely when performed by an experienced neurologist who specializes in movement disorders. Some people have multiple chronic conditions, making it difficult for doctors to identify whether parkinsonian symptoms are caused by a disease or a medication. In some cases, it is possible to have more than one type of parkinsonism.

Parkinson’s disease

The most common type of parkinsonism is Parkinson’s disease (PD), which accounts for about 80 percent of cases. No one is sure what causes most cases of Parkinson’s disease, so it is also known as idiopathic Parkinson’s. Idiopathic means “cause unknown.”

Deep inside the brain, regions called the basal ganglia and substantia nigra work together to ensure that the body moves smoothly. The substantia nigra produces a neurotransmitter – a chemical that helps nerves communicate – called dopamine. Messages sent by the brain to muscles to cause movement pass through the basal ganglia with the help of dopamine. In Parkinson’s disease, cells in the substantia nigra gradually stop producing dopamine and die off. With too little dopamine, the basal ganglia cannot facilitate movement as well. Researchers believe parkinsonian symptoms begin when the level of dopamine falls to about half of normal levels.

Subsets of Parkinson’s disease include:

Late-onset Parkinson’s disease

Symptoms develop after age 50.

Most PD is late-onset.

Early-onset or young-onset Parkinson’s disease

Symptoms develop before age 50.

Accounts for approximately 10 percent of PD cases

Tends to have slower progression, more medication side effects

Dystonia (painful spasms and abnormal postures) is more common in early-onset PD.

Juvenile-onset Parkinson’s disease

Symptoms develop before age 20.

Extremely rare

Often strong family history of Parkinson’s

Familial Parkinson’s

Directly caused by genetic variants inherited from parents

Accounts for 10 to 15 percent of Parkinson’s disease cases

Parkinson’s disease dementia (PDD)

Between 50 and 80 percent of those with Parkinson’s disease eventually develop Parkinson’s disease dementia. On average, most people begin to develop PDD about 10 years after they receive a Parkinson’s disease diagnosis. PDD is often confused with Alzheimer’s and dementia with Lewy bodies. Parkinson’s disease dementia is usually diagnosed when motor symptoms occur first, at least a year before dementia symptoms.

Antipsychotics such as Haldol (Haloperidol) and Thorazine (Chlorpromazine)

Anti-nausea medications such as Reglan (Metoclopramide)

Antidepressants in the serotonin specific reuptake inhibitors (SSRI) class such as Prozac (Fluoxetine) and Zoloft (Sertraline)

Calcium channel blockers such as Flunarizine and Cinnarizine (not approved for use in the U.S.)

Reserpine

PSP: Progressive Supraneuclear Palsy

No… I do not think I have the diagnosis… But since a person in one of the online communities for pwp typed she just has her Diagnosis changed to PSP and the signs and symptoms overlap with other neurodegenerative diseases, I felt I should document it.

Research is now showing that all symptoms of neurodegeneration are likely linked by common pathology, so that research may eventually unlock the secrets of more common illnesses like Alzheimers and Parkinson’s

“Last month, a terrific article was published on progressive supranuclear palsy (PSP) in a nursing journal. The article shares a list of symptoms in the four stages of PSP from thePSP Association, based in the UK. The four stages are:

* early stage
* mid stage
* advanced stage
* end of life stage

The symptoms are copied below. I’m sure you can overlook the British spellings.”

Early stage:
May present via the fracture clinic, falls services, eye specialist or speech and language therapist. The early stage typically spans years 0-1.

> Ambulant.
> Occasional falls.
> Unsteadiness and poor balance.
> Possible visual problems affecting ability to read.
> Voice changes, for example reduced volume.
> Mood changes.
> Reduced socialising.
> Changes in mood and behaviour, including apathy and anxiety.

Mid stage:
Many people reach this stage before diagnosis. Consider discussing advance care planning and advance decisions to refuse treatment. Consider referral to palliative care services. The mid stage typically spans years 2-3.

> Ambulant with aids.
> High risk of falls and injury.
> Visual problems affecting self-care abilities, for example eating and walking as unable to move eyes to see.
> Speech increasingly unintelligible.
> Inability to initiate conversation.
> Impulsivity (risky or impulsive behaviour).
> Apathy.
> Dysphagia.
> High level of supervision required.
> Increasingly socially withdrawn.

Advanced stage:
Patients should be on GP palliative care register and have access to specialist palliative care.
The advanced stage typically spans years 3-6.

> Mobility significantly compromised, probably chair bound requiring a wheelchair for mobility.
> Significant visual problems.
> Significant muscle stiffness.
> Significant communication problems, but probably still able to understand.
> High risk of aspiration and pneumonia as a result of dysphagia.
> Pain.
> Increasing periods of sleepiness.
> Incontinence.
> Severely withdrawn socially.
> Dependent for most or all aspects of care.

End of life stage:
This stage is difficult to detect, but may be indicated by reduced levels of consciousness, inability to eat or drink, acute infection, a fall or major fracture, and rapid and significant weight loss. The end of life stage typically spans 6-8 weeks.

> Severe impairments and disabilities.
> Rapid and marked deterioration in condition.
> Decisions with regard to treatment interventions may be required, considering an individual’s previously expressed wishes (advance decisions to refuse treatment).TH

Orthostatic tremor

I learned about a type of tremor I hadn’t heard about, before… from a team member with a MSA diagnosis, typing on the myparkinsonsteam.com site.

“Orthostatic tremor (OT) is a rare syndrome characterized by unsteadiness on standing due to a high-frequency tremor involving the legs. Symptoms usually start in the sixth decade. Typically, the symptoms rapidly improve on sitting or walking, and the need to sit down or to move can be so strong that patients avoid situations where they have to stand still. A polygraphic recording of a fast and synchronous tremor of the legs, between 13 and 18Hz, is mandatory to confirm the diagnosis of OT. Many patients also suffer from tremor, often involving lower frequencies, of the face, hands, or trunk. Recent studies suggest that this is perhaps due to subharmonics of the high-frequency tremor spreading through the body. Most cases of OT seem to be idiopathic, though symptomatic forms have been occasionally described. Several cases of OT have been reported in Parkinson’s disease.”

…..What follows was written by a DR in the Neurology Dept at Mayo Clinic…..

“The term tremor implies an involuntary, rhythmic body movement. Orthostatic tremor affects the muscles in a person’s legs, and sometimes also radiates from the legs upward to other parts of the body. The term “orthostatic” refers to standing. Orthostatic tremor occurs when a person stands up. The condition can be difficult to diagnose and, although medication helps some people, it can be a challenging condition to treat effectively.

Orthostatic tremor is an uncommon disorder that can significantly affect the quality of life for those who develop it. Usually, the main symptom is a feeling of leg shakiness and unsteadiness when standing still. Orthostatic tremor can create difficulty in performing daily activities that require a person to stand freely without support. For example, standing in line at a store, standing at a kitchen counter to prepare a meal, or standing at a workbench to enjoy a hobby can be very hard or impossible for people who have orthostatic tremor. Most people don’t fall as a result of the condition. However, approximately 15 percent become so unsteady that falling is a problem.

Orthostatic tremor often starts shortly after standing and stops when a person sits or lies down. Contrary to what common sense might normally suggest, typically the tremor decreases when a person is walking. Leaning on an object such as a chair or a countertop when standing also may help reduce the tremor.

Orthostatic tremor is a high-frequency tremor, which means the tremor rhythm is very rapid and there can be as many as 16 to 20 tremor cycles in one second. That’s significantly faster than other tremor types. For example, essential tremor usually involves eight to 12 tremor cycles per second, and the tremors associated with Parkinson’s disease typically occur at a rate of four to eight cycles per second.

Because the tremor is so fast, orthostatic tremor can be difficult to see. That can make the diagnosis challenging. In some cases, when patients report that they feel unsteady on their feet, the physicians may overlook the leg tremor and may pursue other possible causes of unsteadiness. One additional diagnostic strategy is to place a hand on the thigh, feeling for the tremor; however, the clinician must have an appropriate level of suspicion.

If a physician suspects orthostatic tremor, the diagnosis can be confirmed by assessing the electrical activity in the leg muscles. At Mayo Clinic, that analysis is conducted in our Movement Disorders Neurophysiology Laboratory. During orthostatic tremor, the leg muscles show no electrical activity when a person is sitting. When he or she stands up, though, the muscles immediately begin firing rhythmic bursts of electrical activity.

Because the cause of orthostatic tremor is unknown, a cure currently isn’t available. Instead, treatment focuses on the symptoms. Once the condition is diagnosed, the first line of treatment is the medication clonazepam or a related drug. This medication moderately to markedly reduces orthostatic tremor in about one-third of people who have the disorder. For some, it eliminates orthostatic tremor almost entirely.

Unfortunately, for those who don’t respond to clonazepam, no single alternative medication has a high likelihood of decreasing orthostatic tremor. Although numerous other medications may be tried, these may be no more than mildly helpful.

Fortunately, orthostatic tremor tends not to be a progressive disorder. Once the symptoms are fully developed, it doesn’t progress to a more pervasive neurological condition. It does tend to be persistent, however, and usually does not resolve on its own.”

— J. Eric Ahlskog, M.D., Ph.D., Neurology, Mayo Clinic, Rochester, Minn.