Paralysis Agitans: An Assessment Of The Determinants And Therapeutic Tactics

Abstract

Paralysis agitans, often known as idiopathic parkinsonism, is a persistent neurological disease that affects 50 to 328 persons per lakh globally. Paralysis agitans affect more than 1% of the population over the age of 65, and the prevalence and incidence rates rise with age. Tremor, inflexibility, and difficulties in standing, walking, balancing, and synchronizing one's actions are all symptoms of paralysis agitans, a prevalent neurological disease. The primary cause of this condition is presumed to be the inexplicable breakdown of dopamine-secreting cells in the substantia nigra, which is located in the midbrain. Stationary tremor, cogwheel stiffness, and bradykinesia are three "cardinal indicators" of paralysis agitans. Spasticity is the fourth cardinal sign, and it is usually a late symptom of paralysis agitans. Symptoms that appear infrequently and symptomatic responses to L-dopa are also prevalent. The lack
of a gold standard assays makes diagnosing paralysis agitans difficult. While the use of Levodopa is limited due to the occurrence of motor inconsistencies and drug-induced dyskinesias, it is still the basis of therapeutic intervention for paralysis agitans. Dopamine agonists (DAs) are also administered, either alone or in combination with Levodopa. Dopamine agonists stimulate the production of natural dopamine increasingly by acting directly on dopamine receptors. Another class of drugs known as Monoamine oxidase B (MAO-B) inhibitors increases dopamine levels in the basal ganglia by blocking dopamine catabolism. Catechol O-methyl transferase (COMT) inhibitors lengthen the half-life of L-dopa in the peripheral nervous system by reducing dopamine breakdown. Regardless of the several paralysis agitans therapies available, every sufferer needs L-dopa at some point throughout the therapy cycle.
Individuals suffering from paralysis agitans who react to therapies, but experience uncontrolled side effects may choose to consider surgery. Among the surgical options are ablative methods (thalamotomy or pallidotomy), tissue transplantation, and deep brain stimulation (DBS). Although the exact cause of paralysis agitans is unknown, it is suspected that a potentiator is a combination of genetic, oxidative stress, and environmental factors.