Consciousness states Flashcards

1
Q

OUTLINE

A

I. Disorders of consciousness

II. Clinical diagnosis

III. Paraclinical diagnosis
> Active paradigm
> Passive paradigm
> Case report

IV. Treatments
> Pharmacological
> Brain stimulation

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2
Q

Challenges

A

Comment savoir si qq un est conscient, notamment en présence d’une forte activité cérébrale ?

Etablir une évaluation précise de la douleur/nociception chez les patients UWS ou MCS. NCS = first step

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3
Q
  1. Awareness evaluation
A

O/V
Intelligible Words
Vocalization Only
AROUSAL
Sustained Attention Eyes
Open w/o Stim
Eyes Open w/ Stim
MOTOR
Functional Object Use
Object Manipulation
Automatic Movement

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4
Q

I. Disorders of consciousness : Clinical entities

A

Disorders of consciousness

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5
Q

I. Disorders of consciousness : COMA

A

No eyes opening

No sign of consciousness

Lasting min 1 hour

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6
Q

I. Disorders of consciousness : Vegetative state/Unresponsive

A

No sign of consciousness

No environment interaction

No voluntary behavior in response to visual, auditive, tactile and painful stimuli

No language comprehension – no language expression

Wake-sleep cycle

NEW NAME : UNRESPONSIVE WAKEFULLNESS SYNDROME

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7
Q

I. Disorders of consciousness : Minimally conscious state

A

Limited but clearly discernible evidence of self or environmental awareness.

One or more of the following behaviors:
• Following simple commands.
• Gestural or verbal yes/no responses (regardless of accuracy).
• Intelligible verbalization.
• Purposeful behavior, including movements or affective behaviors that occur in contingent relation to relevant environmental stimuli:
– appropriate smiling
– appropriate vocalizations or gestures
– reaching for objects
– touching or holding objects
– visual pursuit or fixation

Emergence from MCS
• Functional interactive communication
• Functional use of two different objects

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8
Q

I. Disorders of consciousness : MCS +/-

A

MCS +
Following simple command

MCS -
Pain localisation
Visual pursuit
Accurate smiling or crying

MCS was recently subcategorized based on the complexity of patients’ behaviours: MCS+ describes high-level behavioural responses (i.e., command following, intelligible verbalizations or non-functional communication) and MCS- describes low-level behavioural responses (i.e., visual pursuit, localization of noxious stimulation or contingent behaviour such as appropriate smiling or crying to emotional stimuli)

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9
Q

I. Disorders of consciousness : Where is consciousness in the
brain?

A

Consciousness # whole brain

Consciousness ≈ frontoparietal

PRECUNEUS
hub in the network

> systematiquement impliqué dans les UWS
> Dans la remission, partie qui se développe

Activité du précuneus
En comparant avec Control > LIS > MCS > UWS = 0

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10
Q

I. Disorders of consciousness : 2 networks

A

Internal awareness network
ACC

External awarness network
Inferior parietal lobule (AG - SMG)

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11
Q

I. Disorders of consciousness : pain

A

Besoin d’une nouvelle façon d’évaluer la capacité à ressentir la douleur afin d’ajuster la sedation.

Nociception Coma Scale

Scores corelated with ACC activation

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12
Q

I. Disorders of consciousness : do they hear us ?

A

Control & MCS : associative areas connected
UWS : nope

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13
Q

II. Clinical diagnosis : misdiagnosis

A

Threshold btw UWS & MCS

Difference entre Volontaire/voulu et Automatic/Reflexe

En fonction de l’échelle employée, le diagnosis posé (et les traitements associés) peut être différents. D’où l’importance de ces échelles.

Glasgow recovery scale : 24/77 MCS
Coma Recovery Scale - Revised : 45/77 MCS
41% of potential misdiagnosis = patients définis comme non conscients alors qu’ils le sont !

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14
Q

III. Paraclinical diagnosis : active paradigm

A

fMRI
> Imagining playing tennis / spatial navigation
Communicatrion is possible “YES” “NO”

Activation studies can predict outcome
Metanalysis - Di et al. - 2008

EEG
MMN sur P3
prenom non familier/ propre prenom
> amplitude correle état de conscience
> pas une onde de cosncience car UWS répondent aussi

EMG
easiest
“move the right hand”

PB : always uses language

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15
Q

III. Paraclinical diagnosis : passive paradigm

A

Aphasia ppl may not be able to understand instructions
=> passive paradigms

Bonne capacité à discerner UWS de MCS ! (74% PET, 56% fMRI prediction outcome)

Default Mode Network
DMN conectivity corelates the degree of consciousness
-> no task, resting state
Vanhaudenhuyse et al, 2010

FDG PET Scan + fMRI
(fluorodeoxyglucose)

Thibaut et al 2012
>> Can predict outcome

TMS/EEG
Wakefulness : complex, long lasting, both hemispheres
→ Integrated information theory

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16
Q

III. Paraclinical diagnosis : Integrated information theory

A

→ Integrated information theory
Consciousness : reseau dense, signaux d’ampleur variables (différentiation), communcation élevée, interconnections nombreuses (intégration)
Perte d’intégration : interconnections très failbles, mini réseau isolés
Perte de différentiation : Tous les signaux d’échanges sont de meme amplitudes (epilepsie)

Perturbational complexity level
Compression : the more is compressible, the less complex (differenciated)

17
Q

III. Paraclinical diagnosis : conclusion

A

Behavioral assesment : 40% misdiagnosis

FDG-PET : en complément des eaminations, peut predire le rétablissement à long terme, mem de patient UWS

Active fMRI/EEG/EMG paradigms are less suited for differential diagnosis but may provide a strong complementary tool

TMS-EEG may provide for the first time a measure of consciousness at a subject level

Encourage to use multimodal assesment of the level of consciousness
-Potential pharmacological and non pharmacological treatments but more validation studies are needed

18
Q

IV. Treatment : Mesocircuit model

A

Giacino et al 2014

Striatum needs an important amount of connections to reach the threshold

A common mechanism for downregulation of the anterior forebrain mesocircuit in severe brain injuries. Reduction of thalamocortical and thalamostriatal outflow following deafferentation and loss of neurons from the central thalamus withdraws important afferent drive to the medium spiny neurons of the striatum, which may then fail to reach firing threshold because of their requirement for high levels of synaptic background activity. Loss of active inhibition from the striatum allows neurons of the globus pallidus interna to tonically fire and provide active inhibition to their synaptic targets, including relay neurons of the already strongly disfacilitated central thalamus, and possibly also the projection neurons of the pedunculopontine nucleus.

19
Q

IV. Treatment

A

Amantadine
(dopaminergic agent)
Stimulates striatum
> Recover faster than placebo
Washout … ?

Zolpidem
GABAergic agent
inhibitates GPi : bypass of the striatum
> Works on specific patients very well but very rare !

Transcranial Direct Current Stimulation
weak direct current btw 2 electrodes - 20 min
Anode : left DLPFC (Frontal cortex)
Double blind, sham
Modulates neuronb activity (not activator as TMS)
> Good result on MCS

Deep brain stimulation
Intraluminar nuclei stimulation (thalamus)
> Induces recovery from MCS