Coma

Abstract

Coma is a state of profound, sustained unconsciousness in which a patient lies with the eyes closed, cannot be roused by vigorous stimulation, and shows no evidence of awareness of self or environment. It reflects a failure of the brain systems that generate *arousal* — the ascending activating pathways of the brainstem and their thalamic and cortical targets — and is therefore distinct from the disorders that follow it, in which arousal returns without awareness. This article defines coma and separates it along the two independent dimensions of *arousal* and *awareness* from the vegetative or unresponsive wakefulness state, the minimally conscious state, the locked-in syndrome, and brain death. It explains bedside assessment with the Glasgow Coma Scale and the FOUR score, the neuroanatomy of arousal, the discovery of *covert* awareness by neuroimaging, and the science of prognosis.

Keywords: consciousness, arousal, disorders of consciousness

Few clinical states press harder on the science of the mind than coma. A person who a day earlier was awake, talking, and planning can, after a cardiac arrest or a head injury, lie utterly unresponsive — eyes closed, breathing perhaps unaided, yet giving no sign that anyone is home. Coma forces a question that cognitive psychology usually takes for granted: what, mechanically, does it take for a brain to be *conscious* at all? The study of coma and the states that follow it has become one of the most productive natural experiments on that question, because it dissociates the two ingredients of consciousness — the *wakefulness* that arousal supplies and the *awareness* that fills it — that in health always travel together (Laureys, Owen, & Schiff, 2004).

The account below moves from what coma is, through the MeSH subtypes and the spectrum of disorders of consciousness it opens onto, to bedside assessment with the Glasgow Coma Scale, the neuroanatomy of arousal, the startling neuroimaging evidence of covert awareness in some behaviourally unresponsive patients, and the science of prognosis. The recurring theme is that consciousness is not one thing but two dissociable capacities, and that coma is specifically a failure of the first — arousal — on which the second depends.

Figure 1

The Two Dimensions of Consciousness: Arousal and Awareness

What Coma Is

Coma is a state of profound unconsciousness from which the patient cannot be aroused: the eyes remain closed, there is no spontaneous sleep–wake cycle, and no purposeful response can be elicited even by vigorous or painful stimulation. It is defined by the *absence* of the two components of consciousness at once — there is neither *wakefulness* (arousal) nor *awareness* (the content of experience) — and by its *sustained* character, conventionally lasting at least an hour, which separates it from the transient unconsciousness of syncope or a seizure (Laureys, Owen, & Schiff, 2004). The comatose brain is not merely asleep; sleep is a reversible, self-terminating state with preserved arousal cycles, whereas coma is a failure of the arousal machinery itself.

The single most important idea for understanding coma and everything that follows from it is that consciousness has *two independent dimensions*. The first is the *level* of consciousness — arousal or wakefulness — supplied by the ascending activating systems of the brainstem and thalamus. The second is the *content* of consciousness — awareness of self and world — supported by widespread activity across the cerebral cortex and its connections. In the healthy brain the two rise and fall together, so it is easy to treat consciousness as a single quantity. The disorders of consciousness prise them apart: coma abolishes both, but the states that follow it can restore arousal while leaving awareness absent, which is what makes them so conceptually and ethically difficult (Laureys, 2005).

Because arousal is the foundation on which awareness is built, a lesion that destroys arousal necessarily abolishes awareness too — there can be no content without a level to carry it. This is why coma is produced either by widespread damage to *both* cerebral hemispheres or by a focal lesion of the *ascending arousal system* in the upper brainstem and thalamus, whereas a lesion confined to one hemisphere, however large, does not by itself cause coma (Laureys, Owen, & Schiff, 2004). Coma is therefore rarely a permanent state in itself: within two to four weeks the arousal systems typically recover enough that the eyes open, and the patient passes into one of the other disorders of consciousness — or recovers, or dies.

Types of Coma

In the Medical Subject Headings (MeSH) vocabulary that indexes the biomedical literature, Coma is filed as a form of unconsciousness, the broader category of states in which awareness is absent. It is worth stressing that a MeSH classification is an *indexing device*, not a clinical theory: the tree records how papers are catalogued, and the descriptors filed beneath Coma are catalogued by *cause* and *context*, which cross-cut the far more important clinical axis — *depth* and *prognosis* — along which coma is actually described at the bedside. The three descriptors MeSH files directly under Coma are listed below for completeness.

These indexing subtypes should not be confused with the clinical typology that actually guides care. Clinically, comas are grouped by *cause* into *structural* (trauma, haemorrhage, infarction, tumour, or herniation damaging the arousal system) and *metabolic or diffuse* (anoxia after cardiac arrest, poisoning, hypoglycaemia, hepatic or renal failure), and this distinction drives investigation and treatment. But the axis that matters most for the patient and family — the *depth* of coma and its *likely outcome* — is captured not by any of these categories but by graded clinical scales and by what the coma resolves *into*, which the next sections address (Bernat, 2006).

Core Features

The defining feature of coma is *unarousable unresponsiveness*. The examiner cannot, by voice or by pain, produce eye opening, comprehensible speech, or purposeful movement. Reflexive responses may persist — a limb may withdraw or stiffen, the pupils may still react — but nothing the patient does is directed, and the eyes stay closed because the arousal system that would open them is offline. This absence of a sleep–wake cycle, visible as continuously closed eyes without spontaneous opening, is the clearest bedside marker separating coma from the states that follow it, in which the eyes open even though awareness has not returned (Laureys, Owen, & Schiff, 2004).

The second core feature is that coma is *time-limited*. Because the arousal systems either recover or fail catastrophically, coma in the strict sense rarely lasts beyond two to four weeks. The eyes then begin to open in cycles that resemble sleep and waking, and the patient is, by definition, no longer comatose — even if no awareness has returned. This transition is not recovery; it is the emergence of *wakefulness without awareness*, the state historically called the vegetative state and now often termed the unresponsive wakefulness syndrome. Understanding coma therefore requires understanding the spectrum of conditions it opens onto, because “coma” in lay usage often refers to these longer-lasting states rather than to true coma (Bruno et al., 2011).

Underlying both features is the dissociation of arousal and awareness with which this article began. In coma both are absent; the value of grading scales and of the spectrum below is that they let clinicians track, separately, whether *arousal* is returning (eye opening, sleep–wake cycles) and whether *awareness* is returning (reproducible, purposeful responses to command). Keeping the two axes distinct is not a theoretical nicety: it is what prevents the return of mere wakefulness from being mistaken for the return of the person (Laureys, 2005).

Disorders of Consciousness

Coma is the entry point to a graded spectrum of *disorders of consciousness*, defined by how much of each dimension has returned. When arousal recovers but awareness does not, the result is the *vegetative state* — eyes open, sleep–wake cycles present, reflexive movements and even grimacing or crying, but no reproducible sign of awareness of self or environment. Because “vegetative” is both pejorative and theory-laden, a European consortium proposed the descriptive term *unresponsive wakefulness syndrome* (UWS) for the same condition, and the two are now used interchangeably (Bruno et al., 2011). The category was itself a mid-twentieth-century clarification: Jennett and Plum coined *persistent vegetative state* to name a condition that until then had no agreed label (Jennett & Plum, 1972), and its natural history and diagnostic criteria were later codified by a multi-society task force (The Multi-Society Task Force on PVS, 1994).

Above the vegetative state sits the *minimally conscious state* (MCS), defined by Giacino and colleagues as a condition of severely altered consciousness in which there is *inconsistent but clearly discernible* evidence of awareness — following a simple command, gesturing yes or no, reaching for objects, or tracking a moving stimulus with the eyes (Giacino et al., 2002). The MCS was a crucial addition because it named the many patients who are neither unaware nor reliably communicative, and because emergence from it — the return of functional communication or object use — is a recognised milestone. Distinguishing MCS from UWS is difficult and error-prone: standardised behavioural assessment reclassifies a substantial fraction of patients judged vegetative on bedside impression as minimally conscious (Schnakers et al., 2009).

Two further states complete the map and are routinely confused with coma. *Locked-in syndrome* is not a disorder of consciousness at all: a lesion of the ventral pons spares the arousal and cortical systems but destroys the motor pathways, leaving a fully aware patient almost completely paralysed, often able to communicate only by vertical eye movements and blinking. *Brain death* is the opposite extreme — the irreversible loss of all brain function, including the brainstem, which is a legal and clinical criterion of death rather than a state of deep coma (Wijdicks et al., 2010). The whole spectrum, from coma through UWS and MCS to emergence, is what recent guidelines organise under the single heading of the *chronic disorders of consciousness* (Bernat, 2006).

Assessment

The depth of coma is quantified at the bedside by graded scales that avoid vague terms such as “stuporous” in favour of observable responses. The most widely used is the *Glasgow Coma Scale* (GCS), introduced by Teasdale and Jennett in 1974, which scores three behaviours independently: *eye opening* (1–4), *verbal response* (1–5), and *best motor response* (1–6), summed to a total from 3 (no response at all) to 15 (fully alert) (Teasdale & Jennett, 1974). Its genius was reliability: by specifying concrete responses, it let different observers — nurses, junior doctors, neurosurgeons — arrive at the same score, making coma depth communicable and trackable over time. Four decades on, the GCS remains embedded in trauma triage and outcome prediction worldwide (Teasdale et al., 2014).

The GCS has a well-known limitation: the verbal score cannot be obtained in an intubated patient, and it does not test brainstem reflexes, which matter most in the deepest comas. The *FOUR score* (Full Outline of UnResponsiveness), developed and validated by Wijdicks and colleagues, was designed to fill both gaps — it grades eye responses, motor responses, brainstem reflexes, and respiration, each from 0 to 4, and so can be applied to ventilated patients and detects the locked-in syndrome and signs of brain death that the GCS misses (Wijdicks et al., 2005). For the longer-lasting disorders of consciousness, standardised *behavioural* assessment — systematically probing for reproducible signs of awareness — is essential, because a single bedside impression misclassifies many patients (Schnakers et al., 2009), a problem that modern diagnostic guidelines address by combining repeated standardised examination with, where available, neuroimaging and electrophysiology (Giacino et al., 2018; Kondziella et al., 2020).

Worked Example

The Glasgow Coma Scale makes coma depth concrete, and working through a score shows both its logic and its pitfalls. The rule is simple: score the *best* response observed in each of the three categories and sum them. Eye opening scores 4 (spontaneous), 3 (to speech), 2 (to pain), or 1 (none). Verbal response scores 5 (oriented), 4 (confused conversation), 3 (inappropriate words), 2 (incomprehensible sounds), or 1 (none). Best motor response scores 6 (obeys commands), 5 (localises pain), 4 (normal flexion/withdrawal), 3 (abnormal flexion), 2 (extension), or 1 (none) (Teasdale & Jennett, 1974).

Consider a patient after a road-traffic head injury. She does not open her eyes to speech but opens them when the examiner presses on the nail bed — *eye opening = 2*. She makes no words, only groaning sounds — *verbal = 2*. When a painful stimulus is applied to the trunk, her hand moves purposefully toward the site — *best motor = 5 (localises)*. Her total is 2 + 2 + 5 = 9. By the conventional bands — severe 3–8, moderate 9–12, mild 13–15 — a total of 9 places her at the boundary of moderate injury, and because localising to pain (motor 5) is a comparatively favourable sign, the motor subscore carries most of the prognostic weight.

Now suppose that, an hour later, she no longer localises but only withdraws in a stereotyped flexion — *motor = 3* — while eye and verbal scores are unchanged. Her total falls to 2 + 2 + 3 = 7, crossing into the severe band. Two lessons follow. First, the *total can mislead*: a drop driven entirely by the motor subscore signals a deteriorating brainstem and demands action that the two-point change in the total understates, which is why the three components are always reported separately (as E2 V2 M3), not merely summed. Second, the score is only as good as the responses are obtainable: sedation, intubation, or paralysis can floor the verbal or motor score artefactually — exactly the limitation the FOUR score was built to address (Wijdicks et al., 2005).

Causes and Neuroanatomy

The neuroanatomy of coma follows directly from the two-dimensional model of consciousness. Arousal is generated by the *ascending reticular activating system* (ARAS), a network of nuclei in the upper brainstem — the pontine and midbrain tegmentum — that projects, via the thalamus and the basal forebrain, to the whole of the cerebral cortex, driving the cortical activation that makes wakefulness possible. Because this system is anatomically compact where it passes through the upper brainstem, a small, strategically placed lesion there can abolish arousal completely, producing coma out of all proportion to its size (Laureys, Owen, & Schiff, 2004). This is why coma has, in essence, only two anatomical routes: destroy the ARAS directly, or destroy so much of both hemispheres (or so profoundly depress their metabolism) that the cortex cannot respond to the arousal it is still receiving.

These two routes map onto the two great classes of cause. *Structural* lesions — a brainstem stroke, a haemorrhage, a tumour, or a mass in one hemisphere that swells and *herniates* to crush the brainstem — damage the arousal system focally or by compression. *Diffuse* or *metabolic* insults — the global oxygen deprivation of a cardiac arrest, poisoning, hypoglycaemia, or the toxins of liver and kidney failure — depress the whole brain at once. The former demands emergency imaging and often surgery; the latter demands correction of the underlying physiology. In the longer-lasting disorders of consciousness that coma resolves into, the critical lesion shifts from arousal to *awareness*: functional imaging shows that the vegetative state is marked by preserved brainstem arousal but grossly reduced metabolism and disconnected activity across the frontoparietal cortical network that supports the content of consciousness (Laureys, 2005). The neural signature of these states is thus one of *disconnection* within a distributed system, not the loss of any single structure.

Covert Awareness

The most striking development in the science of coma is the discovery that the bedside examination can be wrong in a specific and consequential way: some patients who show *no* behavioural sign of awareness are nonetheless aware, their responses hidden by an inability to move. In a landmark study, Owen and colleagues asked a woman who met every clinical criterion for the vegetative state to imagine playing tennis and to imagine walking through her house; her brain, scanned by functional MRI, produced the same distinct activation patterns — in the supplementary motor area and in spatial-navigation regions respectively — as healthy volunteers performing the same imagery, demonstrating command-following that no behaviour betrayed (Owen et al., 2006). The result was extended into a communication channel: patients could answer yes/no questions by choosing which of the two mental images to perform (Monti et al., 2010).

This phenomenon, now termed *cognitive motor dissociation* or covert consciousness, has been found not only in chronic patients but in the acute intensive-care setting. Using EEG rather than fMRI, Claassen and colleagues detected command-related brain activity in about 15% of acutely brain-injured patients who were behaviourally unresponsive, and this early covert responsiveness predicted later recovery (Claassen et al., 2019). The findings raise the possibility that some patients diagnosed as unaware are misclassified — the debate over whether such patients occupy a “cortically mediated state” distinct from the classical minimally conscious state turns on exactly this point (Naccache, 2018). They also raise profound ethical questions about a patient who can think but not act, and they have driven guidelines to recommend that neuroimaging and electrophysiology supplement, rather than merely follow, the behavioural examination (Giacino et al., 2018).

Prognosis and Treatment

Prognosis is the question families ask first and the one coma science exists to answer. Outcome depends heavily on *cause* — coma after traumatic brain injury carries a substantially better prognosis than coma after cardiac-arrest anoxia — on *depth* and *duration*, and on specific examination and test findings. Multimodal assessment now combines the clinical examination with structural and functional neuroimaging and electrophysiology: PET imaging of cortical metabolism, for instance, distinguishes minimally conscious from vegetative patients and predicts recovery more accurately than bedside assessment alone (Stender et al., 2014). No single test is definitive, and modern guidelines stress that prognosis should never rest on one finding in the first days, both because early covert consciousness predicts recovery (Claassen et al., 2019) and because self-fulfilling pessimism can prematurely end care (Kondziella et al., 2020).

Treatment of coma is, first and always, treatment of its *cause* — restore oxygenation and circulation, evacuate a haematoma, correct the metabolic derangement, treat the infection — combined with meticulous supportive care of a patient who cannot protect their own airway or move. For the prolonged disorders of consciousness that follow, the therapeutic record is thinner but no longer empty: the stimulant amantadine has been shown to accelerate functional recovery in the vegetative and minimally conscious states, and experimental approaches from deep-brain stimulation of the central thalamus — which transiently improved responsiveness in a minimally conscious patient in a proof-of-principle study (Schiff et al., 2007) — to transcranial stimulation are under active investigation (Thibaut et al., 2019). The overarching lesson of the recovery literature is that the brain retains more capacity for late reorganisation than the old assumption of a fixed, hopeless outcome allowed (Edlow et al., 2021).

Discussion

The modern science of coma is a story of conceptual clarification driving clinical progress. For most of medical history, unconsciousness was a single undifferentiated darkness. The decisive move was the recognition that consciousness has two separable dimensions — arousal and awareness — which allowed the tangle of “coma” to be resolved into distinct, definable states: true coma, the vegetative or unresponsive wakefulness state, the minimally conscious state, locked-in syndrome, and brain death (Laureys, Owen, & Schiff, 2004). Each of these was named and criterion-defined within living memory — the vegetative state in 1972 (Jennett & Plum, 1972), the minimally conscious state in 2002 (Giacino et al., 2002) — and each refinement improved both communication and care.

That clarification carried practical force. Reliable grading of coma depth by the Glasgow Coma Scale made outcomes comparable across centres and embedded coma assessment in everyday trauma care (Teasdale et al., 2014). The discovery of covert consciousness then delivered the field's most humbling lesson: the behavioural examination, for all its refinement, can miss a conscious mind entirely, and diagnosis must therefore reach beyond behaviour to the brain itself (Owen et al., 2006; Claassen et al., 2019). Coma research has thus repeatedly forced cognitive science to make its concept of consciousness *operational* — to say precisely what would count as evidence of awareness — and in doing so it has sharpened the concept for everyone.

Cognitive Implications

For cognitive psychology, coma and the disorders of consciousness are the clearest available demonstration that consciousness is not a single, indivisible property but a structured capacity that can be taken apart. The dissociation of arousal from awareness — wakefulness with no content in the vegetative state, intact content with almost no output in locked-in syndrome — is a natural dismantling of the machinery that theories of consciousness must explain. It shows that the *level* of consciousness and its *contents* have distinct neural substrates, and it locates the neural correlates of consciousness for awareness not in the brainstem that supplies arousal but in the integrity and connectivity of the widespread cortical networks that the brainstem activates (Laureys, 2005).

The covert-consciousness findings sharpen a methodological point that reaches to the foundations of the field. Cognitive psychology infers hidden mental states from behaviour, but coma exposes the limit of that inference: a patient may follow a command in imagination and produce a reliable, specific brain response while remaining wholly unable to act (Owen et al., 2006). This dissociation of *cognition* from *behavioural output* validates the use of brain activity as a direct measure of mental process, independent of the motor system, and it dovetails with the wider programme of using neuroimaging to read consciousness and covert cognition where behaviour is absent (Monti et al., 2010). It is a striking vindication of the idea that the mind can, in principle, be observed in the brain even when the body is silent.

Current Directions

Current research is converging on the problem of *detecting* consciousness where behaviour cannot. The active-paradigm methods pioneered with fMRI are being adapted to portable EEG so that covert command-following can be screened for at the bedside in the intensive-care unit, where its prognostic value is greatest (Claassen et al., 2019). Alongside them, resting-state and stimulation-based markers — measures of the brain's capacity to sustain complex, integrated activity — are being validated as indices of the *capacity* for consciousness that do not require the patient to perform a task at all, and multimodal batteries combining PET, fMRI, and EEG are being tested against long-term outcome (Stender et al., 2014; Edlow et al., 2021).

A second front is therapeutic and definitional. The modest but real success of amantadine and the proof-of-principle results for central-thalamic and transcranial stimulation have made the prolonged disorders of consciousness a target for treatment rather than only for prognosis, and trials are working to identify which patients might respond (Thibaut et al., 2019). In parallel, the field continues to argue over its own categories — whether covertly aware patients constitute a distinct state, and how the nomenclature of vegetative, unresponsive wakefulness, and minimally conscious should be harmonised (Naccache, 2018) — an unusually productive disagreement, because each redefinition has repeatedly turned out to change what clinicians look for and what they find (Kondziella et al., 2020).

Common Misconceptions

“A coma can last for years.”

True coma — eyes closed, no arousal — rarely lasts beyond two to four weeks. The long-lasting states the public calls “coma” are the vegetative/unresponsive wakefulness state or the minimally conscious state, in which the eyes open and arousal has returned even though awareness has not (Bruno et al., 2011).

“A vegetative patient with open eyes is aware.”

Eye opening reflects the return of arousal, not awareness. In the vegetative/unresponsive wakefulness state the patient is awake but shows no reproducible sign of awareness — the two dimensions have come apart (Laureys, 2005).

“If a patient shows no response, there is no one there.”

Neuroimaging has found covert, command-following awareness in a minority of behaviourally unresponsive patients. Absence of behavioural response is not proof of absence of consciousness (Owen et al., 2006; Claassen et al., 2019).

“Brain death is just a very deep coma.”

Brain death is the irreversible loss of all brain function, including the brainstem, and is a legal and clinical criterion of death. A comatose patient, by contrast, retains brain function and may recover (Wijdicks et al., 2010).

Glossary

Arousal.

The level or wakefulness dimension of consciousness, generated by the ascending activating systems of the brainstem and thalamus; abolished in coma.

Ascending reticular activating system (ARAS).

The network of upper-brainstem nuclei that, via the thalamus and basal forebrain, activates the cortex and sustains wakefulness; a focal lesion here can cause coma.

Awareness.

The content dimension of consciousness — experience of self and environment — supported by widespread cortical networks; can be absent even when arousal has returned.

Brain death.

The irreversible loss of all functions of the entire brain, including the brainstem; a clinical and legal criterion of death, not a deep coma.

Cognitive motor dissociation.

The condition of a behaviourally unresponsive patient who nonetheless shows command-following detectable by neuroimaging or EEG; also called covert consciousness.

Coma.

A sustained state of unarousable unresponsiveness with eyes closed and no sleep–wake cycle, in which both arousal and awareness are absent.

Consciousness.

The state of being aware; analysed in the disorders of consciousness as two dissociable dimensions, arousal (level) and awareness (content).

FOUR score.

The Full Outline of UnResponsiveness, a coma scale grading eye and motor responses, brainstem reflexes, and respiration; applicable to intubated patients the GCS cannot fully score.

Glasgow Coma Scale (GCS).

The standard bedside scale of coma depth, summing eye-opening, verbal, and best-motor responses to a total from 3 to 15.

Locked-in syndrome.

Near-complete paralysis from a ventral pontine lesion with fully preserved arousal and awareness; not a disorder of consciousness, though easily mistaken for one.

Minimally conscious state (MCS).

A state of severely altered consciousness with inconsistent but clearly discernible signs of awareness, such as command-following or visual tracking.

Persistent vegetative state.

The historical term for wakefulness without awareness lasting beyond a set period; now often replaced by unresponsive wakefulness syndrome.

Stupor.

A state of deep unresponsiveness from which a person can be roused only briefly by vigorous, usually painful, stimulation; one step less severe than coma on the continuum of impaired arousal.

Unresponsive wakefulness syndrome (UWS).

The descriptive, non-pejorative term for the vegetative state: eyes-open wakefulness with no reproducible evidence of awareness.

Key Researchers

Joseph T. Giacino

(living). A neuropsychologist at Spaulding Rehabilitation Hospital and Harvard Medical School who defined the minimally conscious state and led the 2018 practice guideline on the disorders of consciousness. ORCID

Bryan Jennett

(1926–2008). A Glasgow neurosurgeon who co-created the Glasgow Coma Scale and, with Fred Plum, named the persistent vegetative state, shaping the modern framework of the disorders of consciousness. Wikipedia

Steven Laureys

(living). A Belgian neurologist who founded the Coma Science Group at the University of Liège and did much to establish the two-dimensional (arousal–awareness) framework and the neuroimaging of the vegetative state. ORCID

Adrian M. Owen

(living). A neuroscientist at Western University whose 2006 study detected covert, command-following awareness by fMRI in a patient diagnosed as vegetative, opening the study of cognitive motor dissociation. ORCID

Fred Plum

(1924–2010). An American neurologist, co-author of *The Diagnosis of Stupor and Coma*, who coined “locked-in syndrome” and co-named the persistent vegetative state. Wikipedia

Graham Teasdale

(living). A neurosurgeon at the University of Glasgow who, with Bryan Jennett, created the Glasgow Coma Scale in 1974 and led its 40-year reappraisal, giving medicine its standard language for coma depth. ORCID

Eelco F. M. Wijdicks

(living). A neurointensivist at the Mayo Clinic who developed the FOUR score coma scale and led the American Academy of Neurology guideline on determining brain death. ORCID

Frequently Asked Questions

What is a coma?

A coma is a sustained state of unconsciousness in which the patient lies with eyes closed, cannot be woken by vigorous or painful stimulation, and shows no sign of awareness. Both dimensions of consciousness — arousal and awareness — are absent (Laureys, Owen, & Schiff, 2004).

How is a coma different from a vegetative state?

In coma the eyes stay closed and there is no arousal. In the vegetative or unresponsive wakefulness state, arousal has returned — the eyes open and sleep–wake cycles resume — but awareness has not. Coma usually resolves within weeks into recovery, this state, or death (Bruno et al., 2011).

How long can a coma last?

True coma rarely lasts beyond two to four weeks, because the arousal systems either recover or fail. The very long “comas” described in the media are almost always the vegetative/unresponsive wakefulness or minimally conscious states, in which the eyes are open (Bernat, 2006).

How is the depth of a coma measured?

Most often with the Glasgow Coma Scale, which scores eye opening, verbal response, and best motor response for a total of 3 to 15. The FOUR score adds brainstem reflexes and respiration and can be used in intubated patients (Teasdale & Jennett, 1974; Wijdicks et al., 2005).

Can someone in a coma hear or think?

Sometimes, in a limited sense. Neuroimaging has shown that a minority of behaviourally unresponsive patients can follow commands in imagination, producing reliable brain responses — a phenomenon called cognitive motor dissociation or covert consciousness (Owen et al., 2006; Claassen et al., 2019).

What is locked-in syndrome?

A condition, usually from a brainstem stroke, in which a fully aware patient is almost completely paralysed and can often communicate only by eye movements. It is not a disorder of consciousness — the mind is intact — but is easily mistaken for coma (Laureys, Owen, & Schiff, 2004).

Is brain death the same as coma?

No. Brain death is the irreversible loss of all brain function, including the brainstem, and is a criterion of death. A comatose patient retains brain function and may recover (Wijdicks et al., 2010).

Can coma be treated?

The first treatment is always to reverse the cause — restore oxygen and blood flow, remove a clot, correct the metabolic problem — with intensive supportive care. For the prolonged disorders of consciousness that may follow, amantadine and experimental brain-stimulation approaches are under investigation (Thibaut et al., 2019).

Support Organizations

• Coma Science Group (University of Liège) — a leading research group on the diagnosis, neuroimaging, and prognosis of the disorders of consciousness.
• Brain Injury Association of America (BIAA) — information and support for patients and families affected by brain injury and prolonged disorders of consciousness.
• American Academy of Neurology (AAN) — the professional body whose practice guidelines cover coma, brain death, and the disorders of consciousness.
• National Institute of Neurological Disorders and Stroke (NINDS) — public information and research funding on coma, traumatic brain injury, and consciousness.

References

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Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness: A practical scale. The Lancet, 304(7872), 81–84. https://doi.org/10.1016/S0140-6736(74)91639-0

The Multi-Society Task Force on PVS. (1994). Medical aspects of the persistent vegetative state (first of two parts). New England Journal of Medicine, 330(21), 1499–1508. https://doi.org/10.1056/NEJM199405263302107

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Laureys, S., Owen, A. M., & Schiff, N. D. (2004). Brain function in coma, vegetative state, and related disorders. The Lancet Neurology, 3(9), 537–546. https://doi.org/10.1016/S1474-4422(04)00852-X

Wijdicks, E. F. M., Bamlet, W. R., Maramattom, B. V., Manno, E. M., & McClelland, R. L. (2005). Validation of a new coma scale: The FOUR score. Annals of Neurology, 58(4), 585–593. https://doi.org/10.1002/ana.20611

Laureys, S. (2005). The neural correlate of (un)awareness: Lessons from the vegetative state. Trends in Cognitive Sciences, 9(12), 556–559. https://doi.org/10.1016/j.tics.2005.10.010

Owen, A. M., Coleman, M. R., Boly, M., Davis, M. H., Laureys, S., & Pickard, J. D. (2006). Detecting awareness in the vegetative state. Science, 313(5792), 1402. https://doi.org/10.1126/science.1130197

Bernat, J. L. (2006). Chronic disorders of consciousness. The Lancet, 367(9517), 1181–1192. https://doi.org/10.1016/S0140-6736(06)68508-5

Schiff, N. D., Giacino, J. T., Kalmar, K., Victor, J. D., Baker, K., Gerber, M., Fritz, B., Eisenberg, B., O'Connor, J., Kobylarz, E. J., Farris, S., Machado, A., McCagg, C., Plum, F., Fins, J. J., & Rezai, A. R. (2007). Behavioural improvements with thalamic stimulation after severe traumatic brain injury. Nature, 448(7153), 600–603. https://doi.org/10.1038/nature06041

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