Parkinson's Reversing FAQ

Featured Image Parkinson's Reversing FAQ

Parkinson's is a disease that affects the nervous system. The condition may affect movement, cause tremors, and may lead to imbalance and lack of coordination. The disease has five main stages. For the first stage, one may barely notice, but as the disease progresses, you get to see some of the symptoms linked to the disease. Most of the people who have the disease are above fifty years and above.

The leading cause of Parkinson's disease is the decrease in dopamine. Dopamine is a neurotransmitter responsible for sending information to nerve cells, thus enabling one to coordinate and control the movement of body parts easily. Parkinson's disease may also be a result of the use of farm chemicals and industrial pollution. The article will help you learn some of the signs associated with the disease, including tremors experienced in the limbs and hands. One experiences muscle rigidity, fatigue, loss of smell, and difficulty speaking, among many others.

There is still no cure for the condition, but you can prevent the disease by avoiding farm chemicals, taking the right foods such as omega-three fats, vitamins, Fruits, and vegetables. The article also highlights how you can show care to a person who has Parkinson's, giving them a friendly listening year, helping the patients in doing exercises, and learning everything that you need to know about the condition, enabling you to assist the person quickly.

You get to learn some of the side effects of Parkinson's disease, which include hallucinations, wearing off, and involuntary body movements. Though there is no known cure for Parkinson's disease, You can use various medications to treat the condition. The most common drugs used include dopamine agonistics, carbidopa-levodopa, and anticholinergics. Doing aerobic exercises, strength training exercises, and balancing exercises also help in managing the symptoms. The article will help you to learn everything that you need to know about the disease.

Frequently Asked Questions

The condition grows in a slow and gradual process, and the symptoms are insignificant at the start. Several symptoms are related to Parkinson's disease, but how the symptoms develop differs with the individual. There are three main signs of the Parkinson's disease which include the following.

  • Tremor

You may experience body shaking that begins from the arms to other body parts. The tremor mostly happens when limbs are relaxed .

  • Muscle rigidity

The muscle becomes stiff and makes it not to be flexible and can be painful at times.

  • Slow body movement

The body movement becomes very slow than normal, and the footsteps while walking become smaller.

Parkinson's disease has other mental and physical symptoms.

The physical symptoms include;

  • Luck of body balance
  • Pain on the nerves
  • Smelling sense getting lost
  • Difficulties during urination
  • Extreme sweating
  • Difficulties in swallowing
  • Insomnia
  • Difficult in speaking
  • Sexual dysfunction for both men and women.
  • Constipation

Mental symptoms include;

  • Anxiety and depression
  • Dementia
  • Memory losses.

Stage 1

Stage one is usually associated with mild symptoms. The symptoms in this stage are there, but they do not affect your daily routine. Most of the time, you may not recognize the signs, but the people around you may notice some change in facial expression, posture, and walking style.  

Stage 2

At this stage, you may notice symptoms of muscle rigidity, lack of balance, difficulty in walking, and difficulty in talking.

Stage 3

It’s mostly referred to as the middle stage, and it is the stage where most symptoms are felt as the disease progresses. Many of the signs in stage 2 are handled, and there may be increased loss of stability. The body movement becomes slower, and your daily routine will be greatly affected.

Stage 4

At this stage, the patient may be able to stand independently but require a walker to assist them in walking. Your daily routine is completely affected, and it is not advised to live on your own.

Stage 5

During this stage, a person may not walk or even stand; hence you may require a wheelchair. People at this stage may be delusional, confused and may start hallucinating. Dementia is another common symptom in this stage.

Some of the main questions that come to the mind of patients diagnosed with Parkinson's disease are how the disease affects your life and how the symptoms progress? Well, it is very hard to tell exactly how the disease symptom will progress.

It is difficult to tell how the disease progresses because Parkinson's disease symptoms come in two buckets. The first bucket comes with motor symptoms and affects the ability to walk and result in tremors and muscle stiffness. The second bucket comes with a non-motor warning sign and has symptoms such as pain, dementia, and loss of smell. Parkinson's disease starts with mild symptoms, and as time goes by, the symptoms become worse. Patients diagnosed with the condition may not experience all the symptoms, and it is not possible to predict how the signs will progress and become worse. The pace at which the disease symptoms progress differs with people.

Vitamin plays a very big role in Parkinson's disease patients. Soluble fat vitamins such as vitamin D and vitamin E have great impacts in reducing Parkinson's disease risks. Vitamin D drops the rate of Parkinson's disease deteriorating and reduces the fracture occurrences in Parkinson's patients. Vitamin D is mostly found in animal liver, egg yolk, red meat, and fish oil.

 Soluble water vitamins such as vitamin C and vitamin B3 has an elaborate role in Parkinson patient. Vitamin C is important in human beings, and it helps improve levodopa concentration in Parkinson's disease patients. It also has a great impact on the psychological functioning of the brain. Vitamin C is found in fresh fruits, animal liver, and vegetables.

 Vitamin B has a great effect on Parkinson's patients as a great improvement in muscle rigidity and bradykinesia. Foods that are rich in vitamin B include milk, vegetable meat, tea, and coffee.

Parkinson's disease is a brain condition triggered by brain nerve cell damage, leading to low brain dopamine. The brain dopamine is responsible for the coordination and control of your body movement. If the level of dopamine in your brain is low, it means you have Parkinson's disease. You may experience

  • Difficulties in walking.
  • Body shaking that starts from arms.
  • Lack of balance.
  • Muscle stiffness.
  • Lack of coordination.

Parkinson's disease starts with mild symptoms and gradually develops and gets worse with time. Parkinson progresses in stages, and as the disease evolves, you may start having difficulties talking and walking. You may also begin showing behavior changes, having problems sleeping, depression, fatigue, anxiety, and memory losses.

Parkinson's disease affects both men and women. However, the research has shown that the disease affects men more than it affects women. Parkinson's disease mostly affects people at the age of 60. However, there is an early form of Parkinson's, and it is mostly inherited, and others are linked to specific genetic mutations.  

We have no permanent cure for Parkinson's disease. Nevertheless, scientists have come up with natural ways that help to manage Parkinson's disease and reduce risks of getting it. These natural ways include;

  • Regular Exercises.

Research has shown that regular exercises help to regulate the production of dopamine in the human brain. Less dopamine in the brain causes brain malfunctioning, thus causing Parkinson's disease.

  • Eat organic foods

Farm chemicals such as pesticides and herbicides rise the risk of getting Parkinson's disease. Taking food that is not grown with these chemicals reduces the chances of getting Parkinson's disease.

  • Practice taking plant-based foods

Plant-based foods such as fruits, nuts, seeds and vegetables are rich in nutrients vital in reducing risks of Parkinson's disease. They are also an important nutrient that helps in managing the disease.

  • Take some minutes in the sun.

Sunlight produces vitamin D nutrients that are vital in managing and reducing the risks of Parkinson's disease.

  • Reduce stress level

Stress can cause brain damage, thus resulting in Parkinson's disease.

There is no definite answer as to how the life expectancy of any patient can be. People have different ways of how the disease can progress to fetal stages. Parkinson's disease progresses slowly. As the nerve cell degeneration progresses, the patient's condition worsens, and behavior changes, slow movement, difficulty talking, and memory losses are seen on the patient.  People with Parkinson's disease have a short life span as compared to normal and healthy people.

Most of Parkinson disease patient starts developing symptoms at the age of 60. The research has shown that people diagnosed with Parkinson's disease live between ten and twenty years. However, the generally healthy and patient age is a factor that affects the life span of a patient diagnosed with Parkinson.

There is no particular cure for Parkinson's disease, people diagnosed with the disease start with a mild symptom, and the symptoms persist as the disease progresses. The disease progression takes place faster on some people than other people. 

The leading cause of Parkinson’s disease is the nerve cell damage in a part of the brain, which is known as substantia nigra. The nerve cells in the substantia nigra produce a chemical known as dopamine, giving the nervous system information that helps coordinate and control the body part's movement. If the nerve cells in the substantia nigra are damaged or dead, the amount of dopamine produced will reduce. Hence, the brain will lose control of the body part's movements, making the body's movement abnormal or slow. The nerve cell losses develop slowly, and Parkinson's disease can only be noticed when the nerve cell damage is about 80 percent.

It is not clear why nerve cell damage is linked to Parkinson's disease, but it is believed that genetic modifications and environmental dynamics can be the cause. Although it is rare, Parkinson's disease can be genetically inherited by children from their parents. It is also believed ecological issues such as industrial pollution and farm chemicals can also lead to the disease.

As the saying goes, prevention is better than cure. You can prevent yourself from getting the condition by,

Avoid farm chemicals

Farm chemicals such as pesticides and herbicides are major causes of Parkinson's disease. It’s important to be aware of the sources of foods that you take. Consider practicing local farming as it is much safer.

  • Eat fresh and raw vegetables.

Fresh vegetables have a significant amount of vitamin B. The vitamins reduce the risk of getting Parkinson's disease. You can get vitamin B in avocados and legumes.

  • Ensure your diet has omega-three fatty acids

Omega 3 fatty acid prevents cell death and degeneration. They have a very big effect on prevention measures of Parkinson's disease.

  • Vitamin D

Research shows that most Parkinson's patients have low vitamin D. Vitamin D intake will boost your immunity and prevent you from Parkinson's disease.

  • Regular exercises

Exercises reduce brain inflammation, thus reducing the chances of getting Parkinson's disease.

Parkinson's disease is a brain disorder that affects the brain nerve cells particular a  part of the brain known as substantia nigra and basal ganglia that are accountable for human body movement. If the nerve cell in your brain is damaged, the amount of dopamine in your brain reduces. If 80 percent of brain dopamine is lost, Parkinson disease symptom starts to appear. Dopamine is responsible for producing neuron that helps in body coordination and control. If the neurons in your brain are damaged or dead, warning signs such as muscle stiffness, tremor, slow movement, and loss of balance start to appear.

The body motion is controlled by nerve cells known as ganglia. That substantia nigra works with the central part of the brain known as the stratum to direct impulse from the spinal cord to the brain. Basal ganglia ensure that the movement is done smoothly. Parkinson's symptoms happen if there is no sufficient dopamine to ensure the message is transmitted.

A patient diagnosed with Parkinson's disease must adhere to the strict measure and timely medications prescribed to have an effective way of managing the disease symptoms. Medication dose up intervals differ with the patient depending on the disease complexity.  The drug is supposed to be administrated on time, depending on the patient's schedule. Suppose the medication is delayed by more than one hour. In that case, the patient's symptom becomes worse, and the patient starts experiencing worse tremor, increased muscle stiffness, lack of stability, becomes confused, problem speaking, and become more agitated. It is always advisable not to change the medication schedule unless advised by a doctor after assessing your condition.

Surgical procedures are very risky for people who are diagnosed with Parkinson's disease. The main reason behind it is that the antiparkinsonian agents are withdrawn from the patient, and surgical anesthesia is introduced into the patient. It may cause serious problems with the status of the patient.

Once you discover that you have Parkinson's disease symptoms, it’s always advisable to see a doctor and start early treatment, which will help to manage the disease early. The signs that you expect to see with Parkinson disease patient include;

  • Tremor

Tremor involves persistent shaking of the chin, legs, and hands.

  • Walking problem

Parkinson's patients might start walking slowly and dragging their feet as they walk.

  • Loss of smell

Smell loss is the most common symptom of Parkinson's disease. Loss of smell appears before the movement problem starts.

  • Problem sleeping

Parkinson affects a person sleeping ability and starts experiencing insomnia, nightmares, sleep apnea, and other sleeping-related problems.

  • Lack of stability

Parkinson affects the brain nerve cell that is responsible for body flexibility and balance.

  • Constipation

Constipation is a non-motor symptom of Parkinson's disease; it appears before the patient start developing motor symptoms.

  • Psychological problems.

Parkinson lowers dopamine levels in the brain, thus causing behavior changes and affecting the patient's psychological health.

When one has Parkinson's, it becomes difficult to control the muscles as the cells responsible for maintaining movement cannot send proper signals to the muscles. People are suffering from this condition experience rigidity. Some of the most noticeable muscle rigidity includes bending of fingers, wrists, neck, and knees. People who have Parkinson's are at a high risk of getting bone fractures and low bone density. The changes are likely to increase over time.

Other effects that one may have in the muscular system after developing Parkinson's disease include muscle stiffness, resulting in one experiencing difficulties in walking, standing, and bodily movements . The legs muscles become weak; hence one may experience joint and muscle pains. It would be best to do exercises to ease the pains.

People with advanced Parkinson's disease may also experience changes in posture. The changes may include leaning forward of the head or the entire body, rounded shoulder, and low back curve.

People who have Parkinson's needs to be shown love and good care. You can offer care to the person.

  • Helping out in the day-to-day activities such as cooking, shopping, cleaning the dishes, picking up medications, and washing the clothes.
  • Exercising plays a major role in reducing Parkinson's exercises. You can encourage the person to become active by doing the activities together. For example, taking nature walks and swimming.
  • Helping the person to get out of the house. Most Parkinson's patients like isolating themselves, and going for coffee or watching a movie will be good for their health.
  • Been a good listener. Most Parkinson's patients experience anxiety and depression; hence, giving them a friendly ear will help them talk about their emotions, thus reducing stress.
  • Learning everything you need to know about the condition. The knowledge will help you understand the symptoms and know what to expect and how you can help.

Parkinson's disease is a slowly developing disease which takes several years before it progresses and becomes serious. The symptom progression is different from one person to the other since the way disease progress differs with a person. Parkinson's disease patient experiences tremor, bradykinesia, muscle and limb rigidity, loss of smell, and lack of balance.

The main cause of Parkinson's disease remains unknown to date. There is still no cure for Parkinson's disease to date, but treatment includes medication and surgery that helps manage Parkinson's disease. The condition is not fatal but the symptom can at times be worse.

Even though we have no cure for Parkinson's illness, people diagnosed with Parkinson's disease can live a quality and good life. The patient is encouraged to follow the doctor's medications and therapy, and they will be closer to having a quality life with Parkinson's. Medication such as dopaminergic is important since they help in treating Parkinson's symptoms.

Parkinson's disease is instigated by damage or loss of the brain nerve cells known as substantia nigra. The nerve cells produce brain dopamine responsible for sending information from the spinal cord and the nervous system. It helps in control and coordinating the movement of the body.  If the nerve cells in the substantia nigra are damaged or dead, the amount of dopamine in the brain reduces, thus causing slow body movement and difficulty while speaking.

Parkinson's disease symptoms may start to appear once a person losses 80 percent of the brain nerve cells. The cause of brain cell losses is unknown yet, but it is believed that environmental factors and genetic changes may be why brain nerve cells get damaged. Parkinson's disease can be passed from parent to child due to faulty genetic factors. Environmental factors such as farm pesticides and herbicides and industrial pollution also contribute to Parkinson's disease.

There is no particular laboratory or imaging test for Parkinson's disease that has been discovered. However, imaging known as DaTscan has been used to allow doctors to assess brain dopamine levels by providing detailed pictures of the person's brain dopamine system. Da Tscan imaging involves injecting a small amount of radioactive drug. A machine similar to MRI, known as single-photon emission computed tomography scanner (SPECT), is used for imaging purposes. The drug impasses the brain dopamine transmitters that show dopaminergic neurons. If the transmitters offer a low level of dopamine, the patient may be diagnosed with Parkinson's disease. However, Da Tscan does not show that you have Parkinson's disease, but it helps the doctor diagnose or avert Parkinson's disease simulations.

In most cases, the doctor diagnoses people with Parkinson's disease based on the person’s health history and checking at the patient's signs and symptoms and neurological and physical examination on the patient.

Some of the side effects which can emerge during Parkinson's disease treatment and extended period of the condition include.

  • Wearing off.

As Parkinson progresses, you are likely to experience wearing off. Frequent wearing off makes it difficult to control motor and non-motor symptoms and predict the most effective medication. Signs of wearing off include tremor, stiffness, and difficulties in movement.

  • Dyskinesia

Dyskinesia entails involuntary body movement, which including jerking, twisting, and twitches. Dyskinesia mostly affects the limbs and the trunks. Not everyone with Parkinson's gets involuntary movement, and the effect varies from one person to another in terms of the frequency, severity, and timing. Dyskinesia is common in people with Parkinson's for a longer period and after long-term use of levodopa.

  • Hallucination

Hallucination is the perception of something that does not exist. It can be in the form of hearing, smelling, or visualizing. Hallucinations are mainly common for people who have had Parkinson's for a longer period.

When a person gets Parkinson's disease, symptoms such as difficulty walking, lack of balance, tremor difficulty speaking becomes part of their day-to-day life. These symptoms get worse with time as the disease progresses. Extra support is needed to ensure the patient stays active and has a healthy and quality life. You can use several ways to help your loved ones who are diagnosed with Parkinson's disease, which may include giving them time and ear to talk to and taking them to take their medications. Below are some of the ways you can offer help to your loved ones to manage the disease;

  • Learn everything you need to know about Parkinson's disease, including symptoms and how to manage the disease.
  • Offer voluntary services to the patient such as cleaning, cooking, and shopping.
  • Help the patient to get active by doing exercises.
  • Help the patient to feel normal and not do concentrate much on the disease.
  • Offer them a friendly listening ear.

Parkinson's ailment was first discovered as a neurological disorder in the year 1817 by a person known as James Parkinson. The disease was refined and expanded by Jean martin Charcot in the mid-1800 AD, explaining and disseminating Parkinson's disease to the international community. He separated Parkinson's disease from other tremor-related disorders and other neurological diseases and classified the disease as Parkinsonism plus disorder.

The early treatments of Parkinson's disease relied on anticholinergic medications and pragmatic observations, and the first trials were done in the early 1990 century. Dopaminergic insufficiencies in Parkinson's disease were later discovered, leading to levodopa's first human trial. Important studies in biochemical, anatomy and physiological research have developed a different neurosurgical and pharmacological approach to managing Parkinson's disease. Today clinicians have been offering therapies that are aimed to improve the quality of life of Parkinson diseases patient and has led to an impact in Parkinson management. The separation of Parkinson's disorder from other neurological diseases and the introduction of therapy have greatly expanded the knowledge of brain cells.

A good diet may have a great impact on a person diagnosed with Parkinson's disease. However, it is not all food that is recommended for patients suffering from Parkinson's disease. Some of the food that should be avoided by these patients include;

  • Food with high protein content.

Protein is very important as it completes a diet to make it a balanced diet. However, it is not advisable for a patient under Parkinson's medication to take food rich in protein. Proteins absorb a good amount of drugs that are supposed to control their symptoms.

  • Dairy products

Consuming a high amount of dairy product increases the chances of Parkinson's disease progression. It’s advisable to reduce dairy produce intake to reduce disease progression.

  • Hard to chew food

It is always advisable to avoid hard-to-chew food as it reduces the risk of patient choking.

  • Processed foods

People with Parkinson's disease experience constipation. Fiber is one of the diets that reduce constipation. Processed food does not have fiber in them.

  • Salty food

Salty food leads to problems like high blood pressure which make symptom of Parkinson to get worse.

  • Acidic food

Acidic food causes nausea which makes Parkinson's symptoms get worse.

It's crucial for doing exercises for people with Parkinson's. Exercises help to improve sleep, reduce depression, and strengthening your joints and muscles. Some of the best exercises include

  • Stretching and flexibility exercises.

Stretching and flexibility exercises help to reduce the rigidity of the muscles hence facilitating easy movement. It would be best to do the exercises at least thrice a week and focus on the areas affected by Parkinson's symptoms, such as the elbows, wrist, lower backs, and legs.

  • Aerobic exercises.

Aerobic exercises help one to lose weight as well as maintaining a healthy heart. Aerobic exercises include jogging, walking, swimming, biking, and running.

  • Strength training exercises.

Strength training exercises help in increasing your body's metabolism and in the burning of calories. The most common strength exercises include pushups, lifting weights, using weight machines at the gym, and squats.

  • Balance exercises.

Balance exercises help to improve mobility and helps in preventing one from falling. You can opt to do single-limb stance, back leg raises, and wall pushups.

Medication helps to manage Parkinson's symptoms and also improves the quality of life. The best medicines for Parkinson's disease treatment include.

  • Carbidopa-Levodopa

 It’s one of the most effective medications for the treatment of Parkinson's disease. It’s a natural chemical that usually passes in your brain to form dopamine. Levodopa combination with levodopa helps to reduce side effects such as nausea.

  • Dopamine agonistics.

The dopamine promoters help in the treatment of Parkinson's by mimicking dopamine effects in the brain. They include apomorphine and Mirapex. However, the medication may have negative side effects such as sleepiness and hallucinations.

  • Inhaled carbidopa levodopa

The medication helps manage symptoms when the oral medications do not work.

  • Anti-depressants.

Using an anti-depressant is the most common method for the treatment of Parkinson's. Anti-depressants such as desipramine, citalopram, fluoxetine, and sertraline work effectively.

  • Anticholinergics

Anticholinergics help in the treatment of tremors linked with Parkinson's disease. The medications help to reduce involuntary movements and to drool.

Parkinson's is painful, and studies show that about forty to eighty percent of the people diagnosed with the condition report that they feel pain. Feeling pain is one of the early signs of Parkinson's, and it's mainly due to the rigidity of the body. However, before jumping to the conclusion that the pain relates to Parkinson's, it's important to consult a doctor as the pain may be related to other health conditions such as arthritis.

You will experience the following pains.

  • Muscle and skeleton pains.

The pain mainly arises due to problems related to muscle joints and bones. The pains are bound to worsen as a result of the rigidity and the stiffness of the muscles.

  • Dystonic pains.

Dystonic pains arise from involuntary muscle contraction, which leads to abnormal posture. The pains are easily notable through the curling of the toes and turning inward of the foot. The pains can be very severe, thus leading to tremors.

  • Nerve pains.

You may experience sharp pains from the nerve root or the nerves.

Parkinson's disease mostly affects people of fifty years and above. The average age for the diagnosis of the condition is usually sixty years. The risks rise as the age increases. It's very rare for people below the age of fifty to acquire the disease. However, they can still be diagnosed with the condition. Young-onset Parkinson's is the term used to refer to Parkinson's disease for people between the age of twenty-one and forty years.

Young-onset Parkinson's may be a result of genetics. Symptoms of the condition include dystonia, increased involuntary body movement, dementia, and memory problems. Most of the patient experiencing this condition tends to have slower progression. You can treat the disease by taking dopamine receptors, anticholinergics, and levodopa medications.

Diagnoses of Parkinson's disease at an early stage may have both advantages and disadvantages. With early diagnosis, you may not be coping with other health problems. On the other hand, it might be more difficult to deal with the condition as you may be at the peak of your career and still parenting.

Genetic mutation and environmental changes are associated with factors that cause Parkinson's disease. Environmental factors such as exposure to herbicides and pesticides cause damage to dopaminergic cells, leading to Parkinson's disease.

Alcohol has been found to have protective effects on neurodegeneration and other vascular disorders. A good example is red wine. It contains flavonoids that have protective effects on vascular diseases and neuro cells. Research has confirmed there is a decrease in Parkinson's risk that is related to alcohol drinking. However, even though it has a protective effect on neurodegeneration, excessive alcohol consumption could lead to neurotoxic impacts on dopamine, resulting in Parkinson's.

Research show that moderate consumption of alcohol increases the chances of getting the condition. However, it doesn’t show the effects of heavy alcohol consumption in reducing the risk of getting the disease. Alcohol disorder has increased diagnosed with the condition, particularly the use of alcohol during the early ages.

Parkinson's disease is mainly characterized by rigidity, tremor, imbalance, and slowness of movement. Illnesses that mimic Parkinson's disease include.

  • Progressive Supranuclear palsy.

You can easily mistake progressive supranuclear palsy with Parkinson's disease, especially during the early stages, as the symptoms are similar. However, as the condition progresses, you may not other additional signs such as difficulties in swallowing and speech.

  • Corticobasal syndrome.

The condition is not that common. It usually starts with symptoms of affecting one limb. The syndrome has similar symptoms as that of Parkinson's disease. Nevertheless, other symptoms difficult in languages, difficulty in motor tasks, and abnormal posturing of the affected limb.

  • Dementia with Lewy bodies.

It's a condition that involves the building up of abnormal protein deposits, known as alpha-syncline, in multiple areas of the brain. The early symptoms of the disease include hallucinations, memory problems, and fluctuation of thinking. After a while, you can easily note Parkinson's symptoms such as rigidity and slowness.

Stress can be destructive in many parts of the human body, including the brain. Long-term stress can damage the brain dopamine, less dopamine in the human brain results in Parkinson's disease. People diagnosed with Parkinson's disease are always advised to reduce their stress level to manage the disease symptoms. Therapy, socializing with people around you, exercises and counseling are some of the best ways of stress management.

Guided breathing and meditation exercises are good options for stress management. The two ways suppress the production of hormones that causes anxiety. The exercises also trigger the production of dopamine in the brain, thus reducing Parkinson's disease.

Excess stress can lead to Parkinson's disease symptoms getting worse. Anxiety and stress cause tremors and other symptoms such as slow movement, loss of balance, difficulty speaking, and muscle and limb stiffness could worsen in Parkinson's disease patients. Some of these symptoms, such as tremors, may not respond to medications, and the only way will be to reduce stress.

A decrease in dopamine levels is the major cause of Parkinson's. Studies show that around fifty to sixty percent of dopamine neurons are usually damaged when diagnosed with Parkinson's. The decrease is mainly linked with a disorder of nerve cells in the brain, which produces the chemical. Dopamine is a neurotransmitter responsible for significant roles in our body, such as movement and memory. Muscle stiffness and tremor may be experienced when dopamine levels are low.

The dopamine neurons are responsible for producing dopamine, usually circulated to various parts, including the caudate and putamen nucleus. When the levels are low, there will be no coordination between the brain and the movement muscles. The lack of coordination sends abnormal patterns to the brain, thus resulting in impaired movement. Treatment of Parkinson's involves increasing dopamine levels to help reduce the symptoms of the Parkinson's condition. The doctor may advise using certain drugs to help improve dopamine levels to help treat the disease.

Anticholinergics are drugs used to treat Parkinson's condition. They work effectively, and you can use them during the early stages of Parkinson's disease, where the symptoms are mild. Anticholinergics help to treat Parkinson's by blocking the chemical messenger known as acetylcholine. The chemical is responsible for sending messages to the brain and from the nerves to the muscles. Excess amounts of acetylcholine may result in the brain becoming overreactive, thus leading to tremor. Taking anticholinergics is beneficial in the following ways.

  • Help to improve Parkinson's symptoms.
  • Anticholinergics help reduce the amounts of acetylcholine and helps to treat tremors where other medications do not work.
  • Improve slowness of movement.
  • Reduce involuntary movement of the eyes and one feeling depressed.
  • Helps in improving writing and speech difficulties.
  • Reduce drooling.

Anticholinergics help reduce the amount of saliva in the mouth, and it's beneficial for people who experience drooling or producing too much saliva.

Parkinson's is a neurodegeneration syndrome that is triggered by brain nerve cell damage. The disease causes slow body movement, loss of balance, muscle and limb stiffness, tremor, and shaking. Parkinson's disease affects affect older people, mostly at the age of 60. The condition is said to be hereditary, although it is rare. Hereditary diseases can be passed genetically from parents to children.

The condition has been found in different genetic mutations. It is possible to inherit genetic illness but not always. About 15 % of Parkinson's disease is related to genetic mutation; the rest are from unknown sources. The research has shown that having a parent or siblings diagnosed with Parkinson's disease increases the disease's risk by about 3 %. The study has also found other sources that may cause Parkinson's disease, including being old, particularly those at the age of 60 and above, being a male, being exposed to herbicide and pesticide.

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Parkinson's Essay on the Shaking Palsy (1817) is often thought to represent his greatest contribution to medi-cine.26 27 The study is based on six cases, some never actually examined by Parkinson but observed on the streets. The five chapters of this 66-page octavo volume include I. Definition History Illustrative Cases, II. Pathognomic symptoms examined Tremor Coactus Scelotyrbe Festinians, III. Shaking Palsy distinguished from other disease with which it may be confounded, IV. Proximate cause Remote causes Illustrative cases, V. Considerations respecting the means of cure. Apologizing for mere conjecture regarding the etiology of the shaking palsy, Parkinson states his duty to submit his opinions to the examination of others, even in their present state of immaturity and imperfection and mission to inspire research on this disease.26 Parkinson recognized the long duration and slowly progressive nature of the disease.

Antiparkinsonian Therapy And Hypersexuality

With the advent of antiparkinsonian therapy, reports of increased libido and sexual performance, hypersexual behavior (with or without concomitant hypomania), and rarely paraphilias have appeared in the literature.11-25 Comparisons cannot be made among studies, as different criteria were used to collect data. Due to the small size of the studies, the incidence of increased sexual drive in patients receiving treatment with antiparkinsonian therapy cannot be determined. The data does not provide a basis for identifying patients who might develop adverse sexual behavior in response to antiparkinsonian medications. Since the initial reports were conducted, medication regimens and dosages have changed. This also affects applicability of reports to current patient care. Not all early reviews found that levodopa increased sexual behavior.61 A review of 152 patients treated for parkinsonism between 11 1 68 and 7 31 69 did not find significant changes in patients' sexual interests.

Is Levodopa Neurotoxic or Neuroprotective

Homeostasis Parkinson Disease

One of the most controversial questions regarding the treatment of PD is whether levodopa is neurotoxic. The results of many in vitro studies have suggested that levodopa may be injurious to dopaminergic neurons (86,87). These findings have raised concerns that chronic levodopa exposure might hasten disease progression in PD patients. Accordingly, some physicians and patients have opted to defer the use of levodopa for as long as possible (28). Other physicians have continued to use levodopa as first-line therapy, arguing that in the absence of clinical evidence of toxicity (88-90), it is inappropriate to withhold the most potent symptomatic treatment for PDO. Until very recently, there was little clinical data to support or refute the possibility of levodopa toxicity.

Amylotrophic Lateral Sclerosis Parkinsonism Dementia Complex of Guam

Interestingly, in Guamanian ALS PDC patients, a-synuclein pathology is often present in multiple brain regions, including the substantia nigra and in the amygdala (47,48). Just as in AD and PD, the presence of multiple forms of brain amyloid in ALS PDC Guam (i.e., a-synuclein and tau filaments) suggests an

Parkinsons Disease After Charcot

Parkinson distinguished the rigidity of paralysis agitans from the spasticity associated with spinal cord damage, mentioning repeatedly his belief that the pathology of paralysis agitans resided in the medulla. In 1871, Dr. Meynert described damage to the corpus striatum and the lenticular nucleus.13 This may have been the first suggestion that the tremor of paralysis agitans as well as chorea might involve the basal ganglia. Drs. Murchison and Cayley described a case in 1871 of paralysis agitans.14 There was shrinkage of the cerebral hemispheres, thickening of the spinal cord and infiltration of the spinal cord with connective tissue and inflammatory cells probably related to typhus. In 1878, Dr. Dowse described a case of a patient who died at age 43.15 No gross lesions were found the central nervous system however, there was pigmented granular degeneration of nerve cells along the spinal cord and diffuse sclerosis in white matter tracts.

Summary of Clinical Phases of Levodopa Therapy

One can usually discern four clinical phases of PD in relation to treatment with levodopa. When levodopa is first introduced, there is a long-duration response from each dose, with few motoric complications. This is the initial period of maximum benefit without adverse motor effects. The duration of this phase varies, but usually lasts two to three years. With continuing treatment, the duration of beneficial response gradually shortens in almost all patients (56), who then need to take levodopa more frequently during the day to minimize the duration of the off (relatively immobile) periods in addition, patients often develop dyskinesias at peak plasma levels of levodopa parallel to the timing of their doses. After approximately five years of levodopa therapy, 75 of patients have either developed troublesome response fluctuations ( wearing-off and on-off phenomena) or troublesome dyskinesias (1).

Dopamine And Treatment Of Parkinsons Disease

Given this pathology, a logical approach to treating Parkinson's disease would be to try to restore the levels of dopamine in the CNS. It was well known that dopamine does not cross the blood-brain barrier because of its positive charge. However, zwitterionic amino acids had the advantage of broadly specific transport systems to carry them across this barrier into the brain. Based on this, a top candidate for increasing dopamine levels in the CNS would be its immediate precursor, L-dihydroxyphenylala-nine or L-dopa. Not only could L-dopa be transported across the blood-brain barrier, it also had the advantage of by-passing the rate limiting step in the synthesis of catecholamines, tyrosine hydroxylase. This, in turn, provided two advantages. First, it avoided the slowest step in the synthetic process. In addition, tyrosine hydroxylase had been shown to be present only in catecholamine-containing neurons in the CNS, the very neurons that were disappearing in Parkinson's disease.

The Hoehn and Yahr Scale 1967

It is a truism that Parkinson's Disease was and is a clinical diagnosis there are no laboratory tests, no imaging techniques, no genetic markers to confirm the diagnosis. It is the clinician's decision. This judgment nicely combines the art and science of medicine but the first attempt to supply a scientific basis for this judgment appeared in Hoehn and Yahr (1967). This is Melvin Yahr's most famous paper (at least 2886 citations by mid-January, 2004) because it laid the foundation for measuring Parkinsonism. and mortality of Parkinson's Disease given the then paucity of information about the natural history of the condition. This would subsequently give the background upon which to judge the effectiveness of the newly introduced L-dopa therapy. Hoehn and Yahr reported on 802 subjects derived from a retrospective clinical sample of 856 patients diagnosed with paralysis agi-tans, Parkinson's Disease and Parkinsonism seen at the Columbia-Presbyterian Medical Center from 1949 to 1964.

Experimental Approaches To Brain Iron Loading

Gsh Transporter Bbb

The neurotoxins (MPTP) and 6-hydroxydopamine (6-OHDA), induce many of the pathological changes that occur in PD and are widely used as animal models of this disease. MPTP induces nigral degeneration in several species including rat, mouse, dog, cat, and monkey (reviewed in 151 ). Essentially, MPTP will cross the BBB to be converted by monoamine oxidase B in glial cells to the active form, 1-methyl-4-phenylpyridinium (MPP+ ) (Figure 23). MPP+ will accumulate in dopaminergic cells prior to its entry into mitochondria, via an energy-dependent mechanism. MPP+ will inhibit mitochondrial activity leading to decreases of ATP levels, thereby inducing cell death. MPTP induces changes in iron metabolism, up-regulating the expression of both transferrin and lactoferrin receptors, as well as increasing free iron content in substantia nigra. Oxidative stress occurs which is associated with cellular changes of both GSH-GSSG ratio and cytoprotective enzymes.

Neuromelanin and Iron

Histochemical studies ascribe the localization of iron in the SN primarily to the glial compartment and changes in glia-associated ferritin have been described in PD. While some iron sequestration appears to occur in a-synuclein in Lewy bodies, the importance of this iron for neurodegeneration is unknown. A more important source of intraneuronal iron involved in the oxidative pathway is neuromelanin, which characterizes the dopaminergic neurons in the human SN. Neuromelanin occurs as granules, possibly inactivated lysosomes, within the neuronal perikaryon. Neuromelanin is a dark polymer pigment produced in specific populations of catecholaminergic neurons in the brain. Interest in this pigment has increased in recent years because of a hypothesized link between neuromelanin and the special vulnerability of neuromelanin-containing neurons in cell death in PD.

Discovery Of Dopamine As A Neurotransmitter

The discovery that dopamine itself is a neurotransmit-ter, similar to norepinephrine and acetylcholine, proved to be a major scientific breakthrough for the understanding of several neurological and psychiatric diseases, including Parkinson's disease and schizophrenia, but it required another 20 years work to establish this. Dopamine was known to be an intermediate in the synthesis of norepi-nephrine and epinephrine, the product of aromatic amino acid decarboxylase acting on L-dihydroxyphenylalanine. Initially, dopamine was thought to be simply a precursor to norepinephrine and epinephrine, since it was found in extremely low levels and norepinephrine had been shown to be the primary transmitter of the sympathetic nervous system.12 The presence of dopamine in greater than trace amounts was demonstrated by Holtz and von Euler in urine, and in the adrenal gland and the heart of sheep by Goodall.13-15 This began to raise the question of whether dopamine was only a metabolic intermediate.

Phosphorylation and Glycosylation

Phosphorylation is a common mechanism for regulating the activity and function of proteins. In AD, phosphorylation of the cytoskeletal protein tau is associated with disease (102), and it is reasonable to suspect that a similar mechanism may be involved with a-synuclein in PD. In vitro, it has been shown that a-synuclein can be phosphorylated at serine 129. In transfected cells, this phosphorylation is insensitive to stimulation of PKC and protein kinase A (PKA), and at steady state the majority of a-synuclein is unphosphorylated (103). In vitro, a-synuclein can be phosphorylated by both casein kinase 1 and casein kinase 2, but not by PKA or PKC. a-Synuclein can also be phosphorylated by G-protein coupled receptor kinases (GRKs), with GRK5 preferentially phosphorylating a-synuclein, while GRK2 A rare glycosylated form of a-synuclein, a-Sp22, has been precipitated from human brain extracts.

Proaggregation Factors

The presence of tau in some Lewy bodies of sporadic PD60 4. A slight but confirmed over-representation of the tau H1 haplotype in patients with PD63 An important clue to the dopaminergic predilection of cellular damage in PD arises from the observation that dopamine inhibits the maturation of toxic protoaggregates to insoluble, probably nontoxic, or less toxic, fibrils by forming adducts.64 Other catecholamines tend to have similar activity, perhaps explaining the involvement of other catecholaminergic nuclei in PD. In light of the reported epidemiological association of PD with exposure to industrial metals, it is intriguing that a-syn interacts with ionic forms of copper, iron, aluminum, and zinc.65-67 Neuromelanin acts as an iron sink and may present a source of that metal to stimulate a-syn aggregation under certain conditions.68,69 Pesticides, a heterogeneous class of chemicals epidemiologically associated with PD, also enhance a-syn aggregation.67

Nigrostriatal Pathway And Pd

Magnetic resonance imaging (MRI) studies of normal subjects reveals a negative correlation of age with estimated midbrain volume, anteroposterior diameter through the substantia nigra, and interpeduncular distance. The linear measurements for the right and left side were found to be almost identical demonstrating symmetry of normal age-related changes between the right and left side of the brain, a laterality finding that is in contrast to idiopathic PD.2 Ultrastructural analysis of neurons of the substantia nigra in four normal aged subjects revealed changes characteristic of apoptosis, including cell shrinkage and chro-matin condensation in 2 of melanized neurons.116 Although the endoplasmic reticulum appears normal, mitochrondria are markedly shrunken. Fragments of mel-anized neurons are found in glial cells. Evidence of autophagic degeneration or necrosis are not detected in melanized neurons.

Rigidity

James Parkinson never mentioned rigidity as a main feature of the disease in his original essay,1 though he did describe features that can be attributed to rigidity. Clinical series have reported that rigidity occurs in 89 to 99 of patients with PD.18-21 The cogwheel phenomenon is a particular type of rigidity occurring in PD, and it refers to rhythmic brief increases in resistance that are palpated during passive movement.17 Cogwheeling is thought to be tremor superimposed on rigidity.22 It is a common misconception that a patient must have cogwheeling on examination to merit a diagnosis of PD. Many instead will have lead pipe rigidity, which is smooth throughout the entire range of motion. Rigidity, like tremor and bradykinesia, often presents unilaterally, progresses Rigidity affects both limb and axial musculature and contributes to the postural deformities seen in PD. The stooped or simian posture and lateral tilt of the trunk are common sequelae of axial rigidity.

Cyp2d6

This CYP has been most often associated with Parkinson's disease CYP2D6 inactivates the neurotoxins MPTP and TIQ as well as a variety of pesticides and endogenous neurochemicals. Genetic variation affects CYP2D6 expression levels in brain in the same way as in liver, for example individuals who are heterozygous for the *4 deletion allele have lower brain CYP2D6 levels than wild type individuals, and individuals homo-zygous for the *4 allele do not express CYP2D6 in brain, as found in liver (Miksys et al., 2002). We have shown that rat brain CYP2D is enzymatically active, and this activity correlates with CYP2D protein expression among brain regions (Miksys and Tyndale, 2004). In human brain, CYP2D6 protein and mRNA expression vary among regions and are restricted to specific cells such as pyramidal neurons in the CA1 region of hippocampus and frontal cortex layer III, and pigmented cells of the substantia nigra (Miksys et al., 2002).

Sensory Symptoms

Numbness is the most common term used by patients with PD to describe unwanted somatic sensations. Other patients describe tingling, others burning, yet others itching or crawling. Some experience focal coldness as though the limb were going to sleep. The extent to which all these different descriptions reflect differing pathophysiology or semantics is uncertain. When asked what they think is the origin or depth of these types of sensations, most patients chose skin rather than muscle or bone. This class of symptoms will be referred to as parasthesias for the remainder of the chapter. These superficial parasthesias are common in the more parkinsonian arm or leg as compared with the contralateral side. They can last for hours at a time or can be continuous. Internal tremors, the subjective experience of rhythmic truncal vibrations in the absence of visible tremor, occur in PD patients only some of whom also have visible limb tremors.

Table of Contents

Chapter 1 James Parkinson Chapter 2 Paralysis Agitans Refining the Diagnosis and Treatment Chapter 3 The Role of Dopamine in Parkinson's Disease A Historical Review Chapter 4 Parkinson's Disease Where Are We Chapter 5 Epidemiology of Parkinson's Disease An Overview Chapter 6 Environmental Toxins and Parkinson's Disease Chapter 7 Rural Environment and Parkinson's Disease Chapter 8 Industrial and Occupational Exposures and Parkinson's Disease Chapter 9 Tetrahydroisoquinolines and Parkinson's Disease Chapter 10 Xenobiotic Metabolism and Idiopathic Parkinson's Disease Chapter 11 Progressive Neurodegeneration in the Chronic MPTP Probenecid Model of Parkinson's Disease Chapter 12 Alpha-Synuclein and Parkinson's Disease Chapter 13 Parkin and Its Role in Parkinson's Disease Chapter 14 Heredofamilial Parkinsonism Chapter 15 Other Mutations Their Role in Parkinson's Disease IV.

Dysphagia

As noted earlier in this chapter, the act of swallowing requires multiple muscles in the mouth, throat, and esophagus to produce a precisely controlled and coordinated cascade of movement. This, perhaps not surprisingly, turns out to be difficult for the individual with PD. Survey studies reveal a rather broad range of positive responses when PD patients are asked whether they perceive difficulty swallowing. While the two large survey studies67 each catalogued a subjective sense of dysphagia in approximately 50 of participants with PD, other studies have suggested that anywhere from 30 to 82 of PD patients may be aware of difficulty swallowing.76-79 The reason for this broad range is uncertain but may simply reflect the degree of detail in the questionnaire.79 While most attention regarding dysphagia in PD has centered on oropha-ryngeal abnormalities, it is clear that esophageal dysfunction may also play a role in the generation of dysphagia in some individuals.

Colonic Dysmotility

Recognition of this definitional revision is important when reviewing reported frequencies of constipation in PD. Older studies indicate the presence of constipation in roughly 50 to 67 of PD patients,6 139 140 but in more recent communications using the contemporary definition, frequencies of 20 to 29 have been reported.7,141 Multiple studies have documented that the physiological basis for decreased bowel movement frequency in PD is slowed colonic transit of fecal material. Colon transit studies, employing radiopaque markers, have indicated that as many as 80 of persons with PD may have abnormally prolonged transit times.142 Reported colon transit times in PD patients have varied rather widely for reasons that are not clear. Jost and Schimrigk initially reported an average colon transit time (CTT) of 5 to 7 days (120 to 168 hr) in a group of 20 persons with PD,142 and in a subsequent study of 22 subjects in whom CTT could be measured, the average time was 130 hr.

Ecogenetic theory

Parkinson's disease is the result of environmental factors acting on genetically susceptible individuals against a background of normal ageing'' (Barbeau, 1985). Intense interest in environmental exposures as risk factors for PD developed in the 1980s after reports confirmed that intoxication with the synthetic meperidine derivative, MPTP, could reproduce the features of PD in humans and animals. This stimulated a search for exogenous or endogenous molecules with similar effect. This also prompted a multitude of epidemiological surveys to assess potential environmental risk factors for Parkinson's disease. It is now clear that a number of classes of molecules have an ability to induce parkinsonism in animals and humans. Examples include the mitochondrial toxin rotenone, proteasomal pathway inhibitors and certain heavy metals. In addition, epidemiological surveys, mostly using a case-control experi That genes are important in the aetiology of PD is unequivocal.

Inhalation Of Convulsant Substances

Sensorimotor Cortex Rats

The pattern of metabolic involvement depends on the seizure type and whether in ictal or postictal state (Veliskova et al., 2005, in press). In immature rats, mild seizures induce decreases in 2DG uptake while severe seizures produce increases in the brain-stem and decreases in the cortex (Szot et al., 2001). In adult rats, c-fos immunoreactivity after flurothyl seizures was found throughout the cortex PN10 rats had immuno-positivity only in the deep neocortical layers (Jensen et al., 1993). This approach is frequently used to create an acute or chronic seizure focus in a particular brain area, usually in the cortex. Additional structures may be injected with a con-vulsant substance, such as the hippocampus, amygdala, substantia nigra, area tempestas, etc. Many of the convulsant drugs can be injected in a solution into the brain ventricular system. Some of these ICV administrations have already been mentioned herein.

Drugs That Interfere With Norepinephrine Storage

The most troublesome untoward effects of treatment with reserpine involve the CNS. Sedation and depression are the most common, although nightmares and thoughts of suicide also occur. Reserpine treatment, therefore, is contraindicated in patients with a history of severe depression. The occasional report of re-serpine-induced extrapyramidal symptoms, which are similar to those seen in patients with Parkinson' s disease, is believed to be a result of dopamine depletion from neurons in the CNS.

Basal Cisterns Cisternogram

Nuclear Cisternogram

Predicting response to dopaminergic therapy in patients with a parkinsonian syndrome might also be possible. The striatal complement of D2 dopamine receptors is normal (or even increased through receptor up-regulation) in Parkinson's disease since the lesion resides in the nigro-striatal fibres (Fig. 8). In diseases such as progressive supranuclear palsy or syndromes producing primary striatal degeneration the D2 dopamine receptor concentration is reduced. The latter are not responsive to dopaminergic therapy since the defect is on the receiving end of the dopaminergic transmission process. This could be quite useful since even in specialised centres Parkinson's disease and parkinsonian syndromes are confused in up to 20 of patients. a Parkinson's Disease Figure 8. Abnormal dopamine neurotransmission in (A) idiopathic Parkinson's disease and (B) primary striatal lesion causing parkinsonism.

Pharmacological Effects Of The Cholinergic Blockers

These drugs are used to treat Parkinsonism, a condition characterized by excessive cholinergic activity in the brain. This condition results in an inability to perform fine motor movements. i. Trihexyphenidyl (Artane ). This drug is used in the treatment of parkinsonism. Side effects that can be caused by trihexyphenidyl include constipation, difficult urination, dizziness, dry mouth, and reduced perspiration. Patients taking this preparation should be told several things. Do not take with alcohol or other central nervous system depressants. Some patients perspire less therefore do not become overheated because of exercise or hot weather. j. Benztropine (Cogentin ). Benztropine is used in the treatment of parkinsonism. The side effects and patient instructions for trihexyphenidyl (Artane ), above, also apply to benztropine. k. Levodopa (Larodopa ). This drug is used in the treatment of parkinsonism.

Terminology Used in Describing Movement Disorders

Affects the hands, but it may also involve the head, jaw, voice, tongue or lower limbs. Resting tremor occurs while the limb is not active. The typical resting tremor is the finger and wrist tremor in Parkinson's disease (PD). This is seen while the hand is resting on the patient's lap. Action tremor can be postural (seen during sustained posture, e.g. hands in the outstretched position), intention (during trajectory movement, e.g. finger-nose-finger), or task-specific (seen while performing a specific activity, e.g. only while writing). Bradykinesia literally means slowness of movement. It is a term used to describe slowness of voluntary movements, such as that seen in PD. The amplitude of fine movements is typically decreased. When there is a lack of movement, the term akinesia is used. Akinesia is frequently used interchangeably with bradyki-nesia. Freezing is an arrest of gait and is usually associated with bradykinesia.

Movement disorders extrapyramidal diseases

Bradykinesia - a loss or slowness of voluntary movement. This is a major feature of Parkinson's disease and produces 2. Postural disturbance - most commonly seen in Parkinson's disease. In Parkinson's disease both positive features, e.g. tremor, and negative features, e.g. bradykinesia, occur.

The memory system that subserves the above

The aforementioned data have been taken to indicate that amnesics can acquire nondeclarative information, and that mediotemporal brain structures damaged in 'global' amnesics ( hippocampus, limbic system) are necessary for declarative but not for nondeclarative tasks. But is this indeed due to the existence of different brain circuits for declarative and nondeclarative information, respectively The argument could still be raised that declarative and nondeclarative memory are subserved by the same circuits, but there is a general impairment in the processing of information in the brain, that affects only declarative memory.4 Compelling evidence against this single-system hypothesis was provided by double-dissociation experiments. 'Double-dissociation' refers to a protocol in which the effect of two different circumscribed lesions, in areas A and B, is tested on two different phenotypes, X and Y (Teuber 1955 control).

Treatment Management And Cost

The discovery of the dopaminergic deficit was the major turning point in the development of rational pharmacotherapeutic approaches to PD leading to the introduction of levodopa and later dopamine agonists. With the exception of anticholinergics and amantadine, all other drugs subsequently developed (dopa-decarboxylase inhibitors, monoamine oxidase inhibitors, catechol-O-methyl transferase inhibitors) act indirectly through dopaminergic mechanisms (1,19). Functional surgery, developed many years ago as a palliative approach to the therapy of PD, has more recently become an important therapeutic option (19, 20). Figure 3.8.1 Cost distribution in Parkinson's disease Figure 3.8.1 Cost distribution in Parkinson's disease Initiation of therapy depends on the age and mental status of the patient and the severity of the disease. In young patients, there is evidence supporting the postponement of more potent medications such as levodopa to prevent early development of motor complications.

Health Promotion And Disease Prevention

Comfort Zone Fear Learning Growth

The concept of disease prevention is more specific and comprises primary, secondary and tertiary prevention (12). Primary prevention is defined as preventing the disease or stopping individuals from becoming at high risk. Universal and selective preventive interventions are included in primary prevention. Universal primary prevention targets the general public or a whole population group without an identified specific risk (e.g. iodine supplementation programmes to prevent neurological and other disorders caused by iodine deficiency). Selective primary prevention targets individuals or subgroups of the population whose risk of developing disease is significantly higher than average, as evidenced by biological, psychological or social risk factors (e.g. prevention of stroke through adequate management of hypertension, diabetes and hypercholesterolemia).

Trimethyltin Neurobehavioral Toxicity and the Learning Performance Distinction

And a review of the sparse clinical literature, was equally discouraging.3738 Use of gangliosides for treatment of human neurodegenerative disorders and CNS trauma has essentially been discontinued or terminated by government decrees because of potential toxicity (i.e., because of its association with neuropathological symptoms appearing after administration of gangliosides to patients), except for perhaps a few clinical trials in the U.S. and elsewhere for Parkinson's disease.

Oxidative stress OS and formation of free radicals

Increased levels of oxidative damage to DNA, lipids, and proteins have been detected in postmortem tissues from patients with PD, AD, ALS, PSP, and related disorders, and at least some of these changes may occur early in disease progression (85,103,110). Recent studies showed that lipid peroxidation is an early event in the brain in amnestic MCI suggesting that oxidative damage occurs early in the pathogenesis of AD (111). Toxic interactions between reactive transition metals and free radicals are regulated by reduced glutathione (GSH). Perturbations of its metabolism are documented in neurodegenerative disorders, associated with abnormalities in copper homeostasis (112) and redox balance (104,113). Oxidative damage has been shown to be the earliest event in AD (106,114,114a,115,116), PD, other neurodegenerative processes, but also in normal aging (101,117).

Nootropic Brain Chemistry 101 - Homeostasis & Neurotransmitters

It is also theorized that people with low Dopamine or dopaminergic activity may be more likely to become addicted to stimulant drugs like cocaine or highly dangerous and daring acts such as gambling and sexual promiscuity. These people are likely seeking the high associated with Dopamine and endorphin release that is missing from their natural chemistry.Although Dopamine sounds great, high levels of Dopamine or a dysfunction of regulation can have extremely negative consequences. Disorders such as Borderline Personality Disorder, Parkinson's disease, Schizophrenia, ADHD and Psychosis have all been linked to Dopamine dysfunction. Apart from these disorders, high Dopamine has also been linked to aggressive and impulsive behaviour.

How Do Nootropics Work?

Excess glutamate levels can accumulate outside of cells and cause toxicity in the brain. Glutamate receptor malfunctions in the brain are thought to be a factor in neurological diseases like Parkinson's and Alzheimer's. ADHD and autism are also thought to be caused in part, by a malfunction of the glutamatergic system

6 Different Types Of Nootropic Stacks

Levodopa (L-Dopa) from the Mucuna plant works to increase dopamine levels and to a lesser extent, serotonin. Increasing both of these monoamine neurotransmitters may improve cognitive function. The dopamine neurotransmitter is related to focus, learning and motivation whilst, serotonin can help to improve mood, memory and promote calmness in some people.

Cdp Choline Vs. Uridine: What's The Difference?

Citicoline is a naturally occurring brain chemical used as a medication for patients who have a wide variety of health conditions such as dementia, Alzheimer's disease, Parkinson's disease, glaucoma, ADHD and head trauma. Research indicates that taking the supplemental form of Citicoline can have a positive impact on the user's cognitive functionality and memory retention. In one study, patients received 500 mg of this nootropic twice a day. They experienced significant differences in memory retention and their body's ability to ward off the decline of their cognitive functionality versus the control group.

New Nootropic Drugs - Meet the Ampakines

This ampakine is being investigated by Eli Lilly and has shown great promise in improving cognitive functioning in animal models. LY-404187 also has possible promise is treating Schizophrenia, Parkinson's disease and ADHD. Not all of these possible applications relate to the primary AMPA potentiation method of action. It is unsure if Eli Lilly will move ahead with LY-404187 as they have a large group of biarylpropylsulfonamide derivatives to work with and may decide to proceed further with any of them. This ampakine has been the most researched by Eli Lilly. Like LY-404187, it also seems to have a stimulation of BDNF in the hippocampus. LY-503430 is a potent ampakine nootropic with neuroprotective effects. It is being investigated for use in Alzheimer's, Parkinson's, Schizophrenia and depression.

6 Nootropics Show Promise In Combating Anxiety And Depression

This nootropic has been looked at primarily as a possible treatment for dementia and Parkinson's disease. But some researchers took the initiative to see if Citicoline could have positive benefits for people who suffer from depression and methamphetamine addiction. The results of this clinical test were very informative, and they offer hope for people with depression and addictive personalities. The number of depressive symptoms that were experienced by patients who were given 2,000 mg per day for 12 weeks was significantly lower than those in the placebo group. In fact, they improved by 28 points on the IDS-C rating scale.

An Intro To Neurotransmitters And Cognition

Dopamine (DA) is well known as the pleasure chemical. It was also initially connected to issues with decision making in Parkinson's patients. Parkinson's is a cognitive impairment that is often rooted in dopamine issues. DA is also involved with focus, vigilance, attention and motivation. Dopamine is released when you have achieved something and is tied in with the reward-feedback circuit in behavior. Dopamine is also implicated in addiction issues and imbalances can be a part of the mental imbalance known as schizophrenia. Norepinephrine (NE) is a catecholamine, like dopamine and serotonin. It is also classed as both a hormone and neurotransmitter. NE is considered to be related to mood, vigilance, focus, memory and stress response. It has been linked with cognitive functions related to mood, arousal, vigilance, focus, memory, and stress response. Some recent research is trained on its role in both post-traumatic stress disorder (PTSD) and Parkinson's disease.

What Is Nootropic Cycling

Velvet bean extract contains l-Dopa, the precursor to dopamine. Even patients who are prescribed l-Dopa for Parkinsons or other conditions are urged to take a drug holiday where they abstain for a day or two on occasion.One trick is, if you notice the same amounts of a compound not offering palpable effects, it is probably time to ease off and take a break. You might want to find another route to get the same effects. For instance, after a couple weeks taking a racetam to boost acetylcholine production for learning and memory, you might want to try something like Huperzine-A or Bacopa monnieri which are acetylcholinesterase inhibitors. Acetylcholinesterase in the enzyme that causes acetylcholine to break down in the synaptic gap. It essentially makes the same amount of acetylcholine last longer, the way it works is somewhat similar to how traditional antidepressant SSRIs (selective serotonin reuptake inhibitors) work.

Amygdala

Amygdaloid Nucleus

Over the years, circumscribed lesions in monkeys and rodents, cases of diseased and injured amygdala in humans, and recently functional neuroimaging, have all been employed to investigate the role of the amygdala in learning and behaviour. The effect of amygdala dysfunction on a number of recognition tasks, including delay tasks and visual and cross-modal associations, was first taken to imply that the amygdala plays a major part in these tasks however, later studies indicated that the impairment was due to damage to the adjacent rhi-nal cortex, which was injured together with the amygdala in the original lesion experiments (Zola-Morgan et al. 1989a,b Murray et al. 1993). In contrast, conclusive evidence for the involvement of amygdala in learning and memory was found in other types of tasks, which engage fear and emotional memory (Adolphs et al. 1995 Maren and Fanslow 1996 Rogan and LeDoux 1996 Scott et al.

Corticosterone

P450 reductase activity, protein (37) and mRNA (37,38) have been reported in the brain. Cytochrome P450 reductase immunoreactivity was detected mainly in neurons, but was also found in some glial populations, and it appears to be expressed widely in the rat CNS (37). Immunocytochemistry and in situ hybridization detected P450 reductase protein and mRNA in many forebrain areas including the olfactory bulb, the cerebral cortex, caudate putamen, globus pallidus, hypothalamus, thalamus, and hippocampus. Cytochrome P450 reductase was also detected in the nucleus of the posterior commissure, superior colliculus, intermediate gray layer, periaqueductal gray, and in the molecular, Purkinje, and granular layers of the cerebellum. In the brain stem, cytochrome P450 reductase was detected in the substantia nigra, nucleus locus coeruleus and raphe nucleus. These are many of the same regions that express P450c17 in the developing rodent CNS (33).