9/16 Consciousness - Rasin Flashcards
components of consciousness
1. content of consciousness: substrate, content
- contribution from all systems (sensory, motor, limbic, etc)
2. level of consciousness
- three distinct but related processes (3xA)
- alertness
- attention
- awareness
levels of consciousness
- conscious
- confused
- delirious
- somnolent
- obtunded
- stuporous
- coma
- conscious: normal attn/wakefulness
- confused: disoriented, slow thinking/response
- delirious: disoriented, restless, marked attn def
- somnolent: sleepy, excessive drowsiness
- obtunded: decr alertness, slowed psychomotor responses
- stuporous: deep sleep, no spont activity, respond by grimace/withdrawal
- coma: unarousable, no resp to stim
disorders of consciousness
main diff b/w brain death and coma?
main diff between coma and veg state?
destruction of localized brain regions manifest as diff disorders of consciousness
- brain death : spinal cord functioning, but brain is not
- coma : severely depressed fx of cerebrum
- locked in syndrome : ventral pons depressed fx
brain death vs. coma
- no brainstem reflexes in brain death
- yes brianstem reflexes in coma
coma vs vegetative state
- diencephalon/upper_brainstem → behavioral/arousal/sleep-wake cycles
- no in coma
- yes in veg state
- (brainstem reflexes intact in both)
abnormal posturing
present in severe lesions
-
decorticate: upper midbrain damage
* brainstem motor centers working BUT no modulation from CST -
decerebrate: upper pontine damage
* no CST, no rubrospinal tract - flaccid: no CST, no rubrospinal tract, no vestibulospinal tract, no reticulospinal tract
progression from decorticate → decerebrate posture can indicate progressive damage!
- can affect medulla and resp arrest rapidly
metabolic encephalopathy
- pt tries to brush examiner away
- asymmetric motor response
- Babinski reflex
coma
definition
potentially dysfx systems
first systems to examin
unarousable unresponsiveness in which patient lies with eyes closed
- min duration: 1 hr
- NOT permanent! within 2-4wk, patients either deteriorate or recover
caused by dysfx of…
- ascending reticular activating system (ARAS)
- bilat regions of cerebral cortex
- bilat lesions of thalamus (medial)
first systems to examine: cardiovasc, respiratory
respiratory system response to injuries to…
- forebrain
- upper brainstem
- medulla
diffuse forebrain impairment without brainstem injury
- waxing/waning depth of resp with interposed apneas: Cheyne-Stokes respiration
- “fast breating, slow breathing, no breathing”
- lesion in upper brainstem*
- fast breathing
- lesion in medulla*
- respiratory arrest/apnea
pupillary effects of coma
next thing to check after resp/CV: pupils!
pontine lesion
- pinpoint pupils, but responsive to light bilat
- PSNS fx and oculomotor nuclei in midbrain are preserved
midbrain lesion/transtentorial herniation
- unilateral or bilateral “blown” pupil
metabolic coma
what is it?
effect on pupils?
coma caused by sedative drugs (NOT opioids)
- small reactive pupils
metabolic encephalopathy
vs
midbrain lesion (bilat)
- head turning results
- cold water test results
metabolic encephalopathy (brain stem intact)
- turn head → eyes move contralat
- cool water in ear → eyes move toward water
midbrain lesion
- turn head → eyes move contralat
- cool water in ear → ipsi eye moves toward water
- abducens nucleus intact!
- oculomotor (medial rectus m.) is not intact
*
neuro exam of unconscious patient
- locomotion assessment
- resp pattern
- examine eyes
- brainstem reflexes
- motor/sensory responses
brain death
extreme, irreversible form of coma
- NO evidence of forebrain/brainstem fx
- NO brainstem reflexes
- might have spinal cord reflexes
- ex. Lazarus reflex
- EEG shows electrocerebral activity
- cerebral perfusion and metabolism minimal
- angiogram shows no blood flow
- “empty bucket” metabolism
tests:
- caloric test + apnea test (brainstem fx)
- at least 2 sep brain death exams within an hour to confirm
- posturing reflexes? criteria not met!
vegetative state
follows coma or certain end-stage dementias, neurodegen, congenital disorders
- regains sleep/wake cycle
- regains primitive responses/reflexes
- remains unconscious
however…
- open eyes & are arousable by stimuli
- might turn eyes/head toward auditory/tactile stimuli
- might produce unintelligible sound and move limbs → not meaningful
implication/evidence: v low basic metabolic fx maintained
persistent vegetative state: > 1 month
minimally conscious state
appearance of visual tracking (one of earliest signs of recovery from veg state)
- minimal/variable degree of responsiveness
- follow simple commands
- say single words
- reach for/hold objects
- no reliable interactive verbal/nonverbal comm
- no reliable fx use of objects
locked-in syndrome
what is it?
classic vs. partial vs. total
why cant they move?
where is the lesion?
can be mistaken for coma, but consciousness is preserved!
- all voluntary muscles except controlling eye movements are PARALYZED
- may be able to communicate through vertical eye movements, eye blinks
no tx or cure
classic (quadriplegia w consciousness/eye movement) vs. partial (classic plus weak hand/arm/facial movements) vs. total (total immobility, inability to comm)
why can’t they move?
- lesion in brainstem motor pathways controlling face, trunk, limbs
- peripheral neuromuscular blockade
where is the lesion?
- lesion of ventral brainstem (motor pathways) at or below trigeminal nerve level
- most freq due to ischemic pontine lesion → stroke of basilar artery
- also poss: traumatic brain injury, demyelinating disease, brain hemorrhage
projection systems
neurotransmitters involved
reticular system has widespread diffuse projections that innervate many structures/whole nervous system
upper brainstem → forebrain
lower brainstem → brainstem, cerebellum, spinal cord
neurotransmitters: HANDS (monoamines)
- Ach
- dopamine
- norepinephrine
- serotonine
- histamine
lesions that block nt systems → confusion/drowsiness (not coma!)
- effect of many psych disorders (dysfx diffuse proj nts)
- target of many psychoactive drugs (diffuse proj)
hemispheric asymmetry
R hemisphere more important for attn mechanisms in most individs
- lesions to R hemisphere → prominent, long-lasting deficits in attn to L side
- lesions to L hemisphere → minimal R neglect
- bilat lesions → severe R neglect
causes: infarct, hemorrhage, seizures, head trauma, tumors affecting parietal/frontal cortex
