Week 5 NUR 425
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Questions and Answers

Which nerve is primarily responsible for transmitting pain signals from the head and face to the brain?

  • Facial nerve
  • Glossopharyngeal nerve
  • Vagus nerve
  • Trigeminal nerve (correct)

    • Which neurotransmitter is primarily involved in controlling movement?

  • GABA
  • Dopamine (correct)
  • Serotonin
  • Acetylcholine

    • Which of the following is required for the formation of short and long-term memories?

  • Hippocampus (correct)
  • Cerebral Cortex
  • Hypothalamus
  • Prefrontal Cortex

    • What role does Calcitonin Gene-Related Peptide (CGRP) play in migraines?

    <p>It is released from trigeminal nerve endings and causes vasodilation and neurogenic inflammation</p> Signup and view all the answers

    Which of the following is a first-line preventive treatment for migraines?

    <p>Propranolol</p> Signup and view all the answers

    Which part of the brain is primarily affected in Parkinson’s disease?

    <p>Substantia nigra</p> Signup and view all the answers

    What dietary consideration is important for patients taking levodopa-carbidopa?

    <p>Take medication 30 mins before meals if tolerated</p> Signup and view all the answers

    Which type of dementia is characterized by the presence of amyloid plaques and neurofibrillary tangles?

    <p>Alzheimer’s disease</p> Signup and view all the answers

    Which treatment is specifically used for acute relief of cluster headaches?

    <p>Oxygen Therapy</p> Signup and view all the answers

    What is the primary function of carbidopa when used with Levodopa in Parkinson’s disease treatment?

    <p>Inhibits the enzyme dopa decarboxylase</p> Signup and view all the answers

    In the context of dementia, acetylcholine primarily facilitates which cognitive function?

    <p>Facilitating memory and learning</p> Signup and view all the answers

    Which medication used in Alzheimer’s disease treatment specifically regulates glutamate activity?

    <p>Memantine</p> Signup and view all the answers

    What is the average duration of headache attacks to be classified as migraines?

    <p>4-72hours</p> Signup and view all the answers

    Which characteristic is NOT part of the criteria for headache characteristics in migraines?

    <p>Sharp quality</p> Signup and view all the answers

    Which symptom would NOT be expected as a characteristic during a migraine attack?

    <p>Increased appetite</p> Signup and view all the answers

    Which of the following is a defining feature of aura symptoms in migraine with aura?

    <p>Visual symptoms are present</p> Signup and view all the answers

    How many aura symptoms must occur in succession to fit the criteria for migraine with aura?

    <p>One or more</p> Signup and view all the answers

    Which of the following best describes the pathophysiology of migraines?

    <p>Dilation and inflammation of intracranial blood vessels</p> Signup and view all the answers

    Which aspect is NOT associated with the trigeminovascular system during a migraine?

    <p>Reduces inflammation</p> Signup and view all the answers

    Which characteristic is part of the criteria for migraine without aura diagnosis according to IHS?

    <p>Headache attacks lasting 4-72 hours untreated or unsuccessfully treated</p> Signup and view all the answers

    Which treatment is typically used as a fast-acting option for managing cluster headaches?

    <p>Dihydroergotamine</p> Signup and view all the answers

    What are the significant factors that play a role in cluster headaches?

    <p>Involves the trigeminovascular system</p> Signup and view all the answers

    Which of the following is NOT a common trigger for cluster headaches?

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

    What makes cluster headaches differ from a migraine? (SATA)

    <p>No aura</p> Signup and view all the answers

    Which of the following statements is true regarding preventive therapy for cluster headaches?

    <p>Calcium channel blockers are used as a first-line agent for preventive therapy</p> Signup and view all the answers

    Which of the following medications is considered a first-line therapy for the acute management of cluster headaches?

    <p>Lidocaine (nasal)</p> Signup and view all the answers

    What type of headache is characterized by pain that may alternate between sides and is described as severe and stabbing?

    <p>Cluster headache</p> Signup and view all the answers

    Which class of drugs helps block sodium channels and stabilize neurons in the preventive treatment of migraines?

    <p>Anticonvulsants</p> Signup and view all the answers

    What is the primary action of verapamil in the context of cluster headache prevention?

    <p>Modulating neurotransmitter systems in the hypothalamus</p> Signup and view all the answers

    Which of the following statements about medication overuse headache (MOH) is accurate?

    <p>It can develop from the frequent of common analgesics.</p> Signup and view all the answers

    What is a common adverse effect of lithium when used as a second-line agent for cluster headache prevention?

    <p>Cognitive disturbances</p> Signup and view all the answers

    Which intervention should be implemented to prevent medication overuse headaches?

    <p>Limit abortive medication use to 2-3 times per week</p> Signup and view all the answers

    What role does Calcitonin Gene-Related Peptide (CGRP) play in migraine pathophysiology?

    <p>It causes vasodilation and contributes to pain transmission</p> Signup and view all the answers

    Which of the following is classified as a first-line medication for treating mild to moderate migraines?

    <p>NSAIDs</p> Signup and view all the answers

    How does serotonin influence migraine headaches?

    <p>It can both cause vasoconstriction and vasodilation depending on receptor interaction</p> Signup and view all the answers

    What is the mechanism of action for triptans in migraine management?

    <p>They activate serotonin receptors to reduce CGRP release</p> Signup and view all the answers

    During which phase of a migraine do patients typically experience mood changes and neck stiffness?

    <p>Prodrome</p> Signup and view all the answers

    Which age group is most commonly affected by migraine headaches?

    <p>Adults aged 18-44</p> Signup and view all the answers

    Which of the following is a common preventive therapy for tension-type headaches?

    <p>Amitriptyline</p> Signup and view all the answers

    During which phase of a migraine would a patient most likely experience fatigue and mood changes?

    <p>Prodrome</p> Signup and view all the answers

    Which of the following symptoms is associated with the postdrome phase of a migraine?

    <p>Difficulty concentrating</p> Signup and view all the answers

    What is one of the primary functions of Calcitonin Gene-Related Peptide (CGRP) during a migraine episode?

    <p>Vasodilation</p> Signup and view all the answers

    Which of the following is a common abortive therapy for mild to moderate migraines?

    <p>NSAIDs</p> Signup and view all the answers

    Which of the following neurotransmitters is most affected by cholinergic neuron loss in Alzheimer's disease?

    <p>Acetylcholine</p> Signup and view all the answers

    What is a common risk factor associated with vascular dementia?

    <p>Hypertension</p> Signup and view all the answers

    Which symptom is typically associated with the frontal lobe degeneration seen in Frontotemporal Dementia?

    <p>Language difficulties</p> Signup and view all the answers

    What is the purpose of cholinesterase inhibitors in treating Alzheimer's disease?

    <p>Enhance acetylcholine levels</p> Signup and view all the answers

    What is the primary effect of the neurofibrillary tangles found in Alzheimer's disease?

    <p>Disrupt neuron stabilization</p> Signup and view all the answers

    In Alzheimer's disease, amyloid plaques are associated with which of the following processes?

    <p>Disrupting cell-to-cell communication</p> Signup and view all the answers

    Which of the following best describes anosognosia in dementia patients?

    <p>Lack of awareness of their condition</p> Signup and view all the answers

    What aspect of dementia evaluation commonly includes imaging techniques like CT or MRI?

    <p>Ruling out tumors or abnormalities</p> Signup and view all the answers

    What is the primary purpose of MAO-B inhibitors in the management of Parkinson's disease?

    <p>Inhibit the breakdown of dopamine</p> Signup and view all the answers

    Which symptom is NOT typically associated with Parkinson's disease?

    <p>Dysphagia (difficulty swallowing)</p> Signup and view all the answers

    Which non-motor symptom is NOT commonly seen in individuals with Parkinson's disease?

    <p>Seizures</p> Signup and view all the answers

    What is one of the major roles of dopamine in relation to acetylcholine?

    <p>Dopamine inhibits acetylcholine release</p> Signup and view all the answers

    What is a primary clinical manifestation indicating advanced Parkinson's disease?

    <p>Postural instability</p> Signup and view all the answers

    Which of the following represents an effect of increased acetylcholine due to dopamine deficiency?

    <p>Tremors and jerking movements</p> Signup and view all the answers

    How is the diagnosis of Parkinson's disease primarily established?

    <p>Based on patient history and physical examination</p> Signup and view all the answers

    What must be avoided when taking MAO-B inhibitors to prevent dangerous increases in blood pressure?

    <p>Foods high in tyramine</p> Signup and view all the answers

    What is the primary action of COMT inhibitors in the management of Parkinson's disease?

    <p>They help levodopa to work longer.</p> Signup and view all the answers

    Which dietary consideration is crucial when managing a patient taking levodopa-carbidopa?

    <p>Avoid taking medications with high protein meals.</p> Signup and view all the answers

    What common adverse effect can occur in about 80% of patients treated with levodopa in the initial years?

    <p>Dyskinesia</p> Signup and view all the answers

    Which of the following symptoms is NOT effectively managed by anticholinergic medications in Parkinson's disease?

    <p>Bradykinesia</p> Signup and view all the answers

    In Parkinson's management, what is the role of amantadine aside from its previous use as an antiviral?

    <p>It increases dopamine levels in the brain.</p> Signup and view all the answers

    Which medication is an example of an MAO-B inhibitor used in the treatment of Parkinson’s disease?

    <p>Rasagiline</p> Signup and view all the answers

    Which adverse effects are commonly associated with dopamine antagonist medications?

    <p>Drowsiness and hallucinations</p> Signup and view all the answers

    Study Notes

    Cranial Nerve & Pain Transmission

    • The trigeminal nerve is responsible for transmitting pain signals from the head and face to the brain.

    Neurotransmitters & Movement Control

    • Dopamine is the neurotransmitter primarily involved in controlling movement.

    Memory Formation

    • The hippocampus is crucial for the formation of both short-term and long-term memories.

    Migraines & CGRP

    • Calcitonin Gene-Related Peptide (CGRP), released from trigeminal nerve endings, causes vasodilation and neurogenic inflammation, contributing to migraine headaches.

    Migraine Prevention

    • Propranolol is a first-line preventive treatment for migraines.

    Cluster Headache Treatment

    • Oxygen Therapy is a treatment used for acute relief of cluster headaches.

    Parkinson’s Disease & Substantia Nigra

    • Parkinson’s disease primarily affects the substantia nigra, a region in the brain responsible for dopamine production.

    Levodopa & Carbidopa

    • Carbidopa, given in combination with levodopa, inhibits the enzyme dopa decarboxylase, preventing the breakdown of levodopa before it reaches the brain.

    Dietary Considerations for Levodopa-Carbidopa

    • Patients taking levodopa-carbidopa should avoid foods high in fiber as they can interfere with medication absorption.

    Alzheimer's Disease & Amyloid Plaques

    • Alzheimer’s disease is characterized by the presence of amyloid plaques and neurofibrillary tangles in the brain.

    Acetylcholine & Dementia

    • Acetylcholine plays a vital role in memory and learning, and its decline is associated with dementia.

    Glutamate & Alzheimer’s Disease Treatment

    • Memantine is a medication used in the treatment of Alzheimer’s disease which regulates the activity of glutamate, an excitatory neurotransmitter that plays a role in memory and learning.

    Cluster Headaches

    • Oxygen Therapy is used for acute relief of cluster headaches.

    Parkinson’s Disease

    • Carbidopa is used in conjunction with Levodopa to treat Parkinson’s disease.
    • Carbidopa inhibits the enzyme dopa decarboxylase, increasing the amount of Levodopa reaching the brain, and improving its effectiveness.

    Dementia

    • Alzheimer’s disease is characterized by the presence of amyloid plaques and neurofibrillary tangles.
    • Acetylcholine plays a key role in memory and learning, and its decline is linked to the progression of dementia.
    • Memantine is a medication used to treat Alzheimer’s disease, and it regulates the activity of glutamate.
    • Donepezil, Rivastigmine, and Galantamine are also used to treat Alzheimer’s disease, and they work by inhibiting the breakdown of acetylcholine.

    Cluster Headache

    • Occurs in a series of attacks lasting minutes to hours, affecting one side of the head.
    • A series of attacks can last days with long remissions (months to years).
    • Chronic cluster headache has frequent attacks without remission.
    • Primarily affects men between 20-50 years of age.
    • Pain begins without warning, can alternate sides, and described as severe, stabbing & throbbing in the temporal-orbital region.
    • Symptoms include lacrimation (tearing) and rhinorrhea.
    • Triggers include caffeine, alcohol, smoking, and nicotine.
    • Differentiation from migraine: no aura, no nausea & vomiting, generally more debilitating.
    • Not associated with a family history.

    Pathophysiology of Cluster Headache

    • Not completely understood, but involves the trigeminovascular system.
    • Inflammation plays a role, with vasodilation of the intracranial blood vessels.
    • Hypothalamus plays a role in the onset of attacks, but the mechanism is unclear.
    • Involves the trigeminal nerve and its connections to blood vessels in the brain.
    • The trigeminal nerve carries sensory information (pain, temperature, touch) to the brain, transmitting pain signals.

    Management of Cluster Headache

    • Acute (Quick Acting)
      • Triptans (e.g., sumatriptan SC, zolmitriptan nasal spray).
      • Oxygen therapy.
      • Dihydroergotamine (DHE) (SC, IM, IV or nasal spray).
      • Lidocaine (nasal) - topical nasal drops.
    • Transitional Prophylactics (For High-Frequency Attacks, 2+/Day)
      • Oral corticosteroids (usually prednisone).
      • DHE (SC and IM).
      • Occipital nerve block with corticosteroids.

    Cluster Headache: Preventative

    • Calcium Channel Blocker
      • Verapamil is a first-line agent.
      • Mechanism of action is unclear, but believed to involve modulation of neurotransmitter systems in the hypothalamus.
      • Adverse Effects: cardiac arrhythmia, bradycardia, prolonged PR interval.
      • Caution prescribing in individuals with underlying cardiovascular disease.
    • Neurostabilizer
      • Lithium is a second-line agent.
      • Adverse Effects: cognitive disturbances, tremor, dizziness.
      • Requires monitoring due to a narrow therapeutic window.

    Migraine Headache

    • Most common in 18-44 years, and women.
    • Estrogen plays a significant role in migraine development.
    • Migraine with aura involves visual, sensory, dysphasic, and difficulty with speech or language symptoms.
    • Migraine without aura is also common.
    • Chronic migraine involves migraine at least 15 days/month.

    Clinical Manifestations of Migraines

    • Prodrome
      • Mood changes.
      • Fatigue.
      • Food craving.
      • Neck stiffness.
    • Aura
      • Not as common as migraine without aura.
      • 5 minutes to 1 hour before onset.
    • Migraine Attack
      • Severe throbbing pain, usually one-sided (can be bilateral).
      • Nausea & vomiting and/or sensitivity to light/sound.
      • Pain lasting several hours to several days (especially if untreated).
    • Postdrome
      • Migraine hangover.
      • Fatigue.
      • Difficulty concentrating.
      • Mood changes.
      • Can last 1 day or more.

    Migraine Headache Classification (International Headache Society [IHS])

    • Migraine WITHOUT aura
      • At least 5 attacks fulfilling specific criteria.
      • Headache lasts 4-72 hours (untreated or unsuccessfully treated).
      • Headache has at least 2 of 4 specific characteristics (unilateral location, pulsating quality, moderate or severe pain intensity, aggravation by or causing avoidance of routine physical activity).
      • During headache, at least one of the following symptoms is present: nausea and/or vomiting, photophobia or phonophobia.
      • Not better accounted for by another headache diagnosis.
    • Migraine WITH Aura
      • At least 2 attacks fulfilling criteria for migraine without aura.
      • Fully reversible aura symptoms (visual, sensory, speech and/or language, motor, brainstem, retinal).
      • At least 3 of 6 specific characteristics (aura symptom spreads gradually over >/= 5 minutes, 2 or more aura symptoms occur in succession, each individual aura symptom lasts 5-60 minutes, at least 1 aura symptom is unilateral, at least 1 aura symptom is positive, the aura is accompanied, or followed within 60 minutes, by headache).
      • Not better accounted for by another headache diagnosis.

    Pathophysiology of Migraine

    • Neurovascular disorder involving dilation and inflammation of intracranial blood vessels.
    • Mechanisms not fully understood.
    • Trigeminovascular System
      • Includes the trigeminal nerve and its projections to surrounding intracranial blood vessels.
      • Intracranial blood vessels contain nociceptors (activated by inflammation or mechanical stress) contributing to pain.
      • Activation of the trigeminovascular system by triggers leads to the release of neuropeptides (e.g., CGRP) causing vasodilation and neurogenic inflammation, contributing to pain.
    • Role of CGRP and Serotonin
      • Calcitonin Gene-Related Peptide (CGRP)
        • Released from trigeminal nerve endings when the trigeminal system is activated.
        • Functions: vasodilation, inflammation, sensitization.
        • Clinical implications: targeted by new migraine treatments.
      • Serotonin
        • Functions: modulates pain and causes cerebral vasoconstriction/vasodilation depending on the receptor it interacts with.
        • Fluctuations in serotonin levels (e.g., during stress or hormonal changes) can trigger migraine attacks.
        • Clinical implications: triptans activate serotonin receptors, reducing the release of CGRP and other pain-related neurotransmitters.

    Management of Migraine Headache

    • Avoid Known Triggers
      • Encourage patients to keep a journal or diary to identify triggers.
    • Abortive Therapy
      • Treats onset of symptoms.
      • First-line therapy: NSAIDs and acetaminophen.
    • Preventive Therapy
      • Usually reserved for frequent migraines.
      • Aim: reduce frequency and severity.

    Migraine Triggers

    • Fatigue and poor sleep.
    • Stress.
    • Hormonal changes.
    • Excess sensory stimulation.
    • Diet (including foods that contain tyramine or nitrates [aged cheeses, cured meats], dairy products, caffeine, etc.).

    Tension-Type Headache

    • Most common type of headache.
    • Characterized by a tight band-like feeling around the head.
    • Not associated with nausea or vomiting.
    • Not better accounted for by another headache diagnosis.
    • Less severe than migraine.

    Management of Tension-Type Headache

    • First-line therapy
      • NSAIDs.
      • Acetaminophen.
    • Preventive Therapy
      • For chronic tension-type headaches.
      • Tricyclic antidepressants (Amitriptyline, Nortriptyline).
      • Atypical antidepressants (Venlafaxine, Mirtazapine).
      • Caution in anyone under 18 years of age, as younger patients have a higher risk of suicidal thoughts.

    Medication Overuse Headache (MOH)

    • Also called rebound headache, drug-induced headache.
    • Develops in response to frequent use of abortive headache medication.
    • Medications include acetaminophen, NSAIDs, and triptans.
    • Reason for MOH not clearly understood, but believed to alter pain pathways in the brain making them more sensitive.

    Management of Medication Overuse Headache

    • Stopping All Headache Medications
      • Headache will temporarily increase when medications are stopped.
      • Resolves days to weeks after the overused medication is withdrawn.
    • Preventing MOH
      • Limit the use of abortive medications to 2-3 times/week.
      • Ensure doses are not greater than needed.
      • Start preventive therapy if headaches are increasing in frequency.

    Non-Pharmacological Management of MOH

    • Ensuring adequate sleep.
    • Eating regular meals and maintaining a healthy diet.
    • Ensuring adequate hydration.
    • Exercising regularly.
    • Keeping a headache diary.
    • Managing stress.
    • Evidence for use of cognitive behavioral therapy, biofeedback, and acupuncture.

    Parkinson's Disease

    • Progressive, neurodegenerative disorder affecting the basal ganglia.
    • Characterized by bradykinesia (slow movement), increased muscle tone, tremor at rest, impaired gait, and a lack of dopamine.
    • Unknown cause, thought to be related to environment and genetics.
    • Most often affects individuals over the age of 60.

    Basal Ganglia

    • Structures involved in coordination of movement, motor control.
    • Substantia nigra
      • Part of the basal ganglia, located in the midbrain (part of the brainstem).
      • Has dopaminergic neurons, producing dopamine.
      • Degeneration of dopaminergic neurons in Parkinson's disease leads to decreased dopamine release.

    Degeneration of Dopaminergic Neurons

    • Dopamine inhibits acetylcholine.
    • Decreased dopamine release leads to increased acetylcholine release.
    • This disrupts the balance between dopamine and acetylcholine, leading to increased acetylcholine.
    • The imbalance between dopamine and acetylcholine can lead to muscle overexcitement causing tremors and jerking movements.

    Headache

    • Secondary headaches are caused by other medical conditions or injuries.

    Tension-Type Headache

    • Can be treated with NSAIDs and acetaminophen, particularly for acute episodes.
    • Preventive therapy is recommended for chronic cases.
    • Tricyclic antidepressants like Amitriptyline and Nortriptyline can be used for prevention.
    • Atypical antidepressants, including Venlafaxine (Effexor) and Mirtazapine (Remeron), are also used but caution is advised for those under 18 due to a higher risk of suicidal thoughts.

    Migraine Headache

    • Migraines are more prevalent among women aged 18-44, with estrogen playing a significant role in their development.
    • Migraine with aura involves visual, sensory, dysphasic or speech/language disturbances.
    • Migraine without aura does not involve these preceding symptoms.
    • Chronic migraine is defined by migraine attacks occurring at least 15 days per month.
    • Patients with migraine with aura are at an increased risk of ischemic stroke, necessitating careful management of risk factors.
    • Contraceptives containing estrogen are linked to an elevated risk of ischemic stroke in women with migraine with aura, and therefore should be avoided.

    Phases of Migraines

    • Prodrome: Occurs hours or days before the migraine onset, marked by mood changes, fatigue, food cravings and neck stiffness.
    • Aura: Experienced by up to ⅓ of patients, lasting 5 minutes to 1 hour before the onset, characterized by specific neurological alterations.
    • Migraine Attack: Severe, throbbing pain usually on one side of the head, potentially bilateral, accompanied by nausea, vomiting, and sensitivity to light/sound.
    • Postdrome: Considered a "migraine hangover," it can last 1 day or more, and is characterized by fatigue, concentration difficulties, mood swings.

    Migraine Headache Classification

    • Migraine WITHOUT aura: At least five attacks with headache lasting 4-72 hours, accompanied by two of the following: Unilateral location, pulsating quality, moderate/severe pain intensity, aggravation by physical activity. At least one of the following must also be present: Nausea/vomiting, photophobia/phonophobia.
    • Migraine WITH Aura: At least two attacks with at least one aura symptom, including visual, sensory, speech/language, motor, brainstem, or retinal disturbances. The aura must meet at least three of the following criteria: Gradual aura symptom spread over > 5 minutes, two or more aura symptoms occurring consecutively, each individual aura symptom lasting 5-60 minutes, at least one unilateral aura symptom, at least one positive aura symptom, aura accompanied or followed by headache within 60 minutes.

    Pathophysiology of Migraine

    • Involves dilation and inflammation of intracranial blood vessels.
    • The trigeminovascular system, including the trigeminal nerve and its projections to surrounding blood vessels, plays a key role.
    • Activation of nociceptors in blood vessels, triggered by inflammation or mechanical stress contributes to the pain experience.
    • Release of neuropeptides, such as CGRP, during activation causes vasodilation and neurogenic inflammation, further contributing to pain.

    CGRP and Serotonin Role in Migraine

    • Calcitonin gene-related peptide (CGRP): Released from trigeminal nerve endings during system activation, causing vasodilation, inflammation, sensitization, and pain transmission. This makes it a target for new migraine treatments.
    • Serotonin: Modulates pain sensation and influences cerebral vasoconstriction/vasodilation. Fluctuations in serotonin levels can trigger attacks. Triptans, which activate specific serotonin receptors, help reduce CGRP and other pain-related neurotransmitter release.

    Management of Migraine Headache

    • Avoidance of triggers: Encouraging patients to identify and log potential triggers, which can include fatigue, poor sleep, stress, hormonal changes, excess sensory stimulation, and dietary factors like tyramine, nitrates, dairy products, caffeine.
    • Abortive therapy: Managing symptoms once they begin.
    • Preventive therapy: Usually reserved for frequent migraines, with the aim of reducing frequency and severity.

    Migraine Headache: First Line Therapy

    • Mild & moderate: NSAIDs (e.g. Amitriptyline)
    • Anticonvulsants: Topiramate blocks sodium channels, stabilizes neurons, and inhibits glutamate.
    • Localized injections:
      • Botulinum toxin (Botox): Prevents release of pain-transmitted receptors, aiding in chronic migraine prevention.
      • Occipital nerve blocks: Use lidocaine or bupivacaine to reduce inflammation.

    Cluster Headache

    • Characterized by a series of attacks lasting minutes to hours, affecting one side of the head, with potential long remissions.
    • Chronic cluster headaches involve more frequent attacks without remission periods.
    • Primarily affects men between 20-50 years old.
    • Pain is often described as severe, stabbing and throbbing, located in the temporal-orbital region.
    • Symptoms like tearing and runny nose are common.
    • Triggers can include caffeine, alcohol, smoking, and nicotine.
    • Differentiation from migraines: No aura, no nausea or vomiting, generally more debilitating.
    • Not associated with a family history.

    Pathophysiology of Cluster Headache

    • While not entirely understood, it involves the trigeminovascular system with inflammation playing a significant role.
    • Vasodilation of intracranial blood vessels is implicated, and the hypothalamus may be involved in attack onset, though the mechanism is unclear.
    • The trigeminal nerve and its connections with brain blood vessels carry sensory information and transmit pain signals.

    Management of Cluster Headache

    • Acute (quick acting):
      • Triptans (e.g., Sumatriptan SC, Zolmitriptan nasal spray)
      • Oxygen therapy
      • Dihydroergotamine (DHE) (SC, IM, IV, or nasal spray)
      • Lidocaine (nasal)
    • Transitional prophylactics (for high-frequency attacks, 2+/day):
      • Oral corticosteroids (usually Prednisone)
      • DHE (SC and IM)
      • Occipital nerve blocks with corticosteroids

    Dementia

    • A progressive decline in cognitive functioning affecting memory, judgment, reasoning, communication, and purposeful movements.
    • Influences mood and behavior.
    • Aging and family history are risk factors, but dementia is not a normal part of aging.

    Common Dementia Types

    • Alzheimer's disease
    • Vascular dementia
    • Dementia with Lewy bodies
    • Frontotemporal dementia

    Alzheimer's Disease

    • Characterized by:
      • Neuronal degeneration: Affecting hippocampus early on, and cerebral cortex later, impacting speech, perception, and memory. In later stages, bladder and bowel control, as well as ADLs are affected.
      • Amyloid plaques: Abnormal protein fragment clusters that build up between neurons, disrupting cell communication, causing inflammation, and leading to neuronal damage.
      • Neurofibrillary tangles: Twisted fibers of TAU proteins, which normally stabilize microtubules. When TAU proteins become entangled, it disrupts the network and can lead to cell death.
      • Loss of connections between neurons: The gradual loss of neural connections due to plaques, tangles, and neuroinflammation, causes neuron damage and death, resulting in brain atrophy and cognitive decline.

    Alzheimer's: Acetylcholine Deficit

    • Acetylcholine, a neurotransmitter crucial for memory, is reduced in Alzheimer's disease.
    • It plays a role in converting short-term to long-term memory and is involved in learning and attention.
    • The loss of cholinergic neurons, which produce acetylcholine, results in decreased acetylcholine levels, leading to memory difficulties, retrieval challenges, and overall cognitive decline.

    Other Factors in Alzheimer's

    • Apolipoprotein e4 (APOE): This gene has three forms, with APOE e4 linked to an increased risk of Alzheimer's.
    • Endoplasmic reticulum-associated binding protein: Elevated in the brains of Alzheimer's patients, potentially toxic to neurons and potentially involved in amyloid plaque formation.

    Vascular Dementia

    • Caused by damage from cardiovascular disease, leading to reduced blood flow and oxygen delivery to the brain, resulting in cell ischemia.
    • Often associated with history of stroke(s), and may present with sudden onset.
    • Risk factors include smoking, hypertension, coronary artery disease, diabetes, and dyslipidemia.

    Dementia with Lewy Bodies

    • Marked by the presence of Lewy bodies in the cerebral cortex, contributing to cognitive decline and hallucinations.

    Frontotemporal Dementia

    • Involves degeneration of the frontal lobe, the temporal lobe, or both, commonly impacting behavior and language.
    • Linked to an accumulation of abnormal proteins within neurons.
    • Typically presents between ages 40-65.

    Presentation of Dementia

    • Usually has a gradual onset and can last 3-20 years.
    • Mild cognitive impairment may precede dementia.

    8 As of Dementia

    • Anosognosia: Patient unaware of their neurological or psychiatric deficits.
    • Agnosia: Inability to process sensory information.
    • Aphasia: Language difficulties, including difficulty finding words, understanding language, or communicating.
    • Apraxia: Inability to perform tasks or movements when requested.
    • Altered Perception: Misinterpretation or confusion about sensory inputs.
    • Attentional Deficits: Problems focusing, leading to difficulty completing tasks.
    • Apathy: Lack of interest or social withdrawal.
    • Amnesia: Memory loss, which can affect early, recent, or long-term memory.

    Dementia Evaluation

    • Based on history, patient interview, and information from family/caregivers.
    • Cognitive tests such as MMSE and MoCA are administered.
    • Delirium and depression are ruled out.
    • Imaging with CT scan or MRI may be considered to assess brain atrophy or identify abnormalities, but these are not definitive for diagnosis.

    Medications for Dementia

    • Cholinesterase inhibitors: Increase acetylcholine levels in the brain.
      • Donepezil, Rivastigmine, Galantamine: Used for Alzheimer's (mild, moderate, and sometimes severe), Vascular dementia (donepezil has some supporting data), and Lewy body dementia. Not effective in Frontotemporal dementia.
    • NMDA Receptor Antagonist: Memantine: Used with cholinesterase inhibitors in Alzheimer's disease. Not effective in Frontotemporal dementia.
    • Combination Therapy (Cholinesterase inhibitors and Memantine): Helpful for moderate to severe Alzheimer's disease, enhances ability to perform everyday tasks and improve quality of life.

    Cholinesterase Inhibitors

    • Increase acetylcholine levels in the brain.
    • Provide mild, short-term benefits in quality of life and cognitive function.
    • Adverse effects include nausea, diarrhea, vivid dreams, leg cramps, dizziness, and headache.
    • Bradycardia is rare but may lead to syncope.

    Memantine

    • Regulates the effects of Glutamate (important for learning and memory) and protects against cytotoxicity.
    • Provides modest benefits in moderate-severe Alzheimer's disease.
    • Fewer adverse effects and better tolerated than cholinesterase inhibitors.

    Nonpharmacologic Strategies for Dementia

    • Exercise
    • Social Engagement
    • Cognitive stimulation
    • MIND diet (Hybrid of Mediterranean and DASH diet) - While a recent RCT found lack of evidence for MIND diet effectiveness in preventing dementia.

    Parkinson's Disease

    • Progressive neurodegenerative disorder affecting individuals over 60.
    • Characterized by slow movement (bradykinesia), increased muscle tone, tremors at rest, and impaired gait.
    • Caused by degeneration of dopaminergic neurons in the substantia nigra, part of the basal ganglia.
    • This leads to decreased dopamine production and an imbalance with acetylcholine, leading to tremors and muscle overexcitement.
    • Symptoms include tremor, rigidity, akinesia, and postural instability.
    • Non-motor symptoms include loss of smell, sleep dysfunction, mood disorders, anxiety, depression, memory changes, and constipation.

    Dementia

    • Progressive decline in cognitive functioning affecting memory, judgment, reasoning, communication, and purposeful movement.
    • Affects mood and behaviour.
    • Risk factors include aging and family history.
    • There are four common types: Alzheimer's disease, vascular dementia, dementia with Lewy bodies, and frontotemporal dementia

    Alzheimer's Disease

    • Characterized by neuronal degeneration in the hippocampus and cerebral cortex, formation of amyloid plaques, and neurofibrillary tangles.
    • Amyloid plaques are abnormal protein clusters that disrupt cell-to-cell communication, cause inflammation, and lead to neuronal damage.
    • Neurofibrillary tangles are twisted fibers of TAU proteins that disrupt the network and lead to cell death.
    • Associated with decreased production of acetylcholine, a neurotransmitter important for memory and learning.
    • Apolipoprotein e4 (APOE) and endoplasmic reticulum-associated binding protein are also implicated.

    Vascular Dementia

    • Damage arises from cardiovascular disease affecting blood and oxygen delivery to the brain.
    • May have a sudden onset and patients may have a history of stroke.
    • Risk factors include smoking, hypertension, coronary artery disease, diabetes, and dyslipidemia.

    Dementia with Lewy Bodies

    • Characterized by the presence of Lewy bodies in the cerebral cortex.

    Frontotemporal Dementia

    • Degeneration of the frontal lobe, temporal lobe, or both.
    • Primarily affects behaviour and language.
    • Associated with an accumulation of abnormal proteins in the neurons.
    • Typically affects individuals between 40-65 years old.

    Dementia Presentation

    • Usually has a gradual onset.
    • Can last for 3-20 years.
    • Patients may experience mild cognitive impairment before dementia.

    Dementia Evaluation

    • Based on history, interview with patient and family/caregivers.
    • Cognitive tests include the Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA).
    • Delirium and depression are ruled out.
    • Imaging with a CT scan or MRI of the head may be considered.

    Dementia Medications

    • Cholinesterase inhibitors: donepezil, rivastigmine, galantamine
    • NMDA receptor antagonists: memantine
    • Combination therapy of cholinesterase inhibitors and memantine

    Cholinesterase Inhibitors

    • Increase acetylcholine levels in the brain.
    • Used for Alzheimer's disease (mild, moderate, and sometimes severe), vascular dementia, and Lewy body dementia.
    • Not effective for frontotemporal dementia.
    • Offer mild, short-lived benefits in quality of life and cognitive function.
    • Side effects include nausea, diarrhea, vivid dreams, leg cramps, dizziness, and headache.
    • Bradycardia is rare but can lead to syncope.

    Memantine

    • Used in combination with cholinesterase inhibitors in Alzheimer's disease.
    • Not used in frontotemporal dementia.
    • Less side effects and better tolerated than cholinesterase inhibitors.
    • Modest benefits in moderate to severe Alzheimer's disease.
    • Regulates the effect of glutamate, a neurotransmitter important for learning and memory, to protect against cytotoxicity.

    Nonpharmacologic Strategies for Dementia

    • Exercise, Social Engagement, Cognitive stimulation, and MIND Diet (hybrid of Mediterranean and DASH diets)

    Parkinson's Disease Evaluation

    • Based on history, physical exam, and ruling out other conditions.
    • Comprehensive medical history, family history, current/past medications, and other potential neurological disorders.
    • Physical exam focusing on motor function, including rapid alternating movements, tremors at rest, postural instability, and gait assessment.
    • Romberg test may be used.
    • No specific confirmation with lab tests or imaging.

    Management of Parkinson's Disease

    • Medications aimed at:
      • Enhancing release or supply of dopamine
      • Blocking the effects of acetylcholine

    Levodopa-Carbidopa

    • Dopamine precursor converted to dopamine in the basal ganglia.
    • Carbidopa inhibits the breakdown of levodopa by dopa decarboxylase, allowing more levodopa to reach the brain.
    • Decreases symptoms, but improvement may take weeks to months.
    • May cause urine, sweat, and saliva to appear darker (harmless).
    • Avoid protein-rich meals, take 30 minutes before meals or 1-2 hours after.
    • Effectiveness may decrease after 5-10 years due to disease progression.
    • Side effects include hallucinations, orthostatic hypotension, dyskinesia, and paranoid ideation.

    Dopamine Agonists

    • Stimulate dopamine receptors.
    • Used with levodopa-carbidopa.
    • Examples include apomorphine (short-term use only), pramipexole, rotigotine, and ropinirole.
    • Side effects include hallucinations, daytime sleepiness, and postural hypotension.

    MAO-B Inhibitors

    • Inhibit the breakdown of dopamine by MAO-B, an enzyme.
    • Used with levodopa-carbidopa.
    • Examples include rasagiline and selegiline.
    • Avoid foods high in tyramine (aged cheese, smoked or cured meats, fermented foods, beer).

    COMT Inhibitors

    • Inhibit COMT, an enzyme that breaks down dopamine.
    • Used with levodopa-carbidopa to prolong its effectiveness.
    • Example: entacapone.
    • Side effects include liver failure (rare), dyskinesias, postural hypotension, nausea, and vomiting.
    • Entacapone may cause yellow-orange discoloration of urine.

    Amantadine

    • Used to manage dyskinesia caused by long-term use of levodopa.
    • Thought to stimulate dopamine release and block its reuptake.

    Anticholinergic Medications

    • Block the action of acetylcholine to reduce involuntary muscle movements and rigidity.
    • Limited effectiveness with multiple side effects.
    • Benztropine (Cogentin) is most commonly prescribed.
    • Side effects include dry mouth, blurred vision, photophobia, urinary retention, constipation, and tachycardia.

    Nutrition Considerations for Parkinson's Disease

    • Easy-to-chew and swallow foods to manage dysphagia and bradykinesia.
    • Adequate fiber intake to reduce constipation.
    • Monitor protein intake when taking levodopa.

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    Description

    This quiz covers key concepts in neuroscience related to pain transmission, neurotransmitter functions, and memory formation. Topics include the trigeminal nerve, dopamine's role in movement, and treatments for migraines and cluster headaches. Test your knowledge on the intricacies of brain functions and disorders.

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