Parkinson's Disease

Table of Contents

Introduction4

Methodology of Literature Search7

Discussion Analysis7

Pathophysiology7

Death of Brain Cells8

Etiology9

The Structures Involved In Parkinson's Disease10

Risk Factors11

Symptoms and Signs12

Other Symptoms14

Typical Progression of Parkinson's Disease16

Diagnosis16

L-Dopa Test17

Imaging18

Autonomic function tests18

Examination for Wilson disease19

Criteria for diagnosis of PD20

Criteria negative (exclusionary) for PD20

Criteria for positive support for the diagnosis of PD (3 or more are needed for diagnosis)21

Inclusion Criteria22

Exclusion Criteria22

Gradual Development of Parkinson's Disease22

Treatment23

Prevention of Progress of Disease23

Symptomatic Treatment24

Mild Symptoms Without Functional Impairment25

Symptoms with Functional Impairment25

Prevention of Motor Fluctuations and Dyskinesias26

Treatment for Patients in Use of Levodopa27

Role of Iron in Pathogenesis of Parkinson Disease28

Comparison of Quantity of Iron in Parkinsonian and Control Substantia Nigra30

Contributions of Central and Systemic Inflammation to the Pathophysiology of Parkinson's Disease32

Systemic Inflammation and Parkinson's disease34

Kinases and Kinase Signaling Pathways: Potential Therapeutic Targets in Parkinson's Disease35

Pathological Role of PINK1 in the Pathogenesis of PD37

Molecular Genetic Basis of Familial Parkinson's disease38

Conclusion41

References43

Appendices64

Parkinson's Disease

Introduction

Parkinson's disease (PD), described in 1817 by James Parkinson, is a neurological disease and intriguing of the most common nowadays. It has worldwide distribution and affects all ethnic groups and socioeconomic classes. It is estimated a prevalence of 100 to 200 cases per 100,000 inhabitants. Its Incidence and prevalence increases with age.

From the standpoint of pathological PD is a degenerative disease whose motor abnormalities arise especially from the death of dopaminergic neurons in the substantia nigra that have inclusions intracytoplasmic familiar with Lewy bodies. Its main motor manifestations include resting tremor, bradykinesia, rigidity with cogwheel and postural abnormalities. However, the changes are not restricted to the substantia nigra and may be present in other brain stem nuclei (For example, dorsal motor nucleus of the vagus), cerebral cortex and even peripheral neurons, such as myenteric plexus.

The presence of degenerative process beyond the nigrostriatal system may explain a series of non-motor symptoms and signs, such as olfaction, sleep disturbances, postural hypotension, constipation, emotional changes, depression, anxiety, psychotic symptoms, cognitive impairments and dementia, among other.

Being a progressive disease, which usually leads to severe disability after 10 to 15 years, has high social and financial impact, particularly in the older population. It is estimated that the cost anti-parkinsonian drugs with annual worldwide is around 11 billion dollars, and the reatment about 3 to 4 times more costly to patients in advanced stages of the disease.

Only in the 60s, after the identification of pathological and biochemical changes in the brain PD patients, came the first successful treatment, paving the way for the development of new effective therapies. The introduction of levodopa represented the greatest therapeutic advance in PD, producing clinical benefits to virtually all patients and reducing mortality from this disease. However, soon after the introduction of medicament, it became apparent that long-term treatment was complicated by the development of side effects, including motor fluctuations, dyskinesia and neuropsychiatric complications. Furthermore, with disease progression, patients spend submit expressions that do not respond adequately to therapy with levodopa, such as episodes of freezing, postural instability, autonomic dysfunction and dementia.

The motor manifestations of PD can be explained by the model in a simplified manner in which the striatum has a ...