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

**[NUR 425 - Test 2 Review Notes ]** **[Week 5: Headache, Parkinson's Disease, & Dementia ]** **[Headache ]** - - Secondary headaches: illness/injury related (e.g. sinus h/a, meningitis, concussion), medication side effect ***Tension Type Headache*** - - - - - ***Management...

**[NUR 425 - Test 2 Review Notes ]** **[Week 5: Headache, Parkinson's Disease, & Dementia ]** **[Headache ]** - - Secondary headaches: illness/injury related (e.g. sinus h/a, meningitis, concussion), medication side effect ***Tension Type Headache*** - - - - - ***Management of tension-type headache*** - NSAIDs and acetaminophen - Preventive therapy (meds) - important to have preventative therapy when it becomes more chronic - Tricyclic antidepressants: Amitriptyline, nortriptyline - Atypical antidepressants: Venlafaxine (Effexor)\*, Mirtazapine (Remeron)\* - \*caution in anyone under 18 - younger pts have higher risk of suicidal thoughts ***Migraine Headache*** - Most common in 18-44 years, and women - Estrogen plays significant role in migraine development - Most well studied - Migraine with aura - Visual (90%), e.g. flashing lights, zigzag lines, blind spots, visual distortions - Sensory, e.g. tingling, numbness, pins-and-needles sensation typically starting in fingers and moving up arm, or affecting the face - Dysphasic, e.g. can't think of words they want to say - Difficulty w speech or language - Migraine without aura - Chronic migraine - migraine at least 15 days/month - *Clinical pearls* - Migraine with aura inc risk of ischemic stroke (important to manage risk factors) - Avoid use of contraceptives (containing estrogen) in women with migraine with aura as this also inc ischemic stroke risk ***Clinical Manifestations of Migraines*** PHASES OF MIGRAINES - Prodrome - Lasts hours or even days before developing migraine - Mood changes - Fatigue - Food craving - Neck stiffness - Aura (up to ⅓ of patients exp an aura) - Not as common compared to no aura - 5 mins to 1 hr before onset - Migraine attack - Severe throbbing pain - Usually one sided, can be bilateral - May have n&v and/or sensitivity to light/sound - Pain can last 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 (more common) A. At least 5 attacks fulfilling criteria B-D B. Headache attacks lasting 4-72 hr (untreated or unsuccessfully treated) C. Headache has at least 2 of the following four characteristics: a. Unilateral location b. Pulsating quality c. Moderate or severe pain intensity d. Aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs) D. During headache at least one of the following: e. Nausea and/or vomiting f. Photophobia or phonophobia E. Not better accounted for by another ICHD-3 diagnosis - Migraine WITH Aura A. At least 2 attacks fulfilling B and C B. One or more of the following fully reversible aura symptoms: a. Visual b. Sensory c. Speech and/or language d. Motor e. Brainstem f. Retinal C. At least 3 of the following 6 characteristics g. At least one aura symptom spreads gradually over \>/ 5 minutes h. 2 or more aura symptoms occur in succession i. Each individual aura symptoms occur in succession j. Each individual aura symptom lasts 5-60 mins k. At least 1 aura symptom is unilateral l. At least 1 aura symptom is positive m. The aura is accompanied, or followed within 60 mins, by headache D. Not better accounted for by another ICHD-3 diagnosis ***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 nociceptor (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 - 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*** - Avoid known triggers - Ask pts to keep a journal or diary to try and identify triggers (some pts don't know their triggers) - Abortive therapy - Treat onset of symptoms - Preventive therapy - Usually reserved for frequent migraines - Aim: reduce frequency and severity ***Migraine Triggers*** - Migraine can be precipitated by triggers - Triggers include: - Fatigue and poor sleep - Stress - Hormonal changes - Excess sensory stimulation - Diet (incl foods that contain tyramine or nitrates \[aged cheeses, cured meats\], dairy products, caffeine, etc.) ***Migraine Headache: First Line Therapy*** - **Mild & moderate:** NSAIDs (ex. ASA high dose, ibuprofen, naproxen) - **Moderate & severe**: selective serotonin receptor agonists (Triptans) - Relieve pain by constricting intracranial blood vessels and reducing inflammation (by suppressing release of inflammatory neuropeptides, incl CGRP) - Available in tabs, inj, and nasal sprays - Ex: 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 AE: 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 pts with inc CV risk - Contraindicated in pts 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 - sudden, brief involuntary twitching - Hyperreflexia - inc or overactive reflex response - Excessive sweating - Tremor - Fever ***Migraines: Second Line Therapy*** - Ergot alkaloids - MOA is not clearly understood - Can be helpful for mod to severe migraines, or migraines that haven't responded to first line tx - Dihydroergotamine (Migranal) is the med available in CAN - SC, IM, or nasal spray - Common AE: N&V (pre-dose antiemetic recommended) - Black box warning for vasoconstriction - inc chance w excessive or prolonged use ***Newer Migraine Treatment*** - CGRP receptor antagonist - 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 - **Cons:** Very expensive, may cause n&v, dry mouth, or drowsiness ***Migraine treatment: Preventive*** - Indications for preventive therapy - 6 + attacks per month - Attacks that are especially severe - Attacks that don't respond adequately to abortive meds - 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) - 1st line therapy: - Beta-blockers - propranolol (nonselective) = most common - Can have 2 pronged effect, prevents excessive dilation of arteries - Antidepressants, e.g. Amitriptyline - Helps with modulating pain pathways - Anticonvulsants, e.g. Topiramate - Blocks sodium channels and stabilizes neurons, inhibits glutamate (excitatory neurotransmitter) - Other treatments: localized injections - Botulinum toxin (Botox) - prevents release of pain transmitted receptors that become activated, helps w chronic migraine prevention - Occipital nerve blocks using lidocaine or bupivacaine - helps reduce inflammation  ***Cluster Headache*** - Occurs in a series of attacks - Lasts mins 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 - Primarily affects men between 20-50 years of age - Attack usually begins 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 - Triggers can include caffeine, alcohol, smoking, nicotine - Differ from migraine: no aura, no n&v, 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 - Involves trigeminal nerve and its connections to the blood vessels in the brain - Trigeminal nerve carries sensory info (pain, temp, touch) to the brain - responsible for transmitting pain signals ***Management of cluster headache*** - Acute (quicker 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) - use transitional prophylactics to stop cluster attacks quickly until they can be put on longer term preventative therapies - high dose oral corticosteroids used - DHE (SC and 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 - MOA in preventing cluster headache is unclear - AE: cardiac arrhythmia, bradycardia, prolonged PR interval - Believed to involve modulation of neurotransmitter systems in hypothalamus - Want to be cautious prescribing these w underlying CVD - Neurostabilizer - Lithium is second-line agent for preventive therapy - AE: 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 MOH is not clearly understood - Don't know why but believed that it alters some sort of pain pathways in the brain making them more sensitive ***Management of Medication Overuse Headache*** - Stopping all headache meds - Pt needs to realize that when meds are stopped, h/a will inc temporarily - Resolves days to weeks after the overused med is withdrawn - Prevent medication overuse h/a by: - Limiting the use of abortive medications to 2-3 times/week - Ensuring doses are not greater than needed - Starting preventive therapy if h/a are increasing in frequency - Pts exp a cycle - they get a h/a, take more h/a meds, then get a rebound h/a ***Non-pharmacological management of MOH*** - Ensuring adequate sleep - Eat regular meals; healthy diet - Ensuring adequate hydration - Exercising regularly - Keeping a h/a diary - Managing stress - Evidence for use of cognitive behavioural therapy, biofeedback and acupuncture **[Parkinson's Disease ]** - Progressive, neurodegenerative disorder - Characterized by bradykinesia (slow movement), inc muscle tone, tremor at rest and impaired gait and a lack of the neurotransmitter dopamine - Unknown cause, thought to be related to environment and genetics - Most often affects individuals over the age of 60 ***Basal Ganglia*** - Group of structures involved in coordination of movement - Motor control - Affected in parkinson's - ***Substantia nigra*** - Part of the basal ganglia - Located in the midbrain (part of the brainstem) - Has dopaminergic neurons, they produce dopamine - In parkinson's disease, there is degeneration of these neurons - Leads to dec release of dopamine - **Degeneration of dopaminergic neurons** - Dopamine inhibits acetylcholine - **Decrease release of dopamine → inc release of acetylcholine** - **Disrupts balance between dopamine & acetylcholine, leading to inc acetylcholine** - The imbalance between dopamine and acetylcholine can lead to muscle overexcitement, which causes tremors and jerking movements. ***Clinical Manifestations*** - Seen with loss or impairments of 60-80% of the dopaminergic neurons - Tremor, rigidity, akinesia, postural instability - Non-motor symptoms: loss of smell, sleep dysfunction, mood disorders, anxiety, depression, memory changes, constipation ***Evaluation*** - Based on patient history and physical exam - Diagnosis is going to begin w/ detailed hx or symptoms - When they started, how long they've been going for, the progression - Looking for key symptoms - tremor, rigidity, etc. - Comprehensive med hx - family hx, current/past meds, and any potential neurological disorders - Physical exam - motor function - Rapid alt movement - Observe tremors at rest - have them put their hands out - Postural instability - assess gait - Romberg test - No specific confirmation with lab tests of imaging - imaging/tests rules out other things that mimic Parkinson's ***Management of Parkinson's Disease*** - Medication therapy - Enhancing release or supply of dopamine - Blocking the effects of acetylcholine ***Levodopa-Carbidopa*** - Dopamine precursor - it is converted into dopamine in the basal ganglia - However, levodopa is broken down (metabolized) by the enzyme dopa decarboxylase (before it reaches the brain) - Carbidopa inhibits the enzyme dopa decarboxylase, and is prescribed with levodopa (allows more levodopa to reach the brain) - L-C decreases symptoms - May take several weeks to months to become effective - improvement can take several weeks to months - Considerations: Urine, sweat & saliva can appear darker (red, brown, or black) - Harmless but frightening to see - Avoid taking with high protein meals (take meds 30 mins before meals or 1-2 hrs after) as this can interfere with drug absorption - If pt exp nausea, take it with light carb snack - Lack of effectiveness after 5-10 years, may be secondary to disease progression - AE: hallucinations, orthostatic hypotension, dyskinesia, paranoid ideation - About 80% of patient can develop dyskinesia (abnormal involuntary movements) within the first few years of treatment ***Dopamine Antagonists*** - Stimulate dopamine receptors - Can be used with levodopa-carbidopa - Ex: apomorphine (not used routinely, short term use only for "off" episode), pramipexole, rotigotine, ropinirole - AE: hallucinations, daytime sleepiness, postural hypotension ***MAO-B Inhibitors*** - Monoamine oxidase type B inhibitors - MAO-B is an enzyme that inactivates dopamine and prevents breakdown of tyramine - Can be used with levodopa-carbidopa - Ex: rasagiline, selegiline - Like all MAO inhibitor meds, must avoid food high with tyramine (aged cheese, smoked or cured meats, fermented foods, beer) - Too much tyramine → release of large amts of norepinephrine → constricts blood vessels and inc bp - Can cause dangerous inc in bp (avoid MAO inhibitor meds with food high with tyramine) ***COMT Inhibitors*** - Catechol-O-methyltransferase inhibitor - COMT breaks down dopamine → COMT inhibitors inc availability of dopamine in the brain - 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*** - No longer used as an antiviral for influenza A - Thought to stimulate dopamine release (inc levels of dopamine in the brain) and block the reuptake of dopamine - Can help to manage dyskinesia caused by long term use of levodopa - Often prescribed with levodopa ***Anticholinergic medications*** - Works 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 - AE: dry mouth, blurred vision, photophobia, urinary retention, constipation, tachycardia ***Nutrition considerations for Parkinson's*** - Dysphagia & bradykinesia highlight need for foods that are easy to chew & swallow - Adequate fibre to reduce constipation (constipation is common issue due to slow GI motility) - Watch protein intake with levodopa - Protein can interfere w levodopa absorption - be mindful of when you're taking the meds vs. when you're eating protein foods **[Dementia]** - Progressive decline in cognitive functioning - Affects memory, judgment, 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 - Hippocampus: early in the disease; plays important role in memory - Cerebral cortex: seen later in the disease; affects speech, perception & memory - Later stages: affects bladder & bowel control, ADLs - Amyloid plaques - Amyloid plaques are abnormal clusters of protein fragments - Build up between neurons and disrupt cell-to-cell communication - Causes inflammation by activating immune responses - Leads to neuronal damage - Neurofibrillary tangles - Neurofibrillary tangles - twisted fibers of TAU proteins - In healthy neurons, TAU helps stabilize microtubules - TAU proteins become broken apart from tangles, disrupts entire network → cell death -  - Loss of connections between neurons - Gradual loss of connections b/w neurons caused by amyloid plaques, neurofibrillary tangles, and associated neuro-inflammation → damage & death of neurons → brain atrophy (cognitive decline) ***Alzheimer's: Decreased production of Acetylcholine*** - Acetylcholine is a neurotransmitter that plays an important role in memory - Helps to convert short term memory into long term memory - Important for learning and attention - Acetylcholine is formed by the cholinergic neurons - There is a loss of cholinergic neurons in Alzheimer's disease - Widespread reduction of acetylcholine levels - causes pts to have difficulty forming memories, retrieving memories, overall cognitive decline - Linked with memory loss in later disease ***Other Factors (involved in Alzheimer's)*** - **Apolipoprotein e4 (APOE)** refers to a gene linked to Alzheimer's disease - 3 different forms - The APOE e4 has been found to inc the risk of Alzheimer's - **Endoplasmic reticulum-associated binding protein** - Elevated in the brains of Alzheimer's patients - Has been found to be toxic to neurons (involved in formation of amyloid plaques) ***Vascular Dementia*** - Damage stems from CVD that leads to decreases in blood & oxygen delivery to the brain, leading to cell ischemia - Patient may have a hx of a stroke or multiple strokes - Can present with a sudden onset - Risk factors: smoking, HTN, CAD, diabetes, dyslipidemia ***Dementia with Lewy Bodies*** - Characterized by presence of Lewy bodies - Found in cerebral cortex contributing to cognitive decline and hallucinations ***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 - Disease can last 3-20 years - May have mild cognitive impairment prior to dementia ------------------------------------------------------------------------------------------------------ ----------------------------------------------------------------------------------------- **8 As of Dementia** **Anosognosia** - pt unaware of their neurological deficit or psychiatric condition **Agnosia** - Inability to process sensory info **Aphasia** - language difficulty, difficulty finding words, understanding language or communicating **Apraxia** - Unable to perform tasks or movements when asked **Altered Perception** - Leads to misinterpretation or confusion **Attentional Deficits** - Problems focusing, leads to difficulty completing tasks **Apathy** - Lack of interest, socially withdrawn **Amnesia** - Memory loss, can be early memory, recent memory, or even long term memory ------------------------------------------------------------------------------------------------------ ----------------------------------------------------------------------------------------- ***Dementia 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 - Imaging won't capture specifics but we may see brain atrophy or tumors/abnormalities - Imaging won't give definitive diagnosis ***Medications*** +-----------------------+-----------------------+-----------------------+ | **Cholinesterase | **NMDA Receptor | **Combination Therapy | | Inhibitors** | Antagonist** | of the 2** | +-----------------------+-----------------------+-----------------------+ | Donepezil | Memantine | Helpful for moderate | | | | to severe disease | | | | | | | | Enhances ability to | | | | do ADLs | +-----------------------+-----------------------+-----------------------+ | Rivastigmine | | | +-----------------------+-----------------------+-----------------------+ | Galantamine | | | +-----------------------+-----------------------+-----------------------+ ***Cholinesterase Inhibitors*** - Leads to inc levels of acetylcholine in the brain - 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 (ineffective) - 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 and better tolerated than cholinesterase inhibitors - Modest benefits in moderate-severe Alzheimer's disease - Memantine regulates effect of glutamate - glutamate is important for learning and memory - protection from cytotoxicity ***Nonpharmacologic Strategies for Dementia*** - 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