Consciousness states Flashcards
OUTLINE
I. Disorders of consciousness
II. Clinical diagnosis
III. Paraclinical diagnosis
> Active paradigm
> Passive paradigm
> Case report
IV. Treatments
> Pharmacological
> Brain stimulation
Challenges
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
- Awareness evaluation
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
I. Disorders of consciousness : Clinical entities
Disorders of consciousness
I. Disorders of consciousness : COMA
No eyes opening
No sign of consciousness
Lasting min 1 hour
I. Disorders of consciousness : Vegetative state/Unresponsive
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
I. Disorders of consciousness : Minimally conscious state
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
I. Disorders of consciousness : MCS +/-
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)
I. Disorders of consciousness : Where is consciousness in the
brain?
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
I. Disorders of consciousness : 2 networks
Internal awareness network
ACC
External awarness network
Inferior parietal lobule (AG - SMG)
I. Disorders of consciousness : pain
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
I. Disorders of consciousness : do they hear us ?
Control & MCS : associative areas connected
UWS : nope
II. Clinical diagnosis : misdiagnosis
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 !
III. Paraclinical diagnosis : active paradigm
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
III. Paraclinical diagnosis : passive paradigm
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
III. Paraclinical diagnosis : Integrated information theory
→ 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)
III. Paraclinical diagnosis : conclusion
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
IV. Treatment : Mesocircuit model
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.
IV. Treatment
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
