Neuroscience of Movement Disorders

<p>By blocking dopamine and serotonin receptors (C)</p> Signup and view all the answers

<p>ALS primarily affects the lower motor neurons. (D)</p> Signup and view all the answers

<p>Amantadine (D)</p> Signup and view all the answers

<p>They inhibit the breakdown of dopamine. (B)</p> Signup and view all the answers

<p>Regular exercise (D)</p> Signup and view all the answers

<p>It acts as an adenosine A2A receptor antagonist. (C)</p> Signup and view all the answers

<p>A mutation in the HTT gene on chromosome 4 characterized by CAG trinucleotide repeats. (C)</p> Signup and view all the answers

<p>More repeats lead to an earlier onset and a more severe form. (A)</p> Signup and view all the answers

<p>Autosomal dominant (A)</p> Signup and view all the answers

<p>It is possible that other factors in tobacco plants, not nicotine itself, may contribute to the protective effect. (D)</p> Signup and view all the answers

<p>Increased Production of Acetylcholine (C)</p> Signup and view all the answers

<p>Destroy free radicals, reducing oxidative stress and damage to cellular components. (A)</p> Signup and view all the answers

<p>Increased calcium influx into neurons, leading to mitochondrial damage and potential neuronal death. (D)</p> Signup and view all the answers

<p>Mitochondrial dysfunction leads to a decrease in ATP production, essential for axonal transport. (A)</p> Signup and view all the answers

<p>They lead to decreased expression of functional SOD1, increasing oxidative stress and potential neuronal death. (C)</p> Signup and view all the answers

<p>Microglial cells release pro-inflammatory cytokines, potentially exacerbating neuronal damage. (A)</p> Signup and view all the answers

<p>The presence of both muscle weakness and spasticity in ALS patients. (B)</p> Signup and view all the answers

<p>Rare (B)</p> Signup and view all the answers

<p>Riluzole blocks glutamate transmission by both stabilizing voltage-gated sodium channels and acting as a non-competitive antagonist of NMDA receptors. (D)</p> Signup and view all the answers

<p>Tetrabenazine acts on the direct pathway, reducing dopamine release and alleviating the hyperkinetic symptoms. (A)</p> Signup and view all the answers

<p>Hyperreflexia (A)</p> Signup and view all the answers

<p>A lack of behavioral and social inhibitions, potentially leading to impulsive and inappropriate behavior. (D)</p> Signup and view all the answers

<p>Edaravone acts as a free radical scavenger, reducing oxidative damage to neurons. (A)</p> Signup and view all the answers

<p>Gradual denervation due to neuronal death (B)</p> Signup and view all the answers

<p>Increased GABA release from the striatum onto the globus pallidus externus. (C)</p> Signup and view all the answers

<p>Tofersen (C)</p> Signup and view all the answers

<p>Decreased inhibition of the subthalamic nucleus, leading to enhanced glutamate release and an increase in thalamic activity. (D)</p> Signup and view all the answers

<p>Respiratory failure (A)</p> Signup and view all the answers

<p>Decreased GABA release, leading to enhanced activity in the indirect pathway and hyperkinetic movements. (C)</p> Signup and view all the answers

<p>It receives excitatory input from the striatum and projects to the globus pallidus internus, regulating thalamic activity. (B)</p> Signup and view all the answers

<p>Difficulty swallowing (C)</p> Signup and view all the answers

<p>All of the above. (D)</p> Signup and view all the answers

<p>Enhanced activity of the direct pathway, contributing to bradykinesia and rigidity. (A)</p> Signup and view all the answers

<p>The GPi receives inhibitory input from the direct pathway and excitatory input from the indirect pathway, thus controlling the overall activity of the thalamus. (A)</p> Signup and view all the answers

<p>Vitamin B12 Deficiency (B)</p> Signup and view all the answers

<p>Diabetic Neuropathy (D)</p> Signup and view all the answers

<p>Guillain-Barre Syndrome (A)</p> Signup and view all the answers

<p>Cytomegalovirus (D)</p> Signup and view all the answers

<p>Heroin (C)</p> Signup and view all the answers

<p>Multiple Sclerosis (D)</p> Signup and view all the answers

<p>Isoniazid (D)</p> Signup and view all the answers

<p>Chronic Inflammatory Response Syndrome (A)</p> Signup and view all the answers

<p>Decreased activation of structures involving myelinated neurons (D)</p> Signup and view all the answers

<p>Disrupted saltatory conduction (D)</p> Signup and view all the answers

<p>Calcium promotes the docking and release of neurotransmitters. (D)</p> Signup and view all the answers

<p>Myelin Basic Protein (D)</p> Signup and view all the answers

<p>Axon terminal (D)</p> Signup and view all the answers

<p>Axosomatic (C)</p> Signup and view all the answers

<p>Neurodegeneration (D)</p> Signup and view all the answers

<p>Acetylcholinesterase (D)</p> Signup and view all the answers

Monoamine oxidase inhibitors that increase dopamine levels by downregulating MAO-B.

A MAO-B inhibitor that helps increase dopamine levels.

Another MAO-B inhibitor used in Parkinson's to boost dopamine.

A drug that enhances dopamine release and inhibits glutamatergic effects.

May have neuroprotective effects but lacks strong clinical support for PD risk reduction.

Acts as an adenosine A2A receptor antagonist, aiding dopaminergic activity.

CAG trinucleotide repeats in the HTT gene cause Huntington’s disease; more repeats indicate earlier onset.

Autosomal dominant; one mutated gene copy from either parent can transmit the disorder.

In early phases of Huntington’s Disease involving striatum destruction, leading to hyperkinetic movements.

Abnormal excessive movements including chorea and athetosis seen in Huntington’s Disease.

Dance-like flailing motions characteristic of hyperkinetic disorders.

Writhing, worm-like movements in limbs or trunk also seen in hyperkinetic disorders.

Part of movement control that is more prominent in late phases, leading to bradykinesia and rigidity.

Symptoms like behavioral, social, and cognitive dysfunction due to Huntington’s Disease.

Medication that prevents dopaminergic effects by inhibiting dopamine release and blocking receptors.

Cognitive and emotional problems in Huntington’s Disease, such as depression and aggression.

Reduction of dopamine D2 receptor activity in the striatum can impact movement control.

A neural pathway that inhibits unwanted movements; decreased activity leads to imbalance in movement regulation.

Enhanced inhibition in the brain leading to reduced activity in the thalamus and cortex, affecting motor function.

Antipsychotic medications that block D2 and 5-HT2A receptors, useful in managing agitation in patients.

A neurodegenerative disease affecting both upper and lower motor neurons, leading to progressive weakness.

A structure made of glycolipids and proteins that insulates the axon of a neuron.

The rapid transmission of electrical impulses along myelinated neurons by jumping between nodes.

The loss of myelin sheath surrounding neurons, leading to decreased electrical transmission.

Tissue damage caused by reduced blood flow leading to inflammation and potential demyelination.

An autoimmune condition where the body's immune system attacks myelin, causing weakness and loss of reflexes.

A lack of vitamin B12 that can lead to peripheral neuropathy and pernicious anemia.

A chronic disease characterized by the immune attack on myelin, leading to neurological symptoms.

The neuron that releases neurotransmitters into the synaptic cleft.

The gap between the pre-synaptic and post-synaptic neuron where neurotransmitter action occurs.

The neuron that receives neurotransmitters from the synaptic cleft.

The process by which neurotransmitters are secreted from the pre-synaptic neuron, dependent on calcium.

A demyelinating disease caused by the JC Virus affecting the brain, particularly in immunocompromised individuals.

A demyelinating condition that follows severe viral infections, presenting with inflammation of the brain and spinal cord.

Effects arising from structural aberrations affecting neurotransmitter release, degradation, or receptor function.

90-95% of ALS cases are sporadic; more common in Caucasian males in their 70s.

Higher risk in those with construction jobs, military history, or exposure to electromagnetic fields.

Increased glutamate binding to NMDA receptors leads to neuronal calcium influx and death.

Mutations in SOD1 gene lead to decreased SOD1 function and increased oxidative stress.

SOD1 normally reduces free radicals, protecting cells from oxidative damage.

Inadequate ATP production from mitochondria impairs axonal transport and action potential propagation.

Increased activation due to pro-inflammatory cytokines can damage neurons.

Presents with both upper and lower motor neuron symptoms.

Characteristics include hyperreflexia, increased spasticity, and uncontrollable emotional expressions.

Includes muscle atrophy, twitches, weakness that leads to paralysis, and loss of reflexes.

Involves difficulty speaking, which can evolve to a complete loss of vocalization.

The most common cause of death in affected individuals due to muscle paralysis affecting breathing.

A drug that blocks glutamate transmission, stabilizes neurons, and may prolong survival by reducing damage.

Works by preventing glutamate release and binding to NMDA receptors, reducing damage and promoting survival.

A free-radical scavenger that reduces oxidative damage to neurons, exact mechanism unknown.

A therapy specifically for SOD1-associated ALS that reduces abnormal protein synthesis to prevent neuronal death.