QUOTE FOR WEDNESDAY:

“April is National Donate Life Month, a time dedicated to raising awareness about organ, eye and tissue donation, while also honoring donors and encouraging individuals to register as donors. Established by Donate Life America, this observance highlights the critical need for donors and celebrates the transformative impact of donation on recipients’ lives.​

As of March 2025, more than 103,000 people in the United States are on the national transplant waiting list, hoping for lifesaving organ transplants. Alarmingly, another person is added to this list every eight minutes. Despite the generosity of donors, the demand continues to outpace the supply, leading to an average of 16 deaths each day among those awaiting transplants.

In 2024, the United States witnessed a record-breaking 48,000 organ transplants, reflecting an ongoing increase in donation and transplantation efforts. Each donor has the potential to save up to eight lives and enhance over 75 more through tissue donation. Kentucky alone has made significant strides in organ donation. In 2023, the Kentucky Organ Donor Affiliates (KODA) reported a 25% increase in organ donations and a 20% increase in organ transplants compared to the previous year. This led to 299 organ donors facilitating 729 transplants, saving 693 lives—the highest number recorded in any given year for the state. However, despite these advancements, more than 1,000 Kentuckians are still awaiting lifesaving organ transplants.

Registering as an organ, eye, and tissue donor is a straightforward yet profound way to contribute. Individuals can sign up through their state’s donor registry or at the Department of Motor Vehicles when obtaining or renewing a driver’s license.”

Ephraim McDowell Health

(National Donate Life Month: A Time to Save Lives Through Organ Donation – Ephraim McDowell Health)

National Donate Life Month – offering organs (ex. eyes or other tissues)!

WHY DONATE:

Organ, eye and tissue donation provides lifesaving and healing opportunities to the nearly 120,000 people waiting for transplants nationwide. Over 2,500 of those people waiting for a lifesaving transplant live right here in our community! Organ, eye and tissue donation allows others to breathe, to see, to move and to live. Donation is a way to give the ultimate gift – the gift of life.

ORGAN DONATION PROCESS:

When the National Organ Transplant Act (NOTA) was signed into law in 1984, it created the national Organ Procurement and Transplantation Network (OPTN) establishing an organ donation process for matching donor organs to waiting recipients. The OPTN standardized the process for donating organs across the country and created the system of federally-designated Organ Procurement Organizations (OPOs), like Donor Alliance.

The OPTN is managed under contract by the United Network for Organ Sharing (UNOS). UNOS establishes allocation policy and manages the national transplant waiting list, matching donors to recipients 24 hours a day, 365 days a year. UNOS also maintains the database that contains all organ transplant data for every transplant that occurs in the U.S.

DIAGNOSIS:

There are numerous laws, regulations and standards that govern how and when a medical professional can make an official declaration of death. What is most important to know is that hospitals and emergency medical professionals will make every effort to save a patient’s life regardless of their status as a donor.

Death can occur in one of two ways: cardiac death, when the heart is no longer able to beat on its own, and brain death, which is the irreversible loss of function of the brain, including the brain stem.

Organ donation after Brain Death:

According to the Uniform Determination of Death Act, brain death is defined as the irreversible cessation of all functions of the entire brain, including the brain stem. A brain-dead person is dead, although his or her cardiopulmonary functioning may be artificially maintained for some time.

Because of the neurological nature of brain death, a controlled and extensive clinical exam occurs to make that final declaration. Brain death is final and finite; it is not in the same thing as a coma or persistent vegetative state.

Brain death determination is rare and occurs only in about 1 out of every 100 hospital deaths.

Organ Donation after Circulatory Death:

Organ donation after circulatory death (DCD) is the type of donation that was used in the early years of organ donation. Before brain death criteria was established, DCD and living related donation were the only options.

This type of donation occurs when a patient has an illness from which he or she cannot recover. The patient is not brain dead, but has no hope of recovery.

If the family is interested in donation and has made the decision to withdraw treatment, that process will occur in the operating room instead of the hospital room. The time from the family authorizing the process to the removal of support is typically no fewer than eight hours, due to the need for blood tests and other arrangements.

Once in the OR, if the patient’s heart stops within the designated time frame for donation, the team waits for several minutes to ensure that the heart has ceased functioning. At this time, a physician from the hospital, not the organ recovery team, will pronounce the patient dead. Then, the surgery to procure the organs for donation begins.

While DCD increases the number of organs available for transplant, this type of donation does not allow for organs other than the liver and kidneys to be procured in most cases. It is rare for the heart and lungs to be recovered.

How to match a donor to the best candidate who needs a organ:

The system uses this information to match the medical characteristics of the candidates waiting against those of the donor. The system then generates a ranked list of patients who are suitable to receive each organ. This list is called a “match run.”

Factors affecting ranking may include:

  • Tissue match
  • Blood type
  • Length of time on the waiting list
  • Immune status
  • Distance between the potential recipient and the donor
  • Degree of medical urgency (for heart, liver, lung and intestines)

The organ is offered to the transplant center for the first person on the list. At times, the top transplant candidate will not get the organ for one of several reasons. When a patient is
selected, he or she must be available, healthy enough to undergo major surgery and willing to be transplanted immediately. Also, a laboratory test to measure compatibility between the donor and potential recipient may be necessary. If the organ is refused for any reason, the transplant center of the next patient on the list is contacted. The process continues until a match is made. Once a patient is selected and informed and all testing is complete, surgery is scheduled and the transplant takes place.

 

QUOTE FOR TUESDAY:

“April is Autism Awareness Month, an international event established to increase understanding and acceptance of individuals with autism. At The Deron School, we provide educational resources for children and young adults with autism.

“History Fact #1: Autism Awareness Month Started in April 1970

Autism Awareness Month was founded in April 1970 by Bernard Rimland, Ph.D., a psychologist and autism researcher. He chose the month of April to coincide with his son’s birthday, as well as the start of spring—a time for new beginnings.

History Fact #2: President Ronald Reagan Was the First to Issue an Official Presidential Proclamation Regarding Autism

In April 1988, President Ronald Reagan issued the first presidential proclamation declaring April as National Autism Awareness Month. This was significant progress and began a new era of awareness, which opened opportunities for people with autism to live fuller and more productive lives.

History Fact #3: The Puzzle Piece Becomes a Symbol of Power for the Autism Community

The Puzzle Piece has become an internationally recognized symbol of power, strength, hope, and unity for those affected by autism spectrum disorders (ASDs). The puzzle piece was first introduced in 1963 by the National Autistic Society as part of their logo. The Puzzle Piece symbolizes the complexity of ASDs and reminds us that we are all interconnected.

History Fact #4: Autism Speaks Steps from 2004.

Autism Speaks is a global organization that works tirelessly to educate and support individuals living with autism. In 2004, they launched the Light It Up Blue campaign to bring awareness to autism. The goal was simple: get everyone worldwide—from businesses and schools to homes and public places—to light up blue in honor of Autism Awareness Month.

History Fact #5: Autism Awareness Month Goes Global

In recent years, Autism Awareness Month has become an international event. More countries are joining the cause to raise autism awareness and increase the acceptance of individuals with ASDs. This is a powerful step forward in creating a brighter future for children living with autism worldwide.

April marks Autism Awareness Month—a time to come together to support individuals living with autism spectrum disorder (ASD). Let’s use this month to celebrate the progress of those facing ASD and recognize how far we have yet to go in providing adequate resources for them.

At The Deron School, we are proud to join forces with organizations like Autism Speaks in celebrating this month.”

The Deron School of N.J., Inc.

(5 History Facts About Autism Awareness Month – Deron School)

 

Part II Autism Awareness – Related Conditions to Autism

Williams Syndrome

Williams Syndrome (also known as Williams-Beuren syndrome) is a rare genetics disorder in which a portion of DNA material on chromosome 7 is missing. The prevalence in the population is somewhere between 1 out of 10,000.

Many people with Williams Syndrome exhibit autistic behaviors. This includes: developmental and language delays, problems in gross motor skills, hypersensitivity to sounds, picky eating, and perseverating.

However, Williams Syndrome includes other symptoms that may require different or additional treatments. A diagnosis is essential to maximize quality of care.

These individuals differ from the typical autistic individual because they also have cardiovascular abnormalities, high blood pressure, elevated calcium levels, and are very sociable. They also have unique pixie-like facial features–almond shaped eyes, oval ears, full lips, small chins, narrow faces, and broad mouths.

Fragile X

Fragile X syndrome (also known as Martin-Bell syndrome) is a sex-linked genetic disorder. The exact frequency of Fragile X syndrome is unclear, but the CDC estimates that roughly 1.4 in 10,000 males and 0.9 in 10,000 females are affected by this disorder. Males afflicted with this syndrome typically have a moderate to severe form of intellectual handicap. Females may also be affected but generally have a mild form of impairment.

Approximately 15% to 20% of those with Fragile X Syndrome exhibit autistic-type behaviors, such as poor eye contact, hand-flapping or odd gesture movements, hand-biting, and poor sensory skills. Behavior problems and speech/language delay are also common features of Fragile X Syndrome.

People with Fragile X syndrome also have a number of recognizable physical features, including a high arched palate, strabismus (lazy eye), large ears, long face, large testicles in males, poor muscle tone, flat feet, and sometimes mild, heart valve abnormalities. Although most individuals with Fragile X syndrome have a characteristic ‘look’ (long face and large ears), there are some who do not have typical features.

Many hospitals and laboratories perform blood tests to diagnose Fragile X syndrome. Several treatments are recommended for individuals with this disorder, including mild medications for behavior problems and therapies for speech and language and sensory improvement. Families are advised to seek genetic counseling to understand the inheritable nature of Fragile X Syndrome and to discuss with family members the likelihood other individuals or future offspring may have this disorder.

Thank  You to Dr. Peter Jacky of Kaiser Sunnyside Hospital in Clackamas, Oregon for his comments on this article.

Landau-Kleffner Syndrome

Landau-Kleffner Syndrome is a rare form of epilepsy that manifests as a form of aphasia, (loss of language), which usually develops between 3 and 7 years. It is twice as common in males than females and is often diagnosed in conjunction with autism. Initially, these individuals have a healthy, problem-free development with normal speech and vocabulary. These individuals first lose their ability to comprehend (i.e., receptive speech) and then their ability to speak (i.e., expressive speech). These changes can occur gradually or suddenly.

People with Landau-Kleffner Syndrome have abnormal EEG patterns (i.e., brain waves) in the temporal lobe (located on the sides of the brain) and in the temporo-parieto-occipital regions during sleep. Diagnosis of this syndrome usually involves examining the person’s EEG patterns during sleep. Approximately 70% develop epilepsy; and these seizures are typically infrequent and can be either with or without convulsions.

One common characteristic of Landau-Kleffner Syndrome is the failure to respond to sounds. Thus, parents may suspect their child of hearing loss. Autistic characteristics seen in Landau-Kleffner Syndrome individuals include pain insensitivity, aggression, poor eye contact, insistence on sameness, and sleep problems.

The cause of Landau-Kleffner Syndrome is not known. Some suggested causes have been a dysfunctional immune system, exposure to a virus, and brain trauma. The prognosis is better when the onset is after age 6 and when speech therapy is started early. Several other treatments have also been shown to be beneficial for many of these individuals, such as anticonvulsant mediations and corticosteroids. There is also a surgical technique in which the pathways of abnormal electrical brain activity are severed.

Prader-Willi Syndrome

Prader-Willi Syndrome is a disorder which is sometimes associated with, but not a subtype of, autism. The classical features of this disorder include an obsession with food which is often associated with impulsive eating, compact body build, underdeveloped sexual characteristics, and poor muscle tone. Because of their obsession with food, many people afflicted with Prader-Willi Syndrome are overweight. Most individuals afflicted with Prader-Willi Syndrome have mild mental deficits.

Some of the behaviors which are common to both Prader-Willi Syndrome and autism are:

  • delays in language and motor development
  • learning disabilities
  • feeding problems in infancy
  • sleep disturbances, skin picking
  • temper tantrums
  • high pain threshold

Prader-Willi Syndrome affects approximately 1 in 10,000 people. Most individuals suffering from this disorder are missing a small portion of chromosome 15 which appears to come from the paternal side of the family. When a small portion of chromosome 15 is missing and comes from the maternal side, the person may suffer from Angelman Syndrome.

The most effective form of treatment for people suffering from Prader-Willi Syndrome is behavior modification. In general, medications do not appear to be very effective for these individuals.

Angelman Syndrome

Angelman syndrome is a genetic disorder that affects the nervous system. Initial symptoms of this disorder typically manifest in the first year of life and become more apparent through early childhood. It is estimated that Angelman syndrome occurs in roughly every one in 15,000 people. Similarly to Prader Willi Syndrome, this disorder derives from a missing portion of chromosome 15, but unlike Prader Willi, this deficit comes from the maternal side.

Angelman syndrome is commonly characterized by:

  • Mental and speech deficits
  • Speech impairment
  • Problems with motor skills and balance
  • Epilepsy
  • Small head size
  • Hyperactivity
  • Smiling, Laughing and Hand flapping
  • Difficulty sleeping

To learn more about Angelman Syndrome, please visit the Angelman Syndrome Foundation

Rett Syndrome

Rett Syndrome was first recognized by Andreas Rett in 1966 and is a neurological disorder affecting primarily females. Autopsies on the brains of these individuals indicate a pathology different from autism; however, children afflicted with Rett Syndrome often exhibit autistic-like behaviors, such as repetitive hand movements, prolonged toe walking, body rocking, and sleep problems. In most cases, there is a regression in cognition, behavior, social, and motor skills throughout their lifetime.

The prevalence of Rett Syndrome is estimated to be between 1 in 10,000 and 1 in 15,000 people.

Typical characteristics:

  • Normal development until 1/2 to 1 1/2 years
  • Behavioral, social, and cognitive regression
  • Shakiness of the torso, and possibly the limbs
  • Unsteady, stiff-legged gait
  • Breathing difficulties (hyperventilation, apnea, air swallowing)
  • Seizures (approximately 80% have epilepsy)
  • Teeth grinding and difficulty chewing
  • Stunted growth and small head
  • Severe mental deficits
  • Hypoactivity

In 1999, Dr. Huda Zoghbi and her colleagues located the gene for Rett syndrome. The gene was located on one of the two X chromosomes that determine sex. Rett syndrome results from the mutation of the gene that makes methyl cytosine binding protein, resulting in excessive amounts of this protein.

For more information about this disorder, visit International Rett Syndrome Association

Tardive dyskinesia

Tardive dyskinesia is a syndrome involving dysfunctional, involuntary movements associated with long-term, chronic use of neuroleptic medications, such as Haldol, Prolixin, and Thorazine. These drugs lead to an apparent general calming or sedative effect on the individual and are considered major tranquilizers.

Tardive dyskinesia may appear anywhere from three months to several years after initial use of these medications, and withdrawal from neuroleptics often exacerbates the symptoms.

Common tardive dyskinesia movements include, but are not limited to:

  • facial tics, grimacing
  • eye blinking
  • lip smacking
  • tongue thrusting
  • moving one’s head back or to the side
  • foot tapping
  • ankle movements
  • shuffled gait
  • head nodding

Tardive dyskinesia may lead to very serious problems, such as respiratory interference, inability to eat, oral ulcerations, and difficulty standing/walking.

Tardive dyskinesia movements may be confused with stereotypy because of the repetitive nature of both behaviors. Stereotypy refers to ritualistic, often complex behaviors, such as body and head rocking, hand-flapping, and complex hand movement patterns. Stereotypy appears to be under voluntary control. In contrast, tardive dyskinesia movements are less complex, less ritualistic, and are not volitional.

Other psychoactive drugs, such as clozaril/clozapine, have similar effects on behavior but do not produce tardive dyskinesia as neuroleptics do.

Is it Autism?

While the behavioral symptoms of the conditions above may overlap with autism, they may require different or additional treatments. Seek a diagnosis and treatment plan from a qualified medical professional before starting any form of treatment.

QUOTE FOR MONDAY:

Though the term “autism” first appeared around 1911, very little was known or medically researched about autism spectrum disorder until the late 20th century. New discoveries and advancements continue to be made today to help individuals on the spectrum achieve their full potential.

Facts about Autism

  1. Autism spectrum disorder affects 1 in 36 children.
  2. Boys are nearly 5 times more likely than girls to be diagnosed with ASD.  Girls are often underdiagnosed with autism and misdiagnosed with other conditions.
  3. Autism spectrum disorder is one of the fastest-growing developmental disorders in the United States. ASD is more common than childhood cancer, diabetes, and AIDS combined.
  4. Autism spectrum disorder affects all nationalities, all creeds, all religions, all races and both sexes. It doesn’t differentiate or affect only one group.
  5. Autism spectrum disorder is a developmental disability that often presents with challenges before the age of 3 and lasts throughout a person’s lifetime.
  6. Early identification, treatment, and support matters! Many important outcomes for children’s lives are significantly improved with early diagnosis and treatment.”

Mass General Brigham Hospital (30 Facts to Know about Autism Spectrum Disorder)

Part I Autism (ASD) Awareness-Learn how’s its diagnosed, what causes ASD, Genes R/T ASD, how s/s change in time, the treatment of ASD!

What disorders are related to ASD?

Certain known genetic disorders are associated with an increased risk for autism, including Fragile X syndrome (which causes intellectual disability) and tuberous sclerosis (which causes benign tumors to grow in the brain and other vital organs) — each of which results from a mutation in a single, but different, gene. Recently, researchers have discovered other genetic mutations in children diagnosed with autism, including some that have not yet been designated as named syndromes. While each of these disorders is rare, in aggregate, they may account for 20 percent or more of all autism cases.

People with ASD also have a higher than average risk of having epilepsy. Children whose language skills regress early in life — before age 3 — appear to have a risk of developing epilepsy or seizure-like brain activity. About 20 to 30 percent of children with ASD develop epilepsy by the time they reach adulthood. Additionally, people with both ASD and intellectual disability have the greatest risk of developing seizure disorder.

How is ASD diagnosed?

ASD symptoms can vary greatly from person to person depending on the severity of the disorder. Symptoms may even go unrecognized for young children who have mild ASD or less debilitating handicaps. Very early indicators that require evaluation by an expert include:

  • no babbling or pointing by age 1
  • no single words by age 16 months or two-word phrases by age 2.
  • no response to name
  • loss of language or social skills previously acquired
  • poor eye contact
  • excessive lining up of toys or objects
  • no smiling or social responsiveness

Later indicators include:

  • impaired ability to make friends with peers
  • impaired ability to initiate or sustain a conversation with others
  • absence or impairment of imaginative and social play
  • repetitive or unusual use of language
  • abnormally intense or focused interest
  • preoccupation with certain objects or subjects
  • inflexible adherence to specific routines or rituals

Health care providers will often use a questionnaire or other screening instrument to gather information about a child’s development and behavior. Some screening instruments rely solely on parent observations, while others rely on a combination of parent and doctor observations. If screening instruments indicate the possibility of ASD, a more comprehensive evaluation is usually indicated.

A comprehensive evaluation requires a multidisciplinary team, including a psychologist, neurologist, psychiatrist, speech therapist, and other professionals who diagnose and treat children with ASD. The team members will conduct a thorough neurological assessment and in-depth cognitive and language testing. Because hearing problems can cause behaviors that could be mistaken for ASD, children with delayed speech development should also have their hearing tested.

What causes ASD?

Scientists believe that both genetics and environment likely play a role in ASD. There is great concern that rates of autism have been increasing in recent decades without full explanation as to why. Researchers have identified a number of genes associated with the disorder. Imaging studies of people with ASD have found differences in the development of several regions of the brain. Studies suggest that ASD could be a result of disruptions in normal brain growth very early in development. These disruptions may be the result of defects in genes that control brain development and regulate how brain cells communicate with each other. Autism is more common in children born prematurely. Environmental factors may also play a role in gene function and development, but no specific environmental causes have yet been identified. The theory that parental practices are responsible for ASD has long been disproved. Multiple studies have shown that vaccination to prevent childhood infectious diseases does not increase the risk of autism in the population.

What role do genes play?

Twin and family studies strongly suggest that some people have a genetic predisposition to autism. Identical twin studies show that if one twin is affected, then the other will be affected between 36 to 95 percent of the time. There are a number of studies in progress to determine the specific genetic factors associated with the development of ASD. In families with one child with ASD, the risk of having a second child with the disorder also increases. Many of the genes found to be associated with autism are involved in the function of the chemical connections between brain neurons (synapses). Researchers are looking for clues about which genes contribute to increased susceptibility. In some cases, parents and other relatives of a child with ASD show mild impairments in social communication skills or engage in repetitive behaviors. Evidence also suggests that emotional disorders such as bipolar disorder and schizophrenia occur more frequently than average in the families of people with ASD.

In addition to genetic variations that are inherited and are present in nearly all of a person’s cells, recent research has also shown that de novo, or spontaneous, gene mutations can influence the risk of developing autism spectrum disorder.  De novo mutations are changes in sequences of deoxyribonucleic acid or DNA, the hereditary material in humans, which can occur spontaneously in a parent’s sperm or egg cell or during fertilization. The mutation then occurs in each cell as the fertilized egg divides. These mutations may affect single genes or they may be changes called copy number variations, in which stretches of DNA containing multiple genes are deleted or duplicated.  Recent studies have shown that people with ASD tend to have more copy number de novo gene mutations than those without the disorder, suggesting that for some the risk of developing ASD is not the result of mutations in individual genes but rather spontaneous coding mutations across many genes.  De novo mutations may explain genetic disorders in which an affected child has the mutation in each cell but the parents do not and there is no family pattern to the disorder. Autism risk also increases in children born to older parents. There is still much research to be done to determine the potential role of environmental factors on spontaneous mutations and how that influences ASD risk.

Do symptoms of autism change over time?

For many children, symptoms improve with age and behavioral treatment. During adolescence, some children with ASD may become depressed or experience behavioral problems, and their treatment may need some modification as they transition to adulthood. People with ASD usually continue to need services and supports as they get older, but depending on severity of the disorder, people with ASD may be able to work successfully and live independently or within a supportive environment.

How is autism treated?

There is no cure for ASD. Therapies and behavioral interventions are designed to remedy specific symptoms and can substantially improve those symptoms. The ideal treatment plan coordinates therapies and interventions that meet the specific needs of the individual. Most health care professionals agree that the earlier the intervention, the better.

Educational/behavioral interventions: Early behavioral/educational interventions have been very successful in many children with ASD. In these interventions therapists use highly structured and intensive skill-oriented training sessions to help children develop social and language skills, such as applied behavioral analysis, which encourages positive behaviors and discourages negative ones. In addition, family counseling for the parents and siblings of children with ASD often helps families cope with the particular challenges of living with a child with ASD.

Medications: While medication can’t cure ASD or even treat its main symptoms, there are some that can help with related symptoms such as anxiety, depression, and obsessive-compulsive disorder. Antipsychotic medications are used to treat severe behavioral problems. Seizures can be treated with one or more anticonvulsant drugs. Medication used to treat people with attention deficit disorder can be used effectively to help decrease impulsivity and hyperactivity in people with ASD. Parents, caregivers, and people with autism should use caution before adopting any unproven treatments

QUOTE FOR THE WEEKEND:

“The effects of parkinsonism depend on why it happens. Most parkinsonian conditions affect parts of your brain responsible for movement. That means you move more slowly. You also may have muscle tremors, causing you to shake.

Under normal circumstances, your brain uses chemicals known as neurotransmitters to control how your brain cells (neurons) communicate with each other. When you have Parkinson’s disease, you don’t have enough dopamine, one of the most important neurotransmitters.

When your brain sends activation signals that tell your muscles to move, it fine-tunes your movements. The neurons that fine-tune your movements need dopamine. Without it, they can’t do their job correctly. That’s why lack of dopamine causes the slowed movements and tremors symptoms of Parkinson’s disease.

With lack of dopamine, the basal ganglia (a key area of your brain) start to deteriorate. As they do, you lose the abilities they once controlled. As Parkinson’s disease gets worse, the symptoms expand and intensify. Later stages of the disease often affect how your brain functions, causing dementia-like symptoms and depression.”

Cleveland Clinic (Parkinsonism: What It Is, Causes & Types)

Part III Parkinson’s Disease-The treatments for this disease from meds to surgery and more; also changes you may make or new lifestyles you may add to your activities of daily living!

Types of Meds Used 

(click box to enlarge writing,if needed)

Part III Parkinson's Disease Part III Parkinson's Disease

Parkinson’s disease is the second most common progressive, neurodegenerative disease after Alzheimer disease. Parkinson’s disease is named after James Parkinson, a 19th century general practitioner in London. Parkinson’s disease is characterised by pathologic intra-neuronal α–synuclein-positive Lewy bodies and neuronal cell loss. Classically this process has been described as involving the dopaminergic cells of the substantia nigra pars compacta, later becoming more widespread in the CNS as the disease progresses. However, recently there has been a growing awareness that the disease process may involve more caudal portion of the CNS and the peripheral nervous system prior to the clinical onset of the disease.1 Parkinson’s disease affects movement, muscle control, balance, and numerous other functions.

MEDS: The combination of levodopa and carbidopa (Brand names Sinemet, Parcopa, Duopa® (as a combination product containing Carbidopa, Levodopa=Rytary® (as a combination product containing Carbidopa, Levodopa).

Levodopa and carbidopa are used to treat the symptoms of Parkinson’s disease and Parkinson’s-like symptoms that may develop after encephalitis (swelling of the brain) or injury to the nervous system caused by carbon monoxide poisoning or manganese poisoning. Parkinson’s symptoms, including tremors (shaking), stiffness, and slowness of movement, are caused by a lack of dopamine, a natural substance usually found in the brain. Levodopa is in a class of medications called central nervous system agents. It works by being converted to dopamine in the brain. Carbidopa is in a class of medications called decarboxylase inhibitors. It works by preventing levodopa from being broken down before it reaches the brain. This allows for a lower dose of levodopa, which causes less nausea and vomiting.

Medications are commonly used to increase the levels of dopamine in the brain of patients with Parkinson’s disease in an attempt to slow down the progression of the disease. Dopaminergic agents remain the principal treatments for patient with Parkinson’s disease, such as Levodopa and Dopaminergic agonist. In many patients, however, a combination of relatively resistant motor symptoms, motor complications such as dyskinesias or non-motor symptoms such as dysautonomia may lead to substantial disability in spite of dopaminergic therapy. In recent days, there has been an increasing interest in agents targeting non-motor symptoms, such as dementia and sleepiness.

As patients with Parkinson’s disease live longer and acquire additional comorbidities, addressing these non-motor symptoms has become increasingly important. Among anti-depressants, Amitriptiline and SSRI are commonly used, while Rivastigmine became the first FDA approved medication for the treatment of dementia associated with PD.

SURGERY:   Surgery for Parkinson’s disease has come a long way since it was first developed more than 50 years ago. The newest version of this surgery, deep brain stimulation (DBS), was developed in the 1990s and is now a standard treatment. Worldwide, about 30,000 people have had deep brain stimulation.

Lifestyle modifications have been shown to be effective for controlling motor symptoms in the early stages of Parkinson’s disease. The surgical treatment options available for Parkinson’s patients with severe motor symptoms are pallidotomy, thalamotomy and Deep Brain Stimulation (DBS).

The novel approaches for treatment of Parkinson’s disease that are currently under investigation include neuroprotective therapy, foetal cell transplantation, and gene therapy.

What is DBS?

For patients whose symptoms are not adequately controlled by medications:

DBS=Deep Brain Stimulation was introduced two decades+ ago and has gained widespread popularity as a surgical treatment for medically refractory Parkinson’s disease. DBS is a reversible procedure that has advantage over surgical lesioning (pallidotomy) and unilateral brain stimulation. DBS is comparable in efficacy to unilateral surgical lesioning while bilateral subthalamic nucleus stimulation is superior to pallidotomy. DBS is FDA approved for the treatment of medically refractory Parkinson’s disease and ET. DBS has proven its efficacy in the treatment of cardinal motor features of Parkinson’s disease such as bradykinesia, tremor and rigidity and it is unresponsive for non-motor symptoms such as cognition, speech, gait disturbance, mood and behavior. Long-term studies have demonstrated that many of these effects last for long as levodopa responsiveness in maintained

During deep brain stimulation surgery, electrodes are inserted into the targeted brain region using MRI and neurophysiological mapping to ensure that they are implanted in the right place. A device called an impulse generator or IPG (similar to a pacemaker) is implanted under the collarbone to provide an electrical impulse to a part of the brain involved in motor function. Those who undergo the surgery are given a controller, which allows them to check the battery and to turn the device on or off. An IPG battery lasts for about three to five years and is relatively easy to replace under local anesthesia.

Is DBS Right for Me?

Although DBS is certainly the most important therapeutic advancement since the development of levodopa, it is not for every person with Parkinson’s. It is most effective – sometimes, dramatically so – for individuals who experience disabling tremors, wearing-off spells and medication-induced dyskinesias.

Deep brain stimulation is not a cure for Parkinson’s, and it does not slow disease progression. Like all brain surgery, deep brain stimulation surgery carries a small risk of infection, stroke, or bleeding. A small number of people with Parkinson’s have experienced cognitive decline after this surgery. That said, for many people, it can dramatically relieve some symptoms and improve quality of life. Studies show benefits lasting at least five years.

Gamma Knife radiosurgery

 Gamma Knife radiosurgery is a painless procedure that uses hundreds of highly focused radiation beams to target deep brain regions to create precise functional lesions within the brain, with no surgical incision. Gamma Knife may be a treatment option for patients with Parkinson’s tremor who are high risk for surgery due to medical conditions or advanced age.

As the nation’s leading provider of Gamma Knife procedures, UPMC has treated more than 12,000 patients with tumors, vascular malformations, pain, and other functional problems.

It is very important that a person with Parkinson’s who is thinking of treatment from meds to surgery to possiby Gamma Knife radiosurgery be well informed about the procedures and realistic in his or her expectations. This means there’s no standard treatment for the disease – the treatment for each person with Parkinson’s is based on his or her symptoms.

Other treatments include:

Lifestyle and home remedies

Some lifestyle changes may help ease your Parkinson’s disease symptoms. But certain medicines can make your symptoms worse. Ask your healthcare team which remedies provide the greatest symptom relief with the fewest side effects.

Healthy eating

No foods are proved to treat Parkinson’s disease, but some may help ease symptoms. For example, eating foods high in fiber and drinking plenty of fluids can help prevent constipation.

A balanced diet also provides nutrients, such as omega-3 fatty acids, that may help people with Parkinson’s disease.

Exercise

Exercising may improve your muscle strength, walking, flexibility and balance. It also may help decrease depression and anxiety.

Ask your healthcare professional to suggest a physical therapist who can help create an exercise program for you. Exercises that may help include walking, swimming, gardening, dancing, water aerobics and stretching.

To improve your balance and gait, try these tips:

  • Don’t move too quickly.
  • Put down your heel first when walking.
  • Look straight ahead, not down, when you walk.

Prevent falls

The following tips may help:

  • Don’t rush.
  • Don’t do too many things at once.
  • Use handrails.
  • Use night-lights.
  • Don’t use throw rugs or rolling chairs and keep cords out of the way.
  • Learn new turning and walking techniques, including landing on your heel first. Also, stand tall and look straight ahead rather than down at your feet when you walk. If you start shuffling, stop. Check your posture and make sure you’re standing up straight.
  • Use a walker or cane if your healthcare professional recommends it.

Daily living activities

These healthcare professionals can help with daily tasks:

  • Occupational therapist. An occupational therapist can show you ways to help with activities such as dressing, bathing and cooking.
  • Speech therapist. A speech therapist may be able to help with swallowing and speech problems.

Your Parkinson’s Disease MD is the best to review what treatment with alternative treatments you should include in your plan.  Always check with your MD!

Last reviewed 4/06/26 by Elizabeth Lynch RN BSN

 

 

QUOTE FOR FRIDAY:

“Parkinson’s disease statistics

  • Parkinson’s disease is the fastest growing neurodegenerative disease in the world, and the second most common after Alzheimer’s disease.
  • There are an estimated 1 million people in the U.S. living with PD and more than 10 million people worldwide.
  • Every 6 minutes, someone is diagnosed with PD.
  • On average, 240 people are diagnosed with PD every day = totaling approximately 90,000 new diagnoses every year.
  • The average age of onset is 60, but 10% of diagnoses occur before age 50 (known as Young Onset Parkinson’s)
  • Men are 50% more likely to get PD than women.
  • The annual economic burden of PD in the U.S. is approximately $52 billion.”

American Parkinson’s Disease Foundation  (What is Parkinson’s Disease | APDA)

Part II Parkinson’s Disease – Know the motor & non-motor signs and symptoms; know how MD’s diagnose PD and what questions to ask your MD about PD!

  part-ii-parkinsons-disease2  part-ii-parkinsons-disease

What are the signs and symptoms (s/s) of this disease?

The early signs and symptoms of Parkinson’s disease that are often overlooked by both patients and doctors because the symptoms are subtle and the progression of the disease is typically slow. S/S of parkinson’s disease are:

Parkinson’s disease does not affect everyone the same way. In some people the disease progresses quickly, in others it does not. Although some people become severely disabled, others experience only minor motor disruptions. Tremor is the major symptom for some patients, while for others tremor is only a minor complaint and different symptoms are more troublesome.

The Motor function symptoms associated with Parkinson’s Disease:

  • The tremors associated with Parkinson’s disease has a characteristic appearance. Typically, the tremor takes the form of a rhythmic back-and-forth motion of the thumb and forefinger at three beats per second. This is sometimes called “pill rolling.” Tremor usually begins in a hand, although sometimes a foot or the jaw is affected first. It is most obvious when the hand is at rest or when a person is under stress. In three out of four patients, the tremor may affect only one part or side of the body, especially during the early stages of the disease. Later it may become more general. Tremor is rarely disabling and it usually disappears during sleep or improves with intentional movement.
  • Rigidity, or a resistance to movement, affects most parkinsonian patients. A major principle of body movement is that all muscles have an opposing muscle. Movement is possible not just because one muscle becomes more active, but because the opposing muscle relaxes. In Parkinson’s disease, rigidity comes about when, in response to signals from the brain, the delicate balance of opposing muscles is disturbed. The muscles remain constantly tensed and contracted so that the person aches or feels stiff or weak. The rigidity becomes obvious when another person tries to move the patient’s arm, which will move only in ratchet-like or short, jerky movements known as “cogwheel” rigidity.
  • Bradykinesia, or the slowing down and loss of spontaneous and automatic movement, is particularly frustrating because it is unpredictable. One moment the patient can move easily. The next moment he or she may need help. This may well be the most disabling and distressing symptom of the disease because the patient cannot rapidly perform routine movements. Activities once performed quickly and easily — such as washing or dressing — may take several hours.
  • Postural instability, or impaired balance and coordination, causes patients to develop a forward or backward lean and to fall easily. When bumped from the front or when starting to walk, patients with a backward lean have a tendency to step backwards, which is known as retropulsion. Postural instability can cause patients to have a stooped posture in which the head is bowed and the shoulders are drooped.

The Non-Motor function symptoms that are often associated with Parkinson’s Disease include:

-Cognitive impairment –Dementia –Psychosis –Depression –Fatigue -Sleep disturbances -Constipation -Sexual dysfunction -Vision disturbances.

As the disease progresses, walking may be affected. Patients may halt in mid-stride and “freeze” in place, possibly even toppling over.  Patients may walk with a series of quick, small steps as if hurrying forward to keep balance. This is known as festination.

A detailed overview of the Unified Parkinson’s Disease Rating Scale that is used by doctors to follow the course of disease progression and evaluate the extent of impairment and disability.

Abstract

The Movement Disorder Society Task Force for Rating Scales for Parkinson’s Disease prepared a critique of the Unified Parkinson’s Disease Rating Scale (UPDRS). Strengths of the UPDRS include its wide utilization, its application across the clinical spectrum of PD, its nearly comprehensive coverage of motor symptoms, and its clinimetric properties, including reliability and validity. Weaknesses include several ambiguities in the written text, inadequate instructions for raters, some metric flaws, and the absence of screening questions on several important non-motor aspects of PD. The Task Force recommends that the MDS sponsor the development of a new version of the UPDRS and encourage efforts to establish its clinimetric properties, especially addressing the need to define a Minimal Clinically Relevant Difference and a Minimal Clinically Relevant Incremental Difference, as well as testing its correlation with the current UPDRS. If developed, the new scale should be culturally unbiased and be tested in different racial, gender, and age-groups. Future goals should include the definition of UPDRS scores with confidence intervals that correlate with clinically pertinent designations, “minimal,” “mild,” “moderate,” and “severe” PD. Whereas the presence of non-motor components of PD can be identified with screening questions, a new version of the UPDRS should include an official appendix that includes other, more detailed, and optionally used scales to determine severity of these impairments.

How Parkinson’s disease is diagnosed:

There isn’t a specific test to diagnose Parkinson’s disease;  it is based on factors such as signs/symptoms, patient history, physical examination, and a thorough neurological evaluation.

A doctor trained in nervous system conditions (neurologist) will diagnose Parkinson’s disease based on your medical history, a review of your signs and symptoms, and a neurological and physical examination.

Your doctor may suggest a specific single-photon emission computerized tomography (SPECT) scan called a dopamine transporter (DAT) scan. Although this can help support the suspicion that you have Parkinson’s disease, it is your symptoms and neurological examination that ultimately determine the correct diagnosis. Most people do not require a DAT scan.

Furthermore, making the diagnosis is even more difficult since there are currently no blood or lab tests available to diagnose the disease. Your health care provider may order lab tests, such as blood tests, to rule out other conditions that may be causing your symptoms.  Some tests, such as a CT Scan (computed tomography) or MRI (magnetic resonance imaging) and PET Scans may be used to rule out other disorders that cause similar symptoms. Imaging tests aren’t particularly helpful for diagnosing Parkinson’s disease.  Given these circumstances, a doctor may need to observe the patient over time to recognize signs of tremor and rigidity, and pair them with other characteristic symptoms.

The doctor will also compile a comprehensive history of the patient’s symptoms, activity, medications, other medical problems, and exposures to toxic chemicals. This will likely be followed up with a rigorous physical exam with concentration on the functions of the brain and nervous system. Tests are conducted on the patient’s reflexes, coordination, muscle strength, and mental function. Making a precise diagnosis is essential for prescribing the correct treatment regimen. The treatment decisions made early in the illness can have profound implications on the long-term success of treatment.

Recommended Related to Parkinson’s

Questions to Ask Your Doctor About Parkinson’s Disease:

Since you’ve recently been diagnosed with Parkinson’s disease, ask your doctor these questions at your next visit.   1.What stage is my illness in now?

2. How quickly do you think my disease will progress?

3. How will Parkinson’s disease affect my work?

4. What physical changes can I expect?

5. Will I be able to keep up the activities, hobbies, and sports I do now?

6. What treatments do you suggest now?

7.Will that change as the disease progresses?

8. What are the side effects of medication?…

Because the diagnosis is based on the doctor’s exam of the patient, it is very important that the doctor be experienced in evaluating and diagnosing patients with Parkinson’s disease. If Parkinson’s disease is suspected, you should see a specialist, preferably a movement disorders trained neurologist.

Revised 4/06/26 by Elizabeth Lynch BSN RN