Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

OS9.2 - Neuro > Sleep, Headache, TBI > Flashcards

Sleep, Headache, TBI Flashcards

1
Q

Non-REM (N1-3) and REM (R) stages of sleep

A

5% - N1 = lightest sleep, waves slow down from wakefulness (theta waves)
50% - N2 = K complexes and sleep spindles
20% - N3 = “deep” sleep with delta waves (slow freq; large amp)
15% - R (REM) = mixed frequency, lots of eye movement, sawtooth waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Process S and C

A

Process S – the sleep drive that increases the longer you’re awake
Process C – circadian alerting signal governed by light; wanes with darkness and increases with light

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Phase Response Curves

A
  • one for each zeitgeber

- depicts how the body responds in terms of sleepiness/wakefulness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Locus coeruleus

A

part of the RAS that makes NE for wake and non-REM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Dorsal raphe nuclei

A

part of the RAS that makes Serotonin for wake and non-REM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Tubomamillary nucleus

A

part of the RAS that makes histamine (blocked → drowsiness)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Suprachiasmatic nucleus

A

part of hypothalamus that senses light and inhibits release of melatonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Lateral hypothalamus

A

part of hypothalamus that makes orexin, stabilizer of wakefulness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Preoptic area

A

part of hypothalamus–ventrolateral and medial preoptic nuclei–that releases GABA/Galanin to cortex to promote sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pineal gland

A
  • releases melatonin (tells you to sleep)

- inhibited by light via signals from SCN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

“REM-on” cells

A

They are in the Cholinergic Pedunculopointine and Lateral dorsal tegmentum.
They release ACh, which inhibits release of 5-HT and NE, and stimulates release of glycine for spinal paralysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Epworth Sleepiness Scale (ESS)

A

assesses likelihood of falling asleep in different scenarios; score >10 (of possible 24) is pathologic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Insomnia

A
  • defined as difficulty falling or staying asleep with daytime consequences; at least 3x/week
  • considered Chronic if >3mo; short-term if
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pathophysiology and complications of Obstructive Sleep Apnea (OSA)

A
  • Small airway, loses extra opening power when asleep, body becomes hypoxic, causes increased respiratory effort and arousal, airway opened, hyperventilation to correct
  • Leads to increased rates of HTN, MI, CHF, stroke, development of a-fib, and all-cause mortality; thought to also contribute to sudden cardiac death
  • Daytime symptoms include depression, fatigue, pain, irritability, HA, lower QOL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What about OSA results in the damage and daytime symptoms?

A
  1. sleep fragmentation → daytime drowsiness, fatigue

2. periods of hypoxemia/hypercapnia → oxidative stress, endothelial dysfunction, SNS surges, metabolic dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Difference between:

  • Central sleep apnea
  • Cheynes stokes breathing
  • Hypoventilation
A
  • CSA = absence of airflow because of no respiratory effort (uncommon to be clinically significant)
  • Cheynes stokes = pattern of waxing/waning respiratory effort and airflow
  • Hypoventilation = just shallow breaths, then a deep breath every few minutes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Narcolepsy is due to?

A
  • hypocretin-1 deficiency
    (seen in CSF sample)
    + there’s a high association with HLA subtypes DR2/DRB1 and DQB1 – but this is not very specific
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Treatment of Narcolepsy

A
  • tx aimed at consolidating and improving overnight sleep, strategic napping, alertness meds
  • First line meds = modafinil and armodafinil
  • 2nd line meds = traditional stimulants
  • the only approved tx for cataplexy and excessive daytime sleepiness is sodium oxybate
19
Q

What is a Circadian Rhythm disorder?

A

symptomatic misalignment between desired sleep/wake cycle and the intrinsic sleep/wake cycle

20
Q

Parasomnias - REM and non-REM

A
  • defined as dissociated state of consciousness (somewhere between sleep and wake)
  • REM = loss of atonia during dreams so they act them out
  • Non-REM = it’s like the inhibition from the frontal cortex is turned off during sleep and the actions revert to instinctual aggressive, locomotive, feeding, and sexual behaviors
21
Q

Categories of Headache

A
  1. Primary (no underlying structural cause; most are subacute) vs. Secondary (underlying structural cause)
  2. Acute onset vs. Subacute onset
22
Q

Pathophysiology underlying all types of headaches

A
  • inflammation or traction of pain nerves
  • this includes:
    • dura/meninges at base of brain
    • med-large arteries at base of brain
    • venous sinuses
    • scalp/cervical muscles
    • periosteum of skull
    • facial/head structures
  • also: stimulation of the nucleus of V or thalamus will trigger a pain response
  • majority of pain is carried through CN 5, 9 and C2/C3; CN7/10 contribute some
  • posterior fossa innervated by C2/C3 and CN 9/10
23
Q

Red flags for possible secondary etiology of bad headache

A
  • abrupt onset (most primary headaches are subacute onset)
  • recent head trauma
  • fever, immunosuppression, AMS, focal deficit
  • new onset above age 50
  • neck pain/stiffness, anti-coag use, progression over days
  • “worst headache of my life”
24
Q

Migraine - clinical features

A

chronic neuro disorder causing recurrent HA with some or all features:
• unilateral; may switch sides or be bilateral
• pulsating, mod-severe intensity
• lasts 4-72hrs
• N, +/-V, photo/phonophobia
• may have prodromal phase (40%) and then aura (20%)
• triggers; family hx (polygenic or Familial hemiplegic migraine)

25
Q

Aura - clinical features

A
  • only 20% of migrainers experience
  • caused by a wave of cortical depression and HA usually occurs w/in 60min (but can also occur and then not get a HA) which stimulates neurogenic inflammation, which excites the hypersensitive periph/central pain pathways
  • usually visual disturbances but of course can be anything that ends up being affected by the wave (limb weakness, aphasia, etc.)
  • scotoma: absence of vision
  • fortification spectra: zigzag lines in periphery
26
Q

Anatomical substrate for migraine

A

Trigeminovascular system:

  • V1 innervates the dura, meninges, med/large cerebral arteries, and veins
  • comes into synapse in the trigeminal nucleus caudalis (then to the trigeminothalamic tract which projects to VPM)
  • there are also projections from ST5 to superior salivatory nucleus which then projects to blood vessels; mediates vasodilation
27
Q

Migraine - Pathogenesis

A

incompletely understood, but comprises:

  1. trigger (maybe)
  2. central generator (brainstem) can cause an aura or go straight to neurogenic inflammation (trigeminovascular)
  3. together with peripheral and central sensitization, there’s central pain (migraine)
28
Q

Aura - Pathogenesis

A
  • wave of depolarization, not following neuronal circuits, travels across the cortex
  • this depolarization means that the tissue is non-functional, thus the net effect is depression of this area of cortex and the malfunction that produces sx of aura
  • likely mediated by syncytium of glial that get depolarized and then the neighboring neurons are also depolarized
29
Q

CGRP and Substance P in the pathogenesis of migraine

A
  1. when trigeminal ganglion cells are activated by CSD/central generator, they have efferent function to release CGRP/SP onto dural/ meningeal vessels, which they VD
  2. CGRP relaxes vessel smooth muscle and degranulates mast cells (local inflammation)
    * triptans block release of CGRP (by being agonists at 5-HT1 receptors); working on CGRP antagonists called Gepants
  3. this process hypersensitizes the nerve terminal; inc. firing back via CN5 which causes central sensitization (self-propagating)
30
Q

Cluster HA - Clinical features

A

chronic neurologic disorder causing recurrent HA with some/all features:

  • pain is always unilateral, frontal, retro-orbital
  • unilateral: conjunctival injection, rhinorrhea, Horner’s, lacrimation
  • constant, severe, non-pulsating, “hot poker”, lasts minutes to 3hrs; daily attacks for weeks/mo, remission for yrs
  • M:F = 4:1
  • triggers - EtOH, tobacco; rare fam hx
  • this makes the patient restless (unlike migraine which seeks quiet dark room)
31
Q

Cluster HA - treatment

A
  • nasal O2 acts on PSNS to inhibit the trigeminovascular activation
  • SQ sumitriptan
  • Prophylaxis = CaChB, lithium, valproate, and prednisone
32
Q

Episodic/Chronic Tension HA - Clinical features

A

chronic neurologic disorder causing recurrent HA with some/all features:

  • pain usually bilateral and bandlike
  • not associated with auras, N/V, photo/phonophobia
  • lasts minutes to 3hr
  • usually awakens without HA
  • Episodic = 15d/mo
33
Q

Idiopathic Intracranial HTN

A
  • patient (fat woman – M:F=9:1) presents with HA, papilledema, +/- visual sx
  • a neurologic emergency b/c permanent vision loss
  • cardinal sign = papilledema (inc. ICP) usually bilateral; loss of peripheral vision first and then blindness within hrs/days
  • categories:
    • primary idiopathic
    • primary sx - from underlying metabolic issues that changes CSF prod/reabs
    • secondary - to something blocking CSF circ/reabs (same as communicating hydro)
  • dx: normal MRI/MRV plus LP opening pressure of >250mmH2O
  • tx: weight loss, acetazolamide/furosemide, maybe shunt or venous stent
34
Q

Temporal arteritis

A
  • caused by AI systemic vasculitis causing granulomatous infiltration of med/small elastic extracranial arteries
  • presents as unilateral HA, scalp tenderness over temporal artery, monocular obscurations, jaw claudication
  • ESR/CRP elevated, do color duplex US of temporal artery
35
Q

What’s a concussion?

A

a mild TBI that results in an alteration of consciousness that lasts less than 24hr

36
Q

What makes a moderate and severe TBI?

A
  • moderate: AOC longer than 24hr; LOC more than 30min and less than 24hrs; PTA 1-6d
  • severe: LOC longer than 24hr; PTA 7d or more
37
Q

Skull fracture

A
  • implies high degree of force
  • depressed - often tears underlying dural tissue, lacerates or compresses brain tissue
  • any fracture may injure bridging veins, which causes SDH
  • occipital and basilar bones are thickest and harder to break; petrous (overlying the MMA) is weakest
38
Q

3 Mechanisms of Brain Injury

A
  1. Coup-ContreCoup - hit front skull then back skull
  2. Diffuse Axonal Damage - shear forces from acceleration/deceleration rips axons, causes swelling
  3. Gunshot wound - laceration plus shock waves with cavitation (temporary stretching)
39
Q

Post-Concussive symptoms

A

Emotional: irritability, mood lability; anxiety, depression; more likely to develop PTSD and depression

Physical: HA, dizzy, balance; N/V, fatigue, vision, photo/phonophobia, tinnitus, sleep probs

Cognitive: concentration and short-term memory problems; problems with processing, attention, word-finding, abstract thinking

40
Q

Concussion recovery and recurrence

A
  • typical 7-10d
  • small portion may have persistent sx for 6-12mo
  • faster recovery in those who come seek treatment earlier
  • having a concussion inc. risk of repeat concussion, and more than 3 concussions inc. severity of next concussion(s)
41
Q

Second impact syndrome

A
  • when the concussion hasn’t recovered all the way and they go back to playing and get hit again
  • this results in a loss of autoregulation which leads to brain swelling, increased ICP, and herniation in 2-5min
  • it’s rare, but RF include M age 17-24 and prior concussion w/in past 4d
42
Q

CTE

A

“Chronic Traumatic Encephalopathy”

  • chronic traumatic injuries result in accumulation of tau proteins
  • kills cells in mood, emotional, end executive regions
43
Q

Concussion treatment

A
  • rest, education about recovery expectations
  • psych testing
  • NSAIDs for HA; avoid narcotics
  • sleep is okay

OS9.2 - Neuro (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions