- Rapid Reference
- Causes of stupor & coma
- Coma neuro exam
- Coma syndromes
- Tests & investigations
- Airway management
- Emergent therapies to consider
- Questions & discussion
coma neuro exam:
approach to stupor/coma:
- Coma is defined as a state of being unawake (closed eyes), unaware, and unarousable.
- Stupor lacks a clear definition, but usually refers to substantially impaired mental status with preservation of some responsiveness to painful stimuli.
- Locked-in syndrome usually results from pontine lesions. Patients are awake and cognitively intact, but paralyzed (only with the ability to blink or move their eyes vertically). It is essential to promptly recognize locked-in syndrome and differentiate this from coma or stupor.
- Coma results from disruption of pathways from the ascending Reticular Activating System. This system originates in the tegmentum of the upper pons and midbrain, projects to the hypothalamus and bilateral thalami, and subsequently diverges widely throughout the bilateral cortexes.
- For a lesion to cause coma, it must have one of the following locations:
- (1) Dorsolateral upper-mid pontine lesion
- (2) Paramedian upper midbrain lesion
- (3) Bilateral thalamic injury
- (4) Diffuse bihemispheric damage
- ⚠️ Coma cannot be attributed to a unilateral cortical lesion alone.(33218655) For example, in order for a unilateral cortical lesion to cause coma it must cause a herniation syndrome that results in damage to the upper midbrain.
causes of stupor & coma
- Intracranial hemorrhage:
- Subarachnoid hemorrhage.
- Thalamic or Pontine hemorrhage.
- Ischemic stroke(s)
- i) Most commonly, basilar artery stroke.
- ii) Severe multifocal infarction (e.g., due to endocarditis).
- Hypertensive encephalopathy, a.k.a. posterior reversible encephalopathy syndrome (PRES).
- Venous sinus thrombosis (thrombosis of the straight sinus may cause bilateral thalamic dysfunction).
- Encephalitis (most notably due to HSV or VZV).
- Brain abscess or subdural empyema that exerts mass effect.
severe metabolic derangements
- Hypoxic/anoxic brain injury.
- Hypercapnia (e.g., pCO2 typically over ~80-100 mm).
- Hypothermia or hyperthermia (e.g., temperature <28C or >40C).(27741988)
- Hypoglycemia (glucose below ~40 mg/dL or ~2.2 mM).(20130300)
- Hyperglycemia (rapid rise in glucose above ~900 mg/dL or ~50 mM).(20130300)
- Hyponatremia (e.g., sudden drop below ~110 mM).(20130300)
- Hypernatremia (e.g., sudden rise above ~160 mM).(20130300)
- Hypercalcemia (e.g., ionized calcium above ~3.5 mM).(20130300)
- Hepatic encephalopathy.
- Severe hyperammonemia.
- Myxedema coma.
- Wernicke's encephalopathy.
- Alcohols (ethanol, methanol, ethylene glycol).
- Sedatives, including baclofen.
- Serotonin syndrome.
- Sympathomimetic intoxication.
- Salicylate poisoning.
- Anticholinergics, including tricyclics.
- Carbon monoxide.
- Hematoma (subdural, epidural, or parenchymal).
- Diffuse axonal injury.
- Fat emboli syndrome.
nonconvulsive status epilepticus
- Functional coma (a.k.a. pseudocoma)
It may be impossible to obtain any information regarding the history. If available, the following are notable:
- Prior medical & neurological history.
- Outpatient medication list and any recent medication changes.
- Preceding symptoms (e.g., confusion, headache, abnormal movements, weakness, depression).
- When was the patient last known to be normal?
- History of substance use?
coma neuro exam
common pupillary abnormalities
bilateral fixed & dilated
- Bilateral midbrain damage causing loss of parasympathetic output from CN3.
- Anticholinergic drugs at high dose (especially atropine).
- Extremely deep metabolic coma (e.g., hypothermia, barbiturates, bupropion, lidocaine, sympathomimetics).
bilateral dilated, reactive
- Anticholinergic drugs.
- Withdrawal from alcohol or benzodiazepines.
- Sympathomimetics (e.g., amphetamine, cocaine, methamphetamines, MDMA).
- Serotonin syndrome.
- Generalized seizure, including the postictal period.
unilateral blown pupil (fixed & dilated)
- Oculomotor nerve paralysis (especially suggested if the involved eye is turned downwards and outwards).
- i) Uncal herniation compressing CN3, which is usually ipsilateral.
- ii) Posterior communicating artery aneurysm compressing CN3.
- Midbrain lesion affecting the CN3 nucleus.
- Focal seizure.
- Albuterol or oxymetazoline got into the patient's eye (following nebulized or intranasal drug administration).
bilateral mid-position, fixed pupils
- Bilateral midbrain damage with loss of sympathetic and parasympathetic output.
- Profound barbiturate coma.
bilateral mid-position, reactive
- This excludes a lesion around the level of the midbrain (where CN2 and CN3 lie). Remaining possibilities include, in roughly descending order:
- (#1) Most likely, this may be toxic/metabolic coma, causing diffuse dysfunction of the cerebral cortex.
- (#2) Lesions in the dorsolateral upper-mid pons.
- (#3) Bilateral thalamic dysfunction.
- Neuromuscular blocking drugs are another possibility (note that smooth muscles of the iris don't get paralyzed).
bilateral small pupils
- Medications (e.g., cholinergic agonists, opioids, clonidine, ACE-inhibitors).
- Bilateral central Horner's syndrome:
- Usually due to extensive pontine hemorrhage (“pontine pupils”).
- May occur in the early phase of central herniation syndromes (either upwards or downwards herniation).
unilateral small pupil
- Unilateral Horner's syndrome (loss of sympathetic outflow, often due to large hemorrhage affecting the thalamus).
spontaneous eye movements
horizontal conjugate deviation
- Cortical injury causes gaze preference. However, eyes are able to cross the midline during cold calorics or doll's eyes.
- Damage (e.g., stroke) –> Eyes deviate ipsilateral to the lesion & contralateral to limb paralysis.
- Focal seizure –> Eyes deviate contralateral to the lesion & ipsilateral to the seizing limb. Active seizure can be associated with nystagmoid jerks. This may subsequently be followed by a Todd's paralysis, wherein the eyes deviate in the other direction.
- Pontine injury causes gaze paralysis. Unlike gaze preference, eyes are unable to cross the midline during doll's eyes or cold calorics.
horizontal conjugate roving eye movements (a.k.a. ping-pong gaze)
- This refers to spontaneous, synchronized movements of the eyes back and forth. Some texts differentiate between “conjugate roving” versus “ping-pong” movements, but they are fundamentally similar phenomena.
- These movements reveal normal function of midbrain and pons. Generally, this indicates that the coma is due to bilateral cerebral hemispheric dysfunction (e.g., a toxic/metabolic coma).
- Lesions in the cerebellar vermis may also cause horizontal conjugate roving eye movements, but such lesions wouldn't be expected to cause coma.(28187795)
ocular bobbing or dipping
- Bobbing (rapid down, slow up) suggests a pontine lesion (video below).(28187795)
- Dipping (slow down, rapid up) localizes to bihemispheric dysfunction (e.g., anoxia or a metabolic disorder)(video below).(28187795)
nystagmus (especially if bidirectional, vertical or rotatory, and non-fatiguing)
- Cerebellar or brainstem lesion.
- Intoxication (e.g., phencyclidine).
- Nonconvulsive status epilepticus (NCSE).
skew deviation (one eye looks up, other looks down)
- Suggests a brainstem or cerebellar lesion.
- Suggests bihemispheric damage (e.g., following severe anoxic injury).
- Thalamic injury (e.g., hemorrhage).
- Midbrain dysfunction (e.g., Parinaud syndrome).
- Bilateral hemispheric dysfunction (e.g., anoxic injury).
- Elevated intracranial pressure.
oculocephalic (doll's eyes) & vestibulo-ocular (cold calorics) reflexes
- Both reflexes test a similar neural circuit involving cranial nerves 3, 6, and 8.
- Oculocephalic Reflex (Doll's Eyes): When the head is rotated, the eyes turn in the opposite direction (thereby staying fixated in roughly the same direction). This is easily tested, as a front-line evaluation of eye movements. Intact oculocephalic reflexes argue strongly against a structural cause of coma. However, this reflex may be muted in deep metabolic coma, so symmetric absence of eye movements doesn't necessarily prove a structural lesion. If the oculocephalic reflex is absent, cold caloric testing can be used to provide a stronger stimulus and test this more rigorously.
- Vestibulo-ocular Reflex (Cold Calorics) involves flushing the ear with 50 ml of ice water, with the head of the bed inclined at a 30 degree angle (to properly align the semicircular canal). In a comatose patient with intact brainstem reflexes, this will cause the eyes to rotate towards the stimulated ear. Cold calorics may elicit nausea and vomiting in awake or mildly somnolent patients.
response seen with intact brainstem and cerebral cortex
- A completely normal response that would be seen in an awake person is deviation of the eyes towards the irrigated side, repeatedly followed by fast-phase nystagmus in the opposite direction.
- If this is found, it suggests:
- Functional coma (pseudocoma).
- Akinetic mutism.
- Less severe toxic/metabolic encephalopathies.
focally abnormal vestibulo-ocular reflexes
- This suggests a focal lesion involving the brainstem, for example:
- (1) With cold caloric stimulation, isolated failure of the contralateral eye to adduct suggests a lesion in the medial longitudinal fasciculus in the pons. This can also occur with a CN3 palsy, but CN3 palsy would also cause pupillary dilation.
- (2) Isolated failure of an eye to abduct (CN6 palsy) may reflect damage to the abducens nucleus in the pons.
symmetrically abnormal vestibulo-ocular reflexes
- This generally indicates brainstem pathology.
- Toxic/metabolic coma can abolish vestibulo-ocular reflexes (e.g., phenytoin, tricyclic antidepressants, or sedatives).
cough & gag reflexes
⚠️ please stop gagging patients
- The gag reflex will almost never provide useful information which isn't revealed by other components of the neurologic examination.
- The presence of a gag reflex does not indicate that the patient is able to protect their airway. Airway protection involves swallowing reflexes, which are far more complex than a simple gag reflex.
- Many normal people lack a gag reflex. Therefore, absence of a gag reflex isn't necessarily pathological, nor does this reveal any definitive information.
- Gagging patients may induce emesis, which could lead to aspiration.
- Further discussion of why gagging patients should be abandoned is here.
cough reflex in intubated patients
- Basics of the cough reflex:
- The cough reflex involves the vagus nerve (CN10, near the medulla). This reflex will be preserved in most coma states (which usually involve higher brain centers).
- Reliably eliciting the cough reflex requires an intubated patient, in whom endobronchial stimulation can be applied by suctioning the endotracheal tube.
- The cough reflex is one of the most durable reflexes, which is generally preserved even in severe brain injury. For example, following anoxic brain injury, lack of a cough reflex after 24 hours carries a likelihood ratio of 85 for poor neurologic outcome.(14970067)
- Causes of an absent cough reflex include:
- Damage to the medulla (e.g., tonsillar herniation, brain death).
- Extremely profound toxic/metabolic coma (e.g., barbiturate or baclofen overdose).
- Neuromuscular paralysis (e.g., lingering effects of rocuronium used for intubation).
- 💡 When encountering a patient who lacks a cough reflex without any obvious cause, always consider the possibility of a lingering neuromuscular paralytic agent. If the patient otherwise appears paralyzed, this should be immediately evaluated at the bedside using a peripheral nerve stimulator (a.k.a. “train of four monitoring”).
how to observe breathing patterns
- Nonintubated patient: simple observation.
- Intubated patient: lift sedation (e.g., propofol) and place the patient on a pressure support mode (e.g., 10 cm pressure support with 5 cm PEEP). This allows patients to drive the rate and depth of respiration without interference, thus revealing their native breathing pattern.
Cheyne-Stokes respiratory pattern
- This is defined as a sinusoidal breathing pattern, reflective of a delayed feedback loop involved in regulating CO2 levels (e.g., commonly seen in severe heart failure with poor cardiac output). Generation of this pattern requires intact brainstem respiratory reflexes.
- In the context of coma, this pattern may result from bilateral forebrain dysfunction (e.g., metabolic etiologies) or bilateral thalamic injury.
- This is a rare pattern that involves end-inspiratory pauses.
- Apneustic breathing suggests pontine dysfunction (especially pontine infarction due to basilar artery occlusion).
- Damage to the medulla may cause irregular breathing patterns.
- High medullary lesions may generate irregular clusters of breaths (this may mimic the Cheyne-Stokes pattern, but it lacks any smooth, sinusoidal transition between apnea and hyperventilation).
increased motor tone or rigidity
- Intoxication (e.g., serotonin syndrome, neuroleptic malignant syndrome, malignant hyperthermia).
- May also result from a subacute or chronic brain disorder.
hyperreflexia or clonus
- Suggests serotonin syndrome, neuroleptic malignant syndrome, malignant hyperthermia.
- May also result from a chronic disorder of the brain or spinal cord.
multifocal myoclonus (diffuse, random, asynchronous jerking of various muscle groups)
- Generally, suggests a toxic/metabolic etiology.
- This should be differentiated from diffuse, synchronous or rhythmic movements – that may suggest anoxic brain injury, nonconvulsive status epilepticus (NCSE), lithium intoxication, cephalosporin intoxication, or pesticides.(20130300)
motor responses to pain
- How to examine:
- Apply painful stimuli to four extremities and bilateral face (either supraorbital ridge or temporomandibular joints).
- Observe for motor response (e.g., purposeful avoidance of the painful stimuli, a “localizing” response to pain) as well as nonfocal grimacing. For example, grimacing without the ability to withdraw suggests an intact sensory response, but the presence of motor paralysis.
- Asymmetric responses suggest a focal lesion.
- Decorticate posturing is loosely associated with damage at the level of the thalamus.
- Decerebrate posturing is loosely associated with damage at the level of the midbrain. This is usually associated with downward herniation or compression of the brainstem by posterior fossa lesions. However, occasionally toxic/metabolic etiologies may also cause decerebrate posturing (e.g., hepatic encephalopathy).
common coma syndromes
bilateral hemispheric dysfunction (e.g., most toxic/metabolic comas)
- The key finding is that brainstem reflexes are usually intact. However, reflexes may be lost in very deep toxic comas (e.g., barbiturate or baclofen overdose).
- Intact vestibulo-ocular reflexes.
- Intact pupillary and corneal reflexes.
- Spontaneous eye movements can occur (e.g., roving conjugate gaze, dipping with slow downgaze followed by rapid upgaze, or ping-pong gaze back and forth).(28187795)
- Upward or downward eye deviation can occur.
- Adventitious limb movements may be seen. If present, multifocal myoclonus, asterixis, or tremor support a metabolic etiology.(28187795) Any motor signs are usually symmetric.
- Ipsilateral blown pupil:
- Initially, the pupil is simply dilated.
- With progression, oculomotor paralysis occurs (causing the eye to be fixed in a down-and-out orientation).
- Contralateral hemiparesis due to compression of the cerebral pedicle
- Ipsilateral weakness can occur if lateral displacement compresses the opposite cerebral peduncle (a “false localizing sign”).
- Hemiparesis may be accompanied by a positive Babinski's sign.
- Impaired consciousness is almost always present by the time the pupil is fixed and dilated.(Gusdon et al., 2020)
- If untreated, this may eventually compress the midbrain (e.g., causing bilateral fixed & dilated pupils, with decorticate or decerebrate posturing).
downward central herniation (a.k.a. downward transtentorial herniation)
- Miotic (small) pupils are initially a prominent sign.
- ⚠️ Initially, this may resemble an intoxication causing small pupils (e.g., cholinergic agonists, opioids, clonidine, ACE-inhibitors). There may initially be conjugate roving eye movements, simulating a toxic/metabolic coma.
- Abnormal motor responses (e.g., posturing) may be an early clue to a structural etiology of the coma.
- With progression of herniation:
- Midbrain dysfunction emerges: pupils may become fixed & mid-position. Vestibulo-ocular reflexes become abnormal.
- Pathological breathing patterns may emerge (including Cheyne-Stokes breathing, irregular ataxic breathing, or neurogenic hyperventilation).
- Decorticate and later decerebrate posturing occur, with bilateral extensor Babinski reflexes.
brainstem displacement from a cerebellar mass
- Cranial nerves:
- Pupillary reflexes are often intact (since these are located in the midbrain, which is above the level of compression).
- Absent corneal reflexes and abnormal vestibulo-ocular reflexes are often seen. Skew deviation may occur (one eye looks up, the other looks down).
- Ocular bobbing can occur, or nystagmus that may be direction-changing or vertical.(28187795)
- Extensor or flexor posturing can occur.
tests & investigations
- Basic labs:
- Electrolytes, including Ca/Mg/Phos.
- CBC with differential.
- Coagulation studies.
- Liver function tests, including ammonia.
- Thyroid Stimulating Hormone (TSH).
- VBG or ABG, if hypercapnia is suspected and the patient isn't intubated.
- Toxicologic labs, depending on clinical context. For example:
- Carboxyhemoglobin level (may be obtained with venous blood).
- Salicylate & acetaminophen levels.
- Ethanol level.
- Urine toxicology screen.
- Blood cultures (if sepsis or meningitis is suspected).
- Creatinine kinase, if the patient is found down with possible rhabdomyolysis.
- Pregnancy test, if relevant.
- (1) Most patients will receive a noncontrast head CT to exclude intracranial hemorrhage or other space-occupying lesions.
- (2) CT angiogram (CTA) and CT perfusion:
- Should be considered if there is suspicion for an acute ischemic stroke (e.g., abnormal brainstem findings on exam suggestive of basilar artery occlusion).
- (3) CT venogram (CTV):
- Thrombosis of the straight sinus may cause thalamic dysfunction, leading to coma.
- CT venogram should be considered if there is suspicion of venous sinus thrombosis.
- Indications to perform an LP:
- (1) Suspicion of meningitis or encephalitis (e.g., based on fever, leukocytosis).
- (2) Lack of any alternative explanations for the coma following review of neurologic examination, labs, and neuroimaging.
- In situations where there is low index of suspicion for meningitis or higher risk from lumbar puncture (e.g., coagulopathy), a contrast-enhanced MRI may be considered as an alternative evaluation for meningitis or encephalitis.(24977138)
- Basic CSF investigations should include the usual chemistries and cell counts, as well as PCR for both HSV and VZV. Immunocompromised patients should be tested more broadly (e.g., including cryptococcal antigen). Cytology should be obtained if leptomeningeal carcinomatosis is suspected.
- Elevated opening pressure may suggest infection (e.g., bacterial or cryptococcal meningitis), venous sinus thrombosis, acute liver failure, or leptomeningeal carcinomatosis.
- Additional fluid should be held for more sophisticated testing if needed (e.g., paraneoplastic or autoimmune antibody screens).
- EEG may be indicated if there are reasons to consider nonconvulsive status epilepticus, such as:
- Seizure history (current or prior).
- Clinical indications of possible nonconvulsive status, for example:
- Focal twitching of the hands or face, nystagmus, eye blinking, or chewing movements.
- Recurrent pupillary hippus (pupils dilating/constricting spontaneously), pupillary dilation.
- Focal neurologic findings despite a normal CT scan (e.g., gaze deviation).(28187795)
- MRI is indicated if the above workup fails to reveal a diagnosis.
- Gadolinium contrast may improve the yield for infection or malignancy, so this may be especially useful if a lumbar puncture hasn't already been performed.(24977138)
- MR angiography (MRA) and/or MR venography (MRV) may be considered, similarly to CT angiography and CT venography (e.g., based on the index of suspicion for cerebral venous sinus thrombosis).
- If the patient isn't already intubated, then intubation should be strongly considered prior to MRI to ensure airway protection. Additionally, intubation with deep sedation (often with propofol) may facilitate a high-quality MRI, without movement artefact.
noninvasive ventilation (e.g., BiPAP)
- This may sometimes be considered if hypercapnia is believed to be the cause of the altered mental status.
- If COPD is the cause of the hypercapnia, then BiPAP may be trialed under close supervision (more on this in the chapter on COPD).
- If hypercapnia is the result of substance intoxication or neurological disease, BiPAP is contraindicated. The management of marked hypercapnia in this context is generally intubation. However, for moderate substance intoxication, if the patient is protecting their airway and they are only moderately hypercapnic, then close observation might be adequate (without either BiPAP or intubation).
- Common indications for intubation in this context:
- (a) Failure to protect the airway.
- (b) Intubation may be required to accomplish diagnostic testing safely (e.g., LP, MRI).
therapies to consider
- Glucose should be checked immediately in any patient with altered mental status.
- If hypoglycemia cannot be excluded immediately, give an ampule of D50W empirically (e.g., while awaiting the return of values from the laboratory).
- Wernicke's encephalopathy should be considered in patients with alcoholism, bariatric surgery, eating disorders, or malabsorption.
- When in doubt, treat empirically with 500 mg IV thiamine Q8hr (more on Wernicke's encephalopathy here).
- Suspect opioid intoxication primarily if the respiratory rate decreased.
- If opioid intoxication is possible, naloxone may be empirically trialed with increasing doses to a cumulative dose of ~4 mg.(26438464)
- Note that patients on chronic opioid will generally experience pain and agitation after naloxone, due to withdrawal of opioid effects. This doesn't prove that their stupor/coma is caused solely by opioid, unless they are able to wake up and mentate normally.
- Increased agitation or pain due to naloxone implies having had exposure to opioid, but doesn't necessarily exclude other pathology.
empiric therapy for meningitis & encephalitis
- If there is a significant concern for meningitis, empiric therapy should be given immediately (even before CT or lumbar puncture).
- A reasonable approach is generally:
- 10 mg dexamethasone, followed by ceftriaxone 2 grams IV q12hr.
- Acyclovir 10 mg/kg IV q8hr.
- The added yield of vancomycin and ampicillin here is extremely low, because most of these patients don't actually have meningitis (and the added benefit from vancomycin and ampicillin in meningitis is minimal).
- More on empiric therapy for meningitis here.
osmotherapy & ICP management
- For patients with evidence of elevated intracranial pressure (e.g., optic disc edema on ultrasonography or clinical features strongly suggestive of a herniation syndrome), the following immediate measures may be considered:
- Elevation of the head of the bed.
- Ensuring the neck is in a midposition.
- One dose of osmotherapy may be considered. Possible treatment options may include two 50-ml ampules of hypertonic bicarbonate (1 meq/ml), or a bolus of ~250 ml 3% saline.
- Attention should also be paid to the PaCO2, with a target pCO2 in the low-normal range (e.g., ~35-40 mm).
- Targeting a higher mean arterial pressure may promote adequate cerebral perfusion pressure (e.g., targeting an initial mean arterial pressure of ~75 mm).
- Fever or hyperthermia may pose a threat to the injured brain.
- When possible, target a temperature of 36 C (i.e., avoidance of fever). This may often be achieved with simple measures (e.g., scheduled acetaminophen 1 gram q6hrs and cooling blankets). If simple measures fail, more aggressive control measures may be considered (e.g., an external adaptive cooling system, such as the Arctic Sun).
- If you're struggling with temperature management, this should also be a reminder to refocus your differential diagnosis on disorders that cause thermal abnormalities:
blood pressure management
- Hypotension may be detrimental to the injured brain. Severe hypotension (e.g., mean arterial pressure below ~60-65 mm) should be treated promptly. Hemodynamic assessment with ultrasonography can guide optimal management. In general, immediate correction of critical hypotension will often require vasopressors (rather than attempting fluid loading).
- Hypertension is more challenging:
- Some patients may have posterior reversible encephalopathy syndrome (PRES), in which the hypertension is the cause of the coma. This is usually associated with a mean arterial pressure >140 mm.
- In other patients (e.g., with ischemic stroke), hypertension may be a beneficial physiologic compensatory mechanism that helps perfuse the injured brain. In these patients, aggressive reduction of the blood pressure can be detrimental.
- Ultimately, clinical judgement is required to determine optimal management for the undifferentiated patient. If the blood pressure is profoundly elevated (e.g., mean arterial pressure >140 mm), then gentle reduction may be reasonable. Ensure that pain and agitation are treated adequately, as these may contribute to hypertension.
- Status epilepticus may be suspected based on the following findings:
- History of seizure or abnormal movements prior to coma.
- Subtle signs of seizure activity (e.g., facial or extremity twitching, eye deviation or nystagmus)
- Elevated lactate that rapidly normalizes.
- Video EEG (vEEG) should be emergently arranged. While awaiting vEEG, the following treatments may be considered:
- For intubated patients: increase propofol to a relatively high dose (e.g., 50-80 mcg/kg/min), even if this requires vasopressor support with norepinephrine.
- Levetiracetam loading dose (e.g., 60 mg/kg up to a maximal dose of 4.5 grams).
functional coma (a.k.a. pseudocoma)
Functional coma may be caused by psychiatric disorder. When in doubt, it is safest to assume that the patient is in a true coma and evaluate them accordingly. However, functional coma may often be suspected or diagnosed on the basis of a thorough neurological examination:
- Eyelid movements
- Patients with functional coma may resist eye opening.
- In a genuine deep coma, eyes are in a resting closed position. They may be easily opened. Subsequently they will close in a smooth, gradual movement that cannot be duplicated by an awake person simulating unconsciousness. (Plum & Posnter 2019; page 69)
- Oculocephalic Reflexes (“Doll's Eyes”)
- In a conscious person, the forebrain will override brainstem oculocephalic reflexes. This makes it difficult to simulate the presence of normal oculocephalic reflexes (e.g., acting as if the eyes were fixed on a point in the distance). Erratic eye movements occurring while moving the head may be a clue to the diagnosis of functional coma. (Plum & Posnter 2019; page 81)
- Demonstration of intact optokinetic nystagmus:
- Play Video #1 below on your phone, and hold this in front of the patient's eyes.
- The normal response to this stimulus is optokinetic nystagmus (depicted on Video #2 below). The presence of optokinetic nystagmus indicates an intact occipital lobe, frontal lobe, and brainstem – suggesting functional coma.
- Cold calorics
- Patients with pseudocoma display a physiologically normal response: tonic deviation towards the irrigated ear, followed by rapid nystagmus in the opposite direction.(27741988) The presence of a normal nystagmus response firmly indicates that the patient is physiologically awake.(Plum & Posnter 2019; page 294)
- In neurologically intact patients, infusion of cold water can stimulate nausea and vomiting.
- 💡 The diagnosis of pseudocoma involves methodical and thoughtful application of standard neurologic examinations. Application of extremely aversive or potentially dangerous stimuli should be avoided.
Video #1: Use this to perform the patient examination.
Video #2: For patients in pseudocoma, you would expect to see intact optokinetic nystagmus, as shown here:
If the diagnosis remains unclear, then further testing may be required. The emphasis should always be on prompt exclusion of possibly life-threatening processes (e.g., with neuroimaging). A normal EEG may support the presence of functional coma.
The optimal treatment of functional coma is unclear. In some patients, this may represent catatonia – which can be a component of an underlying psychiatric disorder. Patients often have a combination of organic and functional abnormalities, which can create a complex picture. Consultation with psychiatry may be helpful.
Follow us on iTunes
questions & discussion
To keep this page small and fast, questions & discussion about this post can be found on another page here.
- Trying to guess the diagnosis and failing to perform a complete evaluation (e.g., skipping a full laboratory panel and missing a diagnosis of carbon monoxide intoxication).
- Satisfaction of search: one abnormality is found (e.g., positive ethanol level), causing other abnormalities to be overlooked (e.g., subdural hematoma).
- Failure to perform a complete coma neurological examination. This examination involves only about seven key parts and can be performed in about five minutes. The examination provides critical information regarding which patients should be risk-stratified for emergent or specialized neuroimaging (e.g., STAT CT angiography to evaluate for basilar artery occlusion).
- There are some rare diagnoses which must be diligently screened for (e.g., primary hyperammonemic disorder, carbon monoxide poisoning), even if they don't seem likely in any particular patient.
- EMCrit Podcast 186: Coma with Eelco Wijdicks
- NeuroEMCrit by Neha Dangayach: Clinical Pearls for Coma
- 14970067 Booth CM, Boone RH, Tomlinson G, Detsky AS. Is this patient dead, vegetative, or severely neurologically impaired? Assessing outcome for comatose survivors of cardiac arrest. JAMA. 2004 Feb 18;291(7):870-9. doi: 10.1001/jama.291.7.870 [PubMed]
- 16251950 Saper CB, Scammell TE, Lu J. Hypothalamic regulation of sleep and circadian rhythms. Nature. 2005 Oct 27;437(7063):1257-63. doi: 10.1038/nature04284 [PubMed]
- 20130300 Wijdicks EF. The bare essentials: coma. Pract Neurol. 2010 Feb;10(1):51-60. doi: 10.1136/jnnp.2009.200097 [PubMed]
- 24977138 Vaswani AK, Nizamani WM, Ali M, et al. Diagnostic Accuracy of Contrast-Enhanced FLAIR Magnetic Resonance Imaging in Diagnosis of Meningitis Correlated with CSF Analysis. ISRN Radiol. 2014 Mar 20;2014:578986. doi: 10.1155/2014/578986 [PubMed]
- 26438464 Stevens RD, Cadena RS, Pineda J. Emergency Neurological Life Support: Approach to the Patient with Coma. Neurocrit Care. 2015 Dec;23 Suppl 2:S69-75. doi: 10.1007/s12028-015-0174-1 [PubMed]
- 27320897 Wijdicks EF. Why you may need a neurologist to see a comatose patient in the ICU. Crit Care. 2016 Jun 20;20(1):193. doi: 10.1186/s13054-016-1372-8 [PubMed]
- 27741988 Traub SJ, Wijdicks EF. Initial Diagnosis and Management of Coma. Emerg Med Clin North Am. 2016 Nov;34(4):777-793. doi: 10.1016/j.emc.2016.06.017 [PubMed]
- 28187795 Wijdicks EF. Management of the comatose patient. Handb Clin Neurol. 2017;140:117-129. doi: 10.1016/B978-0-444-63600-3.00008-8 [PubMed]
- 28913634 Cadena R, Shoykhet M, Ratcliff JJ. Emergency Neurological Life Support: Intracranial Hypertension and Herniation. Neurocrit Care. 2017 Sep;27(Suppl 1):82-88. doi: 10.1007/s12028-017-0454-z [PubMed]
- Gusdon et al. 2020 Gusdon, A. M., Nyquist, P. A., & Nelson, S. E. (2020). Management of Elevated Intracranial Pressure. In Current Clinical Neurology (pp. 3-19). (Current Clinical Neurology). Humana Press Inc.. https://doi.org/10.1007/978-3-030-36548-6_1
- 33218655 Karpenko A, Keegan J. Diagnosis of Coma. Emerg Med Clin North Am. 2021 Feb;39(1):155-172. doi: 10.1016/j.emc.2020.09.009 [PubMed]