Headache, Parkinson's Disease & Dementia NUR 425 Week 5 PDF

Headache, Parkinson’s disease & dementia NUR 425 Week 5  A&P Review Question s Which nerve is primarily responsible for transmitting pain signals from the head and face to the brain? A. Facial nerve B. Vagus nerve C. Trigeminal nerve D.Glossopharyngeal nerve Which neurotransmitter is pri...

Headache, Parkinson’s disease & dementia NUR 425 Week 5  A&P Review Question s Which nerve is primarily responsible for transmitting pain signals from the head and face to the brain? A. Facial nerve B. Vagus nerve C. Trigeminal nerve D.Glossopharyngeal nerve Which neurotransmitter is primarily involved in controlling movement? A. Serotonin B. Dopamine C. Acetylcholine D.GABA Which of the following is required for the formation of short and long-term memories? A. Hypothalamus B. Cerebral cortex C. Prefrontal cortex D. Hippocampus 5 Headache Headache Primary vs Secondary Primary headaches (examples): Tension type headache Migraine headache Cluster headache Secondary headaches (examples): Illness/injury related (e.g. sinus headache, meningitis, concussion) Medication side effect Tension type Headache Most common type of primary headache Headache is typically bilateral and mild, with feeling of a tight band or pressure around the head Episodic: less than 15 days/month Chronic: at least 15 days/month, for at least 3 months Pathophysiology is not well understood (Lewis, 2023, p. 1512) Management of tension-type headache Non-steroidal anti-inflammatory drugs (NSAIDs) and acetaminophen Preventive therapy (medications) Tricyclic antidepressants: Amitriptyline, nortriptyline Atypical antidepressants: Venlafaxine (Effexor)*, Mirtazapine (Remeron)* *caution in anyone younger than 18 years of age Migraine headache Affects about 8.3% of Canadians (Amoozegar et al., 2022) Most common in those aged 18-44 years More common in women https://migrainecanada.org/you-are-not- alone/  Auras - Visual (90%), Migraine headache e.g. flashing lights, zigzag Migraine with aura lines, blind spots, Migraine without aura visual distortions Chronic migraine – migraine - Sensory, e.g. headache at least 15 tingling, days/month numbness, pins- Clinical Pearls and-needles - Migraine with aura ↑ risk of ischemic sensation stroke (important to manage risk factors) typically starting - Avoid use of contraceptives (containing in fingers and estrogen) in women with migraine with moving up arm, aura as this also ↑ ischemic stroke risk or affecting the face - Dysphasic, e.g. Clinical manifestations Phases: Prodrome Aura (up to 1/3 of patients experience an aura) Migraine attack Postdrome (Lewis, 2023, p. 1512) https://www.migrainedisorders.org/migraine-  Migraine headache classification (International Headache Society [IHS]) Migraine without aura (more Migraine with common) aura A. At least five attacks fulfilling criteria B-D A. At least two attacks fulfilling criteria B and C B. Headache attacks lasting 4-72 hr (untreated or B. One or more of the following fully reversible aura symptoms: 1. Visual unsuccessfully treated) 2. Sensory C. Headache has at least two of the following four 3. Speech and/or language characteristics: 4. Motor 1. unilateral location 5. Brainstem 2. pulsating quality 6. Retinal 3. moderate or severe pain intensity C. At least three of the following six characteristics: 4. aggravation by or causing avoidance of routine physical 1. at least one aura symptom spreads gradually over ≥5 minutes activity (e.g., walking or climbing stairs) 2. two or more aura symptoms occur in succession D. During headache at least one of the following: 3. each individual aura symptom lasts 5-60 minutes 4. at least one aura symptom is unilateral 1. nausea and/or vomiting 5. at least one aura symptom is positive 2. photophobia and phonophobia 6. the aura is accompanied, or followed within 60 minutes, by E. Not better accounted for by another ICHD-3 headache diagnosis. D. Not better accounted for by another ICHD-3 diagnosis. https://ichd-3.org/1-migraine/ Pathophysiology of migraine Neurovascular disorder that involves dilation and inflammation of the intracranial blood vessels Mechanisms not fully understood Trigeminovascular system Includes the trigeminal nerve and the projections of this nerve to surrounding intracranial blood vessels Intracranial blood vessels contain nociceptors (which can be activated by inflammation or mechanical stress), contributing to pain Activation of this system by various triggers leads to the release of neuropeptides (e.g. CGRP) which cause vasodilation and neurogenic inflammation, contributing to pain  Pathophysiology of migraine 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 and pain transmission Clinical implications: targeted by new migraine treatments Serotonin Functions: modules pain and can cause cerebral vasoconstriction/vasodilation (depending on which receptors it interacts with) Fluctuations in serotonin levels (i.e. during stress or hormonal changes) can trigger migraine attacks Clinical implications: Triptans activate serotonin receptors, which help reduce the release of CGRP and other pain-related neurotransmitters Management of migraine headache Avoiding known triggers Abortive therapy Preventive therapy Migraine triggers Migraine can be precipitated by triggers Triggers include: Fatigue and poor sleep Stress Hormonal changes Excess sensory stimulation Diet (including foods that contain tyramine or nitrates, dairy products, caffeine, etc.) Migraine headache: First line therapy Mild & moderate: non-steroidal anti-inflammatory drugs (NSAIDs) Examples: ASA high dose, ibuprofen, naproxen Moderate & severe: Selective serotonin1B/1D receptor agonists or Triptans Relieve pain by constricting intracranial blood vessels and reducing inflammation (by suppressing release of inflammatory neuropeptides, including CGRP Available in tablets, injections and nasal sprays Examples: sumatriptan (Imitrex), zolmitriptan (Zomig) These treatments are effective when taken early in the course of a migraine attack Combo of NSAIDs + triptans superior to triptan alone Triptans: Adverse effects Common adverse effects: nausea, facial flushing, tingling, paresthesia, dizziness, fatigue Less common: chest discomfort or tightness (with or without palpitations) Serious side effects (rare): coronary vasospasm, serotonin syndrome Caution in use in patients with increased CV risk Contraindicated in patients with CV or cerebrovascular disease Triptans: Drug interactions Numerous drug interactions Selective serotonin reuptake inhibitors (SSRIs), serotonin- norepinephrine reuptake inhibitors (SNRIs) and tricyclic antidepressants (TCAs) can increase the risk of serotonin syndrome Serotonin syndrome includes: Altered mental status Incoordination Myoclonus Hyperreflexia Excessive sweating Tremor Fever Migraines: Second line therapy Ergot alkaloids Mechanism of action is not clearly understood Can be helpful for moderate to severe migraines, or migraines that have not responded to first line treatments Dihydroergotamine (Migranal) is the medication available in Canada Route of administration: SC, IM or nasal spray Common adverse events are nausea & vomiting (pre-dose antiemetic recommended) Black box warning for vasoconstriction Increased chance with excessive or prolonged use Newer migraine treatment CGRP (calcitonin gene-related peptide) receptor antagonist November 2022: Health Canada approved the first oral CGRP receptor antagonist for abortive therapy - Ubrelvy (ubrogepant) Can be used for mild, moderate and severe migraines Consider use in patients who cannot tolerate triptans or ergots, or who are not responding to standard treatments Generally well tolerated Can be used as part of combo therapy as well Migraine treatment: Preventive Indications for preventive therapy 6 or more attacks per month Attacks that are especially severe Attacks that do not respond adequately to abortive medications Patient experiencing medication overuse headache Most preventive medications take 4-6 weeks to show their full effect Goals of prophylaxis therapy - Decreased migraine severity or frequency by 50% or more - Prevent medication overuse headache (MOH) Migraine treatment: Preventive 1st line therapy: Beta-blockers, Propranolol is used most often Antidepressants, e.g. Amitriptyline Anticonvulsants, e.g. Topiramate Other treatments: localized injections Botulinum toxin (Botox) Occipital nerve blocks using lidocaine or bupivacaine Cluster headache Cluster headache occurs in a series of attacks Attacks last minutes to hours Affects one side of the head A series of attacks can last days There can be long remissions (months to years) Chronic cluster More frequent attacks without any remission Cluster headache Primarily affects men between 20-50 years of age Attack usually beings without warning Pain may alternate between sides of the head Pain described as severe, stabbing & throbbing in the temporal-orbital region Symptoms include lacrimation (tearing) and rhinorrhea (Lewis, 2023, p. 1512) https://commons.wikimedia.org/wiki/File:Trigeminal_Nerve.png Cluster headache Triggers can include caffeine, alcohol, smoking Differ from migraine in several ways No aura No nausea/vomiting Generally more debilitating Not associated with a family history Pathophysiology of cluster headache Not completely understood Involves the trigeminovascular system Inflammation plays a role Vasodilation of the intracranial blood vessels Hypothalamus plays a role in the onset of attacks, but this is unclear Management of cluster headache Acute: Triptans (e.g. sumatriptan SC, zolmitriptan nasal spray) Oxygen therapy DHE (SC, IM, IV or nasal spray) Lidocaine (nasal) Transitional prophylactics (for high-frequency attacks, 2+/day): Oral corticosteroids (usually prednisone) DHE (SC or IM) Occipital nerve block with corticosteroids (e.g. methylprednisolone SC in combo with lidocaine) Cluster headache: Preventative Calcium channel blocker Verapamil is a first-line agent for preventive therapy Mechanism of action in preventing cluster headache is unclear Adverse effects: cardiac arrythmia, bradycardia, prolonged PR interval Neurostabilizer Lithium is second-line agent for preventive therapy Adverse effects: cognitive disturbances, tremor, dizziness Need to monitor drug level as it has a narrow therapeutic window Medication overuse headache Also called rebound headache, drug-induced headache Develops in response to frequent use of abortive headache medication Medications include: Acetaminophen NSAIDs Triptans Reason for medication overuse headache is not clearly understood Management of medication overuse headache Stopping all headache medications Patient needs to realize that when medications are stopped, headaches will increase temporarily Resolves days to weeks after the overused medication is withdrawn Prevent medication overuse headache by: Limiting the use of abortive medications to 2-3 times/week Ensuring doses are not greater than needed Starting preventive therapy if headaches are increasing in frequency Non-pharmacological management Ensuring adequate sleep Eating regular meals; healthy diet Ensuring adequate hydration Exercising regularly Keeping a headache diary Managing stress Evidence for use of cognitive behavioural therapy, biofeedback and acupuncture What role does Calcitonin Gene- Related Peptide (CGRP) play in migraines? A. It causes vasoconstriction and reduces inflammation. B. It is released from trigeminal nerve endings and causes vasodilation and neurogenic inflammation. C. It stabilizes serotonin levels and prevents pain transmission. D. It blocks nociceptors and prevents pain. Which of the following is a first- line preventive treatment for migraines? A. Sumatriptan B. Propranolol C. Dihydroergotamine D.Lidocaine Which of the following treatments is used for acute relief of cluster headaches? A. Amitriptyline B. Topiramate C. Oxygen therapy D.Verapamil Parkinson’s disease Parkinson’s disease Progressive, neurodegenerative disorder Characterized by bradykinesia, increased muscle tone, tremor at rest and impaired gait Unknown cause, thought to be related to environment and genetics Most often affects individuals over the age of 60 Characterized by a lack of the neurotransmitter dopamine  Basal ganglia https://www.flintrehab.com/basal-ganglia-brain-damage/ Substantia nigra Part of the basal ganglia Located in the midbrain (part of the brainstem) Has dopaminergic neurons In Parkinson’s disease, there is degeneration of these neurons https://www.researchgate.net/figure/Substantia-Nigra-and-Dopamine-producing- cells_fig1_345208392 Degeneration of dopaminergic neurons Decreased release of dopamine Degeneration of dopaminergic neurons Disrupts balance between dopamine & acetylcholine, leading to increased acetylcholine https://alzheimersnewstoday.com/news/new-insights-into-dementia-with-lewy-bodies-parkinsons-disease/ Clinical manifestations Seen with loss or impairment of 60-80% of the dopaminergic neurons Tremor Rigidity Akinesia Postural instability Nonmotor symptoms: loss of smell, sleep dysfunction, mood disorders, anxiety, depression, memory changes, constipation Evaluation Based on patient history and physical exam No specific confirmation with lab tests or imaging Management Enhancing release or supply of Medication dopamine therapy Blocking the effects of acetylcholine Levodopa-Carbidopa Levodopa is a dopamine precursor It is converted into dopamine in the basal ganglia However, levodopa is broken down (metabolized) by the enzyme dopa decarboxylase Carbidopa inhibits the enzyme dopa decarboxylase, and is prescribed with levodopa Levodopa-carbidopa decreases symptoms May take several weeks to months to become effective Levodopa-Carbidopa Urine, sweat & saliva can appear darker Avoid taking with high protein meals as this can interfere with drug absorption Lack of effectiveness after 5-10 years, may be secondary to disease progression Adverse effects: hallucinations, orthostatic hypotension, dyskinesia, paranoid ideation About 80% of patient can develop dyskinesia (abnormal movements) within the first few years of treatment Dopamine agonists Stimulate dopamine receptors Can be used with levodopa-carbidopa Examples: apomorphine (not used routinely, short term use only for “off” episode), pramipexole, rotigotine, ropinirole Adverse effects: hallucinations, daytime sleepiness, postural hypotension MAO-B inhibitors Monoamine oxidase type B inhibitors MAO-B is an enzyme that inactivates dopamine Can be used with levodopa-carbidopa Examples: rasagiline, selegiline Like all MAO inhibitor medications, must avoid food high with tyramine (aged cheese, smoked or cured meats, fermented foods, beer) COMT inhibitors Catechol-O-methyltransferase inhibitor Catechol-O-methyltransferase inactivates dopamine Used with levodopa-carbidopa, helps levodopa to work longer Example: entacapone AE: liver failure (rare), dyskinesias, postural hypotension, nausea, vomiting Entacapone can cause yellow-orange discolouration of urine Amantadine (Used as an antiviral for influenza A) Thought to stimulate dopamine release and block the reuptake of dopamine Can help to manage dyskinesia caused by levodopa Anticholinergic medications Work by blocking the action of the neurotransmitter acetylcholine This helps to inhibit involuntary muscle movements, decreases rigidity Little or no effect on bradykinesia Limited effectiveness, multiple side effects Benztropine (Cogentin) most common Adverse effects: dry mouth, blurred vision, photophobia, urinary retention, constipation, tachycardia Nutrition considerations Dysphagia & bradykinesia highlight need for foods that are easy to chew & swallow Adequate fibre to reduce constipation Watch protein intake with levodopa Which part of the brain is primarily affected in Parkinson’s disease? A. Hippocampus B. Substantia nigra C. Cerebellum D.Medulla oblongata What is the role of carbidopa in the treatment of Parkinson’s disease with levodopa? A. Enhances the breakdown of levodopa B. Inhibits the enzyme dopa decarboxylase C. Increases the production of acetylcholine D.Reduces the side effects of dopamine What dietary consideration is important for patients taking levodopa-carbidopa? A. Take medication with high-protein snack B. Avoid foods high in fiber C. Take medication 30 min before meals if tolerated D.Increase intake of dairy products Dementi a Dementia Progressive decline in cognitive functioning Affects memory, judgement, reasoning, ability to communicate, ability to carry out purposeful movements Affects mood & behaviour Risk factors include aging and family history (but not a normal part of aging) Dementia: 4 most common types Alzheimer’s disease Vascular dementia Dementia with Lewy bodies Frontotemporal dementia Alzheimer’s disease Characterized by: Neuronal degeneration Amyloid plaques Neurofibrillary tangles Loss of connections between neurons Neuronal degeneration Early in the disease Hippocamp Hippocampus plays important us role in memory Seen later in the disease Affects speech, perception & Cerebral memory cortex Later stages: affects bladder & bowel control, ADLs  Amyloid plaques & neurofibrillary tangles (Lewis, 2023, p. 1545) https://www.brightfocus.org/news/amyloid-plaques-and- neurofibrillary-tangles Microtubules (Lehne, 2021, p. 209) Loss of connections between neurons Gradual loss Leads to of connections damage & Atrophy between death of neurons neurons Decreased production of acetylcholine Acetylcholine is a neurotransmitter that plays an important role in memory Acetylcholine is formed by the cholinergic neurons There is a loss of cholinergic neurons in Alzheimer’s disease Linked with memory loss in later disease Other factors Apolipoprotein e4 Endoplasmic reticulum- Apolipoprotein (APOE) refers associated binding to a gene linked to protein Alzheimer’s disease This protein is elevated in the 3 forms: APOE e2, APOE e3 & brains of patients with APOE e4 Alzheimer’s disease The APOE e4 has been found Has been found to be toxic to to increase the risk for neurons Alzheimer’s disease Vascular dementia Damage stems from cardiovascular disease that leads to decreases in blood & oxygen delivery to the brain, leading to cell ischemia Patient may have a history of a stroke or multiple strokes Can present with a sudden onset Risk factors: smoking, hypertension, coronary artery disease, diabetes, dyslipidemia  Dementia with Lewy bodies https://alzheimersnewstoday.com/news/new-insights-into-dementia-with-lewy-bodies-parkinsons-disease/ Frontotemporal dementia Degeneration of the frontal lobe, temporal lobe or both Usually affects behaviour & language Associated with an accumulation of abnormal proteins in the neurons Typical age of onset is between 40-65 years of age Presentation of dementia Gradual onset usually 8 As of dementia Disease can last 3-20 Anosognosia Agnosia years Aphasia Apraxia May have mild cognitive Altered Attentional impairment prior to perception deficits dementia Apathy Amnesia Evaluation Based on history, interview with patient & family / caregivers Cognitive tests: MMSE, MoCA Ruling out delirium, depression Imaging with CT scan, MRI of head may be considered Medications Cholinestera NMDA se inhibitors receptor antagoni st Donepezil Rivastigmine Memantin Galantamine e Cholinesterase inhibitors (Lewis, 2023, p. 1549) Cholinesterase inhibitors Indications Alzheimer’s disease (mild, moderate and sometimes severe cases) Vascular dementia (some evidence supporting use of donepezil) Lewy body dementia Not used in frontotemporal dementia (not shown to be effective) Mild, short-limited benefits in quality of life & cognitive function AE: nausea, diarrhea, vivid dreams, leg cramps, dizziness, headache Bradycardia is rare but can lead to syncope Memantine Can be used with cholinesterase inhibitor in Alzheimer’s disease Not used in frontotemporal dementia Less AE than cholinesterase inhibitors Modest benefits in moderate-severe Alzheimer’s disease (Lewis, 2023, p. 202) Nonpharmacologic strategies Exercise Social engagement Cognitive stimulation MIND diet (hybrid of Mediterranean diet & Dietary Approaches to Stop Hypertension (DASH) diet) Recent RCT found lack of evidence for MIND diet (Barnes et al., 2023) Which type of dementia is characterized by the presence of amyloid plaques and neurofibrillary tangles? A. Vascular dementia B. Frontotemporal dementia C. Alzheimer’s disease D.Dementia with Lewy bodies What is the primary role of acetylcholine in the brain, particularly in relation to dementia? A. Regulating blood pressure B. Facilitating memory and learning C. Controlling muscle movements D.Enhancing sensory perception Which of the following medications regulates the activity of glutamate and is used in the treatment of Alzheimer’s disease? A. Donepezil B. Rivastigmine C. Memantine D.Galantamine References Amoozegar, F., Khan, Z., Oviedo-Ovando, M., Sauriol, S., & Rochdi, D. (2022). The burden of illness of migraine in Canada: New insights on humanistic and economic cost. Canadian Journal of Neurological Sciences, 49(2), 249-262. Barnes, L. L., Dhana, K., Liu, X., Carey, V. J., Ventrelle, J., Johnson, K., Hollings, C. S., Bishop, L., Laranjo, N., Stubbs, B. J., Reilly, X., Agarwal, P., Zhang, S., Godstein, F., Tangney, C. C. Holland, T. M., Aggarwal, N. T., Arfanakis, K., Morris, M. C., & Sacks, F. M. (2023). Trial of the MIND diet for prevention of cognitive decline in older persons. New England Journal of Medicine, 389(7), 602-611. Bosma, M. & Nemiroff, L. (2022). Dementia. Compendium of Pharmaceuticals and Specialities (e-CPS)/e-Therapeutics. https://www-e-therapeutics-ca.myaccess.library.utoronto.ca/ Burchum, J. & Rosenthal, L. (2021). Lehne’s pharmacology for nursing care (11th ed.). Elsevier Rogers, J. L. (2023). McCance & Huether’s pathophysiology: The biologic basis for disease in adults and children (9th edition). Elsevier. Tyerman, J., & Cobbett, S. (2023). Lewis's medical-surgical nursing in Canada: Assessment and management of clinical problems (5th ed.). Elsevier.