APPROACH TO COMA What well discuss Basic definitions

APPROACH TO COMA

What we’ll discuss Basic definitions Neuroanatomy of consciousness Key examination points (CNS & General) Investigations Coma mimics

Importance of this topic: Lot of Semantic confusions about the terminology related to coma. Work up of the patient with coma is often complex and always urgent. Examination determines the early management, urgency with which imaging and CSF studies are obtained.

CONSCIOUSNESS: Def: Awareness of one’s own self and his environment and responsiveness to external and internal stimuli. Two Dimensions: Arousal: Primitive function, sense of wakefulness (Brainstem, Medial thalamus). Cognition: Cerebral cortex, Subcortical nuclei. Cognition depends on arousal, but normal

Severity of altered sensorium: Alert Drowsiness Stupor Coma Confusion Delirium.

Definitions: Drowsiness: inability to sustain a wakeful state without external stimuli. Pt can be easily arousable, but falls asleep when left alone. Stupor: A state in which the pt can be aroused by noxious stimuli only ; little motor or verbal activity once aroused. Coma: State of complete loss of consciousness. The pt appears to be in deep sleep and not arousable at all to any kind of stimuli. He won’t attempt to avoid painful or noxious stimuli. No sleep – wake cycle.

Definitons……. Confusion: inability to maintain a coherent sequence of thoughts, usually by inattention and disorientation Delirium : a state of disturbed consciousness with motor restlessness and disorientation. (Confusion + Motor agitation)

Really Simple Neuroanatomy Ascending Reticular Activating System (ARAS) in the brainstem (Upper pons & midbrain). Thalamic nuclei – receiving fibers from ARAS and sending fibers to Cortex. Cerebral cortex.

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 Basics: Coma implies dysfunction of: ARAS or Both hemi-cortices Anatomically, this means central brainstem structures (bilaterally) from caudal medulla to rostral midbrain both hemispheres

Epidemiology of Coma Plum and Posner 1982 500 consecutive cases of coma 326 diffuse or metabolic brain dysfunction (149 drug intoxication) 101 supratentorial (44/101 ICH) 65 subtentorial lesions (40/65 brainstem infarcts)

Etiology: (Metabolic) AEIOU TIPS: They affect cortex or brainstem or both. • A- Alcohol, Anoxia, Acidosis • E- Electrolytes, enviroment • I - Immunity, insulin • O-Opiates • U- Uremia • T- Trauma, toxins • I- Infections • P- Psychogenic, pharmacologic • S- Shock, sepsis

Structural causes: Supratentorial : 1. Bilateral cerebral infarct, concussion , contusion, 2. Postical states, hypertensive encephalopathy, 3. Encephalitis, meningitis, Increased ICP, 4. SAH, hemorrhage , tumor , abscess.

Structural causes …. . Infratentorial : 1. Pontine hemorrhage, Infarct. 2. Cerebellar hemorrhage , 3. Basilar artery occlusion , 4. Brainstem tumors, or traumatic Hge.

Coma Patient Evaluation:

History: To seek historical data from friends , family , or others. The rate of onset of neurologic or behavioral changes: Abrupt onset favors the CNS hemorrhage or ischemia , Gradual onset favors a metabolic problem. The history of trauma or on ongoing medical illness, Suicidal ideation , past attempts at self-harm , History of substance abuse.

First Step: Assess the ABCs Airway & gag reflex, Breathing pattern and sufficiency, Circulation adequacy and hypotension.

The roles of vital signs: Bradycardia : Increased ICP , hypothyroidism, intoxication and cardiac disease. Tachycardia: Hypovolemia, Infection. Hypertension: ICP, ICH, HT encephalopathy, Stroke and toxins. Hypotension: Sepsis, Hypovolemia, Wernicke’s encephalopathy, MI. Hypothermia : sepsis , hypothyroidism , or environmental exposure. Hyperthermia : sepsis , heat stroke , thyrotoxicosis , stroke , toxins.

General examination: Look for external injuries. Skin: needle tracks, rash. Breath odour: fetor hepaticus, uremia, acetone, or alcohol. CVS, RS and ABDOMEN.

Neurologic Exam Cornerstone of assessment, Descriptive, systematic, Reference point for serial assessment.

Components: Level of Consciousness Breathing pattern Pupillary size and reaction Extraocular movements Corneal reflex Motor status

Breathing Abnormalities of respiration can help localize but almost always in the context of other signs. Cheyne-Stokes respiration : Cycles of Hyperapnea alternating with apnea. bilateral dysfunction of the hemispheres or diencephalon. Apneustic: Long inspiratory phase, upper pons lesions. Cluster : high medulla or lower pons. Ataxic : Erratic shallow and deep breathing, medulla.

Level of consciousness: GCS (Glasgow Coma Scale) Eye Opening (4), Verbal (5), Motor (6) 13 -15 Mild, 8 -12 Moderate, 3 -7 Severe Coma. The AVPU scale : A - alert & aware V - responds to verbal stimuli P - responds to painful stimuli U - unresponsive

Cranial Nerve Exam Systematic assessment of brainstem function via reflexes Cranial Nerve Exam Pupillary light response (CN 2 -3) Gaze/Oculocephalic/calorics (CN 3, 4, 6, 8) Corneal reflex (CN 5, 7) Gag refelx (CN 9, 10)

Pupillary Light Responses Afferent Limb: Optic Nerve. Efferent Limb: Parasympathetics via oculomotor. Midbrain integrity/ tectum. Avoid the term ‘PERLA’ State size, before and after light stimulation, Specify right and left. Be aware of drug effects - Systemic and Local.

Pupils: Localizing Value Small, Reactive pupils : Metabolic coma. Unilateral fixed, dilated pupil : uncal herniation, PCOM aneurysm. Bilateral, Large fixed pupils: Midbrain lesion or Death. Bilateral, midposition, fixed pupils: Transtentorial herniation. Pinpoint pupils – Pontine ICH, infarct, Opiate poisoning. Horner’s syndrome- sympathetic dysfunction.

PUPILLARY ABNORMALITIES: Normal Horner’s syndrome Left 3 rd CN palsy

Terminal stage pupil

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.

Eye Movements Eye movements are the cornerstone of the neurologic examinations of the comatose patient , as they closely approximate the ARAS anatomatically. EOM evaluates the cortex, and the MLF in the brainstem.

Eye Movements Note resting position of both eyes: Conjugate Deviation suggests frontal / pontine damage. Frontal – Eyes look toward the side of lesion. Pontine - Eyes look away from the side of lesion. Dysconjugance suggests Cranial Nerve abn. Roving eye movts indicate intact brainstem. Ocular bobbing: Pontine lesion.

Oculocephalic and Calorics Same reflex elicited differently Afferent: Eighth nerve Efferent: 3, 4, 6 via MLF and PPRF Oculocephalics may also involve proprioceptive afferents from the neck

Oculocephalic Reflex (Doll’s eye) Brisk horizontal rotation of head with eyes held open and watch for contraversive movements of eyes. Then flexion of the neck: eyes deviate up, followed by extension: eyes deviate downward – Vertical gaze. If eyes follow movement of head to side, suspect brainstem involvement in coma. Caution with suspected c-spine injury.

DOLL’S EYE MOVEMENT:

Caloric test(Oculovestibular reflex) Ensure TM integrity Elevation of head to 30 degrees (so that lateral semicircular canal is vertical) Instillation of 50 to 120 ml of ice water Awake pt: deviation toward, nystagmus away Comatose: deviation toward, no nystagmus. (Brainstem intact, Cortex is damaged) No Deviation, no nystagmus - (Brainstem

Calorics COWS – Pneumonic. Wait for 5 minutes and test the other ear. To test vertical eye movements Both ears, cold water-downward gaze Both ears, warm water-upward gaze

Caloric test: Normal Abnormal

Corneal Reflex Afferent: Trigeminal Nerve Efferent: Third Nerve (Bell’s Phenomenon and Facial Nerve (Eye closure) Tests dorsal midbrain (Bell’s) and pontine integrity (Eye closure)

Gag Reflex Afferent: Glossopharyngeal Efferent: Vagus Taken in context of other findings

Motor Exam Assess tone, presence of asterixis Response to painful stimuli none abnormal flexor abnormal extensor normal localization/withdrawal Focal weakness.

Decorticate posturing in comatose patient Lesion above the red nucleus Lower limbs extend, upper limbs flex following stimulus Activity in the brainstem flexor center, the red nucleus

Decerebrate posturing in comatose patient Upper and lower limbs extend following stimulus Lesion between red nucleus and vestibular nucleus. Overactivity of Lateral vestibular nucleus.

Clinical Value: Decorticate posturing indicates a higher level of brainstem injury than decerebrate posturing (a good thing) Comatose patients who go from decerebrate to decorticate (ascending progression of impaired area) have a better prognosis than those that go from decorticate to decerebrate (descending progression of impaired area). Descending impairment will be fatal if medullary respiratory and cardiovascular centers are damaged.

Reflexes Deep tendon Biceps, brachioradialis, triceps Patellar, Achilles Plantar Responses Superficial skin Abdominal, cremasteric Meningeal signs.

Goals in Emergency Primary Neurological Process? evidence of raised ICP, focal findings, especially that implicate brainstem structures. Secondary Processes? signs of infection, toxic/metabolic processes relative lack of focality.

Coma classification after examination: Diseases with no focal or lateralizing signs. Diseases with focal brainstem or lateralizing cerebral signs. Diseases with meninigitic syndromes.

Diseases with no focal or lateralizing signs. Symmetrical examination, small reactive pupil, normal eye movements. Predominantly metabolic, toxic or septic Bilateral cerebral hemispheres or brainstem or both are affected.

Diseases with focal brainstem or lateralizing cerebral signs. Focal lesion in the brainstem directly affect the ARAS. Focal lesion in the cortex leading to herniation and indirectly affecting the ARAS. Bilateral cortical lesion can directly cause coma.

Uncal herniaiton Expanding lesions in lateral middle fossa. Compression of hippocampal gyrus over free edge of tentorium. Ipsilateral dilated nonreactive pupil. Ipsilateral hemiparesis due to compression of opposite CST by the midbrain (Kernohan waltman sign).

Uncal herniation:

Transtentorial herniation: Large midline mass Small symmetric pupil or midposition, unreactive pupil. Decorticate posturing. Duret’s hemorrhages in the midbrain.

Transtentorial herniation:

Tonsillar herniation: Posterior fossa lesions Herniated tonsils compress the medullary vital centers. Decerebrate rigidity, apnea, bradycardia Neck rigidity, opisthotonus.

Tonsillar herniation:

Investigations: Blood glucose, urea, electrolytes, ABG etc… Non contrast head CT Acute blood Space occupying lesion MRI Posterior fossa Early infarct LP Xanothochromia Infection EEG – Non convulsive status epilepticus.

Coma Mimics Akinetic mutism Locked-in’ syndrome Persistent Vegetative state Conversion reactions

Akinetic Mutism Silent, immobile but alert appearing Usually due to lesion in bilateral mesial frontal lobes, bilateral thalamic lesions or lesions in periaqueductal grey (brainstem)

Persitent Vegetative state: No evidence of awareness of self or environment and an inability to interact with others Bowel & bladder incontinence Hypothalamic & brain stem autonomic function preservation to permit survival with medical & nursing care Maintainence of intermittent wakefulness and sleep -wake cycles No evidence of language comprehension or expression No response to visual, auditory, noxious, or tactile stimuli

“Locked-In’ Syndrome Infarction of basis pontis (all descending motor fibers to body and face) May spare eye-movements Often spares eye-opening EEG is normal or shows alpha activity

Conversion reactions Fairly rare Oculocephalics may or may not be present. The presence of nystagmus with cold water calorics indicates the patient is physiologically awake EEG used to confirm normal activity