medicine.coma.(dr.muhamad tahir)

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