“Sometimes, it’s just easier to say yes to that extra snack or dessert, because frankly, it is exhausting to keep saying no. It’s exhausting to plead with our kids to eat just one more bite of vegetables.”
“Sometimes, it’s just easier to say yes to that extra snack or dessert, because frankly, it is exhausting to keep saying no. It’s exhausting to plead with our kids to eat just one more bite of vegetables.”
“Today, the Centers for Disease Control and Prevention (CDC) announced that the incidence rate of autism among eight year olds in the United States remains 1 out of 68 children. This updated report occurs every two years, with the previous report being released from the CDC in April 2014.”
Autism Society . Org
Autism spectrum disorder (ASD) refers to a group of complex neurodevelopment disorders characterized by repetitive and characteristic patterns of behavior and difficulties with social communication and interaction. The symptoms are present from early childhood and affect daily functioning.
The term “spectrum” refers to the wide range of symptoms, skills, and levels of disability in functioning that can occur in people with ASD. Some children and adults with ASD are fully able to perform all activities of daily living while others require substantial support to perform basic activities. The Diagnostic and Statistical Manual of Mental Disorders (DSM-5, published in 2013) includes Asperger syndrome, childhood disintegrative disorder, and pervasive developmental disorders not otherwise specified (PDD-NOS) as part of ASD rather than as separate disorders. A diagnosis of ASD includes an assessment of intellectual disability and language impairment.
ASD occurs in every racial and ethnic group, and across all socioeconomic levels. However, boys are significantly more likely to develop ASD than girls. The latest analysis from the Centers for Disease Control and Prevention estimates that 1 in 68 children has ASD.
What are some common signs of ASD?
Even as infants, children with ASD may seem different, especially when compared to other children their own age. They may become overly focused on certain objects, rarely make eye contact, and fail to engage in typical babbling with their parents. In other cases, children may develop normally until the second or even third year of life, but then start to withdraw and become indifferent to social engagement.
The severity of ASD can vary greatly and is based on the degree to which social communication, insistence of sameness of activities and surroundings, and repetitive patterns of behavior affect the daily functioning of the individual.
Social impairment and communication difficulties Many people with ASD find social interactions difficult. The mutual give-and-take nature of typical communication and interaction is often particularly challenging. Children with ASD may fail to respond to their names, avoid eye contact with other people, and only interact with others to achieve specific goals. Often children with ASD do not understand how to play or engage with other children and may prefer to be alone. People with ASD may find it difficult to understand other people’s feelings or talk about their own feelings.
People with ASD may have very different verbal abilities ranging from no speech at all to speech that is fluent, but awkward and inappropriate. Some children with ASD may have delayed speech and language skills, may repeat phrases, and give unrelated answers to questions. In addition, people with ASD can have a hard time using and understanding non-verbal cues such as gestures, body language, or tone of voice. For example, young children with ASD might not understand what it means to wave goodbye. People with ASD may also speak in flat, robot-like or a sing-song voice about a narrow range of favorite topics, with little regard for the interests of the person to whom they are speaking.
Repetitive and characteristic behaviors Many children with ASD engage in repetitive movements or unusual behaviors such as flapping their arms, rocking from side to side, or twirling. They may become preoccupied with parts of objects like the wheels on a toy truck. Children may also become obsessively interested in a particular topic such as airplanes or memorizing train schedules. Many people with ASD seem to thrive so much on routine that changes to the daily patterns of life — like an unexpected stop on the way home from school — can be very challenging. Some children may even get angry or have emotional outbursts, especially when placed in a new or overly stimulating environment.
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:
Later indicators include:
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
Schizophrenia is a serious disorder which effects how a person thinks, feels and acts. A individual with this diagnosis may have difficulty distinguishing between what is real and what is imaginary; may be unresponsive or withdrawn; and may have difficulty expressing normal emotions in social situations. The person with schizophrenia may have difficulty expressing normal emotions in social situations.
Contrary to public perception, schizophrenia is not split personality or multiple ones. The vast majority of people with schizophrenia are not violent and do not pose a danger to others; if anyone they could put a danger to is themselves without supervision around. Schizophrenia is not caused by childhood experiences, poor parenting, lack of will power. The signs and symptoms of the disease are not the same for each person.
The cause of schizophrenia is still not clear.
Some theories about the cause of this disease include: genetics (heredity), biology (the imbalance in the brain’s chemistry); and/or possible viral infections and immune disorders.
One possible cause can be genetics (heredity). Scientists recognize that the disorder tends to run in families and a person inherits to develop the disease. Schizophrenia may also be triggered by environmental events like viral infections or highly stressful situations or a combination of both. Similar to some other genetically-related illnesses, schizophrenia appears when the body undergoes hormonal and physical changes, like those that occur during puberty in the teen and young adult years.
Another possible cause is Substance Use. Some studies have suggested that taking mind-altering drugs during teen years and young adulthood can increase the risk of schizophrenia. A growing body of evidence indicates that smoking marijuana increases the risk of psychotic incidents and the risk of ongoing psychotic experiences. The younger and more frequent the use, the greater the risk. Another study has found that smoking marijuana led to earlier onset of schizophrenia and often preceded the manifestation of the illness.
Another high possible cause deals with chemistry. Genetics help to determine huw the brain uses certain chemicals. People with schitzophrenia have a chemical imbalance of brain chemicals (serotonin and dopamine) which are neurotransmitters. These neurotransmitters allow nerve cells in the brain that send messages to each nerve cell. The brain is made up of nerve cells, called neurons, and chemicals, called neurotransmitters. An imbalance of one neurotransmitter, dopamine, is thought to cause the symptoms of schizophrenia. … The “dopamine hypothesis” has been the main theory regarding the cause of the symptoms of schizophrenia. Dopamine is produced in the dopaminergic neurons in the ventral tegmental area (VTA) of the midbrain, the substantia nigra pars compacta, and the arcuate nucleus of the hypothalamus. With the imbalance these chemicals affects the way a person’s brain reacts to stimuli—which explains why a person with schizophrenia may be overwhelmed by sensory information (Ex. loud music or bright lights) which other people can easily handle. This problem in processing different sounds, sights, smells and tastes can also lead to hallucinations or delusions.
Looking for a moment at Dopamine in different areas of the brain in both low and high amounts see how it effects brain thinking to better understand schizophrenia.
Dopamine in cognition:
Dopamine in the frontal lobes of the brain controls the flow of information from other areas of the brain. Disorders of dopamine in this region lead to decline in neurocognitive functions, especially memory, attention, and problem-solving.
D1 receptors and D4 receptors are responsible for the cognitive-enhancing effects of dopamine. Some of the antipsychotic medications used in conditions like schizophrenia act as dopamine antagonists. Older, so-called “typical” antipsychotics most commonly act on D2 receptors, while the atypical drugs also act on D1, D3 and D4 receptors.
Dopamine in movement
A part of the brain called the basal ganglia regulates movement. Basal ganglia in turn depend on a certain amount of dopamine to function at peak efficiency. The action of dopamine occurs via dopamine receptors, D1-5.
Dopamine reduces the influence of the indirect pathway, and increases the actions of the direct pathway within the basal ganglia. When there is a deficiency in dopamine in the brain, movements may become delayed and uncoordinated. On the flip side, if there is an excess of dopamine, the brain causes the body to make unnecessary movements, such as repetitive tics.
Dopamine in pleasure reward seeking behavior
Dopamine is the chemical that mediates pleasure in the brain. It is released during pleasurable situations and stimulates one to seek out the pleasurable activity or occupation. This means food, sex, and several drugs of abuse are also stimulants of dopamine release in the brain, particularly in areas such as the nucleus accumbens and prefrontal cortex.
Dopamine and addiction
Cocaine and amphetamines inhibit the re-uptake of dopamine. Cocaine is a dopamine transporter blocker that competitively inhibits dopamine uptake to increase the presence of dopamine.
Amphetamine increases the concentration of dopamine in the synaptic gap, but by a different mechanism. Amphetamines are similar in structure to dopamine, and so can enter the presynaptic neuron via its dopamine transporters. By entering, amphetamines force dopamine molecules out of their storage vesicles. By increasing presence of dopamine both these lead to increased pleasurable feelings and addiction.
Dopamine in memory
Levels of dopamine in the brain, especially the prefrontal cortex, help in improved working memory. However, this is a delicate balance and as levels increase or decrease to abnormal levels, memory suffers.
Dopamine in attention
Dopamine helps in focus and attention. Vision helps a dopamine response in the brain and this in turn helps one to focus and direct their attention. Dopamine may be responsible for determining what stays in the short term memory based on an imagined response to certain information. Reduced dopamine concentrations in the prefrontal cortex are thought to contribute to attention deficit disorder.
Dopamine is affected in schizophrenia, just look at the functions of the chemical and the signs and symptoms of schizophrenia.
Signs and symptoms of schizophrenia:
–Deficits in cognitive abilities are widely recognized as a core feature of this disease. The deficits impacting the cognitive function are found in a large number of areas: working memory, long-term memory,verbaldeclarative memory, semantic processing, episodic memory, attention, learning (particularly verbal learning). Deficits in verbal memory are the most pronounced in individuals with schizophrenia, and are not accounted for by deficit in attention. Verbal memory impairment has been linked to a decreased ability in individuals with schizophrenia to semantically encode (process information relating to meaning), which is cited as a cause for another known deficit in long-term memory. When given a list of words, healthy individuals remember positive words more frequently (known as the Pollyanna principle); however, individuals with schizophrenia tend to remember all words equally regardless of their connotations, suggesting that the experience of anhedonia impairs the semantic encoding of the words. These deficits have been found in individuals before the onset of the illness to some some extent and varying degrees.
-Disorganized or catatonic behavior
TREATMENT FOR SCHIZOPHRENIA:
There is no cure for schizophrenia, but it can be treated and managed in several ways.
-Psychotherapy, such as cognitive behavioral therapy and assertive community treatment and supportive therapy.
– Self-management strategies and education
“Highly concentrated sources of oxygen promote rapid combustion and therefore are fire and explosion hazards in the presence of fuels. The fire that killed the Apollo 1 crew on a test launchpad spread so rapidly because the pure oxygen atmosphere was at normal atmospheric pressure instead of the one third pressure that would be used during an actual launch.”
LENNTECH.com http://www.lenntech.com/periodic/elements/o.htm#ixzz48HfY7per Water Treatment and Purification Company
“Oxygen, although it is essential for aerobic organisms for respiration as well as energy production, has been therapeutically used for a long time. It also can be either toxic or lethal for humans if it is continuously inhaled pure for about 60 hours.”
U.S. National Library of Medicine/National Institute of Health http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3231820/
Now don’t get me wrong oxygen is an element that is a must for most creatures that live in the world both now and since it began but there is dangers to any element especially if mixed with some other element causing a negative result in the end. So you wonder how oxygenation can have pros and cons and why oxygen would ever have dangers to it, well let’s take a deeper look.
Oxygenation may refer to:
Oxygen saturation (medicine), the process by which concentrations of oxygen increase within a tissue
Oxygenation (environmental), a measurement of dissolved oxygen concentration in soil or water
–Great Oxygenation Event, an ancient event that led to the rise of oxygen within our atmosphere
–Water oxygenation, the process of increasing the oxygen saturation of the water
–Dioxygen complex, the chemical details of how metals bind oxygen
Of course, oxygen has its good points. Besides being necessary for respiration and the reliable combustion engine, it can be liquefied and used as rocket fuel. Oxygen is also widely used in the world of medicine as a means to imbue the body with a greater amount of the needed gas. But recent studies indicate that administering oxygen might be doing less good than hoped—and in fact be causing harm. No one is immune to the dangers of oxygen, but the people who might most suffer the ill effects are infants newly introduced to breathing, and those who are clinically deceased.
Oxygen regarding the medical view:
There are a variety of injuries and ailments for which modern medicine dictates oxygen therapy. Look at the medical aspect, the common wisdom is that by filling the lungs with pure O2, one is pushing more of the vital gas into the blood, and thus to organs that are weakened and in need of support. It has also long been known that even at partial pressures, pure oxygen can be toxic—a fact with which scuba divers and astronauts are intimately familiar. Recent studies have indicated that the human body responds to pure oxygen, even at normal pressures, in a negative way.
When pure O2 is introduced to the lungs, autonomic reflex increases respiration. The increased rate of breathing means that a much larger load of carbon dioxide is released from the body, which causes the blood vessels to constrict. Despite the increased amount of available oxygen in the lungs, the circulatory system is hampered, and cannot deliver precious O2 as well as it could when breathing normal atmosphere.
Ronald Harper, a neurobiology professor at UCLA, conducted observations on a group of healthy teenagers breathing various gas mixes using functional magnetic resonance imaging (fMRI). His findings showed that in some subjects the pure O2 caused the brain to go clinically bonkers. Brain structures such as the hippocampus, the insula, and the cingulate cortex all displayed an adverse reaction; they in turn spurred the hypothalamus, the body’s main regulatory gland, into a fervor. The hypothalamus regulates a myriad of things, including heart rate, body temperature, and is the master of a variety of other glands. The introduction of pure oxygen prompts the hypothalamus to flood the body with a cocktail of hormones and neurotransmitters which serve to hamper heart rate, and further reduce the circulatory system’s effectiveness. But Harper also found that by adding a mere 5% CO2, all the detrimental effects found in pure oxygen are negated.
There are circumstances, however, where even the proper mix of gases would prove inadequate. Modern medicine has long taught that after respiration stops, the brain can only survive for six to seven minutes without oxygen before its cells begin to die in droves. In order to combat this, standard procedure has been to aggressively attempted to restore breathing and heartbeat immediately upon cessation, CPR. The base premise on which this protocol is designed may be in error but only if continuing longer than the AHA guides us to do CPR. For there is more than just to lack of oxygen in patients who die having CPR done to them for death (Ex Exacerbation of a disease, multi – organ failure, years of CHF, etc… Even thought lack of 02 is part of the reason for the death in the end. There was a cause for it happening and leading to lack of 02 is the prime entity to death of all diseases leading up to this in a human.).
Upon examining heart cells and neurons deprived of oxygen under a microscope, Dr Lance Becker of the University of Pennsylvania found there was no indication that the cells were dying after five or six minutes. In fact, they seemed to endure the state for up to an hour without adverse affect. Given this unexpected observation, the researchers were forced to investigate why human resuscitation becomes impossible after only a few minutes of clinical death. The answer they uncovered was that the body’s cells were not dying of oxygen starvation; they were expiring due to Reperfusion—the sudden reintroduction of oxygen to a dormant cell = Programmed cell death! The cells reintroducing oxygen back into the cell from outside the cell in the bloodstream caused the destruction of the red blood cells, the RBCs carry oxygen to all our tissues sites. You would think that would save the cells in sending more oxygen out to the tissues but like we’re told from childhood too much of almost anything can hurt or kill you (Ex. Food/work/stress…)
Take a patient with severe emphysema they do get oxygen in their body but the problem is that oxygen gets air spaced elsewhere rather than all the 02 breathed in going in the red blood cells at the lungs exchange for 02 at the bottom of the lungs with CO2 (carbon dioxide) sent from the cells to the lungs to leave the body. Than the cells go off throughout the bloodstream having our tissues utilize from the red blood cells the oxygen it needs (a transfer of 02 to our tissues). Upon return of the red blood cells that took the CO2 from the tissues to keep the tissues more oxygenated, so they can do their function as an organ. Oxygen deprivation to a severe state is Oxygen Starvation to our bodies leading to death, if not reversed. Also with the severe COPD emphysema pt their body adjusts to having high C02 levels compared to a person without emphysema. A normal person’s brain functions to sending messages out to cause us to breath when our 02 level is low but to a severe emphysema pt the low C02 levels causes their brain to send out messages to breath, so if you give an emphysema pt over 2L of 02 for several hours if will turn the brain off and the pt deceases (except when a emphysema pt is in respiratory distress since it is needed and temporary support of higher oxygen levels than when stable and out of respiratory distress their at 2L of 02 again).
Inside the cells, the culprit seems to be in the mitochondria, which is the cell’s power plant where sugar and oxygen are converted to usable energy. Mitochondria are also responsible for apoptosis—the organized, controlled self-destruction of a cell. Normally apoptosis occurs in situations such as the cell being damaged beyond repair, infected by a virus, an attempt to prevent cancer, or aiding in initial tissue development. The process effectively kills and dismantles the cell allowing the body’s usual waste management functions to carry the cell’s remains away. For reasons not entirely clear, reperfusion triggers apoptosis—the oxygen intended to save the cell actually causes cellular suicide.
Armed with this new information about how cells react to oxygen, it is clear that current emergency care is not altogether ideal, and new protocols are under investigation. Dr Becker proposes that induced hypothermia may slow cell degradation, and if a means can be found to safely reintroduce oxygen to tissues, a clinically dead person—who still has trillions of living cells—could be resuscitated after being an hour dead.
This glorious future is still on the horizon, but to imagine the practical application leads one to ponder the multitude of accidents and injuries that are currently fatal, but will one day be treatable. Emergency Medical Personnel could arrive on the scene, and inject the patient with a slurry of ice and salt that lowers the body temperature to about 92° F. In a hypothermic state, the patient is hauled to the hospital, where instead of frantically trying to restart the heart, doctors patch up the problem, prevent apoptosis , and then restart the heart. Though it won’t save everyone, these findings may lead to a future where a person made up of perfectly good human cells is not written off as dead merely because their heart has stopped beating. The miracle of modern medicine, it seems, is on the cusp of determining the true distinction between dead and mostly dead.
“When you exhaust all possibilities remember this: You haven’t!”
Thomas Edison (Inventor and Businessman)
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.
DBS 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 lesioning7 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 behaviour. Long-term studies have demonstrated that many of these effects last for long as 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.
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.