Persistent vegetative state Flashcards
What structures in the brain make up the ‘seat of consciousness’?
Lateral PFC
Posterior PFC
Thalamus
*recent studies have suggested that the dorsolateral pontine tegmentum is also part of the seat of consciousness rather than the thalamus
What 3 things does the glasgow coma scale measure? What are the highest + lowest scores? What score would a comatose patient have?
Measures:
- eye opening
- best verbal response
- best motor response
highest score: 15
lowest score (totally unresponsive): 3
Comatose patient: <8
What are the different types of “comas”?
Brain death
Vegetative state
Locked-in syndrome
Recover wakefulness
What are the two subtypes of vegetative state? What are the potential outcomes for each?
- Persistent vegetative state:
- will result in death - Minimally conscious state:
- permanent minimally conscious state
- confusional state
- recovery of consciousness
What is the role of the ascending reticular activating system? What brain structures are involved in this system?
Alerting or arousal (wakefulness/awareness)
Involves rostral brainstem tegmentum, the diencephalon, the projections to the cerebral cortex
Centres for sleep
involves the preoptic region (hypothalamus)
What are the 3 main categories of disorders of consciousness?
- comatose state (asleep + unconscious)
- vegetative state (awake + unconscious)
- minimally conscious state (awake + some consciousness)
What is a comatose state? How is this different from stupor?
Comatose state is complete unresponsiveness
patient’s eyes are closed and they cannot be aroused
Stupor is similar to a coma but the patient will respond with strong stimuli
What is locked-in syndrome? What areas of the brain are usually affected? Which autoimmune disorder/s can cause locked-in syndrome?
State of unresponsiveness - the patient’s eyes are closed and they cannot be aroused, however, they retain eye movement and are fully conscious
This is most often due to injury to the ventral pons to the corticospinal and corticobulbar tracts causing quadriplegia and anarthria (mute)
Guillain-Barre syndrome and motor neurone disease can cause locked-in syndrome
What is akinetic mutism? What areas of the brain are usually affected? What conditions is it commonly associated with?
Condition of apparent alertness along with a lack of almost all motor functions (speech, gestures, facial expression)
Anatomical sites affected:
- frontal lobe (supplementary motor area, cingulate gyrus)
- basal ganglia (caudate, putamen, globus pallidus)
- Mesencephalothalamic regions (midbrain + thalamus)
Often associated with Alzheimer’s, Pick’s disease, Creutzfeld-Jakob’s disease
What is vegetative state? How can the patient present? What is the difference between persistent and permanent vegetative state?
It is spontaneous eye-opening (wakefulness) - no evidence of awareness
Patient can present in two different positions depending on location of injury:
- Decorticate
- Decerebrate - worse as the injury location is closer to the brainstem
Persistent: lasting at least 1 month
Permanent: lasting at least 12 months after traumatic injury
OR
lasting at least 3 months after non-traumatic injury (anoxia, hypoxia)
What is minimally conscious state?
condition of severely altered consciousness - definite, but subtle and inconsistent displays of awareness
Return of which functions indicate a relatively good progonsis?
return of speech
spontaneous eye movement
normal resting muscle tone
ability to follow motor commands
absent brain reflexes = poor prognosis
How can consciousness be assessed?
- Auditory stimulation (measure auditory event-related potential)
- aim to identify a P300: this is a positive component appearing in the PFC and primary auditory cortex around 300 ms after a change in sequence of sounds - Imaging
- Positron emission tomography (uses fluorodeoxyglucose)
- Blood oxygenation level dependent (detects difference between oxygenated Hb and deoxygenated Hb - assesses cerebral blood flow)
What is the current treatment for lack of consciousness?
- sensory stimulation (avoid sensory deprivation + provide enriched environment to promote neuronal plasticity)
- amantadine (weak NMDAR antagonist + blocks dopamine reuptake)
take 100-200 mg twice daily over a period of 4 weeks with traumatic disorders who are at 4-16 weeks of injury
Zolpidem + vagal n. stimulation are potential future treatments.