Demyelination & Synapse Structure
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Questions and Answers

In the direct pathway of the striatum, what is the consequence of decreased GABA release onto the thalamus?

  • Increased GABA release from the GPi onto the thalamus.
  • Increased inhibition of the globus pallidus internus (GPi).
  • Decreased activation of the motor cortex, leading to reduced motor coordination.
  • Increased activation of the motor cortex, leading to enhanced motor coordination and fluidity of movement. (correct)

Which region of the substantia nigra experiences the most significant impact from Parkinson's Disease, resulting in diminished dopamine release?

  • Subthalamic nucleus
  • Pars reticulata
  • Pars compacta (correct)
  • Globus pallidus

Which clinical manifestation is LEAST likely to be observed in the early stages of Parkinson's Disease?

  • Gait abnormalities (shuffling gait)
  • Tremors with voluntary movement
  • Resting tremors (correct)
  • Bradykinesia (slow movements)

Carbidopa is administered alongside levodopa in Parkinson's Disease to accomplish what?

<p>Prevent the peripheral breakdown of levodopa (D)</p> Signup and view all the answers

What is the primary mechanism of action of MAO-B inhibitors, such as selegiline and rasagiline, in the management of Parkinson's Disease?

<p>Promoting increased dopamine levels by downregulating MAO-B mediated dopamine breakdown. (D)</p> Signup and view all the answers

What is the functional consequence of dopamine binding to D1 receptors in the direct pathway of the striatum in the context of motor control?

<p>Decreased inhibition of the globus pallidus internus (GPi). (C)</p> Signup and view all the answers

Which of the following best describes the rationale for using dopaminergic agonists in the treatment of Parkinson's Disease?

<p>To compensate for decreased dopamine production by directly stimulating dopamine receptors. (A)</p> Signup and view all the answers

What is the primary function of dopa decarboxylase in the context of Parkinson's Disease treatment with Levodopa?

<p>Converting levodopa into dopamine within the brain (A)</p> Signup and view all the answers

Tetrabenazine is NOT recommended for late-stage Huntington's disease due to its mechanism of action primarily affecting:

<p>Increased inhibition of the striatum, exacerbating motor dysfunction. (D)</p> Signup and view all the answers

Which of the following describes the combined action of tetrabenazine on dopamine activity?

<p>It prevents dopamine packaging and antagonizes dopamine receptors, reducing dopamine's effect. (D)</p> Signup and view all the answers

In ALS, glutamate toxicity leads to neuronal damage through which specific sequence of events?

<p>Glutamate-NMDA binding, increased calcium entry, mitochondrial damage, increased oxidative stress. (D)</p> Signup and view all the answers

What is the direct consequence of a neuron shifting to anaerobic metabolism in ALS?

<p>Lactic acid accumulation leading to neuronal destruction. (D)</p> Signup and view all the answers

Which combination of physical exam findings would strongly suggest a diagnosis of ALS?

<p>Hyperreflexia, muscle atrophy, and uncontrollable laughing/crying. (B)</p> Signup and view all the answers

A patient presents with gradual muscle weakness, fasciculations, and eventual paralysis but no sensory loss. Electromyography reveals widespread denervation. These findings MOST strongly suggest:

<p>Amyotrophic lateral sclerosis (ALS). (C)</p> Signup and view all the answers

The MOST common cause of mortality in ALS patients is directly related to:

<p>Respiratory failure due to paralysis of respiratory muscles. (D)</p> Signup and view all the answers

In managing ALS, what therapeutic strategy aims to alleviate dyspnea associated with diaphragmatic paralysis?

<p>Initiation of non-invasive positive pressure ventilation (NIPPV). (D)</p> Signup and view all the answers

Which of the following best describes the pathophysiology underlying the hyperkinetic movements observed in the early stages of Huntington's Disease?

<p>Decreased glutamate release from the subthalamic nuclei onto the globus pallidus interna (GPi), resulting in decreased inhibition of the thalamus. (D)</p> Signup and view all the answers

In late-stage Huntington's Disease, the emergence of bradykinesia and rigidity is primarily attributed to the involvement of which of the following structures?

<p>Degeneration of the substantia nigra, leading to decreased dopamine release. (D)</p> Signup and view all the answers

A patient with Huntington's Disease exhibits a lack of social inhibitions and engages in inappropriate behavior. Which of the following best explains the underlying pathophysiology?

<p>Disruption of striatal neurons projecting to the frontal cortex. (B)</p> Signup and view all the answers

Which of the following neuronal mechanisms contributes most directly to the chorea observed in Huntington's Disease?

<p>Decreased activity of the indirect pathway, resulting in reduced inhibition of the thalamus. (B)</p> Signup and view all the answers

In Huntington's Disease, visuospatial deficits arise due to the disruption of striatal neurons projecting to which area of the brain?

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

Which of the following best describes the effect of Huntington's Disease on the basal ganglia circuitry in the early stages?

<p>Increased glutamate release from the subthalamic nuclei onto the GPi. (C)</p> Signup and view all the answers

What is the primary genetic mutation associated with Huntington's disease, and what amino acid does it encode?

<p>CAG trinucleotide repeats, encoding for glutamine. (B)</p> Signup and view all the answers

What is the classic neuroimaging finding associated with Huntington's Disease, and why does it occur?

<p>Enlargement of the lateral ventricles due to gradual degeneration of subcortical tissue. (A)</p> Signup and view all the answers

Which subcortical area, when affected by seizures, is MOST associated with the induction of fear and aggression?

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

A patient experiencing a seizure presents with rhythmic jerking movements of their extremities. Which area of the brain is MOST likely involved?

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

What is the MOST likely characteristic of generalized seizures?

<p>They often affect subcortical areas like the thalamus and brainstem, leading to loss of consciousness. (C)</p> Signup and view all the answers

A patient is observed staring blankly into space, without any significant motor convulsions or post-ictal confusion. Which type of seizure is the patient MOST likely experiencing?

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

In a generalized tonic-clonic seizure, what is the sequence of events that typically occurs?

<p>Tonic phase followed by loss of consciousness, then clonic phase. (C)</p> Signup and view all the answers

Which of the following BEST describes the pathophysiologic definition of status epilepticus?

<p>Continuous seizure activity lasting longer than 5 minutes or recurrent seizures without recovery of consciousness between them. (B)</p> Signup and view all the answers

A patient reports experiencing visual auras prior to some of their seizures. Which lobe is MOST likely involved in the epileptiform activity?

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

Why might seizures NOT always result in a loss of consciousness?

<p>Because seizures can involve brain areas which do not affect consiousness. (B)</p> Signup and view all the answers

Which of the following mechanisms explains how neuronal edema contributes to increased neuronal excitability and potential seizure activity?

<p>By altering the electrochemical gradients of sodium and potassium, promoting increased neuronal excitability. (A)</p> Signup and view all the answers

An athlete presents with a seizure following a marathon. Which of the following underlying conditions is most likely contributing to their seizure?

<p>Hyponatremia secondary to excessive water consumption. (D)</p> Signup and view all the answers

Which of the following best describes the mechanism by which MDMA (ecstasy, Molly) increases the risk of seizures?

<p>Increased glutamate release, resulting in hyperexcitability. (B)</p> Signup and view all the answers

How does the activity of the GABAA receptor lead to neuronal inhibition?

<p>It opens chloride channels, leading to chloride influx and hyperpolarization. (A)</p> Signup and view all the answers

Which of the following mechanisms contributes to decreased inhibition in the pathophysiology of seizures?

<p>Decreased GABA release from the presynaptic neuron. (D)</p> Signup and view all the answers

How does ketamine uniquely induce seizures compared to other drugs that also increase seizure risk?

<p>By potentiating increased norepinephrine and dopamine release from subcortical areas, leading to cortical neuron hyperexcitability. (A)</p> Signup and view all the answers

What distinguishes GABAB receptors from GABAA receptors in terms of mechanism and location?

<p>GABA<del>B</del> receptors are metabotropic and found pre- and postsynaptically, while GABA<del>A</del> receptors are ionotropic and exclusively postsynaptic. (A)</p> Signup and view all the answers

Bupropion, a commonly prescribed medication, increases seizure risk through which primary mechanism?

<p>Increasing membrane permeability for sodium and, therefore, lower seizure threshold. (A)</p> Signup and view all the answers

How does magnesium normally affect NMDA receptor function, and under what conditions is this effect relieved?

<p>Magnesium blocks the NMDA receptor under resting conditions, and this block is relieved upon glutamate binding and postsynaptic neuronal depolarization. (D)</p> Signup and view all the answers

Flumazenil, a benzodiazepine reversal agent, can precipitate seizures. Which of the following mechanisms explains this phenomenon?

<p>Competitive GABA<del>A</del> antagonism, decreasing inhibitory effect on neurons. (B)</p> Signup and view all the answers

Isoniazid-induced seizures are primarily attributed to which of the following mechanisms?

<p>Pyridoxine deficiency decreased GABA production, increased glutamate accumulation glutamate toxicity, resulting in hyperexcitation of neurons and seizure. (D)</p> Signup and view all the answers

Which of the following best describes the role of AMPA receptors in synaptic transmission?

<p>Allowing sodium entry into the postsynaptic neuron. (C)</p> Signup and view all the answers

In the context of seizure pathophysiology, how does neuronal synchronization contribute to the generation of seizures?

<p>It increases the likelihood that other nerve networks within the brain are depolarized simultaneously, resulting in seizure-like activity. (D)</p> Signup and view all the answers

Clozapine increases glutamatergic transmission, resulting in seizures. Clozapine is a D2 antagonist which is utilized in the management of what condition?

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

Which of the following is an example of a metabolic or electrolyte abnormality that can contribute to the pathophysiology of seizures?

<p>Hyponatremia (low sodium levels) (B)</p> Signup and view all the answers

How does presynaptic inhibition mediated by GABAB receptors contribute to reducing neurotransmitter release?

<p>By inhibiting voltage-gated ion channels, leading to decreased synaptic vesicle docking and neurotransmitter release. (D)</p> Signup and view all the answers

Flashcards

CAG trinucleotide repeats

Genetic repeats on chromosome 4 leading to Huntington's disease.

Huntingtin protein

Protein that accumulates in Huntington's disease, encoded by CAG repeats.

Striatum

Brain region (caudate and putamen nuclei) highly affected in Huntington's disease.

Enlargement of lateral ventricles

Classic neuroimaging finding in Huntington's due to tissue degeneration.

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Hyperkinetic phenotypes

Early stage symptoms of Huntington's including chorea and athetosis.

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Bradykinesia

Slowness of movement, a symptom in late stages of Huntington's disease.

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Visuospatial deficits

Difficulty with spatial awareness, a non-motor symptom in Huntington's disease.

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Neuropsychiatric deficits

Cognitive issues and dementia associated with Huntington's disease.

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Direct Pathway of Striatum

Pathway where striatum releases GABA to GPi, increasing motor coordination.

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Role of D1 Receptors

Dopamine binding to D1 receptors increases GABA release from striatum to GPi.

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Effects of GABA on GPi

Increased GABA from striatum inhibits GPi, leading to decreased GABA to thalamus.

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GPi to Thalamus Inhibition

Increased GABA release from GPi results in decreased excitatory output to motor cortex.

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Parkinson's Disease Pathway

Decreased dopamine from Pars Compacta leads to motor symptoms and decreased coordination.

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Clinical Phenotypes of Parkinson's

Bradykinesia, tremors, gait abnormalities, and late-stage cognitive difficulties.

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Levodopa + Carbidopa

Levodopa crosses blood-brain barrier; Carbidopa prevents peripheral breakdown.

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Monoamine Oxidase Inhibitors

MAO-B inhibitors like Selegiline reduce dopamine breakdown, increasing levels.

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Resting Membrane Potential

-70 millivolts; electrical potential difference across the neuron's membrane.

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AMPA Receptor

Glutamate receptor allowing sodium entry, linked to focal seizures.

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NMDA Receptor

Glutamate receptor allowing calcium and sodium entry; linked to generalized seizures.

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GABAA Receptor

Ionotropic receptor that opens chloride channels, causing hyperpolarization.

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GABAB Receptor

Metabotropic receptor that inhibits neurotransmitter release and opens potassium channels.

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Glutamate and Seizures

Excessive glutamate activates receptors, increasing seizure risk.

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Decreased GABAergic Effect

Decreased GABA leads to less inhibition, increasing seizure likelihood.

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Focal Seizures

Seizures beginning in one area, may spread or stay localized, with possible symptoms.

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Tetrabenazine

A medication that decreases dopamine effect at D2 receptors, used in early-stage Huntington's Disease.

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D2 Receptors

Dopamine receptors that are inhibitory and targeted by Tetrabenazine to reduce hyperactivity in Huntington's Disease.

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Glutamate toxicity in ALS

Occurs when glutamate binds to NMDA receptors, increasing calcium, damaging mitochondria, leading to neuronal death.

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Upper Motor Neuron Symptoms

Symptoms in ALS including hyperreflexia, increased spasticity, and uncontrollable laughing or crying.

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Lower Motor Neuron Symptoms

Symptoms in ALS such as muscle atrophy, weakness, and gradual loss of reflexes.

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Respiratory Failure in ALS

The most common cause of death in ALS patients due to paralysis of respiratory muscles.

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Anaerobic Metabolism

Occurs when neurons shift due to mitochondrial damage from increased calcium in ALS, leading to lactic acid buildup.

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Late-Stage ALS Symptoms

Symptoms including slurred speech, swallowing difficulties, and cognitive challenges typically seen in advanced cases.

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Frontal Lobe Seizures

Seizures that involve the primary motor cortex leading to focal motor findings.

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Parietal Lobe Seizures

Seizures affecting the primary somatosensory cortex, impacting sensation.

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Occipital Lobe Seizures

Involves the primary visual cortex, causing visual auras.

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Temporal Lobe Seizures

Most common focal seizures, often involving the hippocampus, affecting memory.

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Generalized Seizures

Involve both hemispheres, causing loss of consciousness and affecting subcortical areas.

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Tonic-Clonic Seizures

Seizures with initial muscle stiffness (tonic) followed by jerking (clonic) movements.

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Absence Seizures

Brief seizures characterized by staring spells without post-ictal confusion.

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Status Epilepticus

Continuous seizure activity lasting longer than 5 minutes or recurrent seizures without recovery.

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Neuronal edema

Swelling of neurons that disrupts sodium and potassium gradients, increasing excitability.

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Primary polydipsia

Excessive thirst often seen in athletes, leading to excessive water intake.

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Illicit drugs increasing seizures

Drugs like amphetamines and cocaine elevate glutamate, leading to neuron hyperexcitability.

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Ketamine mechanism

Ketamine can cause seizures via NMDA-independent pathways, enhancing norepinephrine and dopamine release.

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Bupropion effects

A drug that lowers seizure threshold by inhibiting dopamine-norepinephrine reuptake and causing sodium blockade.

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Flumazenil

A GABA_A antagonist that can increase seizure risk by reversing benzodiazepine effects.

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Isoniazid seizure risk

Antibiotic for TB that can induce seizures due to pyridoxine deficiency, affecting GABA production.

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Clozapine effects

Antipsychotic that may promote seizure development by increasing glutamatergic transmission.

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Study Notes

Pathophysiology of Demyelination

  • Saltatory conduction is the transmission of neuronal electric current from node of Ranvier to node of Ranvier.
  • Pathophysiologic causes of demyelination include JC virus polyomavirus, Cytomegalovirus (CMV), and Epstein-Barr virus (EBV).
  • JC virus (dormant) can reactivate during immunosuppression, leading to progressive multifocal leukoencephalopathy (PML).
  • CMV is associated with retinitis, frequently in patients with weakened immune systems (e.g., CD4 count < 50 in HIV/AIDS).
  • EBV is linked to multiple sclerosis.

Synapse Structure

  • A synapse consists of three parts:
    • Presynaptic neuron: releases neurotransmitters.
    • Synaptic cleft: space between neurons containing enzymes that regulate neurotransmitter activity (e.g., acetylcholinesterase for acetylcholine, monoamine oxidase for dopamine, norepinephrine, and serotonin).
    • Postsynaptic neuron: contains receptors for neurotransmitters, with effects varying depending on the neurotransmitter.

Calcium's Role in Presynaptic Neuron

  • Calcium promotes vesicular docking at the presynaptic terminal through voltage-gated calcium channels, facilitating neurotransmitter release.

Basal Ganglia

  • The basal ganglia is a critical subcortical brain area involved in the integration and fine-tuning of nerve fiber projections to multiple locations.
  • Key components include the globus pallidus (internal and external segments), substantia nigra (compacta and reticulata), striatum (caudate and putamen), and subthalamic nuclei.

Indirect Pathway of the Striatum

  • Without dopamine, the striatum releases GABA onto the globus pallidus external segment (GPe), decreasing GABA release through the subthalamic nuclei.
  • The subthalamic nuclei release glutamate, enhancing GABA release from the globus pallidus internal segment (GPi).
  • Increased GABA from the GPi inhibits the thalamus, reducing motor coordination.
  • With dopamine binding to D2 receptors, the striatum inhibits GABA release onto the GPe, reducing its inhibition on the subthalamic nuclei and increasing GABA release to the thalamus, enhancing motor coordination.

Direct Pathway of the Striatum

  • Striatum releases GABA onto the globus pallidus internal segment (GPi), decreasing GABA release by the GPi onto the thalamus, reducing inhibition of the thalamus, increasing motor coordination, and enhancing fluidity of movement.

Parkinson's Disease

  • Parkinson's disease primarily affects the substantia nigra pars compacta, leading to decreased dopamine release.
  • Clinical features include bradykinesia, tremors, rigidity, and gait abnormalities.

Huntington's Disease

  • The classic neuroimaging finding in Huntington's disease is enlargement of the lateral ventricles.
  • Early stages often exhibit hyperkinetic phenotypes (chorea, athetosis)
  • Later stages transition to a loss of voluntary movements, and cognitive deteriorations.
  • Disease correlates to increases in glutamatergic activity, loss of GABA, and neuronal damage in subcortical zones.

Multiple Sclerosis

  • Often related to the presence of anti-ganglioside autoantibodies.

ALS

  • A disease involving glutamate binding to the NMDA receptor leading to oxidative stress and subsequent neuronal death.
  • Often leading to respiratory failure.

Seizures

  • A variety of causes can lead to seizure.
  • Conditions such as hyponatremia, stroke, and excessive intake of alcohol can lead to seizure.

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Description

Explore the pathophysiology of demyelination, including viral causes like JC virus, CMV, and EBV. Also review synapse structure, covering the roles of presynaptic neurons, synaptic clefts, and postsynaptic neurons in neurotransmission.

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