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Neurophysiological assessment of coma

Neurophysiological assessment of coma. Definitions. Consciousness is the state of awareness of self and the environment and coma is its opposite. That is the total absence of awareness of self and the environment even with external stimulation. Between these poles there is :.

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Neurophysiological assessment of coma

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  1. Neurophysiological assessment of coma AH

  2. Definitions • Consciousness is the state of awareness of self and the environment and coma is its opposite. That is the total absence of awareness of self and the environment even with external stimulation. AH

  3. Between these poles there is : • Confusion…………bewildered but attentive • delerium…………..irritable,out of contact but alert • obtundation……….reduced alertness, slowed responses • stupor……………..responsive only with vigorous and repeated stimuli AH

  4. Other states of importance • Vegetative state……The return of alertness but no evidence of cognitive function • Apallic syndrome…..Essentially the same as vegetative state • Akinetic mutism……Silent alert immobility, minimal motor response to noxious stimulation. • Locked in syndrome..Evidence of cognitive function as distinct from akinetic mutism. AH

  5. The state of consciousness reflects • 1. The level of arousal • Arousal depends on the integrity of brain stem function, in particular the ARAS • 2. Cognitive function • Cognitive function predominantly depends on cortical and thalamocortical integrity. AH

  6. Clinical approach to the comatose patient • Pathology must involve either • Bilateral hemispheres……supratentorial • The ARAS……………….subtentorial • Diffuse…………………...toxic/metabolic AH

  7. Patients can usually be categorised into these groups • History • Assessment of arousal • pupillary responses • eye movements • corneal responses • breathing pattern • motor patterns • deep tendon reflexes AH

  8. Supratentorial • Initiating signs usually of focal cerebral dysfunction • Signs of dysfunction progress rostral to caudal • Motor signs often asymmetrical AH

  9. fig18 AH

  10. Fig 19 AH

  11. Fig 20 AH

  12. Fig 21 AH

  13. Fig 22 AH

  14. Fig 23 AH

  15. Subtentorial • History of brain stem dysfunction or sudden onset coma • Oculovestibular features often precede or accompany coma • Cranial nerve palsies present • Bizarre respiratory patterns common and at onset AH

  16. Toxic/Metabolic • Confusion,delirium,stupor,obtundation precede motor signs • Pupillary responses usually preserved • motor signs usually symmetrical • Asterixis,myoclonus,seizures common • Acid-base imbalance with hypo or hyperventillation AH

  17. Psychogenic unresponsiveness • eyelids actively close • icewater calorics induce nystagmus • EEG normal AH

  18. The role of EEG in diagnosis • Differentiates coma from psychogenic unresponsiveness • Identifies non convulsive status epilepticus • Bilateral delta indicates the patient is either deeply asleep or unconscious • A normal EEG rules out metabolic brain disease as a cause of coma. • A “normal” EEG in delerium strongly suggests an alcohol or drug withdrawal state • The degree of slowing usually reflects the severity of the metabolic encephalopathy AH

  19. In diffuse metabolic encephalopathy the EEG is usually more sensitive than the clinical assessment with slowing still present when the patient has returned to clinical normality. AH

  20. The role of EEG in prognosis of anoxic cerebral injury. • Five Grades AH

  21. Grade 1. “Near normal” • Excellent prognosis unless “locked in”or alpha pattern coma AH

  22. Grade 2. Theta dominant • If reactive the prognosis is very good • If nonreactive survival is usually accompanied by neurological sequelae AH

  23. Grade 3. Delta dominant • If reactive the prognosis can be good • If non-reactive the prognosis is grave provided drugs and hypothermia excluded. AH

  24. Grade 4. Burst suppression & continuous bilateral periodic sharp waves • Prognosis grave if drugs and hypothermia excluded • Often associated with clinical myoclonus. AH

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  28. Grade 5. Isoelectric • Prognosis grave if drugs and hypothermia excluded. AH

  29. Rare Variants AH

  30. Alpha pattern coma • Anterior predominance • Unreactive alpha frequency activity. • Rare survivors but only if brain stem reflexes intact. AH

  31. AH

  32. Theta pattern coma • Usually elderly • 5 Hz theta with low amplitude burst suppression morphology • Grave prognosis AH

  33. AH

  34. Spindle coma • Usually head injury, rarely anoxic injury • resembles stage II sleep • prognostically benign. AH

  35. The role of EEG in coma prognosis in anoxic injury • The difficult group are grade II nonreactives and grade III. These are also the most common groups. • SEPs are useful to further define the prognosis in these groups. AH

  36. The role of EEG in prognosis in severe head injury • EEG is considerably more limited in prognostication in severe head injury. • Reactivity may be the most useful parameter for classifying outcome into “good” vs “bad” • Good being moderately disabled or better • Bad being worse than moderately disabled. AH

  37. Reactivity can be • Attenuation • Paradoxical (high amplitude slow waves) • Doubtful/Uncertain • absent. • 90 + % of patients with preserved reactivity of either type have “good”outcomes • 90 +% of patients with absent reactivity have bad outcomes. • 20 +% have “uncertain” reactivity & 70+ % of these have good outcomes. AH

  38. Fig 1 AH

  39. The role of SEPs in anoxic cerebral injury and severe head injury • The bilateral absent of the “thalamo-cortical” wave forms (N19, N20, N1)signifies that the patient will not recover to better than PVS………….100% specificity • However sensitivity is low (20-30 %). • Hence the interest in the N70 AH

  40. AH

  41. N70 • Madl et al • “Of 113 patients with a bilateral N70 peak latency >130 msec or absent all but one had a poor outcome” • Sensitivity of 94% and specificity of 97% • Sherman et al • Using a bilateral N70 peak latency > 176 msec all had a poor outcome • Sensitivity 78% and specificity of 100% AH

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