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

Study These Flashcards
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

Study These Flashcards
A
  • generally a transitional state which lasts a few weeks are rarely longer than 1 month
25
what is stupor
- similar to a coma but will response to a strong stimuli
26
what is locked in syndrome
- 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
what can cause locked in syndrome
- trauma and ishcemia to the ventral pons causing interruption to the corticospinal and corticobulbar tracts causing quadriplegia - severe cases of guillian barre syndrome
28
What is Gillian barre syndrome
autoimmune disorder which immune system attacks healthy neuroens)
29
how can people in locked in syndrome communicate
- e-tran frame | - brain computer interface
30
define akinetic mutism
- A condition of apparent alertness along with a lack of almost all motor functions including speech, gestures and facial expression
31
what is akinetic mutism often defined as
- Often misdiagnosed as having psychological reasons to not respond such as depression, deliruium, reduced awareness or physically paralysed lcokaedi n syndrome
32
what is akinetic mutism associated with
- Associated with Alzheimer’s disease, picks diseases, Creutzfeldt disease
33
What are the areas that are affected by akinetic mutism
Frontal lobe (supplementary motor area, cingulate gyrus), Basal ganglia (caudate, putamen/globus pallidus) Mesencephalothalamic regions (midbrain-thalamus)
34
what is the definition of vegetative state (unresponsive wakefulness syndrome)
- 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
What is the difference between a persistent vegetative state and a permanent vegetative state
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
What is the definition of minimally conscious state
condition of severely altered consciousness in which there is definite but often subtle and inconsistent behaviour evidence of self or environmental awareness
37
what are the characteristics of minimally conscious state
- 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
what are the characterises of the confusional state
- Interactive communication - Amnesia/confusion - Hypokinetic or agitated - Labile behaviour
39
describe the characteristics of the post confusional state
- 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
what is the prognosis of the vegetative state
- Depends on cause, severity, site of damage, duration and depth of consciousness - Absent brain stem reflexes is poor prognosis
41
what is the diagnostic criteria of the PVS
 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
what are the factors affecting the recovery from the PVS
 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
the earlier these occur the more favourable the prognosis...
- Return of speech - Spontaneous eye movements that can track objects - Normal resting muscle tone - Ability to follow commands
44
what are the ethical issues regarding PVS
- 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
what is the current management of patients with PVS
- 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
How do you assess consciousness
- auditory event related potential - imaging - sensory stimulation
47
Describe how an auditory event related potential works
* 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
what is the issue with the auditory event related potential
• ISSUE: The P300 is absent in 10-20% healthy individual
49
what imaging can you use to detect consciousness
* 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
name a few ways which can be used for current treatment
- sensory stimulation - amantadine - zolpidem - vagal nerve stimulation
51
describe how sensory stimulation works
- 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
describe how amantadine works
- 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
describe how zolpidem works
- 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
what are the down sides of zolpidem as a treatment
* Not effective in all PVS/MCS patients (hypoxia > TBI) | * Can not be replaced by benzodiazepines
55
What is the hypothesis as to why zolpidem works
- 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
describe how vagal nerve stimulation works as a treatment for PVS
- 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
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