Parkinson's Disease

Parkinson disease

Parkinson’s disease is a progressive condition stemming from the degeneration of nerve cells within the substantia nigra, a region in the brain responsible for regulating movement. These nerve cells deteriorate or become compromised, losing their capacity to generate dopamine, a vital neurotransmitter. Dopamine typically maintains a delicate equilibrium with other neurotransmitters to coordinate the intricate interplay of nerve and muscle cells required for motion. Insufficient dopamine disrupts this equilibrium, leading to hallmark symptoms of Parkinson’s: tremors (shaking in the hands, arms, legs, and jaw), rigidity (limb stiffness), slowed movement, and compromised balance and coordination.

The root cause of Parkinson’s remains predominantly unclear. Nevertheless, theories encompassing oxidative damage, environmental toxins, genetic factors, and accelerated aging have been explored as potential triggers for the ailment. In 2005, researchers identified a single mutation in a Parkinson’s disease gene, first detected in 1997. This mutation is believed to contribute to about five percent of hereditary cases of the disease.

Stages of

The progression of Parkinson’s disease can span years to decades before causing significant impacts. In 1967, Margaret Hoehn and Melvin Yahr introduced a staging system for the disease, though its usefulness has waned, as individualized assessment and treatment prove more valuable. Presently, the primary tool for categorizing the condition is the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS). This comprehensive scale evaluates four domains of Parkinson’s impact:

1. Non-motor aspects of daily living: This section addresses non-movement-related symptoms such as mental health issues, pain, fatigue, and gastrointestinal problems.
2. Motor aspects of daily living: It encompasses movement-related effects, like eating, dressing, and speaking.
3. Motor examination: This assesses movement-related impacts on speech, facial expressions, stiffness, gait, balance, tremors, and more.
4. Motor complications: This section gauges the extent of symptom influence on daily life, including their duration and impact on daily activities.


Symptoms of

The most familiar indications of Parkinson’s disease pertain to the deterioration of muscle control. However, contemporary insights affirm that issues related to muscle control are not the exclusive manifestations of the ailment.

Motor symptoms associated with movement in Parkinson’s disease include slowed movements known as bradykinesia, characterized by muscle weakness yet stemming from challenges in muscle control without actual strength loss; resting tremors occurring in about 80% of cases, differentiating from essential tremors by their presence during muscular rest; rigidity or stiffness, encompassing lead-pipe rigidity denoting unchanging stiffness during movement and cogwheel stiffness combining tremors and lead-pipe rigidity in a start-and-stop pattern resembling a mechanical clock’s second hand; and unstable posture or gait, brought about by slowed movement and stiffness leading to a stooped posture, evident in walking through shorter, shuffling strides and reduced arm motion, often requiring additional steps for directional changes. These motor symptoms illustrate the multifaceted impact of Parkinson’s disease on movement and posture.

Additional motor symptoms can include: blinking less often than usual, cramped or small handwriting, drooling, mask-like facial expression or hypomimia, trouble swallowing (dysphagia), or unusually soft speaking voice (hypophonia).

While historically, experts perceived non-motor symptoms as precursors to the disease when preceding motor symptoms, emerging evidence suggests that these symptoms can emerge during the early stages of the condition. This implies that these symptoms might serve as warning signs that emerge years or even decades before the onset of motor symptoms. Non-motor symptoms, including potential early indicators highlighted in bold, consist of autonomic nervous system issues such as orthostatic hypotension (low blood pressure upon standing), constipation, gastrointestinal troubles, urinary incontinence, and sexual dysfunctions; depression; loss of the sense of smell (anosmia); sleep disturbances like periodic limb movement disorder (PLMD), rapid eye movement (REM) behavior disorder, and restless legs syndrome; as well as cognitive challenges and difficulties in concentration known as Parkinson’s-related dementia.

Causes of

While various established factors elevate the risk of developing Parkinson’s disease, like pesticide exposure, currently, the sole confirmed origins of Parkinson’s lie in genetics. In instances where Parkinson’s disease lacks a genetic basis, it is termed “idiopathic,” signifying an ailment with its own distinct cause. This indicates a lack of precise understanding about its inception. It’s important to note that numerous conditions resembling Parkinson’s disease are actually instances of parkinsonism, which refers to conditions resembling Parkinson’s disease but having a specific underlying cause, such as certain psychiatric medications.

Diagnostics of

Currently, diagnosing Parkinson’s disease relies predominantly on identifying the shared symptoms mentioned earlier. No X-ray or blood test exists to definitively verify the condition. Nevertheless, noninvasive diagnostic techniques, like positron emission tomography (PET), can supplement a physician’s diagnosis. Traditional diagnostic approaches encompass:

1. Manifestation of at least two of the three core symptoms.
2. Absence of other neurological indicators upon examination.
3. Lack of history relating to potential alternative causes of parkinsonism, such as the use of tranquilizer medications, head injury, or stroke.
4. Positive response to Parkinson’s medications, like levodopa.

Researchers have discovered potential methods to detect potential markers for Parkinson’s disease. Both of these novel tests focus on the alpha-synuclein protein but employ innovative approaches to identify it. While these tests cannot pinpoint the exact conditions resulting from misfolded alpha-synuclein proteins, this information can still aid healthcare providers in making a diagnosis.

Spinal fluid analysis: One of these tests examines misfolded alpha-synuclein proteins in cerebrospinal fluid, which envelops the brain and spinal cord. This assessment requires a spinal tap, during which a healthcare professional inserts a needle into the spinal canal to obtain cerebrospinal fluid for examination.

Skin tissue biopsy: Another potential test involves a biopsy of superficial nerve tissue. This biopsy entails collecting a small skin sample, including nerves within the skin, from specific areas on the back and legs. Analyzing these samples can offer insights into whether the alpha-synuclein protein exhibits specific malfunction, potentially heightening the risk of Parkinson’s disease development.

Complications of

Parkinson’s disease triggers the deterioration of a specific brain region, the basal ganglia, leading to the loss of functions once governed by these areas. Scientists have unveiled that Parkinson’s disease prompts a significant alteration in brain chemistry.

In normal circumstances, the brain employs neurotransmitters, chemical messengers, to regulate communication between neurons. In Parkinson’s disease, dopamine, a crucial neurotransmitter, becomes deficient, disrupting this communication. Typically, the brain utilizes dopamine-sensitive cells to finely control muscle movement in response to activation signals. The insufficiency of dopamine gives rise to the characteristic slowed movements and tremors observed in Parkinson’s disease.

As the condition advances, symptoms broaden and intensify. In later stages, the disease can impact overall brain function, resulting in symptoms reminiscent of dementia and depression.

Treatment of

Currently, there is no cure for Parkinson’s disease, but there are diverse strategies to address its symptoms. The approaches can differ based on individual symptoms and the efficacy of specific treatments. Medications constitute the mainstay of treatment for this disorder.

Medications for Parkinson’s disease can be classified into two groups: Direct therapies and symptom-specific therapies. Direct treatments aim at addressing the disease itself, while symptom treatments focus on managing particular consequences of the condition. Various medications target distinct symptoms associated with Parkinson’s disease, such as sexual dysfunction, fatigue, constipation, sleep disturbances, and depression.

Another treatment avenue involves a surgical procedure to implant a device that administers a gentle electrical impulse to a brain region (referred to as Deep Brain Stimulation). Additionally, there are experimental possibilities, including treatments utilizing stem cells. Recent studies have also shown that the Transcranial Magnetic Stimulation has a positive effect on motor functioning in patients with Parkinson’s Disease.