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Adult Health > Neurological Disorders > Flashcards

Neurological Disorders Flashcards

1
Q

Alzheimer’s Disease: What is it?

A

A degenerative brain disease that causes progressive decline in neurocognitive functioning that is severe enough to compromise social and occupational functioning

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2
Q

Alzheimer’s Disease: General Considerations

A
  • most common form of dementia
  • after age 60, the prevalence doubles every 5 years
  • half of patients with AD have a family history
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3
Q

Alzheimer’s Disease: Risk Factors

A
  • aging
  • smoking
  • family history
  • Down’s syndrome
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4
Q

Alzheimer’s Disease: Assessment Findings

A
  • gradual worsening ability to remember new information (most common)
  • decline in memory, cognition, language, personality, and mobility
  • impaired judgement, abstract thinking, memory, reasoning, orientation, and attention
  • difficulty with speech and other forms of communication
  • inability to interpret sounds, speech, and use of objects
  • insomnia, daytime sleepiness
  • hyperactivity, wandering, restlessness
  • mood disturbances and emotional outbursts
  • urinary and/or fecal incontinence
  • paranoia, hallucinations, delusions (late findings)
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5
Q

Alzheimer’s Disease: Diagnostic Studies

A
  • Medical and family history
  • APOE 34 presence increases risk
  • Mini mental status exam
  • Rule out reversible causes: CBC, CMP, UA, LFTs, thyroid function tests, B12, and folate levels, consider CT or MRI, syphilis serology, PET scan to rule out Lewy Body Dementia
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6
Q

Alzheimer’s Disease: Prevention

A
  • Regular physical exercise
  • Healthy diet
  • Management of risk factors (control of DM and HTN)
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7
Q

Alzheimer’s Disease: Nonpharmacological Management

A
  • Maintain routines and familiar environment
  • Supportive care
  • Display calendar and clocks in prominent places
  • Display family pictures
  • Promote socialization
  • Fall precautions
  • Wandering and exiting precautions
  • Emotional support from family
  • Respite care for caregivers
  • Maintain healthy nutritional status
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8
Q

Alzheimer’s Disease: Pharmacological Management

A
  1. Cholinesterase inhibitors
  2. NMDA receptor antagonists
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9
Q

Cholinesterase Inhibitors

A

** For treatment of Alzheimer’s
- Donepezil
- Galantamine
- Rivastigmine

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10
Q

NMDA Receptor Antagonist

A

** For treatment of Alzheimer’s Disease
- Memantine

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11
Q

Alzheimer’s Disease: Referral/Consultation

A
  • consult neurologist for new onset dementia
  • consult social services as needed for family
    ** 33% of patients develop depression
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12
Q

Bell’s Palsy: What is it?

A

An acute, unilateral, peripheral paralysis of cranial nerve 7, which controls the lower motor neurons of the face

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13
Q

Bell’s Palsy: Etiology

A
  1. Inflammation
  2. Idiopathic
  3. Herpes simplex or zoster virus
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14
Q

Bell’s Palsy: General Considerations

A
  • most common cause of unilateral facial paralysis
  • peak age of occurrence is 20-40 years of age
  • affects people with DM or upper respiratory infections more commonly and those who are pregnant
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15
Q

Bell’s Palsy: Risk Factors

A
  • Lyme disease
  • Pregnancy
  • DM
  • Family history
  • HTN
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16
Q

Bell’s Palsy: Assessment Findings

A
  • Acute onset of unilateral upper and lower facial paralysis
  • Loss of nasolabial fold on affected side
  • Otalgia
  • Poor eye closure with decreased/excessive tearing, and blurred vision
  • Taste disturbances
  • Drooling, dysphagia
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17
Q

Bell’s Palsy: Diagnostic Studies

A
  • Usually diagnosed on clinical presentation
  • CT to rule out stroke or neoplasm
  • Lyme disease titer if history of tick bite
  • Serologic studies for syphilis and HIV
  • CBC, TSH, ESR, glucose
  • EMG testing (determines severity and extent of nerve involvement)
  • Hearing/vestibular testing (is cochlear or vestibular nerve affected)
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18
Q

Bell’s Palsy: Nonpharmacological Management

A
  • Patient education
  • Warm, moist heat to affected side of face
  • Close and cover affected eye, especially at night
  • Active and passive ROM of eye and facial muscles
  • Majority of cases will recover without treatment
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19
Q

Bell’s Palsy: Pharmacologic Management

A
  1. Corticosteroids
  2. Antivirals (valacyclovir, acyclovir)
  3. Pain relief (ASA, ibuprofen, tylenol)
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20
Q

Bell’s Palsy: Consultation/Referral

A
  1. Obstetrician for pregnant patients
  2. Neurologist for serious comorbid conditions
  3. Ophthalmologist for actual or suspected corneal abrasions
  4. Occupational and/or speech therapy
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21
Q

Bell’s Palsy: Follow Up

A
  • 2 weeks after onset to monitor treatment safety and condition of eye
  • 3 months
  • 6 months
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22
Q

Bell’s Palsy: Expected Course (Resolution of Symptoms)

A

** Varies
- complete recovery of facial nerve function (majority)
- incomplete recovery of facial nerve function with no obvious cosmetic defects
- permanent neurologic sequelae that are cosmetically and clinically obvious (rare)

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23
Q

Bell’s Palsy: Expected Course (Recovery Times)

A
  • Majority have complete resolution within 6 weeks to 3 months
  • Symptoms usually begin to improve within 2 weeks
  • Extent of nerve damage determines extent of recovery
    ** Prognosis is related to severity
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24
Q

Concussion: What is it?

A

A change in mental status or cognitive function as a result of trauma; a mild traumatic brain injury

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25
Q

Concussion: General Considerations

A
  • may or may not involve loss of consciousness
  • usually resolves in 7-10 days with rest and observation
  • head injuries account for almost half of all trauma-related deaths
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26
Q

Concussion: Etiology

A
  1. Direct trauma
  2. Blast
  3. Coup-contrecoup injury
    ** Changes in white matter occur in concussion, likely due to sudden release of excitatory neurotransmitters, quick release of potassium into the extracellular space with resulting calcium entrance into the cells, and decreased cerebral blood flow
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27
Q

Concussion: Incidence

A
  • Underreported because many do not seek treatment
  • Estimated 1.6-3.8 million sports and recreation related concussions per year
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28
Q

Concussion: Risk Factors

A
  1. Sports participation
  2. Fall risk patients
  3. Women have a higher incidence than men
  4. Postconcussive syndrome is more common in women and those with severe initial injury, previous head injuries, and comorbid psychiatric illness
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29
Q

Concussion: Assessment Findings

A
  • Observed or self-reported loss of consciousness lasting < 30 minutes
  • Posttraumatic amnesia < 24 hours
  • GCS greater than or equal to 13
  • Physical exam often normal
  • Battle sign (bruising over mastoid process)
  • Raccoon sign (bruising around the eyes)
  • Clear fluid leakage from nose or ears
  • Visual abnormalities
  • Difficulty in coordination or balance
  • Irritability or labile mood
  • Brain fog
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30
Q

Concussion: Diagnostic Studies

A
  • Acute Concussion Evaluation (ACE) tool for ED
  • CT scan
  • Possible MRI
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31
Q

Concussion: Prevention

A
  • use helmets with sports and play activities
  • use of seatbelts and proper child restraints
  • implement safety measures to prevent falls in the home
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32
Q

Concussion: Nonpharmacologic Management

A
  • physical and cognitive rest
  • early return to nonstrenuous, noncontact activity as tolerated
  • accommodations at school or work
  • PT, vocational rehab, education
  • evacuation of hematoma
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33
Q

Concussion: Pharmacologic Management

A
  • Focused on symptom management
  • Omega 3 fatty acids
  • Drug therapy should target specific symptoms, such as anxiety, depression, HA, and insomnia
  • Nonbenzodiazepines (zolpidem, zalepion, eszopidone)
  • NSAIDs
  • Antiseizure meds (gabapentin, topiramate)
  • SSRIs (sertraline, escitalopram)
  • Nonbenzodiazepine anxiolytics (hydroxyzine, buspirone)
  • Antivirals (amantadine)
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34
Q

Concussion: Prognosis

A
  • average recovery 7-10 days, but can last much longer
  • metabolic changes in brain tissue can last longer than symptoms, increasing risk for repeat injury if another trauma occurs
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35
Q

Concussion: Possible Complications

A
  1. Postconcussive syndrome
  2. Second impact syndrome (second injury after initial concussion, causing severe cerebral edema; can be fatal)
  3. Repeated concussions cause increased risk for multiple diseases (chronic traumatic encephalopathy, Parkinsons, Depression, ALS, Epilepsy)
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36
Q

Concussion: Referral

A
  • Refer immediately to ED for any signs of intracranial hemorrhage, skull fracture
  • Refer to neurology or psychiatry for persistent symptoms not suitable for primary care
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37
Q

Cluster Headaches: What is it?

A

A primary neurovascular headache disorder that causes a grouping of headaches, usually over a period of several weeks

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38
Q

Cluster Headaches: General Considerations

A
  • may be classified as episodic or chronic
  • men affected more than women
  • possible causative factor is release of histamines or serotonin
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39
Q

Cluster Headaches: Risk Factors

A
  1. Heritable tendency in first-degree relatives
  2. Age of onset 20-40 years
  3. Previous head trauma or surgery
  4. Small amounts of vasodilators (alcohol)
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40
Q

Cluster Headaches: Possible Triggers

A
  1. Histamine
  2. Stress
  3. Allergens
  4. Seasonal changes
  5. Nitroglycerin
  6. Tobacco use
  7. Alcohol intake
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41
Q

Cluster Headaches: Assessment Findings

A
  1. Severe unilateral periorbital pain with sudden onset, usually at night, lasting 15 minutes to 3 hours
  2. Ipsilateral nasal congestion, rhinorrhea, lacrimation, redness of the eye, and Horner syndrome
  3. Restless and agitation during attacks
  4. Eyelid and facial swelling
  5. Aural fullness
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42
Q

Cluster Headaches: Diagnostic Studies

A
  • Based on clinical history
  • At least 5 attacks that fulfill the cluster headache diagnostic criteria
  • Lab testing and imaging to rule out other possible causes
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43
Q

Cluster Headaches: Prevention

A
  1. Avoid triggering substance (alcohol, nicotine)
  2. Temper, strong emotions
  3. Maintain usual sleep/wake hours
  4. Pharmacologic interventions for prophylaxis (melatonin)
  5. Avoidance of vasodilators (nitroglycerin, alcohol)
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44
Q

Cluster Headaches: Pharmacological Management

A
  1. 100% oxygen for 15 minutes
  2. Triptans (sumatriptan/imitrex)
    ** oral agents not effective
    ** aborts individual attacks but does not reduce duration of clusters
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45
Q

Cluster Headaches: Consultation/Referral

A
  • refer to neurologist for severe headaches or headaches unresponsive to drug therapy
  • atypical features such as
    1. absence of a periodic pattern
    2. residual headache between exacerbations
    3. bilateral headache
    4. incomplete or minimal response to standard therapy
    5. presence of lateralizing findings on examination
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46
Q

Cluster Headaches: Follow Up

A
  • RTC or ED if headache unresolved after treatment
  • periodically monitory ECG, thyroid function, renal function, and electrolytes
  • Taper of preventative medications
    1. Episodic: completely headache free for 2 weeks and/or moved beyond typical cluster period duration
    2. Chronic: after 6-12 months of therapy, can consider taper, as long as headaches do not recur
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47
Q

Cluster Headaches: Potential Complications

A
  • No real long term complications, but may be excruciating and incapacitating
  • Depression and aggression with suicidal ideation
  • Possibility of self-injury during an attack
  • Risk of addiction to narcotic analgesics
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48
Q

Migraine Headaches: What is it?

A

A common primary headache disorder characterized by recurring headaches that are complex and can be disabling

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49
Q

Migraine Headaches: General Considerations

A
  • Two main types: with aura and without aura
  • More common in white females
  • Strong genetic component
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50
Q

Migraine Headaches: Assessment Findings

A
  • common while awake or upon awakening
  • unilateral; may be pulsating or throbbing
  • if < 18 years old, more commonly bilateral
  • frontotemporal
  • builds over 1-2 hours
  • prodrome may begin hours or days before and cause changes in mental status, photophobia, stiff neck
  • postdrome may last 48 hours (fatigue, difficulty concentrating, neck stiff)
  • nausea and vomiting
  • blurred and/or double vision
  • photophobia/phonophobia
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51
Q

Migraine Headaches: Diagnostic Studies

A
  1. CT, MRI, and/or MRA
  2. Consider sinus series
  3. CBC, CMP, TSH
  4. Cervical xrays
  5. EEG
  6. LP
  7. Sed rate
  8. UDS
  9. UA
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52
Q

Migraine Headaches: Prevention

A

** Avoid triggers
- nitrite containing foods (hot dogs, etc)
- MSG containing foods (Chinese food, etc)
- tyramine containing foods (chocolate, red wine, caffeinated beverages)
- hormonal changes (menstruation, pregnancy, ovulation)
- stress
- medications (vasodilators, OCP)
- excessive/insufficient sleep
- exposure to bright/fluorescent light
- strong odors
- head trauma
- weather changes
- motion sickness
- cold stimulus (ice cream, etc.)
- lack of exercise
- fasting or skipping meals

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53
Q

Migraine Headaches: Nonpharmacologic Management

A
  1. Avoid triggers
  2. Application of ice or cool compresses to head, face, scalp, and neck
  3. Darkened room
  4. Quiet atmosphere
  5. Cognitive behavioral therapy
  6. Relaxation techniques
  7. Biofeedback
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54
Q

Migraine Headaches: Pharmacologic Management

A
  • Abortive:
    1. ASA, tylenol, ibuprofen, naproxen
    2. Ergotamines (all end in “-ergotamine”)
    3. Triptans (all end in “-triptan”)
  • Prophylactic
    1. Beta blockers (propranolol, timolol)
    2. Anticonvulsants (topiramate, divalproex)
    3. Calcitonin gene-related peptide antagonists (end in “-umab”)
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55
Q

Migraine Headaches: Consultation/Referral

A

Refer to neurologist for severe headaches or lack of response to drug therapy

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56
Q

Migraine Headaches: Expected Course

A
  • Most resolve within 72 hours
  • Severity and frequency diminish with age
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57
Q

Migraine Headaches: Possible Complications

A
  • medication overuse
  • risk of addiction to narcotic analgesics
  • status migrainosus
  • persistent aura without infarction
  • migrainous infarction
  • migraine triggered siezures
  • severe nausea/vomiting may lead to shock
  • increased risk of ischemic strokes
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58
Q

Tension Headaches: What is it?

A

Bilateral, nonthrobbing headaches of mild to moderate intensity, without other associated features

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59
Q

Tension Headaches: General Considerations

A
  • most common type of primary headache disorder
  • muscular and psychogenic factors may be the cause
  • affects women and more often than men
  • peaks in 40s
60
Q

Tension Headaches: Risk Factors

A
  1. Emotional stress
  2. Anxiety, depression
  3. Change in sleep pattern
  4. Certain medications (nitrates, antihypertensives, SSRIs)
  5. Overexertion
  6. Poor posture
  7. Jaw clenching/teeth grinding
  8. Hormonal changes
  9. Consumption of high-nitrite foods
  10. Excessive caffeine/alcohol intake
61
Q

Tension Headaches: Assessment Findings

A
  • Bilateral with mild-to-moderate intensity
  • Gradual onset
  • Dull, vice-like, tight
  • Frontal and/or occipital location
  • Muscle tenderness in the head, neck, and/or shoulders
  • May be intermittent or last all day
  • Normal neuro exam, VS normal
62
Q

Tension Headaches: Diagnostic Studies

A
  1. Determined by symptoms and presumed etiology
  2. CT, MRI
  3. Consider sinus series
  4. CBC, CMP, TSH
  5. Cervical xrays
  6. EEG
  7. LP
  8. Sed rate
  9. UA
63
Q

Tension Headaches: Prevention

A
  1. Relaxation therapy
  2. Stress management
  3. Regulation of sleep patterns
  4. Correct posture
  5. Mouth guard for teeth grinding
  6. Food diary to identify triggers
64
Q

Tension Headaches: Nonpharmacologic Management

A
  • Avoid triggers
  • Application of ice, cool compresses to head, face, scalp, or neck
  • Moist heat
  • Ultrasound
  • Electrical stimulation
  • Darkened room
  • Quiet atmosphere
  • Stretching
  • Deep tissue massage
  • EMG biofeedback
  • Relaxation training
  • Cognitive behavioral therapy
  • Acupuncture
  • Spinal manipulation
  • Counseling/psychotherapy
65
Q

Tension Headaches: Pharmacologic Management

A
  1. NSAIDs
  2. Acetaminophen
  3. Tricyclic antidepressants (Amitriptyline)
66
Q

Tension Headaches: Consultation/Referral

A
  • Physical therapy (depending on cause) for exercises/stretches, heat/cold therapy, massage, etc.
  • Refer to neurologist for severe headaches or headaches unresponsive to drug therapy
67
Q

Tension Headaches: Expected Course

A

Most follow a chronic course if stressors are not eliminated

68
Q

Tension Headaches: Possible Complications

A
  • GI bleed from continued use of NSAIDs
  • Impaired renal function from continued use of NSAIDs
  • Rebound headaches, medication overuse headaches
  • Overreliance on nonprescription caffeine-containing analgesics
  • Dependence on/addiction to narcotics
  • May co-occur with migraines
  • Risk of epilepsy 4 times greater in patients with tension headaches than the general population
69
Q

Meningitis: What is it?

A

An inflammation of the brain and spinal cord meninges resulting from infection with bacteria, viruses, or fungi

70
Q

Meningitis: Etiology and Incidence

A
  • Caused by Neisseria meningitidis and Streptococcus pneumoniae
  • Serogroup C is the most common cause of epidemic disease
  • Serogroup B is the most common cause of sporadic disease
  • Approximately 40% of population are carriers
  • Transmitted by droplets
71
Q

Meningitis: Risk Factors

A
  1. Young children, young adults
  2. Crowded living
  3. Immunocompromised
72
Q

Meningitis: Assessment Findings

A
  • High fever, chills, N/V, HA
  • Confusion, seizures
  • Positive Kernig sign (the elicitation of pain or resistance with passive extension of the patient’s knees past 135 degrees)
  • Positive Brudzinski sign (position the patient’s supine and passively flex their neck, if it causes reflex flexion of the hip and knee then the sign is positive)
  • Petechial rash
73
Q

Meningitis: Diagnostic Studies

A
  1. Lumbar puncture
  2. Blood cultures
  3. CBC, CMP
  4. Possible CT/MRI
  5. CXR
74
Q

Meningitis: Prevention

A
  • strict asceptic technique during neurosurgical dressing changes
  • treat URIs promptly
  • vaccinations
75
Q

Meningitis: Nonpharmacologic Management

A
  • good handwashing, supportive care, prevention of dehydration
  • isolation
  • minimize external stimulation
76
Q

Meningitis: Pharmacologic Management

A
  1. Antibiotics specific to culture results
  2. Begin antibiotics early, stop if viral
  3. Dexamethasone
  4. Oxygen
  5. Antipyretics, analgesics, antiemetics, anticonvulsants, sedatives
77
Q

Meningitis: Consultation/Referral

A
  • Refer to emergency department/neurologist immediately
  • Refer to infectious disease specialist
78
Q

Meningitis: Expected Course (Bacterial)

A
  • overall fatality is 14%
  • afebrile in 7-10 days
  • HA and other symptoms may persist intermittently for 2 weeks
  • dependent on timing of antibiotic initiation
79
Q

Meningitis: Expected Course (Viral)

A
  • recovery in 4-10 days
  • HA and other symptoms may persist intermittently for 2 weeks
  • In most cases, not fatal
80
Q

Meningitis: Expected Course (Fungal)

A

Poor prognosis usually related to overall health

81
Q

Meningitis: Expected Course (parasitic)

A

High mortality rate

82
Q

Meningitis: Potential Complications

A
  • epilepsy and seizures
  • septic shock
  • bacteremia
  • cerebral edema
  • hearing loss
  • hydrocephaly
  • renal impairment
  • stroke
  • motor disability
  • cognitive dysfunction
83
Q

Multiple Sclerosis: What is it?

A

A chronic, immune-mediated, inflammatory, demyelinating disease of the CNS that affects gray and white matter

84
Q

Multiple Sclerosis: Etiology and Incidence

A
  • slow and progressive
  • exact cause is unknown
  • most common type is relapsing-remitting MS (RRMS)
  • more common in white women with initial presentation between ages 20-45 years
85
Q

Multiple Sclerosis: Assessment Findings

A
  • Insidious onset with remissions and exacerbations
  • Initial presentation is usually weakness, numbness, tingling or unsteadiness in limb; spastic paresis; diplopia; disequilibrium, urinary urgency or hesitancy
  • Increasing disability, with weakness, spasticity, and ataxia of the limbs; impaired vision; and urinary incontinence
  • Fatigue
86
Q

Multiple Sclerosis: Diagnostic Studies

A
  • Primarily a clinical diagnosis
  • MRI of the brain and cervical cord
87
Q

Multiple Sclerosis: Nonpharmacologic Management

A
  • Avoid factors that precipitate attacks
  • Emotional support and education
  • OT/PT
  • Monitor for depression
88
Q

Multiple Sclerosis: Pharmacologic Management

A
  1. Immunomodulatory agents (interferon, “-umab” meds
  2. Symptom management meds
    - antispasmotics
    - bladder dysfunction: anticholinergics
    - constipation: stool softeners
    - Incontinence/diarrhea: bulk agents, loperamide
    - Depression: SSRIs
    - Fatigue, attention: modafinil, armodafinil, stimulants
    - Seizures: antiseizure meds
    - Pain related to trigeminal neuralgia: NSAIDs, gabapentin, pregabalin, carbamazepine, lamotragrine, baclofen, or misoprostol
89
Q
A
90
Q

Multiple Sclerosis: Consultation/Referral

A
  • Consult neurology for suspected initial diagnosis, follow-up, and long-term management plan
  • Physical, occupational therapy
91
Q

Multiple Sclerosis: Follow-Up

A
  • Depends on severity and frequency of exacerbations
  • Regular follow-up with neurologist
92
Q

Multiple Sclerosis: Expected Course

A
  • Highly variable and unpredictable with periods of exacerbation and remission
  • About 70% of patients lead active lives but should avoid extreme fatigue
  • Average illness lasts more than 25 years
93
Q

Multiple Sclerosis: Possible Complications

A
  • UTIs
  • Urinary retention
  • Depression
  • Severe fatigue
  • ED
  • Pressure injuries if bedridden
  • Optic nerve atrophy
  • Paraplegia
  • Dental caries
  • Dementia
94
Q

Essential Tremor: What is it?

A
  • Postural tremor of hands, head, or voice
  • Family history is common
  • May improve temporarily with alcohol
95
Q

Essential Tremor: Assessment Findings

A
  • Tremor is not present at rest, but emerges with action
  • Typically becomes more conspicuous with time
  • May interfere with manual skills
96
Q

Essential Tremor: Treatment

A
  • Often unnecessary
    1. Propranolol or primidone
    2. Occasionally alprazolam, topiramate, or gabapentin
    3. Deep-brain stimulation
97
Q

Parkinson’s Disease: What is it?

A

Idiopathic, chronic and progressively disabling neurodegenerative disease
- any combination of tremor, bradykinesia, or postural instability

98
Q

Parkinson’s Disease: Etiology and Incidence

A
  • More common in men
  • Incidence increases with age
  • Most commonly idiopathic; an imbalance of dopamine and acetylcholine
99
Q

Parkinson’s Disease: Risk Factors

A
  1. Age
  2. Male sex
  3. Family history
  4. Exposure to pesticides, herbicides, toxins
  5. Ingestion of neuroleptic medications
100
Q

Parkinson’s Disease: Primary Motor Symptoms

A
  1. Bradykinesia (slowness of movement)
  2. Rigidity or stiffness: resistance of major joints to passive movement sometimes referred to as “cogwheel rigidity”
  3. Resting tremor; pill-rolling tremor
101
Q

Parkinson’s Disease: Secondary Motor Symptoms

A

** Caused by rigidity and bradykinesia
1. Dysarthria
2. Hypophonia (decreased volume of speech)
3. Dysphagia
4. Sialorrhea (hypersalivation)
5. Gait freezing
6. Micrographia (smaller handwriting)
7. Expressionless face
8. Tachyphemia (rapid rate speech)

102
Q

Parkinson’s Disease: Nonmotor Symptoms

A

** May precede motor symptoms by several years
1. Autonomic dysfunction
2. Orthostatic hypotension
3. Sweating dysfunction
4. Sphincter dysfunction
5. ED
6. Urinary bladder distension/infections
7. Constipation
8. Depression
9. Anxiety
10. Hallucinations
11. Apathy
12. Lewy body dementia
13. OCD
14. Impulse disorders

103
Q

Parkinson’s Disease: Diagnostic Studies

A
  1. Movement Disorder Society-Unified Parkinson’s Disease Rating Scale
  2. Once parkinsonism is established, diagnosis is made in a neurology setting
  3. Diagnosis of clinical PD requires:
    - Absence of absolute exclusion criteria
    - Presence of at least two supportive criteria
    - No red flags
104
Q

Parkinson’s Disease: Nonpharmacologic Management

A
  • PT/OT, speech therapy
  • Home environment modification
  • Assistive device
  • Support group and palliative care
105
Q

Parkinson’s Disease: Pharmacologic Management

A
  1. Carbidopa-Levodopa
  2. Dopamine agonists (bromocriptine, pramipexole, ropinirole, rotigotine)
  3. NMDA Receptor Inhibitor (amantadine)
  4. Monoamine Oxidase-B Inhibitors (Selegiline, Rasagiline, Safinamide)
  5. Anticholinergics (Benztropine, Trihexyphenidyl
106
Q

Parkinson’s Disease: Consultation/Referral

A
  • All patients suspected of having PD should be promptly referred to a specialist with expertise
  • PT, speech, and language therapy, and/or occupational therapy
  • Support groups
107
Q

Parkinson’s Disease: Follow-Up

A
  • Lifelong neurology follow up and medication adjustment every 6 -12 months
  • Educate to never abruptly withdraw medications
  • Give oral and written information about risks, and record that discussion has taken place
  • Review nonmotor symptoms that can occur
108
Q

Parkinson’s Disease: Expected Course

A

Treatment goals:
- Improve motor function
- maximize functional level
- Manage neuropsychiatry complications
- Chronic, progressive neurological disorder with high mortality

109
Q

Parkinson’s Disease: Possible Complications

A
  • Multiple falls
  • Aspiration pneumonia due to immobility
  • Dementia
  • Depression
  • Injuries from falls
110
Q

Seizure Disorder: What is it?

A
  • AKA, convulsions, epilepsy
  • A transient disturbance of cerebral function due to an abnormal paroxysmal neuronal discharge in the brain
  • Epilepsy is defined as two unprovoked seizures that occur > 24 hours apart or one unprovoked seizure with a condition resulting in a persistent lowered seizure threshold and a high risk seizure recurrence
  • Two seizure types: focal and generalized
111
Q

Seizure Disorder: Etiology

A
  • Idiopathic
  • Alcohol intoxication or withdrawal
  • Metabolic disturbance
  • Brain tumor
  • Hypoxia
  • Acute intracranial events
  • Convulsive syncope
  • Eclampsia
  • Fever
  • Head injury
  • Hyperventilation
  • Meningitis
  • Migraine
112
Q

Seizure Disorder: Incidence

A
  • Highest incidence in children
  • 2 million people in U.S have epilepsy
113
Q

Seizure Disorder: Risk Factors

A
  1. Previous history of seizure
  2. Family history
  3. Brain tumor
  4. History of brain insult
  5. Cardiac dysrhythmias
  6. Arteriovenous malformation
  7. Drug or alcohol-related
  8. Withdrawal from anticonvulsant medications
114
Q

Seizure Disorder: Assessment Findings

A
  • Witness description of seizure
  • Presence of incontinence
  • Eye deviation
  • Seizure with or without loss of consciousness
  • Assess for aura and postictal phase
  • Detailed history to elicit cause of seizure
  • Developmental assessment for delay
  • Full neuro assessment
115
Q

Seizure Disorder: Diagnostic Studies

A
  1. CMP
  2. Toxicology screens
  3. Anticonvulsant levels if patient is taking an anticonvulsant
  4. MRI or CT of brain
  5. Sleep-Deprived EEG
  6. Lumbar puncture indicated for most children younger than 2 years or if CNS infection is suspected in patient of any age
  7. ECG
116
Q

Seizure Disorder: Prevention

A
  1. Usually none
  2. Fever management
  3. Adherence to antiepileptic medication treatment
  4. Manage underlying conditions
  5. Reduce potential seizure triggers
117
Q

Seizure Disorder: Nonpharmacologic Management

A
  1. Monitor anticonvulsant levels
  2. Patient education for anticonvulsant therapy
  3. Provide safe environment during seizures
  4. Discussion about driving, swimming, other activites
  5. Address social and psychological needs
  6. Ketogenic diet (not recommended in adults)
  7. Vagus nerve stimulation
118
Q

Seizure Disorder: Pharmacologic Management (Focal Seizures)

A
  1. Carbamazepine
  2. Lamotrigine
119
Q

Seizure Disorder: Pharmacologic Management (Primary Generalized)

A

Generalized Tonic-Clonic, Myoclonic, Tonic and Atonic Seizures, and Idiopathic Generalized Epilepsy, Absence
1. Valproic acid
** You can also use Ethosuximide for Absence seizures

120
Q

Seizure Disorder: Pharmacologic Management (Status Epilepticus)

A

In the community:
- Buccal midazolam
In the hospital:
- secure airway, O2, blood glucose levels
- lorazepam
- diazepam
- keppra
- rectal diazepam

121
Q

Seizure Disorder: Follow-Up

A
  • Depends on severity and etiology
  • Monitor anticonvulsant levels periodically
  • Epilepsy is considered resolved if patient is seizure-free for 10 years without anticonvulsant medications
122
Q

Seizure Disorder: Possible Complications

A
  • Drug toxicity/side effects from anticonvulsants
  • Hypoxia from repetitive seizures with resultant neurologic manifestations
  • Sudden unexpected death in epilepsy
  • Misdiagnosis
123
Q

Transient Ischemic Attacks (TIA): What is it?

A

A transient episode of neurologic dysfunction due to focal brain, spinal cord, or retinal ischemia, without acute infarction

124
Q

Transient Ischemic Attacks (TIA): Etiology

A
  1. Atherosclerotic disease within the brain and/or carotid arteries
  2. Microemboli from Afib, cardiac valve disorders
  3. Hypercoagulable states
  4. Cerebral artery vasospasm
  5. Use of OCP
125
Q

Transient Ischemic Attacks (TIA): Risk Factors

A
  1. HTN
  2. Advanced age
  3. Prior TIA
  4. Smoking/tobacco use
  5. DM
  6. HLD
  7. CKD
  8. Cardiac disease
  9. Afib
  10. OCP use
  11. Sickle cell disease
  12. Family history
  13. Sleep apnea
  14. Carotid artery stenosis
  15. Obesity
126
Q

Transient Ischemic Attacks (TIA): Assessment Findings

A
  1. Aphasia
  2. Visual field defects
  3. Confusion
  4. Amnesia
  5. Diplopia
  6. Dysphagia
  7. Dysarthria
  8. Unilateral weakness
  9. Symptoms usually last < 60 minutes
  10. Transient global amnesia
127
Q

Transient Ischemic Attacks (TIA): Diagnostic Studies

A
  1. CT/MRI of head
  2. Carotid studies
  3. Neurovascular studies
  4. ECG
  5. 24 hour Holter monitor
  6. Echocardiogram
  7. EEG
  8. CBC, PT/PTT, ESR, glucose, lipid profile, BMP
128
Q

Transient Ischemic Attacks (TIA): Prevention

A
  1. Control BP, HLD, DM
  2. Weight loss if needed
  3. Aerobic activity 3-4 times weekly
  4. Smoking cessation
  5. Limit alcohol
  6. Antiplatelet therapy
  7. Sleep study
129
Q

Transient Ischemic Attacks (TIA): Nonpharmacologic Management

A
  1. Control BP, HLD, DM
  2. Weight loss if needed
  3. Aerobic activity 3-4 times weekly
  4. Smoking cessation
  5. Limit alcohol
  6. Antiplatelet therapy
  7. Carotid endartectomy, angioplasty, and stenting
  8. Reduced sodium intake
  9. Mediterranean diet
  10. Treatment of Sickle Cell
130
Q

Transient Ischemic Attacks (TIA): Pharmacologic Management

A
  1. Platelet aggregation inhibitors (clopidogrel, ticlopidine)
  2. ASA
  3. Factor Xa inhibitors (rivaroxaban, apixaban)
  4. Direct thrombin inhibitors (dabagatran)
131
Q

Transient Ischemic Attacks (TIA): Consultation/Referral

A
  • Cardiologist if underlying cardiac disorders
  • Neurologist
  • Nutritional counseling
  • Sleep study referral
132
Q

Transient Ischemic Attacks (TIA): Possible Complications

A
  1. Stroke
  2. Injury from fall
  3. Bleeding from antiplatelet therapy/anticoagulation
133
Q

Cerebrovascular Accident (CVA): What is it?

A
  • AKA stroke
  • Sudden onset of neurologic deficit of cerebrovascular origin
  • 6th leading cause of death in U.S.
  • Subdivided into infarcts and hemorrhages
134
Q

Cerebrovascular Accident (CVA): Risk Factors

A
  1. HTN
  2. DM
  3. HLD
  4. Cigarette smoking
  5. Cardiac disease
  6. HIV infection
  7. Trigeminal herpes zoster
  8. Recreation drug abuse
  9. Heavy alcohol consumption
  10. Family history of stroke
135
Q

Cerebrovascular Accident (CVA): Diagnostic Studies

A
  1. CT and/or MRI
  2. CT angiography
  3. CBC, blood glucose, fasting lipid panel
  4. ECG and continuous cardiac monitoring
  5. Echo
  6. Possible blood cultures
136
Q

Cerebrovascular Accident (CVA): Treatment

A
  1. IV thrombotic therapy
  2. Endovascular mechanical embolectomy
  3. Symptomatic treatment
  4. Meds
  5. PT/OT/speech therapy
137
Q

Trigeminal Neuralgia: What is it?

A

Recurrent, unilateral, brief, electric shock-like facial pain

138
Q

Trigeminal Neuralgia: Incidence

A
  • more common in women
  • more common in middle and later life
  • more common in people with MS in young adults
139
Q

Trigeminal Neuralgia: Risk Factors

A
  • HTN
  • MS
140
Q

Trigeminal Neuralgia: Assessment Findings

A
  • Shock-like, severe, unilateral facial pain occurring in one or more divisions of the trigeminal nerve
  • Pain is episodic with spontaneous remissions
  • Stimulus-evoked pain: eating, talking, brushing teeth, and shaving
141
Q

Trigeminal Neuralgia: Diagnostic Studies

A
  1. MRI of brain with and without contrast to rule out causative structural brain lesions
  2. CT scan to rule out neoplasm if unable to obtain MRI
  3. Fulfillment of Diagnostic Criteria
142
Q

Trigeminal Neuralgia: Diagnostic Criteria

A

A. Recurrent paroxysms of unilateral facial pain in the distribution of one or more divisions of the trigeminal nerve, with no radiation beyond, and fulfilling criteria B and C.
B. Pain has all of the following characteristics:
1. Lasting from a fraction of a second to 2 minutes
2. Severe intensity
3. Electric shock-like, shooting, stabbing, or sharp in quality
C. Preciptitated by innocuous stimuli within the affected trigeminal distribution
D. Not better accounted for by another ICHD-3 diagnosis

143
Q

Trigeminal Neuralgia: Nonpharmacologic Management

A
  1. Acupuncture
  2. TENS
  3. Biofeedback
  4. Low-impact exercise, yoga, aromatherapy
  5. Surgical management (microvascular decompression, stereostactic radiosurgery, rhizotomy, peripheral neurectomy)
144
Q

Trigeminal Neuralgia: Pharmacologic Management

A

Carbamazepine is first-line therapy
** 70-98% of patients initially respond

145
Q

Trigeminal Neuralgia: Consultation/Referral

A
  • Neurology
  • Neurosurgery
146
Q

Trigeminal Neuralgia: Follow-Up

A
  1. Periodically check carbamazepine levels
  2. Monitor CBC and LFTs if carbamazepine is prescribed
147
Q

Trigeminal Neuralgia: Possible Complications

A
  1. Side effects from medications
  2. Depression/behavior changes from medication and/or from suboptimal pain control
  3. Surgical complications
  4. Facial numbness

Adult Health (13 decks)

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