Lecture:

Unconsciousness and Coma

Dr. Eyad M. Hussein

MD, Ph.D of Neurology
Consultant in Neurology Department,
Nasser Hospital,
Assistant Professor,
Faculty of Medicine, Islamic University
Faculty of Dentistry, University of Palestine
‫الرجاء تحويل الجوال إلى وضع‬
‫الصامت مع الشكر‬
 Consciousness

Consciousness: is regarded as a state of awareness

of self and surrounding.
Impaired of consciousness due to disturbed
wakefulness or awareness of mental function.
 Consciousness

! Wakefulness (arousal, alertness)- brain stem

! Content or awareness (of self or environment)-
cerebral hemispheres
! No awareness without wakefulness
! Wakefulness can occur without awareness
(vegetative state)
 Consciousness

Consciousness:
AWARENESS+
AROUSAL
AWARNESS WAKEFULNESS
 Mental Status

Mental Status = awareness + wakefulness

Awareness (Content) - the sum of cognitive and
affective function: intact of cerebral cortex.
Arousal (level of consciousness)- appearance
of wakefulness: Ascending reticular activating
system (ARAS) projects to diencephalon and
cerebral cortex.
Changes in the level of wakefulness :
➢ Lethargy, stupor, and coma.

Changes in the awareness :

➢“Relatively simple” changes: e.g. speech,
calculations,
spelling
➢More complex changes: emotions, behavior or
personality: confusion, disorientation, hallucination, poor
comprehension, or verbal expressive difficulty
 Mechanism of Coma

Dysfunction of reticular
activating system (direct
and indirect)

COMA OR+

Diffuse bilateral
hemispheric cerebral
damage, or
Both
Disturbance of Consciousness Level

COMA

SEMI COMA

STUPOR

LETHERGY&DROWSNESS

SLEEP

CONSCIOUS
 Disturbances of Consciousness Level
•Conscious (Alert): Appearance of wakefulness,
awareness of the self and surroundings.
•Sleep: is normal mental and physical inactivity from
which the subject can be roused.
•Lethargy or drowsiness: mild reduction in
wakefulness
•Stupor: is an abnormal, sleepy state (deep sleep) from
which the subject can be aroused by repeated stimuli.
Returns to deep sleep when not continually stimulated.
•Semicoma: Sleep like appearance no response to
verbal stimuli but preserved response to painful stimuli
•Coma (Unconscious) : Sleep like appearance and
behaviorally unresponsive to all external stimuli
(Unarousable, unresponsiveness, eyes closed)
 Classification of Coma
Grade Consciousnes External stimulus
s
I. Lethargy or Disturbed Response to verbal and
drowsiness painful stimuli (but not
vigorous)
II. Stupor Disturbed Response to verbal and
painful stimuli (vigorous)

III. Semi-coma Lost No response to verbal stimuli

with preserved response to
painful stimuli
IV. Coma Lost No response to both verbal &
painful stimuli
 Grading of Coma
Grade Grading of Coma
I Alert

II Drowsy but responds to verbal stimulation.

III Unconscious: no response to verbal stimulation, but

withdrawal response to pain.

IV Unconscious: decorticate responses to pain (flexion

of upper limbs and extension of lower limbs).

V Unconscious: decerebrate responses to pain

(hyperextension of both upper and lower limbs).

VI Unconscious: no responses to pain.

 Classification (causes) of Coma

Supratentorial Infratentorial Metabolic Psychogenic

 Causes of Coma

! Diffuse hemisphere damage

! Bilateral thalamic involvement.
! Brainstem lesion.
! Supra- or infratentorial mass lesions causing
midbrain compression and brainstem herniation.
 Causes of Coma

I- Intracranial Causes

! Trauma:
◦ Diffuse white matter injury (Diffuse Axonal Injury)
◦ Intracranial haemorrhage (extradural, subdural, subarachnoid)
! Vascular:
◦ Ischemic stroke
◦ Hemorrhagic stroke
! Infectious:
◦ Meningitis
◦ Abscess
◦ Encephalitis
! Neoplastic:
◦ Tumor with oedema
! Other:
◦ Epileptic status
◦ Hydrocephalus
 Causes of Coma

II- Extracranial Causes
! Endocrine and Metabolic: ! Decrease cardiac output:
◦ Hypoglycaemia, hyperglycaemia, ◦ Vasovagal attack, MI,
DKA cardiac arrhythmias,
valvular disease
◦ Hypothyroidism (myxedema),
◦ Blood loss, hypotensive
hyperthyroidism
drugs
◦ Ca, K, Na disturbances ! Toxin:
◦ Uraemia, hepatic failure ◦ Alcohol, carbon
◦ Hypoxia, hypercapnia monoxide, heavy metals
! Respiratory insufficiency: ! Drugs:
◦ Hypoventilation, perfusion ◦ Sedatives, opiates,
anaesthetic agents
deficiency
◦ Anticonvulsants,
antidepressants
! Psychiatric disorders:
◦ Conversion disorder and
catatonia
 Other states of impaired consciousness

Brain Death A kinetic mutism

Vegetations State Minimally

COMA conscious state

Locked-in Syndrome
Vegetation State (VS) or Apallic syndrome

Coma with return of wakefulness and

develop a persistent unresponsive
state in which sleep–wake cycles
return.

No evidence of language comprehension

or meaningful expression

After severe cortical damage after head

injury, the brainstem function returns with
sleep–wake cycles, eye opening in response
to verbal stimuli, and normal respiratory
control.
 Locked-in Syndrome

Brain imaging with MRI may show

isolated lesions (bilateral infarction,
haemorrhage, or tumour) of the
ventral part of pons.

➢Complete quadriplegia, anarthria and

dysphagia resulting from the disruption
of corticospinal and corticobulbar
pathways
Ventral ➢ Preserved consciousness: Patient is
Pontine awake and alert
Infarction ➢ Preserved eye opening and vertical
eye movement
 Brain Death

! Absent cerebral function

! Absent brainstem function

! Apnea
 Tests for Brainstem Death 

(By two doctors)

➢ No pupillary response to light

➢ Absent corneal reflexes
➢ Absent vestibulo-ocular reflex
➢ Absent gag reflex
➢ Absent cough reflex
➢ No motor response in cranial nerve territory
to painful stimulus (e.g. supraorbital pressure)
➢ Apnea: no respiratory movements when
patient is disconnected from ventilator
Transient Disturbances of Consciousness

➢ Syncope:cardiac arrhythmias, micturation, and

cough syncope
➢ Epilepsy
➢ TIA

➢ Hypoglycemia
➢ Drop attack (falls without warning and without
clear-cut loss of consciousness.
➢ Psychogenic
Examination of the Unconscious Patient
➢ History
➢ General examination
➢ Neurological examination
• Conscious level
• Pupil response
• Fundus examination
• Corneal and limb reflexes
• Facial weakness: failure to ‘grimace’ on one side in
response to bilateral supraorbital pain
• Oculocephalic (Doll’s eye) reflex
• Oculovestibular reflex (caloric testing)
• Limb weakness
 History
! Recent head injury: diffuse brain injury, intracranial
hemorrhage.
! Previous head injury (e.g. 6 weeks): chronic subdural
hematoma)
! Sudden collapse: hemorrhagic stroke
! Limb twitching, tongue biting, incontinence: epilepsy
! Gradual development of symptoms: mass, infectious
! Previous illness: DM, epilepsy, alcoholism, drug abuse, viral
infectious, malignancy, migraine, psychiatric illness
 General Examination
! Temperature: fever, hypothermia (alcohol, barbiturate,
myxedema)
! Pulse: bradychardia with high BP (intracranial hypertension)
! Blood Pressure: high BP (cerebral hemorrhage, hypertensive
encephalopathy), low BP (adissonian crisis)
! Respiration:
◦ Cheyne-Stokes (periodic) respiration is alternating hyperpnoea
and apnoea (bilateral deep cerebral & upper brainstem
dysfunction, metabolic comas, with CO2 retention),
◦ Kussmaul (acidotic) respiration is deep, sighing
hyperventilation ( seen in DKA and uremia),
◦ Central neurogenic (pontine) hyperventilation describes
sustained, rapid, deep breathing seen with pontine lesions,
◦ Ataxic respiration is shallow, halting, irregular respiration. It
frequently precedes death. The medullary respiratory centre is
damaged.
 General Examination

! Odor of breath: alcohol, acetone (DKA), uriniferous odor

(uremic coma).
! Inspection: multiple bruises, CSF leak & internal auditory
meatus bleeding (head trauma), dry skin (DKA, CRF),
sweaty (hypoglycemia), puffiness & flushing (alcohol
intoxication & DKA), rashes (meningococcal meningitis,
endocarditis), jaundice (hepatic failure), tongue biting
(Epilepsy), needle marks on limbs (drug abuse)
 Neurological Examination
! Level of consciousness
! Signs of raised intracranial pressure (ICP).
! Neck stiffness and +ve Kernig’s sign: meningitis, SAH
! Unilateral, dilated, fixed pupil: intracranial mass lesion
! Bilateral, dilated, fixed pupil: brainstem death. They also occur
in deep coma due to barbiturate, atropin and sympathomemitic
intoxication.
! Horner's syndrome.
! Pinpoint pupils: drugs (morphine, parasympathetic), pontine
hemorrhage
! Eye movement absence: severe trauma, ischemia, hemorrhage
! Asymmetric limb response (hemi- or monoparesis): focal brain
damage (tumor, trauma, CVA, encephalitis)
•Oculocephalic (Doll’s eye) reflex: Passive head
turning produces conjugate ocular deviation away from
the direction of rotation (doll's head reflex). This reflex
disappears in very deep coma, brainstem lesions, and
brainstem death.
•Oculovestibular reflex (caloric testing): Slow tonic
ocular deviation (nystagmus) towards the irrigated ear
is seen when ice-cold water is run into the external
auditory meatus . This indicates an intact brainstem.
The test is used in the diagnosis of brainstem death.
 Signs of Lateralization
➢ Anisocoria
➢ Facial asymmetria.
➢ Abnormalities of conjugate gaze
➢ External rotation of one lower limb
Lateralizing signs.
➢ Asymmetry of muscle Tone.
➢ Asymmetrical response to painful stimuli.
➢ Asymmetry of plantar responses.
➢ Asymmetry of tendon reflexes.
➢ Asymmetry of decerebrate and decorticate
posturing.
 Glasgow Coma Scale (GCS)
Category Response Points
Eye opening Spontaneously 4
To speech 3
To pain 2
None 1
Verbal response Oriented 5
Disoriented, confused conversation, able to 4
answer questions
Inappropriate responses (words) 3
Incomprehensible speech (sound) 2
None 1
Motor response Obeying commands 6
Localizes to pain 5
Withdraws from pain 4
Abnormal (spastic) flexion, (decortication) 3
Extensor (rigid) response, (decerebration) 2
None 1
(GCS minimum = 3: maximum = 15)
 Investigations
•Trauma If negative
•Signs of raised ICP Lumbar
•Focal neurological Urgent CT SCAN
puncture
signs
•Meningism

If negative

Metabolic Screen In addition:

Suspected drug
Glucose, ABGs, KFT, Skull X-Ray
abuse or metabolic
disease LFT, electrolytes, drug Chest- X-Ray
• No signs of raised ECG
screen, B1, B12, blood
ICP,
• No meningism culture (fever), TFT EEG
• No focal neurological MRI
signs
 Management of Coma
❖ABCs:
➢Airway: remove any obstruction
➢Breathing: suction of nasal and pharyngeal secretion
O2 mask, intubation with mechanical ventilation and
urgent tracheostomy if needed
➢Circulation: check pulse and BP. Establishing
intravenous access, and replace any blood loss
❖Intubate if GCS ≤8
❖Stabilize cervical spine
❖Supplement O2
❖IV access
❖Blood pressure support as needed
❖Glucose 50% IV 50mL
❖Thiamine 100mg IV
❖Treat definite seizures with phenytoin or equivalent
❖Anticoagulant: DVT prophylaxis.
 Empiric Treatment

➢For possible infection: Ceftriaxone, Vancomycin,

Acyclovir
➢For possible ingestion: Naloxone, Flumazenil (for
suspected benzodiazepine overdose)
➢Gastric lavage/activated charcoal
➢For possible increased ICP: Mannitol
➢For possible nonconvulsive status: Lorazepam,
Phenytoin, Depakine
 Long Term Requirements

➢Bed “Skin care”: change of patient position (every 2

hours), frequent wash of the skin of the back and pressure
points.
➢Oral hygiene
➢Eye care
➢Bladder: F. catheter, suprapubic catheter
➢Bowel “nutrition – fluid balance – defecation”: NGT,
gastrostomy, laxative, daily enema
➢Medical rehabilitation and family training
Thank You