(2)  Decerebrate posturing (upper and lower limb extension, uni- or bilateral) localizes the deficit to the midbrain (red nucleus).

(3)  If required, noxious stimuli include rubbing the sternum, or applying firm but gentle pressure to the forehead or nail beds.

(4)  Asymmetrical limb movements or hypertonia occur with structural brain lesions, whereas symmetrical motor responses are typical with toxi-metabolic conditions.

(5)  Bilateral myoclonic jerks, asterixis, or tremulousness strongly suggest toxi-metabolic causes of coma.

(6)  Asymmetrical or focal, rhythmical movements may be subtle clues when nonconvulsive status epilepticus causes coma.

2.  Respiratory patterns do not strictly correlate with the level of brain dysfunction as once thought and may be obscured if the patient is mechanically ventilated.

a.  Cheyne–Stokes’ breathing is observed as periods of increasing, then decreasing, tidal volumes and respiratory rate, followed by seconds of apnea.

(1)  It occurs more commonly in elderly patients, with or without systemic medical problems or congestive heart failure.

(2)  It may occur from bilateral cerebral lesions or a unilateral lesion with brain shift.

b.  Persistent hyperventilation occurs more often from pulmonary causes like pneumonitis, and rarely from midbrain lesions.

c.  Arrhythmical, irregular respirations accompany dysfunction at the medulla, where critical cardiorespiratory centers are located.

3.  The pupils are typically small but reactive to light in the elderly, as well as those in toxi-metabolic coma, even when other cranial nerve reflexes are absent.

a.  A unilaterally large pupil unreactive to light (“fixed or blown pupil”) in an unresponsive patient represents dysfunction of third cranial nerve pupilloconstrictive fibers.

(1)  Most commonly found with ipsilateral temporal lobe compression of the third cranial nerve (uncal herniation) from hemorrhage or edema.

(2)  Rarely due to a ruptured intracranial aneurysm at the junction of the internal carotid-posterior communicating artery.

(3)  Asymmetrical pupils and decreased pupillary light reflexes are independent predictors of a structural lesion causing coma.

b.  Bilateral midposition to large, unreactive pupils may occur with midbrain lesions or terminal anoxic brain injury.

c.  Pinpoint, reactive pupils are caused by extensive pontine lesions interrupting the descending sympathetic pupillodilator fibers; however,

(1)  pinpoint pupils can also be caused in older patients by cholinergic eyedrops for glaucoma, and

(2)  narcotic overdose can also produce small pupils.

4.  Ocular reflexes, which are cortically suppressible in an awake patient, indicate preserved brainstem function when found in a comatose patient.

a.  The oculocephalic (“doll’s eyes”) reflex occurs when the examiner passively turns the head to one side, eliciting a normal lateral conjugate rolling of the eyes to the opposite side.

b.  The oculovestibular (“cold caloric”) reflex occurs after instillation of 50- to 200-cc ice water into one ear canal, with the head elevated 30 degrees, eliciting a slow, tonic deviation of both eyes toward the irrigated ear, after several seconds delay.

(1)  Ensure that the tympanic membrane is intact, so nonsterile water and debris cannot enter the middle ear.

(2)  Ensure there is no impacted cerumen in the ear canal, causing a false-negative test.

(3)  Lateral jerk nystagmus of the eyes toward the nonirrigated ear occurs in conscious patients, but not comatose patients where cortical function is depressed.

c.  Ocular reflexes

(1)  should not be checked in trauma patients until cervical spine stability is assured,

(2)  may be absent because of previous labyrinthine trauma, mastoiditis or toxicity from benzodiazepines or barbiturates, and

(3)  appear asymmetrical from a structural lesion affecting the brainstem, or from facial bone fractures restricting extraocular muscle function.

d.  In coma,

(1)  the eyes are slightly divergent at rest,

(2)  conjugate lateral deviation of the eyes toward one side occurs from a lesion in the contralateral brainstem or ipsilateral cerebral hemisphere,

(3)  persistent, rhythmical nystagmus may be a subtle finding of nonconvulsive status epilepticus, and

(4)   “ocular bobbing” consists of repetitive downward jerks of the eyes, with slower updrift, because of pontine lesions with poor outcome.

e.  Blinking

(1)  occurs spontaneously if the pontine ARAS is intact and

(2)  along with vertical eye movements may be the only motor functions (and means of communication) in a patient with the “locked-in syndrome” (see section Differential Diagnosis).

ETIOLOGY

A.  Toxi-metabolic coma accounts for almost two-thirds of unresponsive emergency room patients.

1.  A confusional state or delirium occurs initially, followed by symmetrical motor or ocular reflex findings and preserved pupillary light reflex.

2.  Exceptionally, hemiparesis or aphasia may be due to hyperglycemic, hypoglycemic, hyponatremic, or dysosmolar states.

3.  Tremulousness, myoclonic jerks, and asterixis are typical.

4.  Drug intoxication or overdose may also lead to subsequent traumatic brain injury and structural lesions leading to coma.

B.  Structural causes of coma account for about one-third of unresponsive emergency room patients.

1.  Asymmetrical motor or ocular reflex findings occur early.

2.  A unilaterally dilated pupil unresponsive to light indicates uncal herniation until proven otherwise.

DIFFERENTIAL DIAGNOSIS

A.  Brain death.

1.  Irreversible, critical loss of brain and brainstem function.

a.  Comatose patient with absence of all brainstem reflexes, including spontaneous respiration (abnormal bedside apnea test: no observed breaths despite pco₂ ≥ 60 mm, while on 100% oxygen).

b.  The cause of coma is known and sufficient to cause brain death, such as cardiopulmonary arrest.

2.  No improvement occurs during observation and treatment.

a.  Observation is at least 6 hours in adults, 12 hours to 2 days for children.

b.  Hypothermia, hypotensive shock, and drug intoxication have been ruled out or treated.

c.  Ancillary testing may help to confirm the clinical diagnosis (absent cerebral blood flow on radioisotope brain scan, or “flat-line” electroencephalogram [EEG]).

B.  Persistent vegetative state (or “unresponsive wakefulness syndrome”).

1.  After several days of coma, the patient appears intermittently awake, breathes spontaneously, and exhibits primitive reflexes or eye-roving behavior.

2.  Severe cerebral damage persists, however, and no meaningful communication or cortical responsiveness occurs.

3.  Patients showing some impersistent, subtle signs of awareness (visual pursuit, pain localization) are felt to be in a “minimally conscious state” (MCS).

C.  “Locked-in syndrome.”

1.  The patient may appear to be in a persistent vegetative state, and is unable to move the limbs and face, or gaze laterally (“de-efferented”).

2.  Vertical gaze and eyeblinking are preserved, and serve as a means of proving that communication and cortical functions are preserved (the patient accurately blinks once for “yes,” or twice for “no” in response to the examiner).

3.  Caused by an extensive pontine infarction or profound neuromuscular paralysis, such as Guillain–Barré syndrome.

D.  Thalamic lesions.

1.  Bilateral lesions interrupting the projections of the intralaminar thalamic nuclei of the ARAS to the frontal lobes can produce an inattentive, unresponsive, but still wakeful state.

2.  Paramedian thalamic syndrome (see Video 5.1).

a.  Lethargic patient with quadriparesis, impaired vertical gaze, and bilateral asterixis.

b.  Caused by bilateral infarction of the dorsal midbrain and thalamus.

E.  Nonconvulsive status epilepticus.

1.  Occasionally, continual or persistent generalized seizures may occur in the absence of obvious clinical convulsive activity.

2.  Subtle clinical manifestations include rhythmical nystagmus, or twitching of an eyelid or part of the face or limb.

3.  Obtain an emergent EEG recording and assess the response to IV benzodiazepine boluses.

F.  Psychiatric unresponsiveness.

1.  Occurs rarely, and remains a diagnosis of exclusion.

2.  In the absence of drug overdose, brainstem reflexes and spontaneous breathing should be preserved, and no focal neurologic deficits are seen.

3.  EEG brain wave frequencies are more similar to that of the awake state than the diffuse EEG slowing typical of toxi-metabolic coma.

4.  Psychiatric patients may become comatose from other medical or neurologic disorders as well, or from therapeutic drug therapy (neuroleptic malignant or serotonin syndromes).

MANAGEMENT

A.  Initial approach for a comatose patient.

1.  Maintain airway, breathing, and circulation, with intubation, ventilation, and fluid/pressor support as needed.

2.  Urgently correct any hypothermia, which, if profound, can mimic brain death.

3.  If trauma has occurred or is strongly suspected, establish stability of the cervical spine (computed tomography [CT] scan) before moving the head, as occurs with testing the oculocephalic (doll’s eyes) reflex.

4.  Rule out hypoglycemia, especially in diabetic patients, with an immediate fingerstick glucose reading (or empirical infusion of 50% dextrose if immediate testing is not available). Before any glucose infusion in malnourished patients, prevent Wernicke’s encephalopathy with adequate thiamine supplementation, such as 500 mg IV (infused over 30 minutes) tid, followed by 250 mg IV daily for 5 days (see Chapter 63).

5.  Check basic bloodwork (blood count, electrolytes, glucose, renal and liver functions, ammonia level, thyroid functions, protime, activated partial thromboplastin time, arterial blood gas, possibly carbon monoxide [CO] level if CO poisoning suspected) and urine drug screen.

6.  The prognosis of coma following cardiac arrest improves with therapeutic hypothermia initiated within 6 hours, achieving a core temperature of 32° to 34°C for 24 hours, followed by slow rewarming.

B.  Comatose patient with suspected hemorrhage.

1.  After the initial approach above, perform a brain CT scan without contrast in a known or suspected trauma patient to rule out intracranial hemorrhage.

2.  Nontraumatic SAH is suspected with prodromal headache and sudden loss of consciousness.

a.  Rule out SAH with a brain CT scan without contrast.

b.  Perform a lumbar puncture (LP) if SAH is still strongly suspected but not seen on brain CT scan.

c.  If SAH is found, request neurosurgical consultation and urgent conventional cerebral angiogram or CT angiogram.

C.  Comatose patient with fever or septic syndrome.

1.  After the initial approach above, examine the patient for any likely systemic focus of infection, such as abscess or peritonitis.

2.  Panculture blood and urine, obtain chest X-ray.

3.  Perform LP to exclude meningitis (in absence of focal neurologic findings, papilledema, bleeding disorder, or local infection over the lumbar spine) and begin initial broad-spectrum antibiotic coverage plus dexamethasone (see Chapter 63).

4.  If LP is contraindicated, request emergent brain CT scan with and without contrast, and neurosurgery consultation.

5.  Especially in the case of Herpes simplex encephalitis, a brain magnetic resonance imaging (MRI) scan may help reveal typical frontotemporal lesions.

D.  Comatose patient with focal findings on neurologic examination.

1.  After the initial approach above, exclude hemorrhage with a brain CT scan without contrast.

2.  Investigate and treat intracranial hemorrhage or other cause of brain edema or shift.

3.  If brain CT scan is normal, obtain brain MRI with and without contrast, including diffusion-weighted sequences, if patient is stable. MR or CT angiography may be urgently done when there is a strong suspicion of ischemic infarction, because acute interventions (mechanical thrombectomy, intravascular thrombolysis) may be helpful. Basilar artery thrombosis often presents with coma.

4.  If brain CT and MRI scans are normal, perform EEG to exclude electrical status epilepticus or postictal state.

E.  Comatose patient without focal findings on neurologic examination.

1.  After the initial approach above, consider administration of IV naloxone or flumazenil, respectively, for possible narcotic or benzodiazepine overdose. Be ready to treat any drug withdrawal symptoms.

2.  If no toxi-metabolic causes become obvious, obtain a brain CT scan or brain MRI scan if patient is stable.

3.  If brain CT and MRI scans are normal, perform an EEG to exclude electrical status epilepticus or postictal state.

Related posts:

Approach to the Patient with Gait Disturbances and Recurrent Falls Approach to the Patient with Acute Sensory Loss Multiple Sclerosis Approach to the Patient with Lower Extremity Pain, Paresthesias, and Entrapment Neuropathies Approach to the Patient with Chronic and Recurrent Headache Neuroimaging of Common Neurologic Conditions

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