medicine 5th year, 6th lecture/part two (dr. mohammed tahir)
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Evaluation of Patients in Coma
Definitions
Coma: “Unarousable unresponsiveness in which the subjects lie with eyes closed”
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
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
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
Demands of Arousal
Function of ARAS-Thalamic-Cortical system depends on: anatomic integrity of structures metabolic integrity (circulatory
integrity) communicative integrity
(neurotransmitter function)
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
Clues from History
Onset of symptoms sudden onset fluctuations
Associated neurologic symptomsMedications
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)
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)
.Pupillary Light Responses
Afferent Limb: Optic NerveEfferent Limb: Parasympathetics via
occulomotorMidbrain integrity/ tectumUncal Herniation (3rd nerve
dysfunction)Pupillary resistance to insult
Pupillary Light Responses
Be aware of drug effects Systemic and Local
Avoid ‘PERLA’ State size, before and after light
stimulation Specify right and left
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
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
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)
Eye Movements
Before maneuvers attempted note resting position Midline
Deviation suggests frontal/pontine damage
ConjugateDysconjugance suggests CN abn.
MovingRoving, dipping, bobbing
Occulocephalic/ Calorics
Same reflex elicited differentlyAfferent: Eighth nerveEfferent: 3,4,6 via MLF and PPRFOcculocephalics may also involve
proprioceptive afferents from the neck
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
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
Calorics
Watch for conjugance of deviationTo test vertical eye movements
Both ears, cold water-downward gaze Both ears, warm water-upward gaze
Gag Reflex
Afferent: GlossopharyngealEfferent: VagusTaken in context of other findings
Motor Exam
Assess tone, presence of asterixisResponse to painful stimuli
none abnormal flexor abnormal extensor normal localization/withdrawal
Avoid use of decerebrate/ decorticate
Reflexes
BrainstemDeep tendon
Biceps, brachioradialis, triceps Patellar, Achilles Plantar Responses
Superficial skin Abdominal, cresmasteric
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
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
Coma Mimics
Akinetic mutism‘Locked-in’ syndromeCatatoniaConversion reactions
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)
“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
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
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
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