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Evaluation of Patients in Coma
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Definitions
Coma: “Unarousable unresponsiveness in which the subjects lie with eyes closed”
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Consciousness
Two components of conscious behavior content- the sum of cognitive and
affective function arousal- appearance of wakefulness
Content depends on arousal but normal arousal does not guarantee normal content
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Really Simple Neuroanatomy
Arousal: where is it localized? Ascending Reticular Activating System
(ARAS) ‘core of the brainstem’ receives input from numerous somatic
afferents projects to midline thalamic nuclei
(which are in a circuit with cortical structures) and the limbic system
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ARAS
ARAS acts as a gating system, increasing or decreasing thalamic inhibitory influence on the cortex alters effect of sensory stimuli
ascending alters descending cortical stimulation
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Demands of Arousal
Function of ARAS-Thalamic-Cortical system depends on: anatomic integrity of structures metabolic integrity (circulatory
integrity) communicative integrity
(neurotransmitter function)
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Coma Fact Number One
Coma implies dysfunction of: ARAS or Both hemi-cortices
Anatomically, this means central brainstem structures (bilaterally)
from caudal medulla to rostral midbrain both hemispheres
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Clues from History
Onset of symptoms sudden onset fluctuations
Associated neurologic symptomsMedications
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Breathing
Abnormalities of respiration can help localize but almost always in the context of other signs Central-reflex Hyperpnea (midbrain-
hypothalamus) Apneustic, cluster, Ataxic (Lower pons) Loss of automatic breathing (medulla)
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Cranial Nerve Exam
Systematic assessment of brainstem function via reflexes
Cranial Nerve Exam Pupillary light response (CN 2-3) Occulocephalic/calorics (CN 3,4,6,8) Corneal reflex (CN 5,7) Gag refelx (CN 9,10)
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.Pupillary Light Responses
Afferent Limb: Optic NerveEfferent Limb: Parasympathetics via
occulomotorMidbrain integrity/ tectumUncal Herniation (3rd nerve
dysfunction)Pupillary resistance to insult
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Pupillary Light Responses
Be aware of drug effects Systemic and Local
Avoid ‘PERLA’ State size, before and after light
stimulation Specify right and left
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Pupils: Localizing Value
Pons-pinpoint pupils Symp. Dysfinction plus parasymp.irritation
Midbrain-Large fixed pupils unresponsive to light, hippus
Horner’s- symp.dysfunctionUnilateral dilation- parasymp.
Dysfunction usually due to 3rd nerve lesion
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Ciliospinal Reflex
1-2 mm pupillary dilatation evoked by noxious cutaneous stimulation
More prominent in sleep or coma than during wakefulness
Test integrity of symp.pathways in comatose patients
Not particularly useful in evaluating brainstem function
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Corneal Reflex
Afferent: Trigeminal NerveEfferent: Third Nerve (Bell’s
Phenomenon and Facial Nerve (Eye closure)Tests dorsal midbrain (Bell’s) and
pontine integrity (Eye closure)
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Eye Movements
Before maneuvers attempted note resting position Midline
Deviation suggests frontal/pontine damage
ConjugateDysconjugance suggests CN abn.
MovingRoving, dipping, bobbing
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Occulocephalic/ Calorics
Same reflex elicited differentlyAfferent: Eighth nerveEfferent: 3,4,6 via MLF and PPRFOcculocephalics may also involve
proprioceptive afferents from the neck
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Occulcephalic Reflex
Brisk rotation of head with eyes held open
Watch for contraversive movementsNext:
Flexion: eyes deviate up and eyelids open (doll’s head phenomenon)
Extension:eyes deviate downward
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Caloric reflex
Ensure TM integrityElevation of head to 30 degrees (so that
lateral semicircular canal is vertical)Instillation of up to 120 ml of ice water
Awake: deviation toward,nystagmus away Comatose: deviation toward
Wait 5 minutes, do other ear
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Calorics
Watch for conjugance of deviationTo test vertical eye movements
Both ears, cold water-downward gaze Both ears, warm water-upward gaze
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Gag Reflex
Afferent: GlossopharyngealEfferent: VagusTaken in context of other findings
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Motor Exam
Assess tone, presence of asterixisResponse to painful stimuli
none abnormal flexor abnormal extensor normal localization/withdrawal
Avoid use of decerebrate/ decorticate
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Reflexes
BrainstemDeep tendon
Biceps, brachioradialis, triceps Patellar, Achilles Plantar Responses
Superficial skin Abdominal, cresmasteric
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Uncal herniaiton
Expanding lesions in lateral middle fossa
Compression of hippocampal gyrus over free edge of tentorium
Three stages described Early third nerve Late third nerve Midbrain-Upper pons stage
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Goals in Emergency
Primary Neurological Process? evidence of raised ICP focal findings, especially that implicate
brainstem structuresSecondary Processes
signs of infection, toxic/metabolic processes
relative lack of focality
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Coma Mimics
Akinetic mutism‘Locked-in’ syndromeCatatoniaConversion reactions
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Akinetic Mutism
Silent, immobile but alert appearingUsually due to lesion in bilateral
mesial frontal lobes, bilateral thalamic lesions or lesions in peri-aqueductal grey (brainstem)
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“Locked-In’ Syndrome
Infarction of basis pontis (all descending motor fibers to body and face)
May spare eye-movementsOften spares eye-openingEEG is normal or shows alpha
activity
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Catatonia
Symptom complex associated with severe psychiatric disease with: stupor, excitement, mutism, posturing can also be seen in organic brain
diease: encephalitis, toxic and drug-induced psychosis
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Conversion reactions
Fairly rareOcculocephalics may or may not be
presentThe presence of nystagmus with cold
water calorics indicates the patient is physiologically awake
EEG used to confirm normal activity