Neurologic assessment of patients in coma

1. History

(obtained from family, friends, colleagues)

• Onset of coma (gradual, abrupt)
• Medical disease history
• Psychiatric history
• Drug history (legal and illicit)
• Occupational exposure (eg. toxins, CO)
• Exposure to pathogens (arthropods, mosquitoes)
• Recent complaints
• Recent injury

2. Physical examination

• Vital signs
• Evidence of trauma
• Evidence of systemic illness
• Evidence of drug abuse (needle marks, alcoholic fetor)
• Nuchal rigidity

3. Verbal response

1. Oriented
2. Confused
3. Inappropriate
4. Incomprehensible
5. No verbal response

4. Eye opening

1. Spontaneous
2. To verbal stimulation
3. To noxious stimulation
4. None

5. Pupillary reaction

• Evaluate both eyes and record each pupil diameter
• Record the best response to light
• Record asymmetry

Localizing value of abnormal pupillary responses

• Bilateral small, responsive:
  • Metabolic encephalopathy
  • Drug effects
  • Diencephalic insult (bilateral)
• Unilateral small, reactive (Horner’s syndrome)
  • Insult between T1-2 spinal level and carotid bifurcation: loss of sweating in ipsilateral face
  • Insult between ipsilateral hypothalamus and spinal cord: loss of sweating in ipsilateral hemibody
• Bilateral large, fixed: pretectal midbrain insult
• Bilateral midposition or large, fixed: bilateral midbrain tegmentum insult
• Unilateral large, fixed: unilateral midbrain tegmentum or CNIII insult
• Bilateral or unilateral pinpoint, responsive: pontine tegmentum insult

6. Ocular motor examination

• Note position of eyes and eyelids
• Tonically retracted eyelids (Collier’s sign) may be seen in dorsal midbrain or pontine damage
• Slight exophoria is often present in patients with impaired consciousness
• Do not confuse baseline strabismus for dysconjugate gaze - obtain detailed history!
• When passively opened and released, the eyelids of a comatose patient close slowly and gradually in a manner that cannot be imitated. The closed position is maintained by the tonic contraction of orbicularis oculi muscle
• Absence of tone, failure to close, asymmetric speed or depth of closure may indicate facial motor weakness
• Active resistance to opening or rapid closure is usually voluntary but lethargic patients with metabolic or structural insults may also resist opening
• Spontaneous blinking is usually lost in coma but may return in persistent vegetative states
• Blinking in response to loud noise implies intact afferent pathways and brainstem
• Patients with visual cortex insults may retain blink reflex to light but not to threat

Conjugate or non-conjugate eye deviation

Conjugate deviation

1. Lateral

• Most often due to destructive or irritative supranuclear insults
• Destructive insults cause deviation towards side of lesion - an exception may be observed in thalamic hemorrhage (“wrong-way eyes”)
• Irritative insults cause deviation away from side of lesion - an exception may be observed in Todd’s paralysis of gaze after a seizure

2. Vertical

• Mass lesions exerting pressure on the tectal plate may cause conjugate downward deviation of gaze
• Oculogyric crisis or acute bilateral damage in the basal ganglia may cause conjugate upward deviation of gaze

Non-conjugate deviation

• Damage to CN III, IV, VI or their nuclei or brainstem fascicles
• Damage to MLF (intranuclear ophthalmoplegia)
• Skew deviation (vertical dysconjugate gaze) may be produced by insults in:
  • Lateral rostral medulla
  • Lower pons
  • Vestibular system or vestibulocerebellum on the side of the inferior eye
  • MLF on the side of the superior eye

Spontaneous eye movements in absence of stimulation.

Nystagmus

Uncommon in comatose patients (the saccadic component is essentially a corrective movement generated by voluntary gaze). Forms of nystagmus or nystagmus-like movements that may appear in comatose patients include:

• Versive eye movements during seizure
• Retractory nystagmus (simultaneous contraction of all 6 extraocular muscles) seen in dorsal midbrain compression or destruction
• Convergence nystagmus (slow divergence followed by rapid convergence) seen in dorsal midbrain lesions

Roving movements

• Typical of metabolic encephalopathy
• If conjugate, imply intact brainstem ocular motor system

Ocular bobbing

Rapid conjugate downward displacement followed by slow return to primary position.

• Pontine insults
• Metabolic or toxic disorders

Ocular dipping

Slow conjugate downward displacement followed by rapid return to primary position.

• Unreliable for localization, may appear in hypoxic, ischemic or metabolic disorders

Reverse ocular bobbing

Rapid conjugate upward displacement followed by slow return to primary position.

• Unreliable for localization. Predominantly seen in metabolic disorders

Reverse ocular dipping

Slow conjugate upward displacement followed by rapid return to primary position.

• Unreliable for localization. Seen in pontine insults and in AIDS patients

Ping-pong gaze

Horizontal conjugate deviation of the eyes, alternating every few seconds.

• Bilateral cerebral hemispheric insult, toxic insult

Periodic alternating gaze deviation

Horizontal conjugate deviation of the eyes, alternating every 2 minutes.

• Hepatic encephalopathy
• Disorders causing periodic alternating nystagmus and unconsciousness or vegetative state

Vertical “myoclonus”

Vertical 2-3 Hz pendular oscillations.

• Pontine insults

Monocular movements

Small amplitude, rapid, intermittent, vertical, horizontal or torsional movements in single eye.

• Pontine insults
• Midbrain insults
• Often coexistent seizures

7. Oculocephalic response

Rule out cervical injury before manipulating the patient’s head.

While holding the patient’s eyes open with your thumbs, briskly rotate the patient’s head laterally to either side holding it a few seconds in each extreme position. Then rotate the head in the vertical plane (as if nodding).

The normal response (known as the “doll’s eye” response) is for the eyes to:

• Rotate in a smooth and conjugate manner away from the head’s rotation direction - ie the eyes should deviate to the right when rotating the head to the left
• Slowly return to midposition when the head is held in the extreme position on each side
• When rotating on the vertical plane, the eyes may open (“doll’s head”)

An intact horizontal and vertical doll’s eye response implies intact pathways from the vestibule to the brainstem vestibular nuclei, lower pontine tegmentum and upper pontine and midbrain paramedian tegmentum.

In awake patients the vestibulo-ocular response is normally suppressed by voluntary gaze control.

8. Caloric vestibulo-ocular response

More vigorous stimulation of the vestibulo-ocular reflex than the oculocephalic response.

Procedure:

1. Remove cerumen if necessary before performing the test
2. Raising the bed to 30o brings the horizontal semicircular canal in vertical position ensuring maximal stimulation
3. Use a 50 ml syringe filled with ice-cold water with a thin plastic IV catheter inserted just before the tympanic membrane
4. Irrigate at ~10ml/min for 5 minutes or until a response is obtained
5. Wait at least 5 minutes for the response to subside before testing the other side
6. To test vertical movements, irrigate both sides simultaneously

Mechanism:

1. Cold temperature causes convection current in endolymph away from the ampulla within the horizontal semicircular canal
2. The current stimulates the hair cells
3. The stimulation inhibits the tonic discharges of the vestibular neurons
4. The simultaneous activation of the anterior and posterior semicircular canals cancel each other out
5. The net effect is a tonic deviation of the eyes toward the irrigated side, identical to what would be observed if the head was turned to the opposite side
6. Warm stimulation produces the opposite response (“COWS” mnemonic: Cold - Opposite, Warm - Same)
7. Simultaneous bilateral stimulation causes downward deviation with cold stimulation or upward deviation with warm stimulation

Testing an awake patient causes a slow drift toward the irrigated side followed by a compensatory saccade back to the midline (contralateral nystagmus). Nausea and vomiting may also occur.

Testing a comatose patient only elicits the initial tonic response (no compensatory saccade). Eliciting contralateral nystagmus on caloric testing in a “unresponsive” patient suggests that the patient is awake.

Pitfalls

• Phenytoin or tricyclic antidepressant toxicity may obliterate the vestibulo-ocular responses
• Aminoglycoside toxicity may obliterate the caloric response but the oculo-cephalic response might be preserved to some extent (because of vestibulo-ocular reflex stimulation from proprioceptive signals from the neck muscles and joints)

9. Corneal and eyelid responses

1. Remove contact lenses before testing
2. Gently stimulate the side of the cornea with a cotton wisp or by dropping 2-3 drops of sterile saline on the cornea from 4-6 inches (10-15 cm) height

The normal response consists of:

1. Reflexive closure of both eyelids
2. Elevation of both eyes (Bell’s phenomenon)

• Intact corneal reflex implies intact trigeminal nerves, trigeminal spinal nuclei, lateral brainstem tegmentum, oculomotor and facial nuclei and nerves.
• In lesions of the descending corticofacial pathways, blinking may be absent but Bell’s phenomenon may be preserved.
• In mesencephalic insults Bell’s phenomenon may be absent but blinking may be preserved.

10. Respiratory pattern

The respiratory pattern may give clues to the level of brain insult

• Forebrain
  • Cheyne-Stokes breathing (hyperpnea regularly alternating with apnea)
  • “Pseudobulbar” laughing or crying
  • Epileptic respiratory inhibition
  • Breath holding or apraxia for deep breathing
  • Posthyperventilation apnea
• Hypothalamic/midbrain
  • Central reflex hyperpnea
  • Neurogenic pulmonary edema
• Basis pontis
  • Loss of voluntary control (pseudobulbar paralysis)
• Lower pontine tegmentum
  • Ataxic breathing (irregular, gasping respiration)
  • Apneustic breathing (respiratory pause of 2-3 seconds at full inspiration)
  • Cluster breathing (closely grouped respirations followed by apnea)
  • Short-cycle anoxic-hypercapnic periodic breathing
• Medulla oblongata
  • Ataxic breathing
  • Slow, regular breathing
  • Loss of autonomic breathing with preserved voluntary control (“Ondine’s curse”)
  • Gasping
  • Hiccups
  • Yawning
  • Vomiting

11. Motor response

• Obeys commands
• Localizes pain
• Withdraws from pain
• Abnormal flexion posturing
• Abnormal extensor posturing
• No response

12. Muscle stretch reflexes

• Normal
• Increased
• Decreased
• Absent

13. Skeletal muscle tone

Grasp patient’s hand as if in handshake and lift flexing the elbow, while simultaneously turning the patient’s wrist back and forth.

• Normal - mild, smooth, almost constant resistance throughout movement
• Spasticity - increased tone with more rapid movements with a spastic “catch” or “clasp-knife” character
• Parkinsonian - “lead pipe” rigidity that is equally intense throughout movement
• Paratonia - irregular resistance to passive movement that increases with increased speed of movement as if the patient voluntarily resists examiner
• Hypotonia - reduced muscle tone
• Flaccidity - no perceived resistance