Neurology Flashcards

1
Q

What is the most common headache type?

A

Tension

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2
Q

What headache is most common to lead to PCP visit?

A

Migraine

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3
Q

What are the primary headache types?

A

Migraine, tension, cluster, new daily persistent

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4
Q

Migraine

A

episodic attacks of severe headaches often associated with nausea, photophobia and/or phonophobia

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5
Q

Phases of Migraines

A

Prodrome-hours-days prior
Aura-w/in hour before headache
Headache
Postdrome-up to 48 hours after

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6
Q

Migraine Prodrome Symptoms

A

fatigue, difficulty concentrating, neck stiffness, photo/phonosensitivity, nausea, blurred vision, yawning, pallor

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7
Q

Migraine Postdrome Symptoms

A

tired, difficulty concentrating, neck stiffness

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8
Q

Common Migraine Criteria

A

At least5 lasting 4-72 hours
@least 2: Unilateral, pulsating, mod-severe pain, aggravated w/ activity
@least 1: N/V, photo and phonophobia

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9
Q

Migraine w/ Aura

A

Classic migraine WITH
@least 1: visual, sensory, speech, motor, brainstem, retinal
@least 3: aura symptom spreads gradually, 2+ occur in succession, each aura symptom lasts 5-60 minutes, at least 1 symptom unilateral and positive, followed by headache w/in 60 minutes

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10
Q

Aura

A

transient focal neurologic reversible symptoms preceding or accompanying the headache

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11
Q

Brainstem Aura (Basilar migraine)

A

No motor or retinal symptoms w/ @least 2: dysarthria, vertigo, tinnitus, hypacusis, diplopia, ataxia, decreased level of consciousness

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12
Q

Retinal Migraine

A

Aura of fully reversible monocular positive/negative visual phenomena confirmed by clinical visual field or patients drawing of monocular field defect
@least 2: aura spreads over 5 minutes, lasts 5-60 minutes and followed by headache w/in 60 minutes

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13
Q

Hemiplegic Migraine

A

Aura has BOTH: reversible motor weakness and reversible visual, sensory, and or speech symptoms

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14
Q

Menstrual Migraine

A

-2 to +3 days of cycle, aura uncommon, related to decline in estrogen

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15
Q

Menstrual Migraine Treatment

A

Preventative: NSAIDs -7 to +6 days, Triptans -2 to +4 days, Magnesium day 15-menses
Extended-cycle hormonal treatment
Abortive: rest, dark, quiet

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16
Q

Chronic Migraine

A

> 15 days/month for 3 months, at least 8 days/month has features of migraine

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17
Q

Migraine Treatment

A

Rest, quiet, dark

NSAIDs, acetaminophen, triptans, nit-emetics, ergotamine

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18
Q

Mild-moderate Migraine treatment

A

NSAIDs first line (ibuprofen, naproxen, ketorolac (injection))

2nd: acetaminophen/tylenol
3rd: Excedrin (ASA/acetaminophen/caffeine)

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19
Q

Mod-Severe Migraine Treatment

A

1st line: Triptans (canc ombrine w/ naproxen for ^ efficacy)

2nd line: Ergots

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20
Q

Triptans

A

MOA: vasoconstrictors, activate serotonin receptors
Avoid in pregnancy (cat C)
Containdicated: coronary/vascular disease, hemiplegic or basilar migraine, hx of stroke/uncontrolled HTN, prinzmetal angina
Side effects: N/V

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21
Q

Ergots

A

MOA: serotonin agonist
Rectal formulations available
Avoid in CVD, CYP3A4 inhibitors
Pregnancy cat X

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22
Q

Alternative Migraine Treatment (last resort)

A

opioids-can cause tolerance, abuse, dependence

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23
Q

Adjunctive Migraine Therapy

A

Antiemetics/dopaminereceptor blockers for N/V: metoclopramide, prochlorperazine, promethazine
Butalbital containing combo analgesics: high risk of overuse/dependence
Hydration

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24
Q

Preventative Migraine treatment

A

Acupuncture, avoid triggers, behavioral modification, headache diary

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25
Q

Botox

A

FDA approved for chronic migraine

Blocks release of Substance P and CGRP, inhibits peripheral signals to CNS ad blocks central sensitization

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26
Q

Tension Headache Criteria

A

Last 30 minutes-7 days, @least 2: bilateral, pressing/tightening (non-pulsating) band, mild-mod intensity, not aggravated by activity
BOTH: no N/V, no more than 1 of photo/phonophobia

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27
Q

Tension Headache Treatment

A

1st line: NSAIDs, acetaminophen, aspirin; canc combine w/ caffein for ^ effect
Tricyclic antidepressants (amitriptyline), other antidepressants (mirtazapine, venlafaxine), anticonvulsants (topiramate, gabapentin), tizanidine, lidocaine in trigger points, botox
NO: opioids, butalbital, muscle relaxants

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28
Q

Tension Headache Non-pharma treatment

A

Biofeedback, CBT, relaxation techniques, acupuncture, PT

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29
Q

Cluster Headaches

A

Least common primary headache
usually <60 minutes up to 8 times/day, pain unilateral near eye, often at night (awakening), “severe, piercing, boring, exploding, penetrating”
Associated w/ suicide ideations

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30
Q

Forms of Cluster Headaches

A

Episodic (more common): phases last 2-16 weeks, then cluster free for 6 months
Chronic: no cluster free episodes for >1 month

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31
Q

Cluster Headache Criteria

A

Severe unilateral orbital/temporal pain w/ @least 1: conjunctival injection/lacrimation, nasal congestion/rhinorrhea, mitosis/ptosis, eyelid edema, forehead sweating
Sense of restlessness/agitation
Frequency 1 every other day to 8/day for >half the time

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32
Q

Cluster Headache Treatment

A

1st line: 100% O2 or sumatriptan
intranasal lidocaine, ergots, IV dihydroergotamine
Glucocorticoids
Prophylactic: verapamil (not in heart block or arrhythmias), greater occipital nerve block, surgical options

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33
Q

New daily Persistent Headache Criteria

A
Persistent headache (1.5-24 hours/day) present for >3 months with known onset, may be mix of migraine or tension-type, usually bilateral with nausea, photo/phonophobia
Treat like tension or migraine
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34
Q

Headache Red Flags

A

Abrupt/sudden onset, onset >50, new onset when pregnant/post-partum, worst HA of life, change in HA, weight loss, fever, severe hypertension

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35
Q

Pseudotumor Cerebri

A

Elevated intracranial pressure in overweight women of childbearing age
Headache that can be exacerbated with posture changes, relieved w/ NSAIDs
Associated with visual obscurations, pulsatile tinnitus, photopsia, back pain, retrobulbar pain, diplopia, visual loss
Could be caused by growth hormones, tetracyclines, hypervitaminosis A

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36
Q

Pseudotumor Cerebri Diagnosis/treatment

A

Elevated ICP on LP, normal CSF, MRI w/ venography negative
Weight loss, decrease sodium intake, carbonic anhydrase inhibitors (acetazolamide), loop diuretics, serial lumbar punctures, surgery (nerve shunting/fenestration)

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37
Q

Rebound Headache

A

Most commonly due to opioids, butalbital/analgesics, excedrin (ASA/aceta/caffeine)
Least likely with NSAIDs
May have nausea, weakness/lack of energy, difficulty concentrating, memory problems, irritability
Limit acute meds to <10 days/month

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38
Q

Rebound Headache Criteria

A

HA 15+ days/month with pre-existing HA disorder, regular overuse for >3 months (regular intake >10 days/month for most drugs, >15 days/month for simples like NSAIDs, ASA and acetaminophen)

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39
Q

Temporal Arteritis

A

Most common systemic vasculitis, rare <50
Abrupt onset of throbbing continuous HA w/ neck, torso, shoulder and pelvic girdle pain, jaw claudication and fever; association w/ polymyalgia rheumatica
BIOPSY for diagnosis

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40
Q

Temporal Arteritis Treatment

A

High dose corticosteroid prednisone 40-60mg w/ biopsy w/in 1 week, 80-100mg for visual sx
Should improve w/in 72 hours, then taper w/ ESR/CRP
Could be on steroids up to 5 years

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41
Q

Trigeminal Neuralgia

A

MC aberrant loop of artery or vein, compressing trigeminal nerve root
More common in MS patients, often mandibular/maxillary
Extreme “electric shock-like/shooting” pain to light tough (like wind) last seconds-minutes

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42
Q

Trigeminal Neuralgia Treatment

A

Antidepressants and anti-seizure meds (carbamazepine), narcotics rarely effective
Best long term outcome: microvascular decompression

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43
Q

Peripheral Neuropathy

A

Most commonly sensory but cane motor or autonomic
Weakness, sensory loss and/or positive sensory symptoms (burning, tingling); bilateral, gradual onset w/ distal involvement

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44
Q

Peripheral Neuropathy Causes

A

Hereditary: Charcot-marie-tooth disease, porphyria
Acquired: Lyme disease, endocrine (diabetes), vitamin deficiencies (B12, Thiamine), B6-also in excess), inflammatory, rheumatic, organ failure, toxins

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45
Q

Charcot-Marie-Tooth disease

A

Most common hereditary PN-demyelination thats asymptomatic until late>distal leg weakness, foot deformities, muscle atrophy below knee, reduced/absent reflexes, sensory deficits
Treat with PT/OT and braces

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46
Q

Poryphoria

A

Metabolic disorder caused by deficiency in heme biosynthetic pathway
Very rare
Presents w/ sharp abdominal pain, agitation, hallucinations, seizures>days later extremity pain/weakness (asymmetric, proximal or distal)

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47
Q

Diabetes PN

A

Most common PN in developed countries

Distal symmetric sensory or sensorimotor polyneuropathy most common

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48
Q

Diabetic Neuropathy Presentation

A

Sensory loss-+/-, “stock glove”, painless injuries, not along dermatomes
Motor symptoms: distal, proximal or weakness
Autonomic: involves CV, GI, GI and sweat glands, ataxia, gait instability, syncope

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49
Q

Diabetic Neuropathy Treatment

A

Glucose control, foot care education, podiatry referral

Anti-epileptics, anti-depressants, Na channel blockers, other analgesics, meds for autonomic dysfunction

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50
Q

Hypothyroidism Peripheral Neuropathy

A

Most common manifestation is carpal tunnel syndrom

Correct hypothyroidism

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51
Q

B12 Deficient Peripheral Neuropathy

A

Glossitis, paresthesias, sensory loss (starting w/hand), hyperreflexiaw/ absent achilles, behavior changes
Supplement w/ 1000ug IM weekly for one month, then monthly OR 1000ug PO daily

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52
Q

Thiamine (B1) Deficient Peripheral Neuropathy

A

“beri-beri” disease most commonly caused by alcohol abuse
Presents w/ mild sensory loss, burning dysphagia in toes/feet, aching/cramping in calves, distal sensory loss in feet/hands
Treat with thiamine replacement until proper levels restored

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53
Q

Carpal Tunnel Syndrome

A

compression neuropathy of median nerve-most common in arm

Can be extrinsic (work/recreation related) or intrinsic small space, fluid retention)

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54
Q

Carpal Tunnel Presentation

A

Aching radiating to thenar area w/ numbness, weakness/dropping objects, pain worse w/activity and at night
“flick sign”, thenar atrophy, weak thumb opposition

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55
Q

Carpal Tunnel Diagnosis/Treatment

A

Tinnels/Phalens tests, nerve conduction testing prior to sx consult (steroid injection or tunnel release)
Short term NSAIDs, PT, ergonomic changes, wrist splint esp @ night

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56
Q

Ulnar Neuropathy “Cubital Tunnel Syndrome” Presentation

A

Ulnar nerve compression/trauma
Parasthesias, tingling, numbness in last 2 fingers, pain @ elbow/forearm w/ weakness
Atrophy and weakness of pinky/ring fingers

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57
Q

Ulnar Neuropathy Treatment

A

Avoid aggravationg factors, elbow pads

Surgery-after 6-12 weeks of no improvement, progressive palsy/paralysis, long-standing lesion (clawing)

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58
Q

Radial Neuropathy

A

Transient compressive injury (from crutches) presenting with wrist drop, finger weakness (thumb side)
Usually spontaneously recovers in 6-8 weeks but can use cock-up wrist/finger splints to avoid further compression

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59
Q

Lateral Cutaneous Femoral Neuropathy

A

Parasthesias, numbness, pain in lateral thigh increased with standing or walking-normal strength and reflexes
Resolves spontaneously but treat w/ weight loss, lido patch, NSAIDs, neuropathy meds, avoid tight belts

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60
Q

Peroneal Neuropathy

A

Presents w/ foot drop, sensory loss, sudden onset, no pain

Mange w/ weight loss, ankle brace, knee pad, avoid leg crossing-resolves spontaneously

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61
Q

Bells Palsy

A
Facial nerve (CN7) neuropathy, lower motor neuron lesion affection all branches >weakness/paralysis
Diabetes and pregnancy are risk factors
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62
Q

Bells Palsy presentation

A

Sudden onset peaked in 3 days
Unilateral facial muscle paralysis-forhead, facial creases, mouth drooping, eyelid sagging; tearing and loss of corneal reflex
Decreased tasted, numbness, difficulty eating/speaking, face feels stiff

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63
Q

Bells Palsy Diagnosis

A

H&P

Can use electrodiagnostic testing, high res CT, serology testing, audiometry

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64
Q

Bells Palsy Treatment

A

Prednisone w/in 3 days of symptom onset
Valacyclovir for severe palsy or HZV presentation
Eye protection, acupuncture, PT

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65
Q

Complex Regional Pain Syndrome

A

Triad of burning pain, autonomic dysfunction and trophic changes preceded by sx or trauma
Disorder of extremities characterized by autonomic and vasomotor instability

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66
Q

CRPS Presentation

A

Findings localized to arm or leg but not a single nerve-most common in hand
Pain (burning/aching) aggravated by stress or environmental changes, color/temp changes, changes in skin and nails, limited ROM, edema, weakness, tremor, spasm

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67
Q

CRPS Diagnosis

A

Starts 4-6 weeks after limb trauma but no longer explained by the trauma, goes beyond region involved in trauma
Bone changes
Budapest Consensus criteria

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68
Q

Budapest Consensus Criteria

A

Continuing pain disproportional to inciting event

>1 symptom in 3 categories and more than 1 sign in 2 categories: sensory, vasomotor, sudomotor//edema, motor/trophic

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69
Q

CRPS Treatment

A

NSAIDs for mild, Red for severe with edema
Tricyclic antidepressants, anticonvulsants, SNRIs, lido, calcitonin, tramadol, neuromodulation, PT/OT
Prevent with early mobilization after injury/surgery

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70
Q

Tourette Syndrome

A

Neurodevelopmental disorder manifested by motor and phonic tics, childhood onset
Often accompanied by ADHD/OCD

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71
Q

Tourette Manifestations

A

Motor: simple (blinking, shrugging, jerking), complex (gait, kicks, jumping, scratching), echopraxia-mimicking gestures, copropraxia (obscene gestures/flipping off)
Verbal: Simple (sniffing, coughing, grunting), coprolalia (obscene words), Echolalia (repetition of words), Palilalia (repeating phrases/babbling)
Ritualistic Behavior

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72
Q

Tourettes Diagnostics

A

Brain MRI if abnormal neurons exam
EEG if possible seizures
Criteria: both multiple motor and 1+ phonic tics, many times a day most days for more than a year, prior to 18 years old

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73
Q

Tourette Treatment

A
Treat comorbids first
Comprehensive behavioral intervention for tics (CIBT)
First line: Clonidine or guanfacine
Favored: Tetrabenazine
Severe tics: Haloperidol
Botox for focal motor tics
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74
Q

Mallampati Scoring

A

Risk of Sleep Apnea
Class 1: tonsils, uvula, soft palate fully visible
Class 2: Hard/soft palate, upper portion of uvula and tonsils visible
Class 3: soft and hard palate and base of uvula visible
Class 4: only hard palate visible

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75
Q

Polysomnogram

A

Measure sleep stages, respiratory effort and airflow, oxygen saturation, limb movement, heart rhythm, etc
Uses EEG, EOG (electrooculogram) and EMG (surface electromyogram) all in one

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76
Q

Home sleep test

A

Tests for obstructive sleep apnea

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77
Q

Multiple Sleep Latency Test (MSLT)

A

helpful for narcolepsy-measures propensity to sleep during day after restful night of sleep

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78
Q

Wakefulness Test

A

Measues ability to sustain wakefulness during daytime; evaluates efficacy of therapy, narcolepsy and sleep apnea

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79
Q

Epworth Sleepiness Scale (ESS)

A

Score of >10 is significant sleepiness

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80
Q

Insomnia Criteria

A

Symptoms 3x/week, problem with sleep maintenance or initiation w/ adequate opportunity and circumstance to sleep and daytime consequences
Short term <3 months or related to stressor
Chronic >3 months

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81
Q

Insomnia Diagnosis and Treatment

A

Diagnose w/ sleep history, meds, conditions, etc
Treat w/ education of sleep hygiene and stimulus control counseling; relaxation/CBT/sleep restriction therapy
Meds: Benzos, nonbenzos (zaleplan, zolpidem), melatonin agonsists (ramelteon), tricyclics (doxepin) and suvorexant (orexin antagonist)

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82
Q

Obstructive Sleep Apnea Diagnosis

A

Caused by repetitive collapse of upper airway during sleep
15+ events per hour
Can diagnose if: excessive sleepiness/fatigue/insomnia, waking up gasping/choking, habitual snoring, HTN, mood disorder, cognitive disfunction, CAD, stroke, HF, DM, afib

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83
Q

Sleep Apnea Presentation

A

Excessive daytime sleepiness, snoring, choking or gasping during sleep
Obesity, crowded/narrow OP airway, elevated BP, signs of pulmonary HTN or cor pulmonale, mallampati scoring

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84
Q

Sleep Apnea Diagnosis/Treatment

A

Polysomnography
Treatment: weight loss/exercise, sleep positioning, avoid alcohol/benzos; CPAP (20-40% pts don’t use it or only 4 hours/night), upper airway sx, hypoglossal nerve stimulation

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85
Q

Narcolepsy

A

Loss of hypothalamic neurons that produce orexin neuropeptides; difficulty sustaining wakefulness, poor regulation of REM, disturbed nocturnal sleep
Type 1 w/ cataplexy
Type 2 w/out cataplexy

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86
Q

Cataplexy

A

Sudden muscle weakness without loss of consciousness, usually triggered by strong emotions

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87
Q

Hypnagogic Hallucinations

A

dream-like hallucinations at sleep onset or upon awakening (hypnopompic)

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88
Q

Narcolepsy Presentation

A

Excessive/severe daytime sleepiness but feel rested upon wakening, ESS>15, “sleep attacks”
Fragmented sleep, other sleep disorders, obesity, psychiatric comorbidities

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89
Q

Narcolepsy Diagnosis

A

Polysomnogram to rule out other cause

MSLT-sleep latency <8 minutes and REM episodes in at least 2 of the naps

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90
Q

Narcolepsy Treatment

A

Adequate sleep with 1-2 20min naps, screen for depression, anxiety, CV, avoid meds (Benzes, opioids, antipsychotics, alcohol)
1st line: modafinil (wake promoting)
Methylphenidate or amphetamines-CNS stimulants
Sodium Oxybate for cataplexy (CNS depressant) or antidepressants

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91
Q

Shift Work Disorder Presentation

A

Fragmented sleep, difficulty falling/staying asleep, poor sleep quality, reduced sleep duration

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92
Q

Shift Work Disorder Management

A

Improve daytime sleep, regular sleep schedule during off-work periods too, sleep hygiene, CBT
Meds: short acting hypnotics, exogenous melatonin, caffeine,wake promoting agents, provigil

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93
Q

Parasomnias

A

More common in kids
NREM: confusional arousal, sleep walking/terrors/eating
REM: sleep paralysis, nightmare disorder, abberations

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94
Q

NREM Parasomnias

A

Usually occur during N3 stage in first 3rd of major sleep period
Criteria: recurrent episodes of incomplete wakening, absent responsiveness, limited cognition/dream report, partial or complete amnesia for event
Diagnose w/ polysomnogram and history

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95
Q

Sleep Terrors

A

Sudden arousal with sitting up, intense fear, piercing scream, intense autonomic activation (tachycardia, tachypnea, diaphoresis, flushing, mydriasis)
Fightened, confused, inconsolable, no recollection of event, calmly returns to sleep after several minutes

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96
Q

Sleep Walking

A

Slow, quiet movement with eyes open, terminate spontaneously, can be agitated or aggressive when aroused
Activities: making/eating food, cleaning, rearranging, driving, inappropriate behavior

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97
Q

Sleep Related Eating Disorder

A

Variant of sleep walking; involuntary eating w/ diminished LOC during arousal from sleep, not linked to daytime eating disorders

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98
Q

NREM Parasomnia Management

A

Avoid sleep deprivation, alcohol, meds
Maintain consistent sleep schedule, safety intervention but allowed to move freely/not woken up
Anticipatory awakening before event if its regular

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99
Q

Pathways to CNS infections

A

Invasion of bloodstream
Retrograde neuronal pathway
Direct contiguous spread

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100
Q

Lumbar Puncture

A

Opening pressure gives us the intracranial pressure, normal is clear and colorless with water-like viscosity
Tests cell count w/ diff, glucose, protein, culture, gram stain, viral PCR
Done below the level of spinal cord (L3-L5)

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101
Q

Contraindications to Lumbar Puncture

A

Cushing’s triad, decreased LOC, cal neurologic symptoms, papiledema, severe coagulopathy, skin infection/spinal abscess at LP site, mass lesion
IF PRESENT DO CT FIRST-if normal can do LP

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102
Q

Cushing’s Triad

A

ALL 3: respiratory depression, bradycardia, hypertension

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103
Q

CSF Analysis

A

Abnormal may be cloudy, purulent or pigment-tinged
Cloudiness begins with WBC>200 or RBC>400 or protein>150
Visibly bloody has RBC>6,000 (can be hemorrhagic-will clear byte 3, subarachnoid hemorrhage, intracerebral hemorrhage or cerebral infarct)
Elevated WBC indicates infection, vasculitis, leukemia infiltration or traumatic tap

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104
Q

Encephalitis

A

Acute inflammation brain parenchyma causing abnormalities of brain function
70% viral, 20% bacterial
Can be primary (neuronal involvement, virus present) or post-infectious (virus no longer present, demyelination occurs, possible autoimmune, no neuronal involvement)

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105
Q

Encephalitis risk factors

A

Outdoors (forestry workers, campers, hunters), travel to endemic areas, compromised immunity, lack of vaccines

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106
Q

Viral Encephalitis Pathogens

A

Herpes, arthropod-borne (west-nile, st Louis, la cross, Colorado tick fever), rabies, HIV, enteroviruses (coxsackie, polio), measles, flu, mumps, adenovirus

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107
Q

Bacterial Encephalitis Pathogens

A

Borrellia burgdorferi (lyme), M. Tuberculosis, treponema pallidum (syphilis), lots of others

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108
Q

Noninfectious Encephalitis causes

A

Paraneoplastic syndrome, drug toxicity, autoimmune (SLE, sarcoid), radiation, metabolic disorders

109
Q

Encephalitis Presentation

A

Fever, altered mental status, seizures, focal neurologic symptoms (motor/sensory, paralysis, nerve palsies, exaggerated reflexes, speed disorder)
No signs of meningeal irritation

110
Q

Encephalitis Diagnostics

A

MRI (but start with CT w/out contrast if sick to rule out mass lesion)
LP/CSF analysis (lymphocytes, ^WBC, pressure, protein, cloudy, normal glucose)
CBC, serum culture
Brain biopsy is gold standard

111
Q

Encephalitis Treatment

A

Stabilize: ET tube, ventilator, circulatory support, electrolytes
Empiric antiviral (Acyclovir 10mg/kg IV Q8H)
DVT and ulcer prophylaxis
Elevated ICP: elevate bed 30-45*, avid jugular compression, corticosteroids and mannitol

112
Q

Meningitis

A

Inflammatory disease of leptomeninges

113
Q

Meningitis Risk Factors

A

Extremes of age, birth history/maternal infection, immunocompromised, vaccine status, exposure risk, injection drug use

114
Q

Meningitis Presentation

A

Headache, N/V, fever, neck stiffness, photophobia, drowsiness, seizures
Bacterial until proven otherwise

115
Q

Viral Meningitis

A

MC is enterovirus, can be HSV, HIV, WNV
present w/ normal symptoms +URI symptoms, rash or diarrhea
Normal to mild elevations on CSF

116
Q

Bacterial Meningitis

A

Rapid progression
In neonates from birth canal or through placenta, in adults from nearby infection or penetrating injury
Cerebral edema, increased ICP, neurologic damage, death

117
Q

Bacterial Meningitis Pathogens

A

Neonates (<28 days): Group B strep (S. agalactiae)
Babies, children, adults: S pneumoniae
Teens, young adults: Neisseria meningitides

118
Q

Bacterial Meningitis Presentation

A

Rapid or slow onset, fever, meningismus, photophobia, severe headache, N/V, back pain, altered mental status, widened pulse pressure, brudzinski and kerning signs
In babies: “floppy”, rash (petechiae)

119
Q

Bacterial Meningitis Diagnosis

A

Blood cultures, CBC, LP/CT (don’t wait for this before antibiotics though!)
CSF: ^ICP, ^^WBC, ^^^protein, no RBC, low glucose, neutrophils present

120
Q

Bacterial Meningitis Treatment

A

Antibiotics ASAP
Empiric: Ceftriaxone/cefotaxime + vanco+ampicillin (if>50)
Need high doses to cross BBB
Supportive care: fluids, elevate bed, dexamethasone (reduce risk of hearing loss), +/- induced hypothermia

121
Q

Bacterial Meningitis Prognosis

A

Emergency-100% death if untreated, can still be long term probs w/ treatment (hearing loss, intellectual impairment, seizures)
Mortality increases with age and risk factors

122
Q

Bacterial Meningitis Prevention

A

Cipro for close contact (prolonged contact >8 hours or direct exposure to oral secretions)
Antibiotics (cillins) during labor-tested @ 35-37 weeks
Vaccines

123
Q

Encephalitis vs Meningitis

A

Difficult to distinguish, will usually be treated for both (antibiotics plus acyclovir)

124
Q

Fungal Meningitis

A

Rare, consider in immunocompromised
NO person-person spread
cryptococcus, visto, blastomyces, cocci

125
Q

Aseptic Meningitis

A

Clinical and lab evidence of meningeal inflammation w/out signs of bacterial infection
Can be caused by meds (bacterium, NSAIDs, IVIG, chemo, immunosuppressives), malignancy, SLE, head injury, brain surgery

126
Q

Multiple Sclerosis

A

Autoimmune disorder of CNS associated with destruction of myelin and nerve fibers
Unknown cause, can be genetic, environment and immune system factors
Most frequent cause of permanent disability in young adults other than trauma

127
Q

Types of MS

A

Clinically isolated syndrome (first attack)
Relapsing-remitting (RRMS)
Secondary Progressive (SPMS/transitional form)
Primary progressive (PPMS)

128
Q

Relapsing Remitting MS

A

unpredictable attacks that may or may not leave permanent deficits followed by periods of remission
Most common form

129
Q

Secondary Progressive MS

A

Initial RRMS followed by gradual worsening w/ or w/out occasional relapses, remissions and plateaus
10-20 years after disease onset

130
Q

Primary Progressive MS

A

Steady increase in disability w/out attacks

Poor/short prognosis

131
Q

MS Presentation

A

Internuclear ophthalmoplegia , optic neuritis (painful monocular vision loss w/ scatoma), Lhermittes sign (electric shock down spine from neck flexion), diplopia, bladder/bowel dysfunction, Uhthoff phenomena (her sensitivity), fatigue, nystagmus

132
Q

Internuclear ophthalmoplegia

A

Abnormal horizontal ocular movement w/ lost or played adduction and horizontal nystagmus of abducting eye

133
Q

MS Physical exam

A

Psychomotor slowing, asymmetric reflexes, spasticity, weakness

134
Q

MS Diagnosis

A

Brain/spinal cord MRI / gadolinium
CSF-oligoclonal bands present ONLY in MS
MUST HAVE dissemination in space and time (plaques)
McDonald Criteria

135
Q

McDonald Criteria

A

Uses MRI+/- CSF, dissemination in space, dissemination in time

136
Q

MS Treatment

A

High doses of methylprednisolone for attacks
Disease modifying therapy for RRMS
Treatment for SPMS or PPMS vary

137
Q

Disease Modifying therapy in MS

A

Decrease relapse rate, slow accumulation of brain lesions on MRI
Interferon*, alemtuzumab, dimethyl fumarate, fingolimod; available as infusion, injections and orally

138
Q

Myasthenia Gravis

A

Fluctuating degree and variable combination of weakness in ocular, bulbar, limb and respiratory muscles due to antibodies against muscle receptor for acetylcholine
“fatiguable weakness”
Most common disorder or neuromuscular transmission

139
Q

Myasthenia Gravis Presentation

A

Occular symptoms initial/MC presentation (ptosis, diplopia, burred vision), weakness of bulbar muscles (2nd most common; drooling, fatiguable chewing, facial weakness, dysarthria, dysphagia), rare limb weakness-asymmetric/proximal
Thymoma in 10-15%, hyperplasia in 60-70%

140
Q

Types of MG

A

Ocular-weakness limited to eyelids and extra ocular muscles; Ab present in 50%
Generalized- weakness affects ocular, bulbar, limb and respiratory muscles; Ab present in 90%

141
Q

MG Diagnosis

A

H&P, ice pack test for ptosis, repetitive nerve stimulation, single-fiber electromyography, serologic testing (AChR-Ab and MuSK-Ab)
Chest CT to rule out thymoma/hyperplasia

142
Q

MG Treatment

A

Symptomatic- anticholinesterase agents FIRST LINE (pyridostigmine, prolongs effect of ACh)
Immunosuppresive- glucocorticoids (azathioprine or mycophenolate)
Rapid/short acting- plasmapheresis and IVIG
Surgical- thymectomy (can still have symptoms after)

143
Q

Myasthenia Crisis

A

Worsening of myasthenia weakness requiring intubation or ventilation>respiratory failure
Life threatening, precipitated by infection/truma/drugs
Plasmapheresis speeds recovery
Slurred speech, dyspnea, decreased forceful coughing, weak voice

144
Q

Plasmapheresis

A

Blood pumped out of body through machine to remove antibodies, then back into body
Similar to dialysis

145
Q

Lambert-Eaton Myasthenia Syndrome (LEMS)

A

Immune system mistakenly attacks own tissues

Antibodies against the nerve where acetylcholine is released

146
Q

LEMS Presentation

A

Depressed/absent reflexes, autonomic dysfunction (dry mouth, slow pupil response, impotence), postexerise facilitation (recovery of reflexes with VIGOROUS muscle activation like sprinting) but proximal legs fatigue with non-vigorous action

147
Q

LEMS Diagnosis

A

H&P
Serology (VGCC Ab)
Repetitive nerve stimulation-increased amplitude
CT chest/abdomen/pelvis bc of risk of malignancy

148
Q

LEMS Treatment

A

Amifampridine (enhances calcium entry), guanidine, pyridostigmine
Prednisone and azathioprine together or alone for immunosuppression
IVIG (temporary improvement)

149
Q

Guillain-Barre Syndrome

A

Immune mediated polynephropathy; antibodies attack axons and/or myelin
Acute, paralyzing illness provoked by preceding infection by 2-4 weeks (Campylobacter jejuni)

150
Q

Guillain Barre Types

A

MC: acute inflammatory demyelinating polyneuropathy (AIDP)-parasthesias in hands/feet
Acute motor axonal (AMAN)
Acute motor/sensory axonal (AMSAN)
Miller Fisher Syndrome-only one with eye component

151
Q

Guillain Barre Presentation

A

Symmetric ascending muscle weakness and diminished reflexes w/ no visible atrophy
Radicular or spinal pain, sensory symptoms (paresthesia in extremities)
Can present independently or together-often gait disturbance
Can have CN involvement, respiratory failure, autonomic disturbances (unstable HR/BP, hyponatremia, urinary retention)
NO fever, meningeal signs, leukocytosis, papilledema,

152
Q

Guillain Barre Diagnosis

A

LP/CSF: ^^protein w/ normal WBC
Nerv conduction tests
Serology (GQ1b Ab in Miller Fisher)
Spine MRI (enhanced intrathecal nerve roots/cauda equina)

153
Q

Guillain Barre Treatment

A

Supportive Care-hospitalization for respiratory/CV function, DVT prophylaxis
Plasmapheresis, IVIG
No corticosteroids
Usually spontaneous recovery in 3-4 weeks

154
Q

Essential Tremor

A

Most common action tremor in adults, can be familial

155
Q

Essential Tremor Presentation

A

Classically affects hands and arms, bilateral, slightly asymmetric
Most pronounced with movement, absent when relaxed
May also involve head, voice and legs, can be relieved w/ alcohol
Exacerbated by anxiety/stress, illness, meds, NOT caffeine, worsens over time

156
Q

Essential Tremor Diagnosis

A

Clinical
Isolated tremor of bilateral arms for at lest 3 years +/- head, voice or leg tremor with normal neurons exam
Can use DaTscan to rule out Parkinsons

157
Q

Essential Tremor Treatment

A

1st line: propranolol or primidone, often combined after 1 year
Can use Benzes or alcohol for exacerbations
Deep brain stimulator for severe

158
Q

Parkinsons Presentation

A
Rest tremor (pill rolling), rigidity (cogwheel or lead pipe), bradykinesia (most common) and postural instability (pull test)
Cognitive dysfunction/dementia w/ Lewy bodies, sleep disturbance, autonomic (BP) dysfunction, psychosis/hallucinations
159
Q

Parkinsons Diagnosis

A

Gold standard: neuropathologic exam
Can do MRI to rule out other dx
Improved bradykinesia/rigidity with dopaminergic drugs

160
Q

Parkinsons Treatment

A

MAOI type B (rasagiline, safinamide), dopamine agonists (prmiprexole, ropinerole, bromocriptine), Carbidopa/levodopa
@nd line: COMT inhibitors (entacapone, tolcapone)
Deep brain stimulator, continuous carbs-levo infusion (LCIG), continuous subQ apomorphine infusion (CSAI)

161
Q

Huntingtons Disease

A

Autosomal dominant disorder with mid-life onset, high cause of suicide
Caused by >36 repeated of mutated HTT/HD gene (CAG)

162
Q

Huntingon Presentation

A

Chorea (defining symptom), psychiatric illness (paranoia, delusions, hallucinations, depression, irritability), dementia, weight loss/cachexia

163
Q

Juvenile Huntington Disease

A

Presents before 20 years

Myoclonus, seizures, behavioral problems and Parkinsonism are more common, but chorea is absent

164
Q

Huntington Diagnosis

A

Clinical features, family history, confirmatory genetic testing for CAG repeat in HTT gene
MRI may show caudate atrophy

165
Q

Huntington Treatment

A

None; therapy focused on symptom management and supportive care w/ multidisciplinary team and palliative care
Dopamine depleting agents or neuroleptics for chorea
SSRIs for depression, ST for dysphagia, NSAIDs for pain

166
Q

Muscular Dystrophy

A

X-linked recessive defect that impairs normal muscle function
Most common forms are Duchenne (DMD-2/3 from mother 1/3 spontaneous; loss of functional expression, low dystrophin levels) and Becker (BMD-mostly all from mother; reduced functional expression with normal dystrophin and altered protein), some carriers may show mild symptoms

167
Q

Muscular Dystrophy Presentation (DMD)

A

Growth delay in first year, cognitive impairment, Gowers sign (uses hands to get up), toe walking, calf hypertrophy, impaired respiratory function, scoliosis, dilated cardiomyopathy, incontinence
Elevated AST/ALT

168
Q

Muscular Dystrophy Presentation (BMD)

A

Growth delay and cognitive impairment uncommon
Live longer, less muscular and respiratory involvement
Cardiac involvement is prominent feature
Elevated AST/ALT

169
Q

Muscular Dystrophy Diagnosis

A

Serum creatine kinase levels (50-100x normal in DMD, 5x in BMD)
Genetic testing for Xp21 gene mutation
Muscle biopsy (absence of dystrophin in DMD, diminished quality/quantity in BMD)

170
Q

Muscular Dystrophy Treatment

A
Daily prednisone (deflazacort is alternative)
PT, sx for scoliosi/muscle contracture, ambulatory and ventilatory support, cardiac meds
171
Q

Amyotrophic Lateral Sclerosis (Lou Gehrigs)

A

Mixed upper/lower motor neuron disease
UMN: slowness, hyperreflexia, spasticity
LMN: weak, atrophy, fasciculation
Most common motor neuron disease, commonly in sporadic form

172
Q

ALS Presentation

A

Asymmetric limb weakness is most common (split hand syndrome), bulbar symptoms are second most common (dysarthria, dysphagia), spastic gait, tongue fasciculations, jaw clenching, may have cognitive and autonomic symptoms
Neuromuscular respiratory failure is most common cause of death

173
Q

ALS Diagnosis

A

El Escorial Criteria, EMG looking for degeneration or fasciculations, MRI of brain,, C and T spine
Really just ruling out other things

174
Q

El Escorial Criteria (ALS)

A

Evidence of LMN degeneration, evidence of UMN degeneration, progressive spread of symptoms or signs

175
Q

ALS Treatment

A

Riluzole-only impact on survival

Edaravone slows deterioration

176
Q

Restless Leg Syndrome

A

Unpleasant or uncomfortable urge tome legs during periods of inactivity, esp evenings
Primarily white women with uremia and low iron

177
Q

RLS Presentation

A

Sensation of crawling, tingling, restless, cramping, pulling, painful, electric
worsens with age, antihistamines, dopamine agonists and antidepressants

178
Q

RLS Diagnosis

A

Iron and BUN levels, review meds

Criteria: urge to move w/ uncomfortable sensation, worsened during inactivity, received by movement, worse in evening

179
Q

RLS Treatment

A

Dopaminergic agents (pramipexole, ropinerole)
Alpha-2-delta Ca channel ligands (gabapentin, pregabalin)
Benzos
Opioids (only if refractory)
Iron replacement

180
Q

Glascow Coma Scale

A

scale to assess mentation
15 is best score
<8 is comatose
3 is unresponsive/death

181
Q

Altered Mental Status

A

Subjective difficulty thinking clearly to abnormal thought and states of depressed consciousness
Can be medical, neurologic or psychiatric in origin

182
Q

Assessing Mental Status

A

Level of consciousness (response to stimuli; alert, clouded, confused, lethargic, obtunded, stupor, coma)
Orientation to envronment

183
Q

Delirium

A

Reduced ability to focus, reduced awareness, develops over short periods of time (hours-days) and fluctuates throughout the day; additional disturbance in cognition (memory, disorientation, language), not due to neurocognitive disorder or coma
Evidence that disturbance is direct consequence of another medical condition, intoxication/withdrawal, or toxin exposure

184
Q

Causes of delirium

A

Infection is #1 (UTI, pneumonia), medication, catheters, restraints, withdrawal, anemia, uncontrolled pain, electrolyte abnormalities, hypothyroidism

185
Q

Delirium Management

A

Prevention, stop causative drugs
Treat reversible contributors
Maintain behavioral control (sitter, avoid restraints)
Small doses of haloperidol if necessary-NO BENZOS
prevent complications

186
Q

Altered Mental Status Presentation

A

Confusion, agitation, combative, disoriented, delusions, hallucinations, sedation, personality chane

187
Q

Altered Mental Status Causes

A

Hypoglycemia, hypercalcemiasepsis, hypertensive encephalopathy
Drugs, electrolytes, metabolism, emotions, neuro/nutrition, trauma (CT), temperature (hyper/hypothermia), infection, alcohol

188
Q

Wernicke’s Encephalopathy

A

Thiamine deficiency causing medical emergency
Ophthalmoplegia, ataxia and confusion
Treat with thiamine and multivitamins (add Benzos if associated w. alcohol)

189
Q

Altered Mental Status Management

A
Address ABCs, Start interventions early, review meds, treat underlying cause (alcohol withdrawal with Benzos)
SNOT cocktail (sugar, naloxone/narcan, oxygen, thiamine)
190
Q

Dementia

A

Progressive intellectual decline, slow insidious onset, not reversible
4 types: alzheimers (most common), vascular, Lewy bodies, frontotemporal

191
Q

Alzheimers

A

Most common form of dementia
Diagnosis by autopsy or brain biopsy
Treated only symptomatically

192
Q

Dementia with Lewy Bodies

A

Progressive dementia caused by microscopic deposits that damage brain cells over time
present in plaques (deposits of beta-amyloid) or tangles (twisted fibers of tau protein)

193
Q

Vascular Dementia

A

Impaired blood flow to brain (often after stroke)
impairment more sudden than alzheimers
HTN, hyperlipidemia and smoking are risk factors

194
Q

Dementia Presentation

A

Establish time of onset, short-term memory loss, inattention, difficulty planning/organizing, agitations, aggression, depression, inappropriate laughing/crying (frontal)

195
Q

Dementia Diagnosis

A

Neuropsychological exam, Brain imaging-MRI, PET scan
Serum B12, TSH
ApoE gene testing to rule out Alzheimers

196
Q

Dementia Treatment

A

Aerobic exercise, mental stimulation (puzzles)
Memantine for Lewy bodies
Cholinesterase inhibitors for Alzheimers (donepezil for mild-mod, memantine for mod-severe)
SSRIs, Trazodone for insomnia
Avoid paroxetine bc of anticholinergic effect

197
Q

Creutzfield-Jakob disease

A

Most common cause of rapidly progressive dementia

PRNP gene

198
Q

Concussion

A

Complex pathophysiological process affecting brain induced by traumatic biomechanics forces AKA mild traumatic brain injury
Rapid onset of neurologic dysfunction with spontaneous recovery

199
Q

Concussion Presentation

A

+/- loss of consciousness, confusion, memory loss, visual disturbance (diplopia, light sensitivity), vertigo/impaired balance, headache

200
Q

Post-concussive Symptoms

A

Last more than a week, up to months

Chronic HA, short term memory difficulty, fatigue, difficulty sleeping, personality change, sensitive to light/noise

201
Q

Concussion Diagnosis

A

Clinical eval, Head CT (if GCS <15 hours from injury, sign of skull fracture, >65years, bleeding diathesis/anticoag use), sports protocols

202
Q

Concussion Treatment

A

Rest and acetaminophen, return to play after symptoms are gone and no meds required

203
Q

Which tumor is most common in children?

A

Low-grade astrocytoma (Wills tumor)

204
Q

Which tumor is most common in adults?

A

Glioblastoma

205
Q

Clinical manifestation of CNS Tumor

A

Headache, focal seizures, cognitive dysfunction, increased ICP (N/V, papilledema), focal signs/symptoms (weakness, sensory loss aphasia, visual spacial dysfunction)

206
Q

CNS Tumor Eval

A

Physical and Neuro exam
Brain MRI WITH contrast
Screen for systemic malignancy
Lumbar punture

207
Q

CNS Tumor Diagnosis

A

Tissue sample for histopathologic and molecular study

Functional MRI can be used, or frozen section

208
Q

Astrocytoma

A

Glial cells of brain and spinal cord; star shaped cells that help with maintenance, repair and transporting nutrients
Most common primary intra-axial brain tumor

209
Q

Grade 1/2 Astrocytoma

A

Most commonly present with seizures, more common in kids/young adults
Usually benign but can become malignant
Low degree of cellularity w/ preservation of normal brain tissue

210
Q

Grade 1/2 Astrocytoma Treatment

A

Surgical resection curative depending on location, radiation, chemo
Slow growing so best approach is to FOLLOW
Can treat symptoms with antiepileptic drugs

211
Q

Grade 3/4 Astrocytoma

A

Malignant gliomas
3-anaplastic, slower growing w/ slower onset of symptoms, mean diagnosis @30, prognosis 3-5 years
4- glioblastoma, mean diagnosis @64, prognosis 11-15 months

212
Q

Glioblastoma

A

Most common primary brain tumor and most deadly, can spread through CSF but rarely systemically

213
Q

Glioblastoma Treatment

A

Surgery not curative (bc of tentacles), can do resection or lobectomy
Radiation, chemo (temozolomide)

214
Q

Meningioma

A

Slow growing, extra-axial being tumor arising from arachnoid matter
Considered non-malignant, usually non-infiltrating, symptoms from pressure
Such slow onset seems like normal signs of aging

215
Q

Meningioma Diagnosis

A

MRI w/ contrast, surgical biopsy

216
Q

Meningioma Treatment

A

Complete surgical resection
Can observe w/ few symptoms, little swelling, no negative effect on life, older patients
Radiation but no chemo

217
Q

Stroke

A

Sudden focal neurological deficit or acute neurological impairments caused by interruption of blood flow to a specific region of the brain

218
Q

Ischemic Stroke

A

Blood clot causing interruption of blood flow

Commonly cardioembolic, atherosclerosis or lacunar infarction

219
Q

Hemorrhagic Stroke

A

Weakened vessel leaking blood causing reduced blood flow

50% mortality, 80% with permanent disability

220
Q

Risk Factors of Stroke

A

Hypertension, Afib, obesity, cardiac disease, smoking, diabetes
Age, gender, fam history, ethnicity, previous stroke

221
Q

What ethnicities have higher risk of stroke?

A

Black-double whites

Mexicans-higher, less likely to know symptoms

222
Q

Cincinnati Pre-hospital Stroke Scale

A

Facial droop, arm drift, abnormal speech (if all 3 present 100% sensitivity 88% specificity)

223
Q

Signs of Stroke

A

One-sided weakness/numbness.tingling, incoordination, sudden change in speech/language, acute confusion, loss of vision (esp one eye), double vision, sudden severe headache

224
Q

NIHSS Scale

A

Test to measure level of impairment caused by a stroke, and to determine whether its severe enough to warrant use of tPA (0-42; higher is more severe, 15-20 is mod-severe)

225
Q

Thrombotic Stroke

A

Atherosclerosis is the most common vascular obstruction leading to thrombosis

226
Q

Embolic Stroke

A

Left sided cardiac chambers and artery to artery stroke are most common sources of emboli
Smaller than thrombi=otic, many become hemorrhagic

227
Q

Acute Ischemic Stroke vs Transient Ischemic Attack

A

AIS: >24 hours, typically >1 hour, permanent damage
TIA: <24 hours, typically <1 hour, no permanent damage

228
Q

Transient Ischemic Attack

A

Transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia without acute infarction
High risk of stroke later in life

229
Q

Risk of Stroke after TIA

A

10% in first 90 days after TIA

1/4 to 1/2 that occur within the first 3 months are usually within the first 2 days

230
Q

ABCD2 Score

A

Determines whether a TIA patient needs to be hospitalized

Age, BP>140/90, symptoms, duration >/<60 minutes, diabetes

231
Q

Diagnostic Testing for TIA

A

Vessel imaging, cardiac eval, lab testing, MRI w/ DWI

Class 2: ECG, echo

232
Q

Penumbra

A

Zone of reversible ischemia around core of irreversible infarction, salvageable in first few hours after ischemic stroke onset
Damaged by hypo perfusion, hyperglycemia, fever, seizure

233
Q

Stroke/BP Relationship

A

Arterial occlusion increases BP, high BP is not a cause of stroke so we don’t want to lower it-worsens outcome of penumbra and can cause hemorrhage (red infarcts)
If BP>200 you can lower it, want it below 185 but >120

234
Q

Tissue Plasminogen Activator

A

Must be given within 3-4.5 hours from last known normal before stroke but LOTS of contraindications

235
Q

Predictors of hemorrhagic transformation

A

size of infarction, afib, NIHSS, hyperglycemia, thrombocytopenia

236
Q

Arteriovenous Malformations

A

Directly divert blood from artery to vein, may bypass brain tissue ad cause chronic ischemia, can increase risk of rupture

237
Q

Hemorrhagic Stroke Symptoms

A

Diastolic BP>110, headache, vomiting, coma, neck stiffness, seizures

238
Q

Common CNS Herniations

A

Subfalcine-common, HA contralateral leg weakness
Transtentorial-oculomotor paresis (dilated pupil, EOMs), contralateral hemiparesis
Tonsillar-obtundation/comatose

239
Q

Brain herniation

A

Life threatening, causes by increased intracranial pressure

Cushing reflex: HTN, bradycardia, abnormal respirations

240
Q

Treatment of Cerebral Aneurysm

A

Endovascular (coil embolization-nickel and titanium), surgical (clip)

241
Q

Subarachnoid Hemorrhage Presentation

A

Sudden increase in ICP, associated with valsalva

242
Q

Cause of subarachnoid hemorrhage/Diagnosis

A

aneurysm in circle of willis, familial causes

Diagnose w/ CT without contrast, LP-xanthochromia (golden yellow blood in CSF)

243
Q

Treatment of Subarachnoid Hemorrhage

A

Decrease ICP with stool softeners, cough suppressant, anxiolytics, analgesics, antiemetics
Treat/monitor vasospasm

244
Q

Subdural Hematoma

A

Blood in skull outside of brain, crescent shaped, CT to distinguish

245
Q

Epidural Hematoma

A

round hematoma

246
Q

Stroke Management Supportive Care

A

Prevent complications: aspiration, DVT, UTI, constipation (use docusate), decubitus ulcers, UGI blee (use PPI/H2B, fever)

247
Q

Post Stroke Depression

A

Often resolves in one year

SSRIs, but if patient takes warfare use escitalopram, citalopram or sertraline

248
Q

Secondary Stroke Prevention Procedures

A
Carotid endarterectomy (CEA) if 70-99% stenosis
Carotid angioplasty/stent only in high risk (re-stenosis, radiation induced stenosis, high risk for CEA, contralateral carotid occlusion
249
Q

Carotid Revascularization

A

Men, older pts, recent cerebral ischemia and ulcerated plaque benefit from CEA the most
CEA has lower risk of periprocedural stroke/death, less risk ofrestenosis but stunting has lower risk of cranial nerve injury, MI

250
Q

Stroke Management Meds

A

Every pt gets a statin
antithrombotic agent based on cause
AVOID estrogen, sympathomimetics, NSAIDs, PPI

251
Q

Epilepsy

A

2 or more unprovoked seizures >24 hours apart, 1 seizure w/ risk of recurrent seizures, tendency to unprovoked seizures not caused by any unknown medical condition
Most common <1 or >65

252
Q

Epilepsy Treatment

A

Most people respond to first drug but 30-40% are unresponsive to meds (tried at least 2 meds)
Start low go slow, only one drug at a time (try not to do combos)

253
Q

What is the most common cause of death in epilepsy?

A

Sudden unexpected death

254
Q

Seizure

A

Sudden urge of abnormal electrical discharges from complex chemical changes in brain cells

255
Q

Temporal Lobe Epilepsy

A

Most common focal epilepsy, good outcome with surgery

Chewing, licking/smacking lips

256
Q

Frontal Lobe Epilepsy

A

Often mistaken for psychiatric conditions, less favorable outcome, only some good for surgery
Bicycle kicking

257
Q

Juvenile Myoclonic Epilepsy

A

lifelong, genetic basis, choice of drugs is critical

258
Q

Lennox-Gastaut Syndrome

A

drug resistant seizures, progressive cognitive/behavioral decline

259
Q

Epilepsy Diagnostics

A

Labs (tox screen, low glucose, low sodium, rule out infection), EEG (evaluate risk of future seizure), Imaging (MRI w/ cuts through temporal lobe
Gold standard is video EEG

260
Q

Common Causes of epilepsy

A

Genetics, structural (stroke, head trauma, tumor), metabolic (glucose, sodium), infection (encephalitis, abscess), most are unknown

261
Q

Comorbidities of epilepsy

A

Mood disorders (depression/anxiety, short term memory loss)

262
Q

When to treat with ONE seizure?

A

Abnormal EEG, significant brain abnormality on imaging, nocturnal seizures, older age, social factors (driving, job)

263
Q

What is the worst thing to do for seizures?

A

Sleep deprivation, need at least 8 hours

264
Q

What epilepsy drugs are not okay in pregnancy?

A

Valprioc acid, phenobarbital, topiramate

265
Q

What epilepsy drugs can be used in pregnancy?

A

Lamotrigine and levetiracetam?

266
Q

When can you stop epilepsy meds?

A

Seizure free for 2+ years with normal neurons exam and EEG

“cured” if off drugs for 5 years and seizure free for 10

267
Q

Status Epilepticus

A

Continuous seizures for >5 minutes without return to baseline
EMERGENT must get to hospital or rescue med (diazepam)
biggest risk is hypoxia

268
Q

Status epilepticus Treatment

A

Benzos in first 30 mins, IV AED 30-120 mins, general anesthesia >120 mins