This document discusses consciousness and disorders of consciousness. It begins by explaining that normal consciousness depends on interaction between the cerebral hemispheres and rostral reticular activating system in the brainstem. Disorders that disrupt these areas can cause altered consciousness states like unconsciousness, confusion, delirium, and coma. Coma is defined as an unarousable, unresponsive state. The causes, assessments, and management of disorders of consciousness like coma are then outlined.

1. DR. SHREEDHARA NS
10/06/2016

2.  A normal level of consciousness depends on
the interaction between the cerebral
hemispheres and the rostral reticular
activating system (RAS) located in the upper
brainstem.
 RAS- located between the rostral pons and
the diencephalon.
 Thus anatomical bilateral hemispheric lesions
or brainstem lesions may result in an altered
conscious state.

3. Unconsciousness is a state in which:-
• Unable to responds to people and
activities.
• Lacking awareness and the capacity for
sensory perception.
• Temporarily lacking consciousness

4. • Without conscious control.
• Not awareness of one’s actions, behaviour etc.
• Lacking normal sensory awareness of the
environment.
• Unconsciousness can be brief, lasting for a few
seconds to an hour or few hours or longer.

5. To produce unconsciousness, a disorder must-
o Disrupt ascending RAS extends length of brain
stem and up in to the thalamus .
o Disrupt the function of both cerebral
hemisphere.
o Metabolically depress over all brain function, as
in drug overdose.

6.  Disorders of consciousness
Confusion
• Inability to think
with customary
speed and clarity,
associated with
inattentiveness,
reduced
awareness and
disorientation
Delirium
• Confusion with
agitation and
hallucination
Stupor
• Unresponsiveness
with arousal only
by deep and
repeated stimuli
Coma
• Unarousable
unresponsiveness
Locked in
Syndrome
• Total paralysis
below third CN
nuclei.
Persistent
vegetative state
• Prolonged coma
>1 month some
preservation of
brainstem and
motor reflexes

7. Akinetic mutism
•Prolonged coma
with apparent
alertness and
flaccid motor tone
Minimally conscious
state
•Preserved
wakefulness,
awareness and
brainstem
reflexes, but
poorly responsive

8.  Aetiology –Multifactorial
1. Diseases that produce focal or lateralising
signs
2. Coma without focal or lateralising signs, but
with signs of meningeal irritation.
3. Coma without focal or lateralising signs or
signs of meningeal irritation.

9.  To assess the depth of coma and to locate the
site of lesion.
 General examination and Neurological
examinations.
 Particularly evaluating the level of
consciousness, brainstem signs and motor
responses in coma.

10. 1. Skin changes-
 carbon monoxide poisoning-cherry-red
discolouration of skin,
 alcoholic liver disease-telangiectasia, clubbing,
 Hypothyroidism-puffy facies
 Hypopituitarism-(sallow complexion).
 Cutaneous petechiae or ecchymoses may point
to meningococcaemia, rickettsial infection or
endocarditis as possible causes of coma.

11.  Needle puncture marks may suggest substance
abuse.
 Periorbital haematomas (raccoon eyes) indicate
an anterior basal skull fracture.
2. Hepatomegaly or Stigmata of chronic liver
disease- Hepatic encephalopathy.
 Enlarged kidney- Uremic encephalopathy,
should suspect for SAH.
3. Breath may smell- Alcohol/
Organophosphorous compound( garlic odour)/
Hepatic and uremic foeter are rare.

13.  FOUR (Full Outline of UnResponsiveness) Score-
 The components are
 Eye movements,
 Motor score,
 Brainstem reflexes and Respiration.
 Each subscomponent is scored out of a
maximum of four and therefore the maximum
score is 16.
 It does not include verbal response and may be
more suitable in the intubated patient.

14.  Normal-2.5mm, equal and brisk
 Demonstrate both direct and consensual light
reflexes and confirms the integrity of the
pupillary pathway.
 Size- Balance between sympathetic(dilatation)
and parasympathetic (constriction) systems.
 Abnormalities- Localising and diagnostic value.

16.  Horizontal eye movements to the contralateral
side are initiated in the ipsilateral frontal lobe
and closely coordinated with the corresponding
centre in the contralateral pons.
 Vertical eye movements are under bilateral
control of the cortex and upper midbrain.
 Spontaneous roving eye movements excludes
brainstem pathology as cause of coma.

17.  In a paralytic frontal lobe pathology the eyes will
deviate towards the side of the lesion,
 In pontine pathologies the eyes will deviate away
from the side of the lesion.
 Occular bobbing- Verticle downward beating
seen in pontine lesions.
 Upward rolling of the eyes after corneal
stimulation (Bell’s phenomenon) implies intact
midbrain and pontine function.

18. OCULO-CEPHALIC REFLEX
 Also called Doll`s-eye movement.
 Elicited by briskly turning or tilting the head.
 Response in coma of metabolic origin or that due to bihemispheral
structural lesions consist of conjugate movements of eyes in the
opposite direction.
 Positive response indicates-
i. Oculomotor, abducent, midbrain and pons are intact.
ii. There is loss of cortical inhibition on brainstem that normally
holds these movements in check.
Absent reflex indicates damage within brainstem but also
can be due to profound overdose of sedatives or
anticonvulsants.

19.  Basal ganglia lesions- Choreoathetotic or
ballistic movements.
 Metabolic disorder- Myoclonic movements, post
anoxic origin.
 Asterixis is seen with metabolic
encephalopathies.
 Hiccup is a nonspecific sign and does not have
any localising value.

20.  Decerebrate rigidity- is characterised by stiff
extension of the limbs, internal rotation of the
arms and plantar flexion of the ankles.
opisthotonos and jaw clenching.
 Seen in midbrain lesions, certain metabolic
disorder- hepatic coma, hypoglycemic.
 Decorticate Posturing- characterised by
 flexion of elbows and wrists and extension of
the lower limbs.
 Seen in lesions in cerebral white matter.

21.  Respiratory failure in comatose patients may
result from hypoventilation, aspiration
pneumonia and neurogenic pulmonary oedema,
a sympathetic nervous system mediated
syndrome seen in acute brain injury.
 Rate and pattern – The precise localising value
is uncertain.

23.  Hypothermia (<35°C)- alcohol or barbiturate
intoxication, sepsis with shock, drowning,
hypoglycaemia, myxoedema coma and
exposure to cold.
 Hyperthermia may be seen in pontine
haemorrhage, intracranial infections, heat
stroke and anticholinergic drug toxicity.

24.  These take precedence over any diagnostic
Investigation.
1. Ensure adequate airway and oxygenation.
2. Secure intravenous access and maintain
circulation.
3. Administer 50% dextrose after drawing a
sample of blood for serum glucose levels.
4. Thiamine must always be administered in
conjunction with dextrose to prevent
precipitation of Wernicke’s encephalopathy.

25. 5. Naloxone- When narcotic overdose is
suspected with impending respiratory failure.
6. Mannitol- With Raised ICP,
7. Treat Suspected meningitis with emperical
antibacterials and antivirals.
8. Control seizures with appropriate AEDs.
9. Treat extreme body temperatures
10. Stabilization of cervical spine if trauma is
suspected.

26. 1. ROUTINE INVESTIGATIONS:
 Toxicology screen- paracetamol, salicylates,
opioids, BZDs, TCAs,
 A sample of serum should be stored for later
analysis for uncommon drug ingestions.
2. NEUROIMAGING:
 a) CT SCAN- CNS trauma, subarachnoid (SAH)
and
 intracerebral hemorrhage, hemorrhagic and
nonhaemorrhagic strokes, cerebral edema,
hydrocephalus and the presence of a space-
occupying lesion (SOL).

27. Limitations-
 Need to shift patient to Ct suite where
resuscitation and monitoring facilities are
limited.
 Low sensitivity to demonstrate an abnormality
in the acute phase of a stroke
 Its low sensitivity for detecting brainstem
lesions

28.  Provide superior contrast and resolution of the
grey and white matter.
 MRI is more sensitive than CT for the detection
of acute ischaemia, diffuse axonal injury, and
cerebral oedema, tumour and abscess.
 Brainstem and posterior fossa structures are
better visualised.
 Non-ionising radiation.

29. Limitations-
 The need for special equipment
 Long imaging times
 Risk of dislodgement of metal clips on blood
vessels and resetting of pacemakers.
 Need for sedation and intubation as needed.

30.  Useful for the assessment of cerebral blood
flow and oxygenation and in the
prognostication of neurotrauma.
 By determining the concentration of the various
tracers in the brain and constructing
tomographic images, cerebral blood flow and
metabolism can be measured by PET scanning.
 Not routinely available

31.  CSF analysis
 Done after excluding raised ICP, clinically and
radiologically.
 Mainly used to diagnose intracranial infections
and to detect abnormal cytology in cases of
suspected malignant meningeal infiltration.
 In SAH, with strong clinical suspicion with
negative CT.

33.  Visual, brainstem and somatosensory evoked
potentials
 Test the integrity of neuroanatomical pathways
within the brain and the spinal cord.
 They may be used in the diagnosis of
blindness in comatose patients and in the
assessment of locked-in states.

34.  These include neuronspecific enolase
(cytoplasm of neurons), S-100B protein
(astroglial cells), CK-BB fraction (astrocytes),
glial fibrillary acidic protein (glial origin),
calpain and caspase.
 Early studies showed S-100B as a reliable
marker of traumatic brain injury, concerns
remain about their sensitivity and specificity for
assessment of severity and prediction of
outcome.

35. THANK YOU