Essay on Parkinson’s Disease and Action of Drugs on Movement

Parkinson 's disease is a progressive neurologic degenerative disease of the Central Nervous system. The brain produces Dopamine and Norepinephrine, which are chemicals needed for smooth muscle movement and coordination, heart rate, and blood pressure. Dopamine and Norepinephrine are released by basal ganglions that are produced in a bundle of nerve cells in the brainstem called substantia nigra. In Parkinson 's patients, the substantia nigra are destroyed and neither of the chemicals can be released into the body. (3) The decrease in Norepinephrine causes heart arrhythmia and low blood pressure, causing the person to get dizzy upon standing or tire easily. The lack of Dopamine, the smooth muscle movement and coordination controller is now gone, or significantly decreased, resulting in the first signs of Parkinson’s disease, pill-rolling, a one handed tremor and a decreased appetite. (2)

Sayer begins to consider LDOPA as a possible cure for the patients. Sayer considers LDOPA due to its reputation as a “miracle drug” in Parkinson’s patients. LDOPA functions as a precursor to the catecholamines dopamine, epinephrine, and norepineprine and, as a precursor, serves to treat Parkinson’s patients by increasing their levels of dopamine.

The major support and refutation of the dopamine hypothesis has come from the examination of dopamine receptors in these regions of the brain. There are two main types of dopamine receptors, D1 and D2. However, within the category of D2 receptors, there are three subtypes, D2, D3, and D4. (5) Through PET scan analysis of dopamine usage in the brain and post-mordum molecular analysis of brain tissue, researcher were able to determine relative levels of dopamine receptors in patients with schizophrenia compared to non-schizophrenics. Overall analysis of dopamine

Parkinson disease (PD), also referred to as Parkinson’s disease and paralysis agitans, is a progressive neurodegenerative disease that is the third most common neurologic disorder of older adults. It is a debilitating disease affecting motor ability and is characterized by four cardinal symptoms: tremor rigidity, bradykinesia or kinesis (slow movement/no movement), and postural instability. Most people have primary, or idiopathic, disease. A few patients have secondary parkinsonian symptoms from conditions such as brain tumors and certain anti-psychotic drugs.

PD is the second most common neurodegenerative disease featured pathologically by the progressive loss of dopaminergic neurons in the substantia nigra. The typical symptoms of PD include slowness of movements (bradykinesia), muscle stiffness (rigidity), tremor, and balance disturbance. Etiopathologically, PD is considered to be caused by the significant loss of dopaminergic neurons in the substantia nigra pars compacta and the subsequent dopamine depletion at the striatum. To date, there are only symptomatic treatments available for PD, particularly in the early stages of the disease. No therapy has been found that can cure or halt the progression of the disease.

Parkinson’s and Alzheimer’s disease are two degenerative brain diseases that differ in their symptoms, causes, treatment, physical and biological indicators. Per Hooley et al. (2017), Parkinson’ disease is thought to be caused by an extended reduction of dopamine, which the absence of constrains normal neural impulses in the brain. After some time, movements such as tremors, stammered speech, diminished or unintentional body movements are demonstrated. Those that suffer from Parkinson’s disease often have an incapability to swallow and muscle stiffness that affects muscles in their faces with mental deterioration occurring as the disease progresses. Parkinson’s disease can be traced to gender and genetics and most of those affected are men that have a family history of the disease (APA, 2013). Treatment for Parkinson’s disease encompasses dopamine precursors to increase the presence of dopamine.

Parkinson’s Disease is a long-term progressive neurodegenerative disease consisting of motor system impairment, neuropsychiatric, and nonmotor features. The disease is characterized by the following key clinical features: bradykinesia, resting tremor, postural instability, and rigidity. These symptoms are due to the diminishing of dopamine in the nigrostriatal pathway and substantia nigra, which causes inhibition of the thalamus decreasing excitatory input to the motor cortex.1 Along with the key manifestations an individual with Parkinson’s Disease will experience problems associated with the disease or the antiparkinson medications. These co-occurring problems are hallucinations, dementia, daytime sleepiness, fatigue, depression, and pyschosis.2 Psychosis is a common problem in Parkinson’s Disease, and is characterized by paranoid delusions and hallucinations that are visual in nature.2 Risk factors for psychosis consists of advancing age, dementia, sleep disorders, and high doses of antiparkinson drugs.1

Dopamine is a brain chemical/Neurotransmitter that work as messenger signal between the Substantia Nigra to the next relay station of the brain, the corpus striatum which helps to produce smooth coordinate movement and also plays a major role to help control muscle’s movement. With Parkinson’s disease, the brain cells that produce dopamine slowly die, which lead to decrease production of Dopamine. The loss of dopamine causes abnormal nerve firing with brain and the cells that control muscle’s movement by sending the messages to the muscles; due to this it becomes really hard to control muscles movement and cause tremors and various other symptoms such as rigidity and difficulty walking and performing daily tasks. Dopamine is not the only neurotransmitter involved in Parkinson’s Disease. Norepinephrine is very relatively close to dopamine and is also involved in Parkinson’s Disease. Individuals with Parkinson’s Disease have loss of nerve ending that produce norepinephrine. Norepinephrine is a major neurotransmitter for sympathetic nervous system, which control many autonomic functions of our body; it causes increase in blood pressure and heart rate. Loss of norepinephrine can help us explain the non-motor symptoms associated with Parkinson’s Disease such as fatigue, decrease in gastric stability and disruption in cognition. Parkinson’s Disease can be hereditary

Focus Statement: Levodopa (L-DOPA) is a drug which enters the brain and changes its composition to dopamine, a neurotransmitter that is low in Parkinson's disease.It is a most popular treatment to control the symptoms of Parkinson’s disease.

Parkinson’s disease is affected by the degeneration of dopaminergic neurons which is responsible to produce dopamine. Dopaminergic neurons have their cell bodies in substantia nigra pars compacta (SNpc) in basal ganglia (O’Sullivan and Schmitz, 2007). Basal ganglia are a collection of interconnected gray matter nuclear masses deep within the brain”. These gray matter masses are caudate, putamen, globus pallidus, subthalamic nucleus and the substantia nigra. Basal ganglia receive its input through striatum (O’Sullivan and Schmitz, 2007).

In the basal ganglia, one of the crucial neuro modulator is dopamine. It interacts with basal ganglia output nuclei and regulates the motor activity. In Parkinson’s disease dopaminergic neuron Substantia Nigra Pars Compacta(Snc) degenerated which is the main provenience of dopamine origination. The authors of this paper performed in vivo studies on primates and the experimental results showed that how the pallidum (GPi, Gpe) react to the dopamine

Parkinson’s Disease is a very common disorder these days. Over 10 million people live daily with Parkinson worldwide. Parkinson’s Disease was named after an English surgeon James Parkinson who wrote a detailed description essay called Shaking Palsy in 1817. The average age for Parkinson’s Disease is between 45 to 70 years old but you can also have juvenile or young onset as well. Most common symptoms of Parkinson are tremors, bradykinesia or akinesia, or rigidity or stiffness, and balance disorder. Parkinson’s Disease doesn’t have a cure and the cause is unknown it could be a number of things genetics, environmental triggers, age, or gender. Parkinson’s Disease happens because the dopaminergic neuron dies and

Dopamine is a neurotransmitter in the brain that is extremely important in the functions of movement, memory, pleasurable reward, behavior and cognition, attention, inhibition of prolactin production, sleep, mood, and learning (Mandal, 2015). There are consequences of having too much or too little of dopamine in the body; it can cause several disease conditions such as Parkinson’s disease and drug addiction. According to Dr Anaya Mandal, “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”. Basal ganglia is part of the brain that controls and regulates movement (Mandal, 2015). It helps a number of functions such

Parkinson 's disease is a chronic progressive movement disorder of the central nervous system. Early in the course of the disease, the most obvious symptoms are movement-related; these include shaking, rigidity, slowness of movement and difficulty with walking and Parkinson’s like gait (leaning forward, small fast pace steps, shuffling, etc.). Parkinson’s involves the malfunction and death of nerve cells in the brain, entitled neurons. Although damage can be spread about, it primarily affects neurons in an area of the brain called the substantia nigra. The substantia nigra controls voluntary movement, produces the neurotransmitter dopamine, and regulates mood. When taking an in-depth look into the changes a Parkinson’s patient goes through, we see symptoms clearly connecting to that of the substantia nigra malfunctioning. Parkinson’s disease is a chronic and progressive disorder of the brain primarily affecting the motor system, but also affecting thinking and emotion.

Parkinson disease (PD) is a progressive neurodegenerative disorder characterized mainly by physical and psychological disabilities. This disorder was named after James Parkinson, an English physician who first described it as shaking palsy in 1817 (Goetz, Factr, and Weiner, 2002). Jean- Martin Charcot, who was a French neurologist, then progressed and further refined the description of the disease and identified other clinical features of PD (Goetz, Factr, and Weiner, 2002). PD involves the loss of cells that produce the neurotransmitter dopamine in a part of the brain stem called the substansia nigra, which results in several signs and symptoms (Byrd, Marks, and Starr, 2000). It is manifested clinically by tremor,