COMA AND CONSCIOUSNESS
DEFINITIONS
Confusion
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Patient is alert but disoriented
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Drowsiness/lethargy
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Patient is no longer alert but is sleepy
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Stupor
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Patient does not respond to verbal stimulus but does respond to pain
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Coma
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Patient no longer responds to pain
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Characteristics of different conditions:
Condition
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Self awareness
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Sleep-wake cycles
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Experience of suffering
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Prognosis
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Comments
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Persistant veg. state
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-
|
+
|
-
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Depends
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Brainstem autonomics are still intact
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Coma
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-
|
-
|
-
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Recovery, PVS, or death in 2-4 wks.
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Brainstem may or may not be affected
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Brain death
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-
|
-
|
-
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No recovery
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No brainstem
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Locked-in synd.
|
+
|
+
|
+
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Unlikely recovery, Possible persistant quadraplesia
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Awake, alert, completely paralyzed except vertical eye movements. Destroyed corticospinal/corticopontine tracts
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Akinetic mutism
|
+
|
+
|
+
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Unlikely reovery
|
|
Anoxic coma – factors associated with unfavorable prognosis
Clinical parameters
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Unfavorable prognosis
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Duration of anoxia
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More than 8 mins
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Duration of CPR
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More than 30 mins
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Pupillary light rxn.
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- on day 3
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Motor response to pain
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- on day 3
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Brainstem reflexes
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-
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Blood glucose on adm.
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More than 300
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3 day glascow score
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More than 5
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Coma type
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Cause
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Symptoms
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Focal structural
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Primary: vascular, trauma,tumor, infection, inflammation
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SUBTENTORIAL: abrubt or eveolving LOC, brainstem dysfunction, which is bilateral but not nec. Symmetric or complete, papillary and occulomotor abnormalities
SUPRATENTORIAL: hemiparesis, hemisensory, hemianopia, focal cognitive defects, aphasia; lethargy or stupor w/o brainstem signs; gradual LOC; LOC more prominent than confusion; 3rd nerve palsy precedes coma, rostral-to-caudal brainstem deterioration.
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Diffuse
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Global ischemia, hypoxia, deficiency disease, hepatic encephalopathy, uremic encephalopathy, toxins
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Partial, bilateral dysfunction at many levels; not nec. Uniform or symmetric, gradual onset following an acute confusional state; papillary light reflex preserved; asterixis, myoclonus, paratonic resistance.
Intention myoclonus = Lance-Adams syndrome
|
UNCAL SYNDROME – caused by herniation of medial temporal lobe into tentorial opening
Early changes –
1. Respiration – becomes irregular
2. Pupils – dilated ipsilateral pupil – get consensual but not direct response to light. Both pupils dilate in response to noxious stimulus on neck (mediated through medulla)
3. Oculocephalics – intact, but ipsi eye won’t cross midline (MR innervated by III)
4. Calorics – stronger stimulus, may overcome MR weakness
5. Pain response – ipsi movement, contra paralysis
6. Plantar reflex – babinski sign present contralaterally.
Late changes –
1. Respiration – cheyne-stokes or central neurogenic hyperventilation
2. Pupils – further dilation of ipsi pupil
3. Pain response – non-purposeful movement on ipsi side, decerberate on contra.
PUPILS IN COMA
Large, fixed
|
Midbrain lesion (tectum) destroying 3rd nerve complex
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Mid-position, fixed
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Midbrain – affecting both 3rd nerve and sympathetics
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Horner’s syndrome
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Sympathetic pathway – anywhere from hypothal to orbit (brainstem, SCG, along carotid artery)
|
Pinpoint
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Pons
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Unilateral horners
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Wallenberg’s – lateral medullary plate lesion
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Unilateral dilated
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Uncal hemorrhage
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Respiratory patterns with brainstem lesions:
SLEEP
Neurophysiology
Brainstem
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Ascending cortical activation, REM/SWS switch
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SCN
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Circadian clock
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Hypothalamus
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Sleep/wake switch
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Thalamus
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Cortical activation, sleep spindle, EEG synchronization
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Stages of Sleep
NREM
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Stages 1-4
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Body’s rest and metabolic restoration
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REM
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Phasic eye movements, loss of muscle tone, EEG neutral
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Active state – functions in learning and memory
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NARCOLEPSY
-
Excessive sleepiness, often associated with cataplexy and other REM sleep phenomena (sleep paralysis, hypnagogic/pompic hallucinations) and fragmented sleep
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Prevalence = 1/2000, equal in men and women
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Can present at any age, but most commonly between 15-30. 6% younger than 10 yrs old.
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Burden: ↓ performance, ↑ interpersonal difficulty, ↓ social interaction, ↑ accidents/injury, ↑ depression, ↓ self esteem
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Genetics
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Mostly sporadic
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Familial forms have been ID’d, but environment plays huge role
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1-2% chance in 1st degree relative
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17-36% chance in monozygotic twins
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HLA-DQB1*0602 association
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Present in 25% of population, 40% of narcoleptics w/o cataplexy, 90% of narcoleptics w/ cataplexy
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Neurochemical abnormalities
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Excessive daytime sleepiness due to ↑ dopaminergic transmission
-
Chronic pervasive fatigue; sleep attacks, accidental naps; automatic behavior
-
Occurs in 100% of narcoleptics
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Cataplexy due to ↓monoaminergic tone (dopaminergic or adrenergic) and ↑ cholinergic hypersensitivity
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REM-related phenomenon
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Sudden hypotonia/atonia of voluntary muscles, triggered by emotions
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Usually less than 2 minutes – ranges from fleeting weakness to complete paralysis
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Medically stable, with consciousness and ocular movement preserved
-
Pathognomonic of narcolepsy
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Hypocretin = orexins
-
Hypothalamic peptides which project widely in CNS; important fx in arousal, locomotion, metabolism, ↑BP/HR
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In narcolepsy – decreased or absent levels in CSF with marked reduction of hypocretin-containing neurons
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CSF levels may have diagnostic role in future
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Assesment of sleepiness
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Epsworth Sleepiness Scale – subjective
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Multiple Sleep Latency Test – measures minutes to sleep onset and to REM onset.
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Increased sleep latency = increased alertness, decreased latency = increased sleepiness
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Sleep deprivation reduces sleep latency
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Diagnostic criteria:
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1. EDS or sudden muscle weakness
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2. recurrent daytime sleepiness for at least 3 months
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3. cataplexy
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4. Associated features (sleep paralysis, hypnagogic hallucinations, automatic behavior, disrupted sleep)
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5. Polysomnography findings: Sleep latency ≤ 10 min, REM latency≤ 20 mins, MSLT: mean sleep latency ≤ 5 min
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6. Medical, psychiatric and other sleep disorders are not primary causes of symptoms
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Need 2+3 OR 1+4+5+6
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Management:
-
structured naps,
-
antidepressants for cataplexy (TCAs and SSRIs)
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amphetamines, methylphenidate, pemoline to stimulate dopamine systems
-
Modafinil – activates hypothalamic regions, does not act through dopaminergic system but may inhibit GABA release
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