Neurologic disorders Flashcards
What are the twelve CNs?
- CN I - olfactory
- CN II - optic
- CN III - oculomotor
- CN IV - trochlear
- CN V - trigeminal
- CN VI - abducens
- CN VII - facial
- CN VIII - auditory
- CN IX - glossopharyngeal
- CN X - vagus
- CN XI - accessory
- CN XII - hypoglossal
What are the functions of CNs I-III?
- CN I - smell
- CN II - vision
- CN III - eyelid and eyeball movement
What are the functions of CNs IV-VI
- CN IV - innervates superior oblique, turns eye downward and laterally
- CN V - chewing, face and mouth, touch and pain
- CN VI - turns eye laterally
What are the functions of CNs VII-IX?
- CN VII - controls most facial expressions, secretion of tears and saliva, taste
- CN VIII - hearing, equilibrium, sensation
- CN IX - taste, senses carotid blood pressure
What are the functions of CNs X-XII?
- CN X - senses aortic blood pressure, slows heart rate, stimulates digestive organs, taste
- CN XI - controls trapezius and sternocleidomastoid, controls swallowing movements
- CN XII - controls tongue movements
What is Bell’s palsy?
AKA idiopathic facial paralysis
- Acute paralysis of CN VII (facial) that is seen without other s/s
Bell’s palsy clinical presentation
- Sudden onset unilateral facial paralysis
- Inability to raise eyebrow or smile on affected side
- Decreased lacrimation
- Difficulty closing eyelid
- Biting on side of cheek
What is the prognosis of Bell’s palsy?
Bell’s palsy is temporary
Symptoms improve within a few weeks with complete recovery by 6 months
How would you differentiate Bell’s palsy from other differentials (e.g. stroke, facial tumor, brain tumor)?
Remaining neurological examination is normal including visual fields, EOM, sense of smell, etc.
Bell’s palsy diagnostic testing
Diagnosis made based on HPI and physical exam findings
- Can order EMG or imaging to rule out tumor/head injury
- Consider Lyme disease in NE states
Bell’s palsy treatment
- Systemic oral corticosteroids (prednisone) within 72 hours of onset to improve facial function
- Eye patch and tear substitute/lubricant
- Facial PT
What are primary headaches? What are the three types?
Not associated with other diseases (likely complex interplay of genetic, developmental, and environmental factors)
Examples: migraine, tension-type, cluster
What are secondary headaches? What are examples?
Associated with other conditions
Examples: brain tumor, intracranial bleeding, inflammation, etc.
What are the two most common types of primary headaches seen in primary care?
Associated with a family history of headaches
- Migraine with or without aura
- Tension-type headache
Tension-type headache clinical presentation and diagnosis
Lasts 30 minutes to 7 days with 2+ of the following:
- Pressing, nonpulsatile pain
- Mild to moderate in intensity
- Bilateral
- One of the following: nausea, photophobia, phonophobia
Migraine without aura clinical presentation and diagnosis
Lasts 4-72 hours with 2+ of the following:
- Unilateral (can be bilateral)
- Pulsating quality, moderate to severe in intensity
- Aggravation by normal activity such as walking (or causes avoidance of these activities)
- 1+ of the following: N/V, photophobia, phonophobia
Migraine with aura clinical presentation and diagnosis
Focal dysfunction of cerebral cortex or brainstem causes aura symptoms to develop over 4 minutes, or 2+ symptoms occur in succession (no aura should last longer than 1 hour)
Symptoms:
- Feeling of dread or anxiety
- Unusual fatigue
- Nervousness or excitement
- GI upset
- Visual or olfactory alteration
When is neuroimaging with head CT or MRI indicated for patient’s presenting with primary headaches?
If they present with headache “red flags”
SSNOOPPP mnemonic
- Systemic symptoms - fever, unintended weight loss
- Secondary headache risk factors - HIV, malignancy, pregnancy, anticoagulation, marked BP elevation
- Neurological signs - confusion, impaired alertness, nuchal rigidity, etc.
- Onset - sudden, split second (“thunderclap”), onset with exertion (sexual activity, coughing, sneezing = increased ICP)
- Onset (age) - >50 years, <5 years
- Prior headache history - change in quality/frequency
- Positional
- Papilledema - visual problems
Lifestyle modifications to treatment primary headaches
- Consider menses, ovulation, or pregnancy
- Birth control/HRT
- Illness of virtually any kind
- Intense or strenuous activity/exercise
- Sleeping too much/too little/jet lag
- Fasting/missing meals
- Bright or flickering lights
- Excessive or repetitive noises
- Odors/fragrances/tobacco smoke
- Weather/seasonal changes
- High altitudes
- Medications
- Stress/stress letdown
Example of a selective serotonin receptor agonist that is used for abortive/acute migraine headache therapy
Triptans
- Can be used in conjunction with NSAIDs for full relief of pain
- Helps with photophobia, phonophobia
Triptan contraindications
Contraindications:
- History of prinzmetal angina
- CAD
- Uncontrolled HTN
- Pregnant women
- Recent ergot use
- Concurrent use with MAOIs, high dose SSRIs/SNRIs
What should the provider look out for if prescribing long term use of NSAIDs for primary headache therapy?
Rebound headaches
- Lower risk with ibuprofen and naproxen; higher risk with ASA, acetaminophen, OTC products that contain caffeine, aspirin, acetaminophen (Excedrin migraine)
If triptans are contraindicated for headache therapy, what other medication can be prescribed? What warnings should also be mentioned?
Fioricet - combination of caffeine, butalbital (barbiturate), acetaminophen
- Frequent of excessive use should be discouraged because of potential for barbiturate dependence
When is the onset of action if headache therapy is taken PO?
Takes 30 minutes to 1 hour before relief of pain
- Best for patients with headache and no GI distress
What are examples of injectable headache therapy? What is its onset of action?
Best for patients with rapidly progressing headache accompanied by significant GI upset
- Examples: sumatriptan, DHE, ketorolac
- Rapid onset of action (15-30 minutes)
What is considered prophylactic/prevention therapy for primary headaches (migraines, tension-type)?
Considered if abortive or acute headache is used frequently or if inadequate symptom relief is obtained from appropriate use of these therapies
What is the goal of prophylactic/preventative therapy for headaches?
Minimum of 50% reduction in number of headaches, easier to control headaches that respond more rapidly to standard therapies, require less medication
What are important considerations before initiating prophylactic/preventative therapy for headaches?
- Discontinue headache provoking medications (e.g. estrogen, progestin/progesterone, vasodilators)
- Implement lifestyle changes to avoid headache triggers
True/false: Patients, while working with the provider, can consider tapering prophylaxis once headaches are better controlled and lifestyle modifications are in place to minimize headache risk
True
What medications can be used for prophylaxis/prevention therapy for headaches?
- Beta blockers
- Antiepileptic drugs → divalproex sodium, sodium valproate, topiramate
- Antidepressants → TCAs (amitriptyline), SNRIs (venlafaxine)
- Calcitonin gene related peptide (CGRP)
What class of medication is first line for prophylaxis/prevention against tension-type headaches?
TCAs
What are cluster headaches?
Primary headache - AKA migrainous neuralgia
- Common in middle aged men, especially with heavy alcohol and tobacco use
Cluster headache clinical presentation and diagnosis
- Tendency to occur daily in groups or clusters
- Clusters last several weeks to months then disappear for months to years
- Occurs at characteristic time of year at the same time of day (typically when sleeping, “alarm clock” headache)
- Located behind one eye with steady, intense severe pain
- Unilateral pain that lasts 15-180 minutes, once to eight times/day
Cluster headache treatment
- Reduction of triggers (e.g. tobacco, alcohol)
- Start prophylactic and abortive therapy
- Abortive treatment can include high low oxygen, triptans, ergot alkaloids, local anesthetics
- Preventive treatment includes CCBs, mood stabilizers, anticonvulsants
True/false: Cluster headaches are often called the “suicide headache” because of the severity of the pain
True
Secondary headache clinical presentation
- Abnormal neurological examination
- Increased ICP - worse upon wakening and gets better as the day goes on
- In tension headaches, pain worsens as the day goes on
What is meningitis?
Infection of the meninges, CSF, and ventricles
- Can be bacterial, viral, fungal, or other
What vaccine has helped to reduce the incidence of meningitis in adults?
Hib
Meningitis mode of transmission and risk factors
Direct contact or respiratory droplets from infected people
Risk factors:
- People living in closed environments (e.g. military, college students, prison)
- Younger than 20 years
- Pregnancy
- Immunocompromised
Meningitis clinical presentation
- Classic triad: fever, headache, nuchal rigidity
- N/V, photophobia, change in MS (drowsiness, confusion, delirium, coma)
- Purpura or petechial rash if n. meningitidis
- Positive brudzinski and kernig signs
What are the brudzinski and kernig sign?
Suggestive of nuchal rigidity and meningeal irritation seen in meningitis
- Brudzinski → passive neck flexion in supine patient results in flexion of knees and hips
- Kernig → patient lying supine and hip flexed at 90, positive when extension of knee elicits resistance or pain in lower back/posterior thigh
Meningitis diagnostic testing
LP with CSF evaluation in febrile patients with an abnormal neuro exam
- Pleocytosis (WBC >5 cells/mm3)
- Elevated CSF opening pressure
- Reduced CSF glucose
- Elevated CSF protein
Meningitis treatment
- Pneumococcal vaccines (PCV13 and/or PPSV23)
- Hib for children under 2 years old
When should the MCV4 and MenB vaccines be administered in pediatrics?
MCV4 at 11 or 12 years then booster at 16 years
- Students should receive MCV4 five years before starting college
MenB at 16 to 18 years
- Priority given between 16 to 23 years old
What is multiple sclerosis (MS)?
Recurrent, chronic demyelinating disorder of the CNS characterized by episodes of focal neurologic dysfunction
Symptoms occurring acutely, worsening over a few days, lasting weeks, followed by period of partial to full resolution
Multiple sclerosis risk factors
- Ages 20-40 years
- Female
- Family history
- Northern European ancestry
- Previous viral infection (e.g. EBV)
- Presence of autoimmune disorder
What are the two types of multiple sclerosis?
- RRMS
Relapsing, remitting MS (RRMS) → episodes resolve with improvement of neurological function between exacerbations and minimal to no cumulative defects
What are the two types of multiple sclerosis?
- PPMS
Primary progressive MS (PPMS) → episodes do not fully resolve, there are cumulative defects
Multiple sclerosis clinical presentation
Symptoms vary and depend on location of affected nerve fibers
- Weakness or numbness of a limb
- Monocular visual loss
- Diplopia
- Vertigo
- Facial weakness or numbness
- Sphincter disturbances
- Ataxia
- Nystagmus
Multiple sclerosis diagnostic testing
- Head MRI → demyelinated plaques, can monitor disease progression in brain and spinal cord
- LP → pleocytosis (increased WBCs), abnormal proteins, increased monocytes
Multiple sclerosis treatment
- What are the three categories of treatment?
- Therapy for relapses
- Long term disease-modifying medications
- Symptomatic management
Multiple sclerosis treatment
- Exacerbations
- Treat underlying precipitating illness (e.g. UTI) and
- Systemic high dose corticosteroid (can shorten course of exacerbation)
What medications can be prescribed for long term control of multiple sclerosis?
Immunomodulatory therapy
- Interferon beta-1b (betaseron, extavia)
- Interferon beta-1a (avonex, rebif)
- Peginterferon beta-1a (plegridy)
Immunosuppressive therapy
- Mitoxantrone (novantrone)
What is Parkinson’s disease and its cause?
Slowly progressive movement disorder that is caused by loss of pigmented dopaminergic neurons in substantia nigra pars compacta
Parkinson’s disease clinical presentation
- Common initial sign
- Four cardinal features
- Most common initial sign → resting tremor of upper limb
- Four cardinal features: tremor at rest, rigidity, bradykinesia, postural instability
- Shuffling gait, reduced arm swing
- Hyposmia (reduced sense of smell)
- Mask-like facies
Parkinson’s disease treatment
- Dopamine agonists → ropinirole (requip), pramipexole (mirapex)
- Levodopa-carbidopa (sinemet)
- Exercise and PT
Considerations before prescribing levodopa-carbidopa (sinemet)
- Long term use (5-10+ years) can lead to dyskinesia
- “Wearing off” phenomenon
- Can add MAO-B inhibitor or COMT can prolong effect of levodopa
Important questions to ask patients with a history of seizure disorder
- Was a warning event present?
- What actually happened during the seizure?
- Did the patient relate to the environment?
- Does the patient have any recollection of the seizure?
- How did the patient feel after the seizure?
- How long was the recovery following the seizure?
- what is the frequency and duration?
- Is there a known trigger?
Characteristics of absence (petit mal) seizure
- Blank staring lasting 3-50 seconds accompanied by impaired LOC
- Age of onset: 3-15 years
Characteristics of myoclonic seizures
- Awake state or momentary LOC with abnormal motor behavior lasting seconds to minutes
- 1+ muscle groups causing brief jerking contractions of limbs and trunk
- Age of onset: 2-7 years
Characteristics of tonic clonic (grand mal) seizures
- Rigid extension of arms and legs followed by sudden jerking movements with LOC
- Bowel and bladder incontinence with postictal confusion
- Age of onset: any age
- Adult onset with brain tumor, head injury, alcohol withdrawal
Characteristics of simple partial or focal seizure
- Awake state with abnormal motor, sensory, autonomic, or psychic behavior
- Movement of any part of the body (localized or generalized)
- Age of onset: 3-15 years
Characteristics of complex partial seizures
- Aura characterized by unusual sense of smell/taste, visual/auditory hallucination, stomach upset
- Followed by vague stare and facial movements, muscle contraction and relaxation, autonomic signs
- Age of onset: any
Seizure disorder diagnostic testing
- Prolactin level within 20 minutes of seizure (elevated following generalized tonic clonic or complex partial seizure)
- Video EEG (especially for unprovoked seizures)
Examples of anti-epileptic drugs
- Older products → phenytoin, carbamazepine, clonazepam, ethosuximide, valproic acid
- New products → gabapentin, lamotrigine, topiramate
What two AEDs have a narrow therapeutic index?
- Phenytoin
- Carbamazepine
If used concurrently, phenytoin use increase ___ clearance by increased CYP 450 enzyme activity leading to levels of both drugs decreasing by 40%
Theophylline
True/false: Carbamazepine induces estrogen metabolism
True - If taking birth control pills with carbamazepine, can lead to contraceptive failure
How can you differentiate a TIA from a stroke based on presentation?
TIA is an acute neurological event that resolves within minutes to 24 hours
If neurologic changes persist beyond 24 hours, consider stroke
TIA and stroke clinical presentation
- Unilateral weakness
- Numbness
- Paralysis of face or limb
- Slurred or garbled speech
- Blindness or diplopia in one or both eyes
- Dizziness and loss of balance
- Sudden onset severe headache
TIA and stroke diagnostic testing
- Labs: BG, CBC, electrolytes, coagulation studies, 12 lead ECG
- Head CT or MRI within 24 hours
- Vascular imaging → doppler US, CT angiography, MRA
TIA management and treatment
- Long term antiplatelet therapy (ASA, clopidogrel)
- If high risk for stroke or TIA associated with cardio embolism from afib or valvular disease, start anticoagulation therapy
- DOAC or warfarin
Symptoms that help differentiate ischemic from hemorrhagic stroke
Hemorrhagic strokes can present with N/V, headache, sudden change in consciousness
Acute stroke clinical presentation
- Alteration in consciousness (confusion, memory loss, agitation)
- Headache
- Unusual or severe neck or facial pain
- Aphasia, facial weakness or asymmetry
- Altered coordination, ataxia
- Visual loss
Stroke diagnostic testing
- Head CT to identify acute hemorrhage
- MRI to identify acute phase of ischemic stroke
How soon after an ischemic stroke should fibrinolytic (alteplase, tPA) be used?
Within 3 to 4.5 hours of stroke onset
Medications for secondary prevention against ischemic strokes
- Antiplatelet therapy with ASA or clopidogrel (plavix)
- If cardiac embolus d/t afib, DOAC therapy or warfarin
- Antihypertensive therapy
- Goal BP 130/80
What is giant cell arteritis?
Autoimmune vasculitis involving medium and large vessels with resulting arterial inflammation that affects parts of an artery with sections of normal artery in between
Giant cell arteritis clinical presentation
- Severe unilateral headache (stabbing, located in frontal, vertex, or occipital area)
- History of recent respiratory symptoms (cough, sore throat, hoarseness)
- Jaw claudication
- Acute reduction or change in vision
Giant cell arteritis diagnostic testing
- Confirmatory arterial biopsy (multiple site d/t skips in vessel)
- Color duplex US of temporal arteries
- Elevated ESR and CRP
Giant cell arteritis treatment
As soon as diagnosis is made, start on high dose systemic corticosteroid to prevent risk of blindness
- Add misoprostol, PPI, bisphosphonate, calcium/vitamin D supplement to minimize steroid AEs
- Can add tocilzumab (actemra) with tapering of corticosteroid
