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Related Concept Videos

Parkinson's Disease: Treatment01:24

Parkinson's Disease: Treatment

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Neurodegenerative disorders, such as Parkinson's Disease (PD), involve the gradual and irreversible destruction of neurons in particular brain areas. These disorders exhibit standard features like proteinopathies, selective vulnerability of some neurons, and an interaction of intrinsic properties, genetics, and environmental influences in neural injury.
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of...
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Prokinetic agents are specialized medications that stimulate gastrointestinal (GI) motility, promoting food movement through the GI tract. Dopamine, an inhibitory neurotransmitter, plays a significant role in this process, reducing GI motility and indirectly controlling the speed of digestion. Dopamine receptor antagonists, such as metoclopramide and domperidone, offer a unique advantage as prokinetic agents. By blocking the dopamine receptors, these drugs increase GI motility, improving food...
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Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

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Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
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Dysrhythmias IV: Characteristics of Bradyarrhythmias01:18

Dysrhythmias IV: Characteristics of Bradyarrhythmias

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Bradyarrhythmias are cardiac rhythm disorders characterized by a slower-than-normal heart rate, typically defined as fewer than 60 beats per minute. Some of which are discussed here:Sinus BradycardiaSinus bradycardia presents a heart rate lower than 60 beats per minute, with a regular rhythm originating from the SA node. The ECG typically shows normal P waves preceding each QRS complex, a normal PR interval (0.12 to 0.20 seconds), and a normal QRS duration (0.06 to 0.10 seconds).First-Degree AV...
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Dysrhythmias I: Introduction01:15

Dysrhythmias I: Introduction

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Dysrhythmias refers to abnormalities in the heart's rhythm. They result from disruptions in the heart's electrical conduction system, which includes the sinoatrial(SA)node, atrioventricular(AV) node, the bundle of His, bundle branches, and Purkinje fibers.Definition and PathophysiologyDysrhythmias result from disorders of impulse formation, impulse conduction, or both. The heart contains specialized cells in the sinoatrial node, atrioventricular node, and the bundle of His and Purkinje fibers...
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Antiepileptic Drugs: Potassium Channel Activators01:20

Antiepileptic Drugs: Potassium Channel Activators

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Ezocgabine or retigabine, an antiepileptic drug of remarkable efficacy, has revolutionized the management of seizures. It is a potassium channel activator, explicitly targeting the family of Q subtype potassium channels. It enhances the transmembrane potassium currents, regulating neuronal excitability. This action stabilizes the resting membrane potential, a pivotal factor in mitigating the hyperexcitability that characterizes epilepsy.
Ezogabine has gained approval as an adjunctive treatment...
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Updated: Oct 25, 2025

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease
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[Paroxystic dyskinesia].

Sonja Holm-Yildiz1, Tina Dysgaard Jeppesen

  • 1Sonja.desiree.holm-yildiz@regionh.dk.

Ugeskrift for Laeger
|August 6, 2021
PubMed
Summary
This summary is machine-generated.

A genetic variant in the PRRT2 gene caused a patient's epilepsy and choreoathetosis. Initially diagnosed with infantile convulsions and myopathy, the condition evolved, highlighting PRRT2's role in neurological disorders.

Area of Science:

  • Neurology
  • Genetics
  • Case Reports

Background:

  • A patient presented with early-onset epilepsy (atypical infantile convulsions) and later developed unspecific myopathy.
  • Diagnostic re-evaluation at age 25 shifted focus from myopathy to neurological symptoms.

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