Coma and consciousness     A/Prof Andrew Zacest      FRACS, FFPMANZCA    Royal Adelaide Hospital
Overview•   Why is this important ?•   Historical considerations•   Normal consciousness•   Impairment of consciousness an...
Consciousness - historical•   Greeks – impaired consciousness = brain failure•   Philosphers – Aristotle, Descartes, John ...
Consciousness• State of full awareness  of the self and one’s  relationship to the  environment• Arousal• Awareness
NORMAL CONSCIOUSNESS• Arousal  wakefulness   –Thalamic ascending system   –Extrathalamic ascending system• Awareness   –D...
CEREBRAL CORTEX Primary        Secondary Sensory     Sensory Cortex          Association    Association Cortex      in eac...
Primary             Secondary  Sensory          Sensory Cortex       Association       Association  Cortex           in ea...
Disorders of consciousness• DOC• Continuum• Unique definitions and  criteria• Require detailed and  sometimes repeated  ex...
Mild TBI- concussion• Most common form of  TBI 22:1• Does not require LOC• Evidence of head  impact• GCS 13-15• Neurosurgi...
Axonal injury in mild TBI•   5 patients with mild TBI•   Death from other cause•   Autopsy•   APP -axonal injury•   No fra...
Impact force and TBI                    I     CONFUSION         Normal consciousness without amnesia                    II...
Coma - definition• Gk – deep sleep• Unresponsiveness• Eyes closed• Does not respond to  stimuli• No awareness of  outside ...
MECHANICAL FORCES – coma and sequelae   CONCUSSIVE SYNDROMES                    COMA                      “INSTANTANEOUS” ...
MINIMALLY CONSCIOUS STATEPatients who are unable to follow instructionsreliably or communicate, but who demonstrateinconsi...
VEGETATIVE STATE• Complete unawareness of self and  environment• Preservation sleep-wake cycles• Complete or partial prese...
"ROADSIDE DEATH"                                MECHANICAL INJURYForces of great magnitude suchas in high speed MVAs disru...
PERMANENT VEGETATIVE         STATE• Implies an irreversible state• A patient in a persistent vegetative state  becomes per...
BRAIN DEATH Permanent absence of all brain  functions (including brain stem) Brain-dead patients are irreversibly  comat...
LOCKED-IN SYNDROME• State of alert wakefulness  associated with paralysis of the  body and inability to speak• Communicati...
AKINETIC MUTISM   Marked diminution in drive (global inertia) with complete or near-    complete loss of spontaneity and ...
Causes of coma in humans• Evidence from lesions, head injury, medical• Either extensive areas of cerebral hemisphere  or a...
Brain lesions that cause coma
Neuropathology
TBI – vegetative state• Recovery of arousal in unresponsive patient• Autopsy of 49 patients, 35 blunt TBI, 14 non  TBI• Di...
Clinical approach to reduced level of                consciousness•   Brain failure•   What is the cause ? History ?•   St...
Structural causes (surgical)• Supratentorial mass lesion impairing  diencephalon• Infratentorial lesion damaging arousal s...
Intracranial pressure• ICP = cerebral venous  pressure• CPP = MAP – ICP• Mass lesions ↑ ICP• ICP > 20mmHg  abnormal• Uncon...
Brain herniation• Arises from compensatory shifts of brain due  to raised ICP• Vicious cycle leading to death• ↑ ICP → ↓ C...
Herniation syndromes• Uncal – pupil dilatation then oculomotor failure• Central – diencephalic - ↓ alertness        - midb...
Clinical assessment - History•   History is important•   History of trauma ?•   PMH ?•   Collateral history ?•   Alcohol ?...
Clinical examination• A,B,C• Pupil and ocular motility• Motor response
Pupils and EOM
Motor response
Glasgow Coma Score• Teasdale & Jennett  1974• 3 components• early assessment• monitoring progress• paediatric coma scale
Investigations•   Electrolytes, LFT, glucose, creatinine•   Blood gas, CXR,ECG•   Lumbar puncture•   Toxicology•   CT/MRI
Neuroimaging•   CT•   MRI•   fMRI•   PET•   Lesions•   Function – CBF•   Limitations•   Can they predict    outcome ?
Why is the patient drowsy ?
Medical causes of coma  Often multifactorial• Hypoxia  Ischaemia  Hyper/hypothermia  Metabolic  Drugs/alcohol  Organ failu...
Differential characteristics of Coma• Supratentorial mass lesions  Focal dysfunction early, progression, localising neurol...
Management of Coma• Identify cause of coma if possible• A,B,C – stabilise patient and get help• Assume a structural cause ...
Prognosis• Depends on diagnosis• Coma after TBI – 15% PVS                 - 45% moderately disabled                 - 7% g...
PROGNOSIS FOR NEUROLOGIC RECOVERYComaUsually recovery, persistent vegetative state, or death in 2 to 4 weeksBrain DeathNo ...
Interventions for DOC•   Systemic review of literature•   At least 6 mos (T), 3 mos (NT) for MCS, VS•   16 of 5852 papers ...
Conclusions• Impaired consciousness is brain failure• Longer coma exists the poorer the prognosis• Prompt diagnosis is imp...
Coma and consciousness 2
Coma and consciousness 2
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Coma and consciousness 2

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Coma and consciousness 2

  1. 1. Coma and consciousness A/Prof Andrew Zacest FRACS, FFPMANZCA Royal Adelaide Hospital
  2. 2. Overview• Why is this important ?• Historical considerations• Normal consciousness• Impairment of consciousness and coma• Pathology• Clinical assessment• Neuroimaging• Treatment• Outcome• Future
  3. 3. Consciousness - historical• Greeks – impaired consciousness = brain failure• Philosphers – Aristotle, Descartes, John Locke• 1800s – cerebral hemispheres – consciousness• 1890 – Wernicke’ s – periventricular lesions• 1916 – encephalitis lethargica - autopsy• 1917 – von Economo - proposed arousal circuit from midbrain• 1929 – Berger – EEG in humans• 1935 – Bremer – EEG in animals with lesions• 1949 – Moruzzi - RAS lesions in animals• 1951 – Starzl – electrical stim of RAS in animals
  4. 4. Consciousness• State of full awareness of the self and one’s relationship to the environment• Arousal• Awareness
  5. 5. NORMAL CONSCIOUSNESS• Arousal  wakefulness –Thalamic ascending system –Extrathalamic ascending system• Awareness –Distributed neuronal networks –Modular organization –Thalamo-cortical-thalamic circuitry• Awareness requires wakefulness but wakefulness can be present without awareness
  6. 6. CEREBRAL CORTEX Primary Secondary Sensory Sensory Cortex Association Association Cortex in each Modality Cortex Cortex LIMBIC SYSTEM BASAL THALAMUS FOREBRAIN HYPOTHALAMUSTHALAMIC EXTRATHALAMICASCENDING BRAIN STEM ASCENDINGAROUSAL AROUSAL SPINAL CORD
  7. 7. Primary Secondary Sensory Sensory Cortex Association Association Cortex in each Modality Cortex Cortex THALAMUSINTRA SENSORY ASSOCIATIONLAMINAR RELAY NUCLEI BASAL FOREBRAINNUCLEI NUCLEIRETICULAR LIMBICNUCLEUS NUCLEI EXTRA THALAMIC THALMIC AROUSAL ASCENDING BRAIN STEM AROUSAL ? RETICULAR FORMATION ACh PEDUNCULOPONE NUCLEUS NA LOCUS COERULEUS 5HT ROSTRAL RAPHE COMPLEX
  8. 8. Disorders of consciousness• DOC• Continuum• Unique definitions and criteria• Require detailed and sometimes repeated examination• Prognostic implications• Differential diagnosis Bernat et al Annu Rev Med 60 :2009
  9. 9. Mild TBI- concussion• Most common form of TBI 22:1• Does not require LOC• Evidence of head impact• GCS 13-15• Neurosurgical intervention not required• Common in sport• Cumulative effect
  10. 10. Axonal injury in mild TBI• 5 patients with mild TBI• Death from other cause• Autopsy• APP -axonal injury• No fracture-hematoma• Axonal injury in all cases• Fornix injured in all• Reticular system injury Blumbergs P, Scott G. Lancet 334 :1994
  11. 11. Impact force and TBI I CONFUSION Normal consciousness without amnesia II CONFUSION Confusion Normal consciousness + Amnesia with posttraumaticImpact III amnesia (PTA) onlyor Shear CONFUSION + AMNESIA Normal strainsImpulse consciousness IV with PTA + retrograde amnesia V COMA PARALYTIC Confusion + Amnesia VI COMA Vegetative State DEATH
  12. 12. Coma - definition• Gk – deep sleep• Unresponsiveness• Eyes closed• Does not respond to stimuli• No awareness of outside or self• Graduation in depth of coma but no arousal cycle
  13. 13. MECHANICAL FORCES – coma and sequelae CONCUSSIVE SYNDROMES COMA “INSTANTANEOUS” DEATH GCS 13-15 GCS 9-12 Moderate TBI Forces of great magnitude Minor TBI GCS 3-8 Severe TBI as in high speed MVAs Mild TBI disrupting neural tissue Different spectrum of brain lesions in this forensic populationRecovery Mild Moderate Severe Vegetative Minimal Death Disability Disability Disability State (VS) Conscious (spectrum State psychologic & neurologic Persistent VS dysfunction) Permanent VS Spectrum Spectrum Spectrum Spectrum Spectrum Spectrum focal + focal > focal + diffuse > diffuse > focal + diffuse diffuse diffuse focal focal diffuse injury injury injury injury injury injury
  14. 14. MINIMALLY CONSCIOUS STATEPatients who are unable to follow instructionsreliably or communicate, but who demonstrateinconsistent but reproducible behaviouralevidence of self-awareness or awareness ofthe environment.American Congress of Rehabilitation Medicine, 1995
  15. 15. VEGETATIVE STATE• Complete unawareness of self and environment• Preservation sleep-wake cycles• Complete or partial preservation of hypothalamic and brain stem autonomic functions
  16. 16. "ROADSIDE DEATH" MECHANICAL INJURYForces of great magnitude suchas in high speed MVAs disruptingbrain tissue CONCUSSION  Death (rare)Different spectrum of brain lesions (Grades 1 to 3)  Recoveryin this forensic population  Postconcussion syndrome COMA  Death (Grades)  Brain death  Recovery  Spectrum of neurologic and psychologic disability including minimally conscious state VEGETATIVE STATE  Death  Recovery with spectrum of neurologic and psychologic disability  Minimally conscious state PERSISTENT VEGETATIVE STATE  Death  Recovery with spectrum of neurologic and psychologic disability  Minimally conscious state PERMANENT VEGETATIVE STATE  Death  ? Recovery  disability
  17. 17. PERMANENT VEGETATIVE STATE• Implies an irreversible state• A patient in a persistent vegetative state becomes permanently vegetative when the diagnosis of irreversibility can be established with a high degree of clinical certainty• Based on probabilities, not absolutes
  18. 18. BRAIN DEATH Permanent absence of all brain functions (including brain stem) Brain-dead patients are irreversibly comatose and apnoeic and have lost all brain stem reflexes and cranial- nerve functions
  19. 19. LOCKED-IN SYNDROME• State of alert wakefulness associated with paralysis of the body and inability to speak• Communication possible via eye movements or eyeblinks
  20. 20. AKINETIC MUTISM Marked diminution in drive (global inertia) with complete or near- complete loss of spontaneity and reduced action, ideation, speech and emotion Well-preserved smooth pursuit eye movements, coupled with occasional speech and movement to command Intact sleep-wake cycles (normal arousal) Bilateral lesions of orbito-mesial frontal cortex, limbic system including the septum and anterior cingulum and paramedian meso- diencephalic reticular formation
  21. 21. Causes of coma in humans• Evidence from lesions, head injury, medical• Either extensive areas of cerebral hemisphere or ascending reticular system• Autopsy studies
  22. 22. Brain lesions that cause coma
  23. 23. Neuropathology
  24. 24. TBI – vegetative state• Recovery of arousal in unresponsive patient• Autopsy of 49 patients, 35 blunt TBI, 14 non TBI• Diffuse axonal injury most common (71%)• Thalamus abnormal in 80% -96%• Ischaemic damage, haematomas• Non TBI ischaemia in 64%, thalamus always• Either subcortical white or thalamic lesions J Adams, Graham D, Jennett B Brain 123 2000
  25. 25. Clinical approach to reduced level of consciousness• Brain failure• What is the cause ? History ?• Structural or metabolic ?• What investigations are necessary ?• What emergency measures are necessary ?• Time is important
  26. 26. Structural causes (surgical)• Supratentorial mass lesion impairing diencephalon• Infratentorial lesion damaging arousal system• History may be limited• Clinical diagnosis depends on recognition of signs of injury to arousal pathways• Neurological signs tends to progress as intracranial pressure ↑ and brain herniation
  27. 27. Intracranial pressure• ICP = cerebral venous pressure• CPP = MAP – ICP• Mass lesions ↑ ICP• ICP > 20mmHg abnormal• Uncontrolled ICP leads to brain herniation and death
  28. 28. Brain herniation• Arises from compensatory shifts of brain due to raised ICP• Vicious cycle leading to death• ↑ ICP → ↓ CPP → hypoxia → edema → ↑ ICP → death Diagnosis of Stupor and Coma. Plum and Posner 2007
  29. 29. Herniation syndromes• Uncal – pupil dilatation then oculomotor failure• Central – diencephalic - ↓ alertness - midbrain – oculomotor failure - posturing (extensor) - pontine – flaccid - medulla – autonomic failure
  30. 30. Clinical assessment - History• History is important• History of trauma ?• PMH ?• Collateral history ?• Alcohol ?• Drugs ?• ? SAH ? Stroke ? Fever ?• Prior neurological exam
  31. 31. Clinical examination• A,B,C• Pupil and ocular motility• Motor response
  32. 32. Pupils and EOM
  33. 33. Motor response
  34. 34. Glasgow Coma Score• Teasdale & Jennett 1974• 3 components• early assessment• monitoring progress• paediatric coma scale
  35. 35. Investigations• Electrolytes, LFT, glucose, creatinine• Blood gas, CXR,ECG• Lumbar puncture• Toxicology• CT/MRI
  36. 36. Neuroimaging• CT• MRI• fMRI• PET• Lesions• Function – CBF• Limitations• Can they predict outcome ?
  37. 37. Why is the patient drowsy ?
  38. 38. Medical causes of coma Often multifactorial• Hypoxia Ischaemia Hyper/hypothermia Metabolic Drugs/alcohol Organ failure Infection Epilepsy Head injury Psychogenic Locked in syndromeDon’t delay imaging if in doubt(Neither the neurological exam or examinerIs infallible)
  39. 39. Differential characteristics of Coma• Supratentorial mass lesions Focal dysfunction early, progression, localising neurological deficit, assymetry• Infratentorial mass lesions History of brainstem dysfunction, immediate coma, pupil, oculomotor, respiratory abnormality• Metabolic/diffuse Delirium common, motor signs symmetric, pupils often normal, seizures• Psychogenic Lids actively closed, inconsistent but normal exam
  40. 40. Management of Coma• Identify cause of coma if possible• A,B,C – stabilise patient and get help• Assume a structural cause until proven otherwise• Control glucose, treat seizures, electrolyte and temp disturbance, give thiamine, treat infection• Control agitation• Surgical - call neurosurgical registrar• Metabolic/Stroke – medical registrar
  41. 41. Prognosis• Depends on diagnosis• Coma after TBI – 15% PVS - 45% moderately disabled - 7% good recovery - <1% chance of awareness > 1yr• Coma after anoxic-ischaemic injury - 53% dead - 32% PVS - 15% awakened - <1% chance of awareness > 3mo
  42. 42. PROGNOSIS FOR NEUROLOGIC RECOVERYComaUsually recovery, persistent vegetative state, or death in 2 to 4 weeksBrain DeathNo recoveryPersistent Vegetative StateDepends on cause (acute traumatic or non-traumaticinjury, degenerative or metabolic condition, or developmental malformation)Locked-In SyndromeRecovery unlikely: persistent quadriplegia with prolongedsurvival possible
  43. 43. Interventions for DOC• Systemic review of literature• At least 6 mos (T), 3 mos (NT) for MCS, VS• 16 of 5852 papers eligible for review• Levodopa, amantadine, zolidepm• PNS, SNS (124), ECS, DBS (1), ITB• Heterogeneity, methodology problems• Schiff et al 2007 – DBS- central thalamus target• Investigational therapies Georgiopoulos et al Stereotact Func Neurosurg 88 : 2010
  44. 44. Conclusions• Impaired consciousness is brain failure• Longer coma exists the poorer the prognosis• Prompt diagnosis is important• Clinical assessment can expedite diagnosis and treatment• Prompt treatment gives the best chance of recovery
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