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Brain and Behaviour Year 2 > Persistent vegetative state > Flashcards

Persistent vegetative state Flashcards

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1
Q

define consciousness

A

This is a state of full awareness of the self and environment

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2
Q

define wakefulness

A
  • the ability to have basic reflexes such as open eyes, cough, swallow, suck
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3
Q

define awareness

A
  • the ability to carry out complex thought processes
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4
Q

In terms of the global workspace theory what is the difference between consciousness and non consciousness

A
  • Conscious – when the signals are broadcast to a wider network of neurones called the global workspace
  • Non conscious – when all signals are localised
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5
Q

describe how global workspace theory works

A

Integrate all senses into a single picture and filter out conflicting information

Non-conscious experiences are processed locally within separate regions of the brain

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6
Q

What two areas are responsible for high level complex thought

A
  • Lateral prefrontal cortex (BA8, 9, 10, 45, 46, 47)

- Posterior parietal cortex ( BA5, 7, 39, 40)

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7
Q

what control the sleep states and levels of arousal and vigilance

A

• Not thalamus, but midbrain and/or pontine tegmentum

  • The Pontine tegmentum controls sleep states and levels of arousal and vigilance
  • lesions cause coma or stupor
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8
Q

what happens in the pontine tegementum becomes damaged

A

lesions cause coma or stupor

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9
Q

what are the three important brain structures for arousal

A
  • Ascending reticular activation system (ARAS)
  • Hypothalamus
  • Circadian clock
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10
Q

what is the ascending reticular activation system important for

A

• Important for alerting or arousal (wakefulness/awareness)

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11
Q

What structures does the ascending reticular activation system involve

A

Involve a number of structures:
• rostral brain stem tegmentum (i.e. pontine tegmentum)
• via diencephalon (i.e. thalamus)
• projections to the cerebral cortex (i.e. LPFC)

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12
Q

what structures does the hypothalamus involve and what do they do

A
  • Tuberomammillary nucleus (TMN) – promote arousal

- Ventrolateral preoptic nucleus (VLPO) – promotes sleep

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13
Q

what structures does the circadian clock involve and what does it do

A
  • Suprachiasmatic nucleus (SCN) – promote arousal
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14
Q

name some disorders of consciousness

A
  • Structural brain lesions
  • Metabolic and nutritional disorders
  • Exogenous toxins
  • CNS infection and septic illness
  • Seizures
  • Temperature related effects
  • Trauma
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15
Q

Name a medical scale that is used to measure consciousness

A

Glasgow Coma scale

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16
Q

what are the 3 big subheadings of the Glasgow coma scale

A
  • eye opening response
  • best verbal response
  • best motor response
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17
Q

describe the Glasgow coma scale

A 
Eye opening response 
score 
4 = spontaneously 
3 = to speech 
2 = to pain 
1 = no response 
Best verbal response 
5 = orientated to time, place and person 
4 = confused
3 = inappropriate words
2 = incomprehensible sounds 
1 = no response
best motor response 
6 = obeys commands 
5 = moves to localised pain 
4= flexion withdraws from pain 
3 = decorticate
2 = decerebrate
1 = no response

Best response = 15
Coma 8 or less
totally unresponsive 3

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18
Q

describe the severity of consciousness using the Glasgow coma scale

A 
mild = 13-15
moderate = 9-12
severe = 3-8
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19
Q

AVPU stands for

A
  • Alert 15GCS
  • Verbal stimuli 12 GCS
  • Painful stimuli - 8GCS
  • Unresponsive - 3GCS
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20
Q

describe the pathway of a coma to either ending up dead or getting better

A

Coma

  • can either end of brain dead, vegetative state, locked in syndrome, recover wakefulness
  • Vegetative state either become a permanent vegetative state or minimally conscious state
  • Permeant vegetative state = death
  • Minimally conscious state – permanent minimally conscious state, confusional state, recovery of consciousness
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21
Q

what are the three main categories for the level of consciousness

A

1, comatose state
2, vegetative state
3, minimally conciseness state

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22
Q

describe the three main categories for the level of consciousness

A
  • 1, comatose state = asleep and unconscious
  • 2, vegetative state (unresponsive wakeful syndrome) (awake and unconscious)
  • 3, minimally conscious state (awake and some consciousness)
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23
Q

what is a comatose state

A
  • A state of complete unresponsiveness in which patient lies with eyes closed and cannot be aroused to respond appropriately to any stimuli
24
Q

how long does a comatose state last

A
  • generally a transitional state which lasts a few weeks are rarely longer than 1 month
25
Q

what is stupor

A
  • similar to a coma but will response to a strong stimuli
26
Q

what is locked in syndrome

A
  • A state of unresponsiveness in which patient lies with eyes closed and cannot be aroused to respond to appropriately any stimuli
  • However the patient retains eye movement and are fully conscious
27
Q

what can cause locked in syndrome

A
  • trauma and ishcemia to the ventral pons causing interruption to the corticospinal and corticobulbar tracts causing quadriplegia
  • severe cases of guillian barre syndrome
28
Q

What is Gillian barre syndrome

A

autoimmune disorder which immune system attacks healthy neuroens)

29
Q

how can people in locked in syndrome communicate

A
  • e-tran frame

- brain computer interface

30
Q

define akinetic mutism

A
  • A condition of apparent alertness along with a lack of almost all motor functions including speech, gestures and facial expression
31
Q

what is akinetic mutism often defined as

A
  • Often misdiagnosed as having psychological reasons to not respond such as depression, deliruium, reduced awareness or physically paralysed lcokaedi n syndrome
32
Q

what is akinetic mutism associated with

A
  • Associated with Alzheimer’s disease, picks diseases, Creutzfeldt disease
33
Q

What are the areas that are affected by akinetic mutism

A

Frontal lobe (supplementary motor area, cingulate gyrus),

Basal ganglia (caudate, putamen/globus pallidus)

Mesencephalothalamic regions (midbrain-thalamus)

34
Q

what is the definition of vegetative state (unresponsive wakefulness syndrome)

A
  • Spontaneous eye opening signalling wakefulness but not evidence of purposeful behaviour suggested awareness of self or environment
  • No purposeful behaviours when exposed to stimuli; visual, auditory, tactile, or noxious and no language comprehension or expression
  • Have decorticate or deceberate positioning (cortex is involved in inhibiting the red nucleus, if you don’t have input from the cortex the red nucleus is not inhibited)
35
Q

What is the difference between a persistent vegetative state and a permanent vegetative state

A

Persistent vegetative state
- Vegetative state persisting for at least 1 month after TBI or non-TBI

Permanent vegetative state

  • Persists for at least 12 months after traumatic injury
  • Vegetative state persisting for at least 3 months after non traumatic causes such as anoxic hypoxia or others
36
Q

What is the definition of minimally conscious state

A

condition of severely altered consciousness in which there is definite but often subtle and inconsistent behaviour evidence of self or environmental awareness

37
Q

what are the characteristics of minimally conscious state

A
  • Recognise verbeal or gestural yes or no responses
  • Provide simple verbal
  • Follow simple commands
  • Provide purposeful movements
  • Often after passing through coma and vegetative state
38
Q

what are the characterises of the confusional state

A
  • Interactive communication
  • Amnesia/confusion
  • Hypokinetic or agitated
  • Labile behaviour
39
Q

describe the characteristics of the post confusional state

A
  • Resolution in amnesia/confusion (months to years)
  • Cognitive impairments in higher levels, attention, memory retrieval and executive functioning
  • Deficits in self-awareness, social awareness, behavioural and emotional regulation
  • Achieve functional independence in daily self care
40
Q

what is the prognosis of the vegetative state

A
  • Depends on cause, severity, site of damage, duration and depth of consciousness
  • Absent brain stem reflexes is poor prognosis
41
Q

what is the diagnostic criteria of the PVS

A

 Cycles of eye opening and closing (appearance of sleep/wake cycle)
 Complete lack of self or environment
 Complete/partial preservation of hypothalamic and brainstem autonomic functions.

42
Q

what are the factors affecting the recovery from the PVS

A

 Time spent in vegetative state.
o Inverse relationship with recovery.

 Age.
o Younger = better recovery.

 Type of brain injury.
o Traumatic better outcome than anoxic.

43
Q

the earlier these occur the more favourable the prognosis…

A
  • Return of speech
  • Spontaneous eye movements that can track objects
  • Normal resting muscle tone
  • Ability to follow commands
44
Q

what are the ethical issues regarding PVS

A
  • continue to receive clinically assisted nutrition
    cost £90,000
  • 2/3 will have an unfavourable long term funtioncal outcome
  • have to now provide hydration and pain relief
45
Q

what is the current management of patients with PVS

A
  • Immediate stabilisation airway, breathing, circulation
  • Admission to an ICU
  • Supportive measures such as control intracranial pressure if TBI, artificial ventilation via endotracheal or tracheostomy tube
  • Establish the cause of the coma (e.g. TBI, blood glucose level in diabetes, opioid overdose reversal with naloxone via blood tests and imaging
  • Taking care of patient (feeding via CANH, prevent bed sores, prevent muscle atrophy)
46
Q

How do you assess consciousness

A
  • auditory event related potential
  • imaging
  • sensory stimulation
47
Q

Describe how an auditory event related potential works

A
  • Aim to identify a mismatch negativity (MMN, a negative component appearing in the primary auditory and prefrontal cortices around 100-250 ms after an auditory change in a monotonous sequence of sounds
  • Aim to identify a P300 (a positive component appearing in the primary auditory and prefrontal cortices around 300 ms after an auditory change in a monotonous sequence of sounds
  • The P300 appearance corresponds to activation of a frontoparietal network
48
Q

what is the issue with the auditory event related potential

A

• ISSUE: The P300 is absent in 10-20% healthy individual

49
Q

what imaging can you use to detect consciousness

A
  • Positron emission tomography (PET) imaging: use radioactive Fluorodeoxyglucose (FDG) to see increase glucose uptake, a proxy to brain activity
  • Blood oxygenation level dependent (BOLD) fMRI imaging: detects difference between oxyHb and deoxyHb, to see cerebral blood flow, a proxy to brain activity
  • can use tactile and sensory stimulation while imaging the patient
50
Q

name a few ways which can be used for current treatment

A
  • sensory stimulation
  • amantadine
  • zolpidem
  • vagal nerve stimulation
51
Q

describe how sensory stimulation works

A
  • idea is to provide an enriched environment to promote neural plasciticty such as axonal growth, dendritic branching an dsynaptogenssi
  • this is in order to avoid sensory deprivation
  • not sure if it really works
52
Q

describe how amantadine works

A
  • Weak NMDA antagonist and block dopaminergic reuptake but mechanism not completely understood
  • 100-200mg twice dialy over a period of 4 weeks in patients (16-65 years old) with traumatic disorders of consciousness who are 4-16 weeks of injury
  • Improves functional recovery rate in the early stages – faster recover reduces the burden of disability
53
Q

describe how zolpidem works

A
  • Used orally as a short term treatment (2-6 weeks) for insomnia (improve sleep osnet and staying asleep) overdose lead to coma or death
  • Indirect GABAA receptor agonist
  • Half life of 2.4 hours with no active metabolite or accumulation
  • PET scans show an increase in glucose metabolism after taking this drug
54
Q

what are the down sides of zolpidem as a treatment

A
  • Not effective in all PVS/MCS patients (hypoxia > TBI)

* Can not be replaced by benzodiazepines

55
Q

What is the hypothesis as to why zolpidem works

A
  • there is loss of active inhibition from the striatum which means the the GPI is allowed to tonically inhibit the thalamus and pedunculopontine nucleus
  • zolpidem activates GABAa in GPI and restores the normal inhibition
  • by substituting the normal inhibition from the striatum therefore it allows an increase in thalamic excitation and this projects to the prefrontal cortex
56
Q

describe how vagal nerve stimulation works as a treatment for PVS

A
  • you can use the vagal nerve to activate the thalami-cortical network and pontinetegmentum
  • it is implanted to the vagus nerve at the neck level for stimulation and then it takes 1 month to recover
  • can cause progress from the PVS to the minimally conscious state

Brain and Behaviour Year 2 (36 decks)

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