Sleep, Headache, TBI Flashcards
Non-REM (N1-3) and REM (R) stages of sleep
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
Process S and C
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
Phase Response Curves
- one for each zeitgeber
- depicts how the body responds in terms of sleepiness/wakefulness
Locus coeruleus
part of the RAS that makes NE for wake and non-REM
Dorsal raphe nuclei
part of the RAS that makes Serotonin for wake and non-REM
Tubomamillary nucleus
part of the RAS that makes histamine (blocked → drowsiness)
Suprachiasmatic nucleus
part of hypothalamus that senses light and inhibits release of melatonin
Lateral hypothalamus
part of hypothalamus that makes orexin, stabilizer of wakefulness
Preoptic area
part of hypothalamus–ventrolateral and medial preoptic nuclei–that releases GABA/Galanin to cortex to promote sleep
Pineal gland
- releases melatonin (tells you to sleep)
- inhibited by light via signals from SCN
“REM-on” cells
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.
Epworth Sleepiness Scale (ESS)
assesses likelihood of falling asleep in different scenarios; score >10 (of possible 24) is pathologic
Insomnia
- defined as difficulty falling or staying asleep with daytime consequences; at least 3x/week
- considered Chronic if >3mo; short-term if
Pathophysiology and complications of Obstructive Sleep Apnea (OSA)
- 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
What about OSA results in the damage and daytime symptoms?
- sleep fragmentation → daytime drowsiness, fatigue
2. periods of hypoxemia/hypercapnia → oxidative stress, endothelial dysfunction, SNS surges, metabolic dysfunction
Difference between:
- Central sleep apnea
- Cheynes stokes breathing
- Hypoventilation
- 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
Narcolepsy is due to?
- 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
Treatment of Narcolepsy
- 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
What is a Circadian Rhythm disorder?
symptomatic misalignment between desired sleep/wake cycle and the intrinsic sleep/wake cycle
Parasomnias - REM and non-REM
- 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
Categories of Headache
- Primary (no underlying structural cause; most are subacute) vs. Secondary (underlying structural cause)
- Acute onset vs. Subacute onset
Pathophysiology underlying all types of headaches
- 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
Red flags for possible secondary etiology of bad headache
- 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”
Migraine - clinical features
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)
