Altered consciousness
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approach to the patient with altered consciousness, how to decide the prognosis and how to map out the outcome
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Altered consciousness
- 1. Altered Consciousness Approach to Patient Assessment Dr Mukhtar PG Neurosurgery HMC, Peshawar
- 2. Road Map • Basic Taxonomy • Discussion of; • Coma • Vegetative State • Minimal Conscious State (MCS) • Akinetic Mutism • Physiologic & Anatomic Considerations • Guide to Prognosis • Recent Developments & their applications
- 3. Introduction
- 4. Consciousness Content Arousal Cognitive + Affective responses Interaction with environment
- 5. • Altered consciousness is the most common clinical finding encountered by the neurosurgeon • Clinical syndromes associated with brain injury include; • Coma • Vegetative State (VS) • Minimally Conscious State (MCS) • Akinetic Mutism and others • Knowledge of forebrain arousal mechanisms; • formulating probabilities & recovery time frames • Spectral knowledge of Coma, VS or MCS
- 6. • The aim of this presentation is; • NOT to present the details of numerous diagnoses; • Rather; • To conceptualize the neurologic disorders of consciousness • And formulation of an organized & physiological approach towards a patient with altered consciousness • Approach to patients with altered consciousness require; • Foundation of the basic principles underlying maintenance of normal wakeful state • Knowledge of the forebrain arousal mechanisms • Effects of various types of neurologic injury on consciousness
- 7. Taxonomy Schiff & Plum’s working definition for normal wakeful conscious state • At its least, normal human consciousness consists of a serially time- ordered, organised, restricted and reflective awareness of self and the environment. Moreover, it is an experience of graded complexity and quantity.
- 8. • Neuropsychological components of conscious brain state are organized in a hierarchical architecture. Arousal Memory Mood-emotion Awareness Attention Intention
- 11. Coma
- 12. • Total absence of patterned behavioural arousal or EEG features of sleep-wake architecture • By definition the term implies that; • The state has endured for at least 1 to six hours • It is a transient condition and does not persist beyond 10 to 14 days; unless complicated by concurrent systemic illness
- 13. • Motionless patient in eyes-closed state without spontaneous eye opening periods • Deep forceful stimulation may produce facial grimace or withdrawal reflexes from the spine • Lack of localisation and absence of organised sequence of movements • Lack of primitive reflexes
- 15. Vegetative state
- 16. • first described in 1940 by Ernst Kretschmer who called it apallic syndrome • The term was introduced by Jennett & Plum in 1972 and defined it as; “The clinical syndrome of ‘persistent vegetative state’, identified by dissociation of an apparent recovery of behavioural wakeful arousal associated with periods of eye opening alternating with eye closure and where the patient does not show any evidence of awareness of self or environment” • Earlier use of the term implied a VS lasting longer than 30 days as ‘Persistent Vegetative State’.
- 17. • VS typically follows an initial coma produced by the initial insult to brain • Two most common causes of VS; • Severe TBI • Cardiac Arrest • Loss of thalamic neurons and thalamocortical connections especially the central thalamic intralaminar nuclei and components of thalamic association nuclei • Bilateral injuries to these areas produce coma
- 18. • Cardiac arrest is associated with widespread neocortical neuronal death as compared to Diffuse Axonal Injury due to trauma (64% vs 11%) • No significant brainstem damage on autopsy, which implies that VS is primarily a disorder of corticothalamic system integration • Stereotyped limbic responses, such as grimaces are preserved.
- 20. • First level of behavioural recovery beyond VS • Definition • a condition of severely altered consciousness in which minimal but definite behavioural evidence of self or environmental awareness is demonstrated • consistent and sustained visual tracking or fixation • Intermittent spoken language responses, verbal output & gestures
- 23. Akinetic Mutism
- 24. • MCS patients who functionally can communicate, however, demonstrate a severe reduction in spontaneous behaviour or extremely slowed interactive responses • Highly attentive, vigilant patient with wide opening eyes and deliberate visual tracking and no other spontaneous behaviour • Injury patterns; bilateral anterior medical regions of cerebral cortex, bilateral caudate injury, bilateral central thalamic lesions, basal forebrain injuries, mesencephalic reticular formation damage
- 25. • Two types; Apathetic AM and Herpathic AM Or Mesencephalic and Frontal AM • Classic finding after Anterior communicating artery aneurysm rupture • Slow Syndrome; severe memory loss, slowed behavioural responses, listless, apathetic appearance
- 27. MRI showing bilateral paramedian thalamic infarction. Shetty A C et al. Age Ageing 2009;38:350-351
- 28. Anatomic and Physiologic Considerations Basis of assessment strategies
- 29. • Disorders of consciousness could belong to one of the following two categories, functionally & anatomically; i. Diffuse functional impairment of both hemispheres due to direct injury ii. Selective impairment of midline or paramedian upper brainstem & basal forebrain regions • Three categories of patients; i. Significant structural injury with poor predictors for death/disability ii. Patients with early steady recovery with good predictors iii. Patients with mixture of structural/functional disturbance
- 30. • Category 1 patients: • Bedside exam with clinical judgment • Large size prospective studies supporting predictors for death or permanent VS (loss of motor responses/pupillary and corneal reflexes) • Category 2 patients: • No realistic characterisation exist, in terms of stages and time frame • Early achievement of consciousness/high cortical functions
- 31. • Category 3 patients: • Significant diagnostic/prognostic challenge • Known structural injury to critical brain areas but without indicators of poor outcome or permanence of their disability • At present no reliable measures/clinical judgment for better predictability of their condition • Establishment of exact diagnosis (Coma, VS, MCS) • Most common transitional signs from VS to MCS are visual fixation and visual tracking
- 32. Approach to the Patient clinical pearls
- 33. • GCS; • technically, a scale for measuring impaired consciousness • ‘Coma’, simply implies ‘unresponsiveness’ • 90% patients below GCS 8 & none above GCS 9 signifies the above definition of COMA • Therefore, GCS 8 is the operational definition of coma • Slight modification for children
- 34. • Pseudocoma • Locked-in Syndrome • Psychiatric • Neuromuscular weakness
- 35. • ABC… • Initial baseline investigations • RFTs, Electrolytes, CBC, ABGs • Toxicology, calcium, ammonia, AEDs level (as appropriate) • Initial resuscitation (if the cause is obvious) • I/V Glucose bolus • Naloxone • Flumazenil • Thiamine
- 36. • Core Neurologic Exam • Respiratory rate & Pattern • Cheyne-Stokes • Hyperventilation • Cluster breathing • Apneustic • Ataxic • Pupils • The light reflex is useful in distinguishing metabolic from structural coma • Metabolic causes of fixed dilated pupils include glutethionoid toxicity, anoxic encephalopathy, anticholinergic
- 37. • Pinpoint pupils in narcotics overdosage • Unequal size (anisocoria) • Fixed & dilated pupil (Oculomotor palsy, Herniation syndrome) • Horner syndrome • Bilateral pupillary defects • Pinpoint with very little reaction (pontine lesion) • Bilateral fixed & dilated (7 – 10 mm) • Subtotal medullary damage/hypothermia/anoxia • Midposition fixed (4 - 6 mm) • Extensive midbrain damage
- 39. • Extraocular Muscle function A. Bilateral conjugate deviation • Frontal lobe lesion (towards affected side) • Pontine lesion (away from the lesion) • Medial thalamic haemorrhage (wrong way gaze) • As a rule supratentorial lesions cause deviation towards the lesion side while infratentorial lesions cause deviation away from the lesion side except in ‘wrong way gaze’
- 40. B. Unilateral outward deviation on side of larger pupil • Uncal herniation C. Unilateral inward deviation (VI nerve palsy) D. Skew deviation • III or IV nerve/nucleus lesion • Infratentorial lesion
- 42. • Manoeuvres to test brain stem • Oculovestibular reflex (Ice Water Caloric) • Patient with intact brainstem deviate towards side of the caloric • Oculocephalic reflex (doll’s eyes) has similar objective but dangerous for C-spine if it is not cleared
- 44. • One mnemonic used to remember the FAST direction of nystagmus is COWS. • COWS: Cold Opposite, Warm Same. • Cold water = FAST phase of nystagmus to the side Opposite from the cold water filled ear • Warm water = FAST phase of nystagmus to the Same side as the warm water filled ear • In other words: Contralateral when cold is applied and ipsilateral when warm is applied
- 48. • No response in case of; • NMBAs, toxins • Metabolic cause • Brain death • Massive infratentorial lesion • Asymmetric in case of infratentorial lesion • Nystagmus without tonic deviation diagnostic of psychogenic coma • Contralateral eye adduction failure: Internuclear ophthalmoplegia
- 49. • Motor • Babinski • Appropriate: corticospinal tracts/cortex intact • Asymmetric: supratentorial lesion • Inconsistent/Variable: Seizures, Psychogenic • Symmetric: metabolic, asterixis, tremor • Hyporeflexia: consider myxoedema coma
- 51. • Patterns: • Decorticate Large cortical or subcortical lesion • Decerebrate Brainstem injury at or below midbrain • Arms flexed, legs flaccid: pontine lesion • Arms flaccid, legs normal: anoxic injury (man in the barrel syndrome) • Ciliospinal reflexes • Pupillary dilatation to cutaneous noxious stimuli) • Tests integrity of sympathetic pathways • Bilateral present: metabolic • Unilaterally present: lesion III if on side of larger pupil • Bilaterally absent: not diagnostic
- 52. Formulating Prognosis A Brief Guide
- 53. • Outcome is always dependent upon the clinical findings, time from the injury and cause of injury • Disorders of consciousness are transitional states with increasingly long time windows • (i.e., coma to VS, VS to MCS) • Step 1: Locate the patient temporally in the natural history of a disorder • (e.g., VS in the first month after a severe traumatic brain injury is not comparable to VS at 6 months or 1 year) • Step 2: Identify the cause
- 54. • Coma is an inherently grave illness associated with very high mortality; • 40% to 50% of patients in a coma after brain trauma • 54% to 88% of patients comatose after cardiac arrest • Outcome always depends upon negative clinical predictors • Bilateral loss of pupillary and corneal reflexes • Recovery from TBI coma is higher than coma after cardiac arrest
- 55. • Prognosis of VS depends on injury mechanism • Non-traumatic VS for 3 months is permanent VS • These timeframes are longer for traumatic VS, • usually longer than 1 year to declare permanence • Transitions from one state to another are not equally distributed across a continuum
- 56. • Prognosis in MCS is least well characterised because this diagnostic category is relatively new • Studies suggest that significant recovery after 1 year may occur in some patients • Patients with MCS show faster changes in rate of recovery during the first year post-injury
- 57. Emerging role of Neuroimaging
- 58. • The use of functional MRI for differentiation of various states of altered consciousness • Ruling out false positive VS or MCS patients • Limitations of this technology include; • Cost, availability, expertise, legal implications • Obtaining reliable fMRI data from severely brain injured patient • Misinterpretation and lack of generalisation due to limited patient data
- 59. Thanks!
Editor's Notes
- Consciousness has two major components: content and arousal. The content of consciousness represents the sum of all functions mediated at a cerebral cortical level, including both cognitive and affective responses
- The arousal level appears to influence all neuropsychological functions in humans and animals and absence of an aroused state precludes behaviour Complete loss of patterned arousal is seen only in coma (and in brain death) In VS Limited recovery of arousal patterning occurs without evidence of the other neuropsychological components of human consciousness Fragmentary elements of specific neuropsychological components are evident in these syndromes For example, fragments of attentional function are evidently preserved in all forms of Akinetic Mutism, with varying levels of impairment in other components. Complex brain injuries typically produce a mix of the clinical features observed in these classic syndromes.
- (A) Brain arousal for neurocognitive and neuro-affective function is promoted by ascending brain stem, forebrain and hypothalamic projections to the cortex and midbrain. Neurotransmitter and neuropeptide systems involved in brain arousal and therefore in cognitive and affective function include the monoaminergic neurotransmitters histamine (His) from the tuberomammillary nucleus (TMN), norepinephrine (NE) from the locus coeruleus (LC), serotonin (5-HT) from the midbrain raphe nuclei, dopamine (DA) from the ventral tegmental area (VTA), and substantia nigra (not shown); the cholinergic neurotransmitter acetylcholine (ACh) from the basal forebrain (BF) and the pedunculopontine (PPT), and laterodorsal tegmental nuclei (LDT); the peptide orexin (ORX), also referred to as hypocretin, from the lateral hypothalamus (LH); the excitatory amino acids glutamate (GLUT) and aspartate; vasopressin (VP), and vasoactive intestinal polypeptide (VIP) from the suprachiasmatic nuclei (SCN). (B) The master circadian clock located in the SCN has modulatory input to many of the ascending arousal pathways, some through direct projections from the SCN (not labeled, see text) and many through indirect projections relayed by the dorsomedial hypothalamus (DMH). Through such projections, the SCN can modulate circadian rhythms in brain arousal to promote wakefulness. (C) The SCN has modulatory input to the sleep systems via relay projections to the DMH, onto the sleep promoting VLPO as well as midbrain and brain stem arousal systems. Through such projections, the SCN can modulate circadian rhythms in brain arousal to promote sleep.
- Laureys S, Owen AM, Schiff ND (2004). "Brain function in coma, vegetative state, and related disorders". The Lancet Neurology 3 (9): 537–546
- The syndrome was first described in 1940 by Ernst Kretschmer who called it apallic syndrome The longest documented case of survival in a persistent vegetative state was Elaine Esposito,[32] who remained PVS for thirty-seven years and 111 days from 1941 to 1978 However, the probability of permanence could only be assessed by knowing the mechanism and elapsed time from the injury. permanent vegetative state (PVS) after approximately one year of being in a vegetative state This condition differs from a coma: a coma is a state that lacks both awareness and wakefulness. Patients in a vegetative state may have awoken from a coma, but still have not regained awareness
- causes of PVS, which are as follows: Bacterial, viral, or fungal infection, including meningitis Increased intracranial pressure, such as a tumor or abscess Vascular pressure which causes intracranial hemorrhaging or stroke Hypoxic ischemic injury (hypotension, cardiac arrest, arrhythmia, near-drowning) Toxins such as uremia, ethanol, atropine, opiates, lead, colloidal silver[12] Trauma: Concussion, contusion Seizure, both nonconvulsive status epilepticus and postconvulsive state (postictal state) Electrolyte imbalance, which involves hyponatremia, hypernatremia, hypomagnesemia, hypoglycemia, hyperglycemia, hypercalcemia, and hypocalcemia Postinfectious: Acute disseminated encephalomyelitis (ADEM) Endocrine disorders such as adrenal insufficiency and thyroid disorders Degenerative and metabolic diseases including urea cycle disorders, Reye syndrome, and mitochondrial disease Systemic infection and sepsis Hepatic encephalopathy
- In these studies, VS patients showed a reproducible reduction in resting metabolism to typically 30% to 50% of normal metabolic rates across cerebral structures Comparable reductions in cerebral metabolic rates are found in normal subjects in the pharmacologic coma produced by surgical anaesthesia These emotional displays most probably reflect isolated limbic networks tightly linked to brainstem and basal forebrain structures that operate without functional connection to the thalamocortical systems that are typically severely damaged in VS patients
- Prior to the mid-1990s, there was a lack of operational definitions available to clinicians and researchers to guide the differential diagnosis among disorders of consciousness. As a result, patients were lumped together into broad categories often based on the severity of the disability (e.g. moderate, severe, extremely severe). These diagnoses were performed without regard to salient differences in behavioural and pathological characteristics. In a three-year period spanning from 1994–1996, three position statements regarding the diagnostic criteria of disorder of consciousness were published. The “Medical Aspects of the Persistent Vegetative State” was published by the American Academy of Neurology (AAN) in 1994. In 1995, “Recommendations for Use of Uniform Nomenclature Pertinent to Patients With Severe Alterations in Consciousness” was published by the American Congress of Rehabilitation Medicine (ACRM). In 1996 the “International Working Party on the Management of the Vegetative State: Summary Report” was published by a group of international delegates from neurology, rehabilitation, neurosurgery, and neuropsychology
- The first level of behavioural recovery beyond VS is operationally defined as MCS. Definition: a condition of severely altered consciousness in which minimal but definite behavioural evidence of self or environmental awareness is demonstrated MCS patients show evidence on bedside examination of contingent responses to environmental stimuli or self-initiated behaviour that provides unequivocal but inconsistent evidence of awareness of self or the environment For example, consistent and sustained visual tracking or fixation may be the only behavioural evidence of responsiveness in an MCS patient Alternatively, an MCS patient may exhibit intermittent spoken language responses or inconsistent and inaccurate communication with gestural or verbal output. Recovery of functional communication (operationally defined as the ability to consistently and accurately answer simple contextual yes or no questions) defines the upper boundary of MCS Beyond MCS, varying levels of severe disability are not currently subcategorized Even though only subtle findings may distinguish VS and MCS patients at the bedside, a wide separation in underlying functional cerebral substrates associated with the two conditions is indicated by neuroimaging and electrophysiologic and pathologic studies
- Autopsy studies of patients with clinical histories consistent with MCS demonstrate reduced overall levels of cerebral cell death and, in some MCS patients, no evidence of significant thalamic cell loss or severe diffuse axonal injury—a pattern never observed in VS patients Neuroimaging studies generally show widespread preservation of distributed cerebral network activation in response to sensory stimuli, including passive language stimuli and auditory and somatosensory stimuli Electrophysiologic studies typically show recovery of a broad range of frequency content on the electroencephalogram and, in some MCS patients, preservation of high-level passive semantic processing of spoken language The presence of recruitable large scale cerebral networks in some MCS patients suggests a potential substrate for further recovery in these patients
- The syndrome of Akinetic Mutism includes patients who fulfil the criteria for MCS and patients who can functionally communicate when formally assessed yet demonstrate a severe reduction in spontaneous behaviour or extremely slowed interactive responses. Patients with Akinetic Mutism may appear highly attentive and vigilant with wide eye opening, deliberate visual tracking of the examiner around the room, but no other types of behaviour These patients are included in the MCS spectrum. Other patients sometimes described as Akinetic mutes may appear awake but somnolent with apparent psychomotor retardation similar to a variety of subcortical dementias The patterns of brain injury most commonly associated with these syndromes are bilateral damage to the anterior medial regions of the cerebral cortex, bilateral injury to caudate nuclei (or unilateral dominant hemisphere caudate nucleus), bilateral central thalamic lesions, large basal forebrain injuries, or damage to the mesencephalic reticular formation Frontal lobe damage Thalamic stroke Cingulate gyrus ablation Other causes of akinetic mutism are as follows: Respiratory arrest and cerebral hypoxia [6] Acute cases of encephalitis lethargica[3] Meningitis[3] Hydrocephalus[3] Trauma[3] Tumors[3] Aneurysms [3] Olfactory groove meningioma Cyst in third ventricle [1] Toxical lesions and infections of central nervous system [10] Delayed post-hypoxic leukoencephalopathy (DPHL) [6] Creutzfeldt-Jakob Disease (mesencephalic form)
- Akinetic Mutism is a classic finding after rupture of an anterior communicating artery aneurysm Some authors have defined “slow syndrome” to identify this subgroup of patients as a related behavioural phenotype characterized primarily by severe memory loss, severely slowed behavioural responses, and a listless, apathetic appearance sometimes referred to as “abulia.”
- MRI showing bilateral paramedian thalamic infarction.
- If psychogenic processes are excluded, observed alteration of consciousness in all settings implies one of the following possibilities: (1) diffuse functional impairment of both hemispheres as a result of direct injury and toxic/metabolic alterations associated, for example, with cardiopulmonary dysfunction, infection, poisoning, or a variety of other processes producing bilateral cerebral dysfunction, such as antibody-mediated alteration of neurons or axons, and (2) selective impairment of midline and paramedian upper brainstem and basal forebrain regions containing nuclei associated with ascending arousal input to the anterior forebrain, often damaged in combination with central thalamic nuclei (or isolated to the central thalamus if the lesions are bilateral and relatively large in rostrocaudal extent) The severity of a disturbance in consciousness directly reflects the functional disturbance produced in cerebral neurons diffusely or within the relatively restricted network of subsystems involved in forebrain arousal and regulation of arousal. Broadly speaking, there are three categories of patients with marked alteration of consciousness encountered by the neurosurgical or neurological consultant: (1) patients with overwhelming structural brain injury and known clinical predictors of death or permanent VS; (2) patients who show a pattern of early, steady recovery and are predicted to have outcomes better than severe disability with relative certainty; and (3) patients with a mix of structural brain injuries or more diffuse alterations (e.g., hypoxia, infection, inflammation), low-level behavioural responses, and relatively prolonged recovery in which available tools can confirm severe cerebral dysfunction but provide little insight into the patient’s future.
- Identification of patients in the first category—those with overwhelming structural brain injury—can frequently be done by inspection and clinical judgment (e.g., a patient with complete infarction of the dominant hemisphere and central herniation but not quite meeting brain death criteria). Prospective studies of large numbers of patients in coma have codified a number of strong clinical predictors of death or outcomes limited to permanent VS after the two most common causes: cardiac arrest and severe traumatic brain injury. For example, coma associated with loss of motor response and pupil and corneal reflexes initially and enduring over the first 48 to 72 hours is invariably associated with outcomes no better than permanent VS after cardiac arrest once potential confounding variables are excluded. The second group of patients, those with early and steady patterns of recovery, are well known but not well characterized in terms of the stages and time frames of their recovery because this is of more scientific than clinical interest. These patients recover consciousness and higher brain function within the first days or weeks after their initial events, and the details of their underlying brain mechanisms of recovery are a secondary concern to clinicians not directly involved in cognitive or motor rehabilitation.
- It is the third group of patients who provide a significant challenge to the neurosurgical and neurological consultant. These patients will have sufficient evidence from their clinical history, structural injury to critical brain structures evident on imaging, or electrophysiologic markers of diffuse neuronal dysfunction to raise concern of futility, but they do not demonstrate known clinical or laboratory indicators that predict permanence of their condition. In formulating a clinical judgement in such cases it is important to recognize that all existing indicators are surrogate markers for overwhelming neuronal death and disconnection within the cerebrum. Estimation of the likelihood of further functional recovery and the ultimate functional level of recovery in patients who lack negative predictors presents significant uncertainty. At present, no measurements reliably allow an assessment of whether the underlying remaining brain structures in such patients may allow recovery of consciousness and higher level cognitive functions. Thus, it is most important to have a reasoned and systematic strategy to assess these patients. An organized approach to this subpopulation of patients with severe brain injury and marked alteration of consciousness begins with an accurate diagnosis. It is absolutely critical to determine whether the patient is in coma, VS, or MCS; this is true whether the assessment is performed in the acute care setting once a comatose patient is stabilized in the emergency room or in more subacute contexts of inpatient units or even nursing facilities. The bedside diagnosis immediately provides an indication of the level of functional integration of cerebral subsystems within the forebrain and should anticipate the results of standard clinical functional assessments such as electroencephalograms, evoked responses, and other tracking measures. For example, comatose patients should show severe diffuse cerebral dysfunction with structural imaging that provides correlative information consistent with the history and cause of the condition. A subtle change in a patient who has remained comatose for 2 weeks (e.g., recovery of intermittent visual fixation when closed eyes are held open) will often correlate with objective findings on electroencephalographic evaluation, such as an increase in the mix of background frequencies or evident reactivity of a still poorly organized record. When the available information does not support the inference that the patient’s functional level is due to overwhelming neuronal death or disconnection, it should prompt consideration of functional disturbances at both the neuronal subcellular and the population (“circuit”) level The most common transitional signs from VS to MCS are visual fixation and visual tracking
- PSEUDOCOMA Differential diagnosis; Locked-in syndrome: ventral pontine infarction Psychiatric: Catatonia, conversion reaction Neuromuscular weakness: Myasthenia Gravis, Guillain Barre
- The uncertainty of outcome for an individual patient in coma, VS, or MCS will vary considerably, depending on the details of clinical findings obtained from bedside examinations, time from the initial injury, and the specific cause of the injury. It is first important to recognize that coma, VS, and MCS are often transitional states with increasingly long time windows that allow further recovery as each transition is achieved (i.e., coma to VS, VS to MCS) The first step is always to locate the patient temporally within the expected natural history of a disease process (e.g., VS in the first month after a severe traumatic brain injury is not comparable to VS at 6 months or 1 year) The next step is to identify the cause, but outside of anoxic encephalopathy or severe traumatic brain injury (roughly 80% of coma/VS/MCS causes), there are few specific outcome data.
- Coma is an inherently grave illness associated with very high mortality; studies indicate that 40% to 50% of patients in a coma after brain trauma and 54% to 88% of patients comatose after cardiac arrest die However, if no strong negative clinical predictors are identified, such as bilateral loss of both pupillary and corneal responses at the time of the initial injury, outcome prediction becomes far less certain A general conclusion is that comatose patients who suffer traumatic brain injury have a significantly higher likelihood of recovery than do comatose patients after cardiac arrest The younger age of patients with traumatic brain injury and the delayed mechanisms of neuronal death after brain trauma may contribute to this well-known difference.
- The prognosis of VS patients similarly depends on the mechanism that underlies the brain injury A patient who remains in VS for 3 months after cardiac arrest or other non-traumatic, diffuse brain injury that produces loss of blood flow or brain oxygen is considered to be in a permanent VS For example, patients with encephalitis are difficult to assess with these guidelines Time frames for recovery after posttraumatic VS are considerably longer, and 1 year is required to expect permanence After diffuse axonal injury, the widespread neuronal death in thalamic neurons is an indirect result of more delayed trans-neuronal degeneration, unlike the immediate effects of oxygen deprivation, which induces rapid neuronal death after roughly 6 minutes of oxygen loss Although a continuum of outcomes after an initial transition from coma to VS is well recognized, the outcomes are not equally distributed across a continuum Anoxic brain injuries produce relatively sharp cut-offs associated with global neuronal death and frequently lead to VS with an underlying anatomic pathology similar to that of brain death Recovery after prolonged traumatic coma and VS is well described, and unlike VS after cardiac arrest, unconsciousness for 3 months does not necessarily preclude significant recovery
- Prognosis in MCS is the least well characterized because the diagnostic category is relatively new and the available studies suggest that significant further recovery may occur in some patients after 1 year in MCS Importantly, MCS patients typically show faster changes in the rate of recovery within the first year after injury from either traumatic or non-traumatic injury than do VS patients. In the small cohorts of MCS patients studied, some attain outcomes better than severe disability at 1 year despite remaining in MCS for 1 to 3 months It is essential that the often small clinical finding that distinguishes VS from MCS be identified on bedside examinations performed within the first few months after injury.
- Several recent neuroimaging studies of VS and MCS patients suggest that functional imaging tools may become part of the comprehensive assessment of neurological disorders of consciousness Owen and colleagues used fMRI to demonstrate unambiguous evidence of command following in a single patient with no visible behavioural response who fit the behavioural criteria for VS