Disorders_of_Consciousness_Lecture_Illustrated(1).pptx

.

1. Disorders of Consciousness Prof. Dr. Aylin Yaman Istinye University, Faculty of Medicine Lecture for Medical Students

2. Learning Objectives • Define consciousness and its components • Differentiate types of disorders of consciousness (DOC) • Understand diagnostic criteria • Review clinical assessment and imaging • Discuss management and prognosis

3. Definition of Consciousness Consciousness is awareness of self and environment, with the ability to respond to stimuli. Components: - Arousal (wakefulness) - Awareness (content of consciousness)

4. Anatomy of Consciousness Key structures: • Reticular activating system (RAS) • Thalamus • Fronto-parietal cortex All must function together for normal consciousness.

5. Classification of DOC 1. Coma 2. Vegetative State (UWS) 3. Minimally Conscious State 4. Locked-in Syndrome 5. Brain Death

6. Coma State of unarousable unresponsiveness >1 hour. Causes: trauma, metabolic, infection, stroke. No wake-sleep cycles; brainstem reflexes may persist.

7. Vegetative State Wakefulness without awareness. Sleep-wake cycles present, eyes may open. No purposeful responses or communication.

8. Minimally Conscious State Minimal, but definite behavioral evidence of awareness. May follow simple commands inconsistently.

9. Locked-in Syndrome Consciousness and cognition intact. Loss of voluntary motor control except vertical eye movement.

10. Brain Death Irreversible cessation of all brain functions. Confirmed by EEG silence and absent brainstem reflexes.

11. Etiologies of DOC • Traumatic brain injury • Hypoxia • Stroke • Metabolic or toxic causes • Infections

12. Pathophysiology Disruption of RAS or diffuse cortical dysfunction impairs awareness. Thalamo-cortical disconnection central to DOC.

13. Clinical Assessment • Glasgow Coma Scale • FOUR Score • CRS-R • Neurological reflexes and pupils

14. Neuroimaging in DOC CT/MRI – identify lesions PET/fMRI – assess brain metabolism DTI – evaluate white matter connectivity

15. EEG and Evoked Potentials EEG shows cortical activity. Evoked potentials test residual responses (SEP, AEP, P300).

16. Metabolic Causes Hypoxia, hypoglycemia, hypernatremia, toxins, liver/renal failure.

17. Traumatic Brain Injury Diffuse axonal injury → DOC. Outcome depends on white matter integrity.

18. Hypoxic-Ischemic Encephalopathy After cardiac arrest or respiratory failure. MRI: cortical laminar necrosis, thalamic damage.

19. Infectious Causes Meningitis, encephalitis, sepsis-associated encephalopathy.

20. Structural Causes Stroke, tumors, hemorrhage.

21. Diagnostic Workflow 1. Stabilize ABCs 2. Neuro exam 3. Exclude reversible causes 4. Perform imaging & EEG

22. Management Principles • Maintain perfusion and oxygenation • Prevent secondary injury • Treat underlying cause • Early rehabilitation

23. Pharmacologic Therapy Amantadine, Zolpidem (rare paradoxical effect), dopaminergic stimulants.

24. Rehabilitation Multidisciplinary approach including physical therapy, communication training, family involvement.

25. Ethical and Legal Issues Withdrawal of life support, brain death, and patient autonomy.

26. Prognosis Better in trauma than hypoxia. Recovery possible from MCS; rare from VS >12 months.

27. Recent Advances • fMRI detection of covert awareness • Brain–computer interfaces • TMS for stimulation studies

28. Case Example 25-year-old post-TBI male (GCS 6) transitioned to MCS after 3 weeks. EEG: reactive. fMRI: partial activation in command task.

29. Summary DOC = spectrum from coma to MCS. Clinical + neurophysiological assessment guides diagnosis and prognosis. Rehabilitation and ethical considerations crucial.