Consciousness and disorders

one

Coma and other disorders of

consciousness
Definitions: consciousness,
somnolence, stupor, coma,
vegetative state and inactivation
Physiopathological mechanisms
leading to consciousness change
Coma differential diagnosis,
metabolic coma and causes of
structural coma and clinical
differences
Coma etiology. Main reasons
Algorithm to be considered in
approaching comatose patients
Evaluation of the motor,
respiratory, pupil, and eye
movements which are important in
the etiology of the neurological
aspect of the comatose patient and
in the lesion localization
2nd

2nd

Coma and disorders of altered

consciousness
Learning objectives and goals
Define the following terms:
consciousness, somnolance, stupor,
coma, vegetative state, locked in
syndrome
Understand the pathophysiologic
mechanisms of impaired consciousness
Be aware of the differential diagnosis
of coma. Distinguish between "structural"
and "metabolic" causes / manifestations
of coma.
Discuss the major categories of
etiologies which can cause a diminished
level of consciousness
Be familiar with the basic clinical
evaluation of the comatose
patient. Memorize an algorithm for the
management of a comatose patient
Discuss the techniques for eliciting
and localization of the following
neurologic exam: a motor, respiratory,
pupillary response, eye movements
3

consciousness
4
Being awake, being aware of himself and his
surroundings
The level of consciousness - be vigilant, to
maintain alertness, ability to continue or
move state
The content of consciousness - be aware, can
be stimulated to make an assessment, to be
able to react
4

Reticular formation
5
 Structure extending from the
observer to the thalamus in the
brainstem
Loose network style neuronal
placement
Lateral reticular formation
Medial reticular formation
5

Reticular formation
6
Lateral reticular formation
Local connection
Medial reticular formation
Sub-inclinations, overtaking long
projections
6

Reticular formation - lateral

7
Short axonal small neurons make
local connections
 Brainstem cranial nerve nucleus
MLF, etc.
7

Reticular formation - medial

8
[Reticulo-spinal tract]
RFI received in the
projection bulb 'also extends to the
anterior horn of the spinal cord
Bulbar tonus at RF warning, DTR is
reduced
bulbar RF's top warning tone, DTR
increases (pontine / mezensefal k)
8

Reticular formation - medial

9
[ascending reticular activator
system - ARAS]
top with the
projection pontine (paramedian) /
mesencephalic (tegmental) RF in the
upper neuronal structures
Responsible for the level of
consciousness, namely alertness and
alertness
9

Reticular formation - medial

10
ARAS 's projections are associated with
three of consciousness
1. thalamic reticular nucleus and
here's the specific thalamic nuclei
through the cortex
[The medial region of posterior
paramedian, parafasiculors, centromedians and
intralaminal nuclei]
2. hypothalamus and anterior to the
brain through the limbic system
3. a diffuse way neocortex
10

Reticular formation - medial

11th
RF-associated thalamus nuclei
Inhibitory effect on cortex
[The medial region of posterior paramedian,
parafasiculors, centromedians and
intralaminal nuclei]
ARAS Although from projections reduce
the effects of these thalamic
nuclei - duplicating provides
wakefulness or sleep
11th

Reticular formation - medial

12

Control and modulation of reticulo-thalamic

sleep-wake regulation
(Cortico-fugal) reaching the cerebral
cortex to the reticular formation
Warning from reticular formation from
various organs
 Deafferentation can lead to disorders of
consciousness at various levels
12

Reticular formation - medial

13

Almost all cerebral hemispheres are

responsible for consciousness content
especially
Primary sensory cortex
Associated cortical cortexes
Intra and interhemispheric pathways
connecting them to each other
Subcortical nuclei associated with them
13

consciousness
14
A sound one
[Central tegmental fascicle]
Proper operation of direct afferent
systems
 Locus coeruleus- epinephrine
Raphe nucleus-serotonin
Basal nucleus-acetylcholine
14

COMA
15
ARAS 's affecting cortical and
subcortical structures responsible
for the content of consciousness
Metabolic (hypoglycemia etc.)
Any structural change (brain
hemorrhage etc.)
Leads to coma
Coma is not a disease,
A clinical picture that is related to
various etiologies, resulting in
different pathological processes
15

CONFIDENTIAL LEVELS
 Consciousness
>> Somnolans
>> Stupor
>> Coma

Confusion and delirium

Rather than being discerned, the evaluation of more

relations and the impression of being in a coherence deteriorates

16

16

Somnolans (Laterji)
17
Patient is sleepy-prone
Aroused by a voice stimulus
Answer the question correctly
Sleep again when left to his own
DEATH

CONSCIOUSNESS

COMA

UNAWARE

NO ANSWER
 STUPOR

SOMNOLANS

17

Stupor
18
The patient does not wake up
with a voice stimulus
But it opens its eyes with a
strong, repetitive stimulus
It does not fulfill oral orders or
makes it very slow and inadequate
DEATH

CONSCIOUSNESS

COMA

UNAWARE

NO ANSWER

STUPOR

SOMNOLANS

18

Coma
19.
The patient can not be
awakened by oral stimuli
With a strong painful stimulus
Mild to moderate coma patient
localized or prompted to remove the
stimulus
Deep coma patient does not
respond to painful warning
DEATH

CONSCIOUSNESS

COMA

UNAWARE

NO ANSWER

STUPOR

SOMNOLANS

19.

Coma
20
Table of consciousness full or
close to the thalamus
 Deep coma
The patient can not be awakened
by painful stimuli
Cornea, pupil, pharynx, DTR and
no plantar response
DEATH

CONSCIOUSNESS

COMA

UNAWARE

NO ANSWER

STUPOR

SOMNOLANS

20

G lasgow coma scale

21
Eye opening:
1. no
2. With painful stimuli
3. Verbal stimulation
4. Spontaneous
Motor response
1. no
1 Extensor response
2 Flexor response
3 Withdraw
4 Localizer
5 Voluntary movement
Verbal response
1. no
2. Incomprehensible sounds
3. Inappropriate response
4. Scattered confusion response
5. Oryze response
21

Brainstem
22
Cranial midbrain III
[Pupil, eye movement]
Pons IV, V, VI cranial
 [Conjugate eye movement,
Corneal reflex]
Spinal IX, X cranial
[Pharyngeal reflex -Gag,
tracheal - cough reflex, Respiratory]
22

Pupil examination in a
comatose patient
23
Light reflex
Direct and indirect
Pupil diameter
Bilateral myotopic pupil
Bilateral mydriatic pupil
Anisocoric
23

Pupil examination in a
comatose patient
24
Bilateral myotopic pupil
Pontine hemorrhage, infarct i
morphine, heroin
use macrographic
Pilocarpine, intoxication
24

Pupil examination in a
comatose patient
25
Bilateral mydriatic pupil
Hypoxia-anoxic encephalopathy
atropine drops then I lmas
i i n common brain stem lesion
25

Pupil examination in a
comatose patient
26
Anisocoric pupil
Press nervous I 3.kranial
 With an aneurysm or mass
Temporal lobe hern. with
demi brain , other requirements
BAS K I.
26

Coma - head and eyes

position
27
In supratentorial lesions, the
patient looks to the lesion side
(vulpian)
Pons lesions on the opposite
side of the lesion
Schoolboy bobbing
The eyeballs splashed down first
in a fast and conjugate manner,
then up-primed
This movement is repeated
irregularly in 5-30 seconds.
Pons showing destruction
 27

Examination of a coma
patient
28
Oculocephalic reflex (tachycardia)
The head is quickly turned from one
side to the other by keeping the patient's
eyes open
Positive response, conjunctive
deviation of eyes to opposite side
This maneuver should not be done to
the patient who is thought cervical
pathology
If there is no movement in the
eyeballs during this maneuver, a lesion at
the level of pons or mesencephalon
should be considered
28

Examination of a coma
patient
29
Okulovestibuler reflex:
The head is raised 30 degrees
and the iced water is slowly
pumped out of the syringe to the
outer ear tract
Nystagmus occurs in the
direction of the normally slow-
cooled channel
Nystagmus does not occur in
brain stem lesions
29

Examination of a coma
patient
30
Ciliospinal reflex:
It is enlarged to the side of the
pupil with the warning of painful
neck pain
Uninvolved in lower brain stem
lesions
 30

Coma respiratory disorders

31
Cheyne-stokes respiration:
Hyperpnea and apnea periodic
breathing pattern
Breathing gradually deepens on
each inspiration
It slowly fades after reaching the
peak) and stops
Bilateral deep hemisphere lesion
31

Coma respiratory disorders

32
Central neurogenic
hyperventilation:
A hyperventilation up to 40 per
minute
There is no localization value
Long prognosis sign
32
Coma respiratory disorders
33
Apneic respiration:
In the form of a deep inspiration
and a temporary pause of
respiration
Pons showing destruction
33

Coma respiratory disorders

34
Ataxic respiration (biot respiration)
Deep and superficial breathing are
irregular and randomly seen
It is impossible to predict the depth
of the next breath
The bulbous shows the destruction
of the respiratory center
34

Coma motor system

examination
35
eyelids
Facial asymmetry
Positions of extremities
The answer to the limbs to
gravity
Motor responses to painful
stimuli
Deep tendon reflexes
Pathological reflexes
35

Coma motor system

examination
36
Facial asymmetry
Decorticated response
Deserebre response
36
Coma motor system
examination
37
Decorticated response
Flexion and adduction with
stimulation
Leg extension
Lesion just above the
mesencephalon or deep
hemispheric
37

Coma motor system

examination
38
Deserebre response
Extension, adduction and
internal rotation
Leg extension
Lesion on upper brainstem
38
Acute unconsciousness -
medical approach
39
Very serious cerebral damage
Priority goal is to reduce, limit,
deepen as much as possible
cerebral damage
Investigation of the cause of loss
of consciousness secondary
importance
39

Acute unconsciousness -
medical approach
40
Check respiration and circulation
Get venous lead, get venous
blood sample
Take arterial blood for blood
gases and pH
 Get ngs and foley probe, urine
sample
Treat convulsions
Treat if there is indication (IV
mannitol 20%)
Treat if agitation
Plan treatment if there is an
infection
40

Short episodic loss of

consciousness
41
syncope
Akinetic or absence seizure
Drop attack
Transient global amnesia
Hypoglycemia
Psychiatric disorders
41

Causes of coma
42
Symmetric
Symmetrical
Asymmetric, structural
42

Causes of coma
[symmetrical, non-
structural]
43
trauma
Concussion, diffuse axonal injury
Vascular
diffuse hypoxic - ischemic,
hypertensive encephalopathy
hypotension
Infections
Sepsis, meningitis, encephalitis
epileptic
Postcontrast period, nonconvulsive
status epilepticus
 Psychiatric charts
43

Causes of coma
[symmetrical, non-
structural]
44
metabolic
Electrolyte abnormality
PH disorder
Hyper or hyponatremia
Hyper or hypoglycemia
Hyper or hypocalcemia
Organ failure
Liver, kidney
Thiamine or b12 vit. Failure
Drug intoxication or sudden
withdrawal
Toxins
44
Causes of coma -
symmetrical, structural
45
Bilateral internal carotid artery or
Anterior carotid artery occlusion
Subarachnoid hemorrhage
Brainstem lesions
[Occlusion occasions]
45

Causes of coma -
symmetrical, structural
46
Bilateral internal carotid artery or
Anterior carotid artery occlusion
Subarachnoid hemorrhage
Brainstem lesions
[Occlusion occasions]
46
Causes of coma -
asymmetric, structural
47
mass
Cerebrovascular event
Subdural, epidural hemorrhage
Intracerebral abscess
Multiple sclerosis
47

Causes of coma -
asymmetric, structural
48
mass
Cerebrovascular event
Subdural hemorrhage
Epidural hemorrhage
Intracerebral abscess
Multiple sclerosis
48
Herniation Syndromes
49
Subfalsiyel
Unkal
Transtentory
Extradural
Tonsiller
49

Unkal herniation
50

50

Acute unconsciousness -
medical approach
51
Severe cerebral damage may
occur
Priority target
Reduce, limit, deepen cerebral
damage as much as possible
Secondary goal
Investigation of the cause of loss of
consciousness
51

Comedy patient story

52
Patients will reveal the cause of
the coma close to important points
should be tried to be learned
The beginning of the coma
(sudden / progressive)
Is there a trauma?
Is there any known
disease? (DM, renal, cardiac,
hepatic)
Is there a psychiatric illness
story?
Do you use medication (due to
abuse, suicide, treatment)
52

Comatose examination
53
priority in a patient with clinical
and neurological examination
methods, loss of
consciousnessassociated with the
situation
Complex biochemistry examination,
blood gases, ECG, chest X-ray,
intoxication studies should be done if
there is doubt
Nervousness, fever, LP
If the convulsion is the first
opportunity EEG
If lateralization is present, brain CT or
MRI
If there is trauma the relevant region
must be displayed
53

Acute unconsciousness -
medical approach
54
Check respiration and circulation
Get a venous lead, get a venous
blood sample
Take arterial blood for blood gases
and pH
Attach NGS and Foley probe, take
urine sample
Treat conviction
Treat KIBAS if indicated (IV
mannitol 20%)
Treat if there is an agitation
Plan treatment if you have an
infection
54

Coma - Story
55
1. Sudden coma
2. Fast developing coma
3.Slowly developing (days /
weeks) coma
55

Coma - Story
56
1. Fast developing coma
2. Slowly developing (days /
weeks) coma
3. Sudden coma
Brain stab infarction, subarachnoid
hemorrhage
56

Coma - Story
57
1. Sudden coma
2. Slow developing (days / weeks)
coma
3. Fast developing coma
There are unilateral findings - SVO
(ischemic, hemorrhagic)
 57

Coma - Story
58
1. Sudden coma
2. Fast developing coma
3. Slowly developing (days /
weeks) coma
Unilateral finding - tumors, apseler,
chronic subdural hematoma
Coma with confusion, delirium,
agitation before unilateral finding
and toxic, metabolic causes,
meningitis
58

Confusion
59
The patient is not asleep, but
around
Indifferent
Can not evaluate
 Can not respond appropriately
Significant deterioration
Orientation / attention /
concentration
59

Delirium
60
Acute mental disorder
Hours elapse within days
Show fluctuating course
Especially in the elderly
There is often a change in the
level of consciousness
60

Delirium
61
Characterized by attention
deficit and positive symptoms
Disarray in thought
 Disorientation and memory
impairment
Detection disorders
Illusions, horrifying hallucinations,
very vivid dreams, strange and absurd
fantasies
Sleep-wake cycle disorder
Convulsions
Intense excitement disorders,
agitations
61

Vegetative state
62
The condition in which the patient
has returned to awaken after coma
but has completely lost his
cognitive functions
Eyes open
There is sleep-wake cycle
BP and respiratory normal
 No significant response to visual,
auditory, and tactile stimuli
Understandable and consistent
word, meaning and signs
It does not match the given order
Can not break but can swallow
There is incontinence
62

Vegetative state
63
Seen in common bilateral
cerebral hemisphere lesions in
which the brain stem is intact
Most commonly in hypoxic-
ischemic encephalopathies
82% mortality in adults over 3
years
GCS score 4: 4: 2 or less
63

Akinetic mutism (coma vigil)

64
Vegetative
There is no movement from the
vegetative state to the patient
Basilar artery thrombosis, upper
brain stem lesions, encephalitis,
bilateral frontal lobe lesions
GCS score is less than 4: 1: 1
64

Locked-in syndrome
65
Pons lesion (basis yada ventral)
develops as a result
Corticospinal and corticobulbar
pathways are bilaterally involved
Reticular formation and sensory
pathways are intact.
Vertical eye movement and blink
protection
Consciousness is open but patient
is unresponsive
 No movement and no talk with the
cause of bilateral paralysis
65

Locked-in syndrome
66
Bifacial plejia
Tetraplegia
Consciousness preserved
Eye movements free
66

67
Mark the wrong thing about
consciousness change? (True B)
In delirium, the clinical picture
has acute headaches, attention,
detection defects
Unkal herniation is observed in
infratentorial cerebellar lesions
 There is a lesion at the level of
the brainstem in locked-in
syndrome
Cerebral hemispheres should be
bilaterally affected in order to lose
consciousness
Brainstem lesions
ARAS 's (ascending reticular
activating system) effects by
causing changes in consciousness
67

68
Which of the following
structures does not contribute
to the formation of
consciousness?(True)
Lateral portion of reticular
formation
The medial part of the reticular
formation
 Pontin paramedian part of
reticular formation
The tegmental part of the
mesacense of the reticular
formation
Thalamic nuclei associated with
reticular formation
Original Turkish text:

coma and disorders of altered consciousness

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