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Level of consciousness chapter 3
1. LEVEL OF CONSCIOUSNESS
Mse IN NEUROLOGY (s&b)LESSON 3
Dr amala Emani
Consultant psychiatrist
Columbus hospital, begumpet.
2. Basic elementary brain function determines pt’s ability to relate to self and environment.
Alteration indicates brain dysfunction
In testing it is important to distinguish content of consciousness and basic arousal
Content refers to higher cognitive and emotional functioning.
Content refers to activation of cortex from ascending activating system
Final level of consciousness is dynamic balance between cortical and ascending reticular
formation.
This chapter deals with basic arousal
3. TERMINOLOGY AND EVALUATION
Many terms used to describe basic levels of consciousness
Represents points on a continuum from full alertness to deep coma
Five principal levels
➢ Alertness
➢ Lethargy or somnolence
➢ Obtundation
➢ Stupor or semicoma
➢ Coma
4. Alertness:
Pt is awake and fully aware of normal external and internal stimuli.
Barring paralysis, pt can respond appropriately to any normal stimuli
Alert pt is able to interact in a meaningful way with the examiner
In case of total paralysis eye contact or eye movement may be adequate to establish
this interaction.
5. LETHARGY
Pt is not fully alert and tends to drift off to sleep when not actively stimulated
Spontaneous movements are decreased and awareness is limited
Pt unable to pay close attention to examiner.
Eyes are open yet appear dull and without animation
Loses train of thought and wanders from topic to topic
Summarize response, movement, conversation.
6. Obtundation
Transitional state between lethargy and stupor.
Difficult to arouse(compare with lethargy where drifts to sleep)
When aroused is confusional.
Constant stimulation is required to elicit even marginal cooperation from the pt.
Obtunded pt is characteristic of acute confusional state
7. Stupor and semicoma
Repeated and vigourous stimulation is needed for the pt to respond.
Respondes with groan or mumble and move restlessly in bed.
8. Coma
Pt respond neither to internal stimuli nor external stimuli spontaneously.
Defined as a state where no evidence of behavioural response to stimulation is present,
the term can serve as an absolute end point on the scale of consciousness or
arousability.
Sometimes can be subdivided as light coma and deep coma
Light coma : Reflex motor activity(glasgow coma scale score 3/2) present.
Deep coma : No motor response
9. Aforementioned terms are qualitative and lack objectivity and reliability.
Can be amended with less subjective assessment scheme and replaced with short
statements, instead of terms such as “lethargy”, that describe both level of stimulus
necessary to arouse the pt and actual behavioral response elicited.
10. First the intensity of the stimulation needed to arouse the patient should be
indicated
1)Calling the pt’s name in normal conversational tone
2)Calling in a loud voice
3)Light touch on the arm
4)Vigourous shaking of the pt’s shoulder
5)Painful stimulation
11. Second pt’s highest level responses should be described
1) Degree and quality of movement
2) Presence and coherence of speech
3) Presence of eye opening and eye contact with the examiner
Finally what the pt does on cessation of stimulation should be described.
Eg: Patient lethargic: Name called in a normal tone of voice; pt opened eyes , pulled
self part way up in bed, mumbled “ why ya bothering me?” then closed eyes and
went back to sleep.
Pt obtunded: Responds to loud shouting with restless movements of all extremities
and brief eye opening, speech is mumbled and incoherent; when stimulation
discontinued, pt returns to sleep.
12. Pt stuporous: Doesnot respond to voice but will respond to vigourous shaking of shoulder
accompanied by loud calling of pt name, pt responds with groan and aimless movement of left
extremities; eyes remain closed.
13. Anatomy and clinical implications
Brain structure –responsible for –arousal –ascending reticular activating system.
Origin –brainstem reticular formation (input)
Diffuse or nonspecific thalamic projection system (mediator or connector)
Cortex (output)
14. A group of specialized (reticular) neurons in the tegmental portion of midbrain and upper pons –
has specific capacity to activate higher centers (cortex).
Perimeridian portion of brainstem (reticular formation and locus ceruleus) receive collateral
inputs from most of ascending and descending fiber systems.
Cortex receives steady input from reticular activating system, without this input cortex cannot
function efficiently.
Any damage or suppression to this system makes person difficult to arouse.
15. Infarction or hemorrhage or RAS (input) lead to total disruption of arousal, coma.
Pressure on the midbrain from hippocampal or uncal herniation causes change in level of
consciousness and progresses to coma.
Drug intoxication, metabolic imbalance and sepsis alters reticular and cortical functioning.
This leads to alteration in arousal but also content of consciousness.
16. Damage to extension of brainstem reticular system at thalamus (mediator) disconnect the reticulocortical
and reticulolimbic pathways, leads to unusual comalike like state, with eye opening but lack cortical
activation.
Termed as akinetic mutism/ persistent vegetative states.
In these state pt has - uncanny (strange) appearance of being like aware,
- lie on bed and look around room
- variable eyecontact ,sometimes seem like random sometimes genuine interpersonal
eye contact appear to take place.
- other than this “visual scanning” pt is immobile and mute.
This dichotomy (?no correlation) between “apparent” visual alertness and lack of speech or motor activity
differentiates with stupor or coma.
17. Input (RAS) is intact, output (cortex) is working but the mediator or projections are not working
leading to comalike state.
Arousal mechanism works, cortical function works but no coordination.
18. Akinetic mutism is reserved for cases –damage in – midbrain or subthalamic region or to septal
region.
Midbrain region causes “apathetic akinetic mutism”
They are --difficult to arouse but when aroused can move all extremities
--mutter few intelligible words
--look directly at the examiner few moments
--turn away or drift back to sleep
Subtle muscle stretch reflex changes, extensor toe signs, extraocular muscle involvement and
pupillary abnormality may be seen.
Occlusion of small vessels entering brainstem from tip of basilar artery.
Leison interrupts ascending reticular activating system.
19. Pts with lesion involving septal area, ant hypothalamus, cingulate gyri, bil orbito frontal cortex are also
akinetic and mute, but they appear much more alert.
Awake most of the day and insomnia at night.
Eyes remain open when awake.
These pts often have violent outbursts during arousal (septal rage).
Coma vigil is used to describe these pts.
This syndrome is seen with rupture of anterior communicating artery aneurysms, deep frontal lobe
tumors and ant cingulate gyrus tumors.
20. Hyper reflexia with Babinski sign +nt from corticospinal tract involvement
Difficulty in temperature regulation from anterior hypothalamic damage
Primitive reflexes (snout and grasp)from mesial(medial) frontal
No pupillary or extra ocular muscle palsy.
21. Diffuse cerebral cortex (output) damage from anoxia, hypoglycemia, circulatory or metabolic
embarrassment frequently survive in a clinical state similar to coma vigil
Bil decortication with double hemiplegia and primitive reflexes is seen
Brain stem remains intact
Condition called aphallic state, due to diffuse damage of neocortex.
22. “Persistent vegetative state” term used to describe pts surviving severe head injury is
similar to aphallic state.
Term persistant vegetative state is used more widely than aphallic state with spread cortical
damage and no ability to interact meaningfully with environment.
23. Locked in syndrome another comalike state
Leison (haemorrhage or infarct) is in upper pontine tegumentum
All corticospinal and corticobulbar fibers at the level of abducens and facial nuclei are dissected.
Central nervous system above the lesion are intact .
Leading to paralysis of all motor muscles except those controlling eye movements.
Cannot use any voluntary muscle, except ocular muscles (mostly vertical movement), eye and
eyelids.
24. Akinetic mute
(apathetic –
midbrain)
Akinetic mute
(coma vigil –
septal)
Aphallic state
(decorticate)
Persistent
vegetative state
Locked –in
syndrome
Level of
consciousn
ess
Lethargy Wakeful, with
occasional
outbursts
Awake, with no
meaningful
interaction with
environment
Awake; no or
little interaction
with
environment
Awake and
alert
Able to
communicate
meaningfully
with eye
movement
Voluntary
movement
Little and infrequent,
but when sufficiently
stimulate can move
all extremities
purposefully.
Little but
purposeful; arms
usually move
much better than
legs.
No or little
purposeful
movement;
mostly reflex or
mass movemnts
Usually little or
none,
depending on
areas of brain
damaged,
mostly primitive
postural reflex
None except for
eye movement
Speech With stimulation can
produce normal,
short phrases.
Little,
occasionally
normal phrases,
None or
occasional
grunting
None or
occasional
grunts or groans
none
25. Akinetic mute
(apathetic –
midbrain)
Akinetic mute
(coma vigil –
septal)
Aphallic state
(decorticate)
Persistent
vegetative state
Locked –in
syndrome
Eye responses Open, when
stimulated;
good eye
contact
Open during
much of the
day in most pts;
eye contact
variable
Open,
searching, but
no real eye
contact
Open,
searching, but
no real eye
contact
Open, with
normal following
and good eye
contact; some
pts have
restricted lateral
gaze
Limb tone Usually normal Often increased
in legs
Increased in all
extremities
Usually
increased,
variable
Increased
Reflexes Can be normal Hyperreflexia in
legs, babinskis
+nt, snout and
grasp +nt
Increased in all,
pathological
reflexes +nt
Usually
increased
Increased in all
26. Psychogenic unresponsiveness(hysterical coma like state)
Examination reveals normal respiration, heart rate and blood pressure
Muscle tone usually normal, but inconsistent response is frequent.
All bulbar reflexes(gag, corneal, pupil, caloric reflex, dolls phenomenon) intact.
Muscle stretch reflex are symmetric.
Inconsistent reponses are not sign of organic coma.
Should not be diagnosed hastily.
Misdiagnoses of true coma as hysterical coma is far more serious
27. Final note
Not all alterations in level of alertness are pathologic.
Sleep represents a natural fluctuation in the level of consciousness.
Any pt with organic condition have inherent normal sleep wake cycle
So altered consciousness, one must rule out normal sleep.
28. Summary
Consciousness is most rudimentary of all mental functions
And its level must be determined first in any MSE
Alteration will impact all other subsequent tests
Only more obvious changes can be validly documented.