Different states of unconsciousness

1. Different states of
unconsciousness
Dr. Sachit Koirala
Resident, 2nd year
Department of Surgery, KISTMCTH

2. • Determine the disease causing diminished state of
unconsciousness
• Determine the direction in which it is evolving
To protect the brain against irreversible damage

3. Most common causes of diminished consciousness
1. Metabolic and diffuse disorders (65%)
• Drug poisoning
• Ischemia or anoxia
• Hepatic encephalopathy
• Encephalomyelitis and encephalitis
• Subarachnoid hemorrhage
• Endocrine disorders (including diabetes)
• Acid-base disorders
• Uremic encephalopathy

4. Most common causes of diminished consciousness
2. Supratentorial mass lesions (20%)
• Intracerebral hematoma
• Subdural hematoma
• Cerebral infarct
• Brain tumor
• Brain abscess
• Epidural hematoma
• Thalamic infarct
• Pituitary apoplexy

5. Most common causes of diminished consciousness
3. Subtentorial lesions (13%)
• Brainstem infarct
• Pontine hemorrhage
• Cerebellar hemorrhage
• Cerebellar tumor
• Cerebellar infarct
4. Psychiatric disorders (3%)

6. Consciousness
State of awareness of self and environment
AND
normal responsiveness to external stimulation and inner need.
Normal consciousness may fluctuate during the day
BUT
the normal individual can be brought immediately to a state of full
alertness and function.

7. Confusion
Inability to think with customary speed, clarity, and coherence.
Some degree of inattentiveness and disorientation i.e. Distractibility
and imperceptiveness.
“Clouding of sensorium”
Results most often from process that influences the brain globally, such
as a toxic or metabolic disturbance or dementia or sleep deprivation.

8. Salient features of a confused individual:
• Severely confused and inattentive persons are unable to do more
than carry out the simplest commands.
• Speech may be limited to a few words or phrases but some confused
individuals are voluble (~Talkative).
• Disoriented in time and place
• Do not grasp their immediate situation
• Do not understand the predicament of their own confusion
• May misidentify people or objects.
• These illusions may lead to fear or agitation.
• Loss of capacity to recall events of the past hours or days
• Deficit in working memory

9. Delirium = Confusion (Adams and Victor)
Delirium: Acute confusional state (Harrison’s)

10. Drowsiness
Inability to sustain a wakeful state without application of external
stimuli.
Sustain alertness for at least some brief period, without the further
necessity of external stimuli
Some degree of inattentiveness and mild confusion are present,
improving with arousal.
The patient shifts positions somewhat naturally and without
prompting.
The lids droop; there may be snoring, the jaw and limb muscles are
slack, and the limbs are relaxed.

11. Stupor
A state in which the patient can be roused only by vigorous and repeated
stimuli
Arousal cannot be sustained without repeated stimulation.
Responses to spoken commands are either absent or slow and inadequate.
Restless or stereotyped motor activity is common.
Reduction or elimination of the natural shifting of body positions.
When left unstimulated, these patients quickly drift back into a deep sleep-
like state.
The eyes are usually found to be displaced outward and upward, a feature
that is shared with sleep.

12. Vegetative state
• Person is awake but is showing no signs of awareness.
• Preserved autonomic and respiratory function without cognition
• Open their eyes
• Wake up and fall asleep at regular intervals
• Have basic reflexes (such as blinking when they're startled by a loud
noise or withdrawing their hand when it's squeezed hard)
• Able to regulate their heartbeat and breathing without assistance.
BUT
the patient regains neither awareness nor purposeful behavior.

13. Persistent Vegetative State
• Vegetative state for 3 months after non traumatic brain injury
• Vegetative state for 12 months after traumatic brain injury
• Also known as Apallic syndrome or Neocortical death
Multi-Society Task Force on PVS concluded that the outcome from a
vegetative state is better in traumatic as compared to nontraumatic
cases.

14. Vegetative state vs Coma
• A coma is when a person shows no signs of being awake and no signs
of being aware
• A vegetative state is when a person is awake but is showing no signs
of awareness

15. Minimally conscious state
• Patient is capable of some rudimentary behavior
• Following a simple command, gesturing, or producing single words or
brief phrases
• Demonstrate a degree of awareness
• Inconsistent from one examination to other
• Transitional or permanent state
• Continuum of vegetative state. Less severe but profound dementia

16. Locked in syndrome (Deefferented state)
• Little or no disturbance of consciousness
• Inability to respond adequately with motor activity and speech
• Most often caused by a large lesion of the ventral pons (basis pontis),
usually as a result of occlusion of the basilar artery
• Spare both the somatosensory pathways, and the ascending neuronal
systems responsible for arousal and wakefulness
• Spare certain midbrain elements that allow the eyelids to be raised in
wakefulness
• Interrupts the descending corticobulbar and corticospinal tracts
• Can respond by voluntary vertical gaze and blinking

17. Akinetic mutism
• Inert (akinetic) and silent (mutism)
• Bilateral lesions in anterior part of frontal lobe or thalamus
• Motor and sensory pathways are intact
• Profoundly apathetic
• Marked delay in verbal and motor response (Abulia)
• Intense stimulation  May speak normally and relate the events

18. Catatonia
• Unresponsive
• Can simulate stupor, light coma or akinetic mutism
• No signs of structural brain damage (Normal pupillary reaction,
normal reflexes)
• Oculocephalic reflex is muted.
• Resistance to eye opening
• Waxy flexibility to passive limb movement
• Long periods of uncomfortable limb positions (Catalepsy)
• EEG shows normal alpha activity that is attenuated by stimulation

20. Electroencephalogram (EEG) in states of
impaired consciousness
Confusion/Drowsiness
• Disappearance of normal alpha rhythm
• Replacement by random slow waves of low to moderate voltage
Stupor
• Regular slow waves (2-3 Hz) of high voltage
Deep coma
• Slow, low voltage waves
• Intermittent suppression of electrical activity
Brain death
• Complete absence of electrical activity

21. EEG in impaired consciousness due to
metabolic disorders
Hepatic or renal failure (Uremia)
• Slow waves
• High voltage
Coma due to sedatives intoxication
• Beta activity replaces normal rhythm
Delta pattern
Triphasic waves

22. Deeply comatose patients
• Diffuse transient alpha activity
• Also known as alpha coma
• Can be mistaken for normal activity
BUT
• No reactivity to sensory stimuli
Associated with pontine or diffuse cortical lesions
Poor prognosis

23. Alpha coma

24. Anatomy and neurophysiology of alertness
and coma
Reticular Activating System (RAS)
• Indistinct boundaries
• Neurons are interspersed
• Locus coeruleus: Upper dorsolateral pons of the brainstem. Activated
directly by orexin from the lateral hypothalamus. Nor-epinephrine
• Raphe nuclei: midline throughout the brainstem within the pons, midbrain,
and medulla. Serotonergic
• Tuberomamillary nucleus: located within the posterior aspect of the
hypothalamus. Histaminergic
• Lateral and dorsal pedunculopontine tegmentum: Primarily cholinergic
neurons in neighboring groups within the midbrain and pons. Cholinergic
neurons project to the thalamus and cortex.

25. Diffusion tensor tactography

26. RAS receives collaterals from the spinothalamic and trigeminal–
thalamic pathways
Project to the whole of the cerebral cortex, not just to the sensory
cortex of parietal lobe
Cerebral cortex also modulates afferent sensory stimulus towards the
RAS through corticofugal projections

27. Pathologic basis of vegetative state
• Diffuse cerebral injury as a result of closed head trauma
• Widespread necrosis of the cortex after cardiac arrest or other form
of anoxia
• Thalamic necrosis
Prominent pathologic changes are often in the thalamic and
subthalamic nuclei rather than solely in the cortex.

28. In traumatic cases, the pathologic findings are often of diffuse
subcortical white matter degeneration (described as diffuse axonal
injury), prominent thalamic degeneration, and ischemic damage in the
cortex.
Anatomic findings indicate that PVS is a state in which the cortex is
either diffusely injured or effectively disconnected and isolated from
the thalamus, or the thalamic nuclei are destroyed

29. Pathologic anatomy of coma
Two broad processes
1. Structural, or morphologic, consisting either of a discrete structural
lesion in the upper brainstem and lower diencephalon (which may
be primary or secondary to compression) or of more widespread
destructive changes throughout the hemispheres.
2. Metabolic or submicroscopic, resulting in suppression of neuronal
activity in the cerebrum and reticular activating system.

30. Structural or morphological
1. A large mass in one cerebral hemisphere— tumor; abscess; massive
infarct; or intracerebral, subdural, or epidural hemorrhage.
Cause coma by secondary compression of the midbrain and central
thalamic region of the RAS.
Displacement or direct compression of these structures by the
advancing medical temporal lobe which is forced into the tentorial
opening.
OR
cerebellar lesion may compress the adjacent upper brainstem reticular
region by displacing it forward and upward

31. Structural or morphological
2. Destructive lesion is located immediately within the thalamus or midbrain,
in which case the neurons of the RAS are damaged directly.
Brainstem stroke from basilar artery occlusion, thalamic and upper brainstem
hemorrhages, and some forms of traumatic damage.
3. Widespread bilateral damage to the cortex and cerebral white matter, the
result of traumatic damage (contusions, diffuse axonal injury), bilateral
ischemic strokes or hemorrhages, encephalitis, meningitis, hypoxia, or global
ischemia.
The coma in these cases results from interruption of thalamocortical impulses
or from generalized destruction of cortical neurons. It is only if the cerebral
lesions are bilateral and extensive that consciousness is impaired. Many of
the diseases in this category also cause severe thalamic damage.

32. Coma in concussion
• Transient but large increase in intracranial pressure
• 200 to 700 lb/in2 (10000-36000 mmHg)
• Lasting a few thousandths of a second
• Vibration set up in the skull and transmitted to the brain was for many
years thought to be the basis of the abrupt paralysis of nervous function
that characterizes concussive head injury (commotio cerebri).
• Sudden swirling motion of the brain induced by acceleration or
deceleration from a blow to the head produces a rotation (torque) of the
cerebral hemispheres around the axis of the upper brainstem.
If severe: multiple shearing lesions or hemorrhages in diencephalon and
brain stem.

33. ‘In the largest group of cases of coma, no structural lesion is
revealed by any technique of conventional pathology.’

34. Metabolic and toxic encephalopathies
• Cerebral Blood Flow (CBF): 55mL/min/100g
• Reduction in cerebral blood flow
• Cerebral blood flow may stay near normal while metabolism is greatly
reduced

35. Clinical approach to comatose patient
• Often, comatose patient is brought to the hospital and little pertinent
medical information is available.
• BLS/ACLS
• If history or suspicion of trauma: ATLS (ABCDE) approach.

36. • Patient’s airway is cleared and blood pressure is restored.
• Patient’s airway is cleared and blood pressure is restored.
• With hypotension, placement of a central venous line and administration
of fluids, pressor agents and blood.
• If respirations are shallow or labored, or if there is emesis with a threat of
aspiration, tracheal intubation and mechanical ventilation are instituted.
• An oropharyngeal airway is otherwise adequate in a comatose patient who
is breathing normally.
• Deeply comatose patients with shallow respirations require endotracheal
intubation.
• The patient with a head injury may also have suffered a fracture of the
cervical vertebrae, in which case caution must be exercised in moving the
head and neck.

37. • Circumstances in which the person was found.
• Previous health, whether there was a history of diabetes, a head
injury, convulsion, alcohol or drug use, or a prior episode of coma or
attempted suicide.
• Sedatives, antiepileptic drugs, opiates, certain antibiotics,
antidepressants, and antipsychotic drugs.

38. General examination : Vitals
Temperature
Fever
• Systemic infection (eg. Pneumonia, meningitis, viral encephalitis)
• Temperature >107.6F: Heat stroke, anticholinergic drug intoxication
• Central fever is rare
Hypothermia
Alcohol or barbiturate intoxication
Drowning
Cold exposure
Advanced TB meningitis

39. General examination : Vitals
Respiration
Slow breathing: opiate or barbiturate intoxication, hypothyroidism
Deep rapid (Kussmaul respiration) : pneumonia, diabetic or uremic
acidosis, pulmonary edema, or the less-common occurrence of an
intracranial disease that causes central neurogenic hyperventilation.
Slow, irregular, or cyclic (Cheyne-Stokes respiration) : Raised ICP

40. General examination : Vitals
Respiration
Apneustic breathing (Pause 2-3s after inspiration) : Low pontine lesion
Biot breathing/Ataxia of breathing (chaotic, being irregularly interrupted
and each breath varying in rate and depth) : Dorsal medulla lesion

41. Cheyne-Stokes respiration
• Isolation of the brainstem respiratory centers from the cerebrum,
rendering them more sensitive than usual to carbon dioxide
(hyperventilation drive)
• Signifies bilateral dysfunction of cerebral structures
• Intoxication or a metabolic derangement
• Bilateral structural lesions such as subdural hematomas

42. General examination : Vitals
Blood pressure
Hypertension: cerebral hemorrhage, hypertensive encephalopathy and in
children with markedly elevated intracranial pressure.
Hypotension: Alcohol or barbiturate intoxication, DKA, internal
hemorrhage, myocardial infarction, dissecting aortic aneurysm,
septicemia, Addison disease, or massive brain trauma.

43. General examination : Vitals
Heart rate
Bradycardia
• Heart block from medications such as tricyclic antidepressants or
anticonvulsants
• If combined with periodic breathing and hypertension, an increase in
intracranial pressure.

44. Neurological examination
Inspection
• Predominant postures of the limbs and body
• Presence or absence of spontaneous movements on one side
• Position of the head and eyes
• Rate, depth, and rhythm of respiration

45. Brainstem function
Pupillary size and reactivity
Ocular movements
Vestibulo-ocular reflexes
Pattern of breathing

46. Pupillary reaction
• Loss of light reaction usually precedes enlargement of pupil
• Unilaterally enlarged (“Hutchinson”) pupil : Early indicator of
stretching or compression of the third nerve. Presence of an overlying
ipsilateral hemispheral mass.
• The light-unreactive pupil continues to enlarge to a size of 6 to 9 mm
diameter and soon, there is slight outward deviation of the eye.
• As midbrain displacement continues, both pupils dilate and become
unreactive to light as a result of compression of the oculomotor
nuclei in the rostral midbrain.

47. Pupillary reaction
• Pontine tegmental lesions (eg. Pontine hemorrhage) : extremely
miotic pupils (<1 mm in diameter) with barely perceptible reaction to
strong light.
• Ipsilateral pupillary dilatation from pinching the side of the neck (the
ciliospinal reflex) is usually lost in brainstem lesions.
• The Horner syndrome (miosis, ptosis, and reduced facial sweating):
ipsilateral to a lesion of the brainstem or hypothalamus or as a sign of
dissection of the internal carotid artery.

48. Coma caused by drug intoxications and intrinsic metabolic disorder
• Pupillary reactions are usually spared
Exceptions
• Serum concentration of opiates that are high enough to cause coma
 Pinpoint pupils
• Systemic poisoning with atropine or with drugs that have atropinic
qualities, especially the tricyclic antidepressants or SSRI: dilatation
and relative unresponsiveness to light

50. Movements of eye, eyelids and corneal
reaction
• Stupor or light coma of metabolic origin:
Eyes rove conjugately from side to side in seemingly random fashion.
Disappears as coma deepens  motionless and exotropic
• Lateral and slight downward deviation: third-nerve palsy on that side
• Medial deviation : Sixth-nerve palsy on that side

51. Movements of eye, eyelids and corneal
reaction
Conjugate deviation of the eyes away from the side of the paralysis: large
cerebral lesion (looking toward the lesion)
Toward the side of the paralysis: unilateral pontine lesion (looking away from
the lesion)
Retraction and convergence nystagmus: lesions in the tegmentum of the
mid-brain
Ocular bobbing: lesions of the tegmentum of the pons
Down and inward (looking at the nose): hematomas or ischemic lesions of
the thalamus and upper midbrain (a variant of Parinaud syndrome)
“Ocular dipping,” (eyes move down slowly and return rapidly to the
meridian) : Anoxia and drug intoxications

52. Vestibulo-ocular reflex

53. Elicitation of these ocular reflexes in a comatose patient:
1. evidence of unimpeded function of the midbrain and pontine
tegmental structures that integrate bi-ocular eye movements
2. intactness of the CN nerves (III, IV, and VI) on both sides

54. Caloric test / vestibulo-ocular test
More vigorous stimulus for ocular movements in coma is accomplished
by irrigation of one ear with 10 mL of cold water (or room-temperature
water if the patient is still arousable).
Causes slow conjugate deviation of the eyes toward the irrigated ear,
followed in a few seconds by compensatory nystagmus (fast
component away from the stimulated side).
In comatose patients, the fast “corrective” phase of nystagmus that is
mediated by the frontal lobes is lost and the eyes are tonically
deflected.

55. Reduction in the frequency and eventual loss of spontaneous blinking
 Loss of response to touching the eyelashes  Lack of response to
corneal touch (the corneal reflex afferent limb travels in the trigeminal
nerve and efferent limb travels in facial nerve) : signs of deepening
coma

56. Sequentially increasing stimuli
• calling his name
• simple commands
• noxious stimuli such as tickling the nares, supraorbital or sternal
pressure, pinching the side of the neck or inner parts of the arms or
thighs, or applying pressure to the knuckles

57. Vocalization may persist in stupor and will be the first response to be
lost as coma appears.
Grimacing and deft avoidance movements of stimulated parts
of the body are preserved in stupor.
Yawning and spontaneous shifting of body positions indicate a minimal
degree of unresponsiveness.

58. Hemiplegia
• Lack of restless movements of the limbs
• Inadequate protective movements in response to painful stimuli.
• The weakened limbs are usually slack and, if lifted from the bed, they
“fall flail.”
• The hemiplegic leg lies in a position of external rotation
• Affected thigh appears wider and flatter than the nonhemiplegic one.
In expiration, the cheek and lips puff out on the paralyzed side of the
face.
A lesion in one cerebral hemisphere causes the eyes to be turned away
from the paralyzed side (toward the lesion).
The opposite occurs with brainstem lesions.
In most cases, a hemiplegia and an accompanying Babinski sign are
indicative of a contralateral hemispheral lesion.

59. Posturing
Decerebrate rigidity
• Opisthotonos
• clenching of the jaws
• stiff extension of the limbs
• internal rotation of the arms and plantar flexion of the feet
Lesions that interrupt the fibers of the red nucleus lead to inhibition of
the rubrospinal tract (To flexor muscles) and constant excitation of the
vestibulospinal and pontine reticulospinal tracts (To extensor muscles)

60. Posturing
Decorticate rigidity
• Arms in flexion and adduction and legs extended.
• Lesions at a more rostral level of the nervous system—in the cerebral
white matter or internal capsule and thalamus.
If preceded by decorticate or decerebrate postures, the coma is
profound and usually progresses to brain death.

61. Clinical signs of raised ICP
• History of headache before the onset of coma
• Vomiting,
• Severe hypertension beyond the patient’s static level
• Unexplained bradycardia
• Retinal hemorrhages

62. • Papilledema
Develops within 12 to 24 h in cases of brain trauma and hemorrhage
If seen at presentation with coma, signifies brain tumor or abscess
(lesion of longer duration)
Absence of papilledema does not exclude the presence of increased
intracranial pressure, particularly in the elderly.

63. Acute Hydrocephalus
• Subarachnoid hemorrhage or from obstruction of the ventricular
system by a tumor in the posterior fossa
• Abulia  Stupor  Coma
• Pupils: small and the tone in the legs is usually increased or there may
be extensor posturing.

64. Classification of Coma
1.Diseases that cause no focal or lateralizing neurologic signs, usually
with normal brainstem functions. CT scan and cellular content of the
CSF are normal
A. Exogenous intoxications: alcohols, barbiturates and other sedative
drugs, opiates
B. Endogenous metabolic disturbances: anoxia, diabetic acidosis,
uremia, hepatic failure, nonketotic hyperosmolar hyperglycemia, hypo-
and hypernatremia, hypoglycemia, addisonian crisis, profound
nutritional deficiency, carbon monoxide poisoning, thyroid states,
hypercalcemia
C. Severe systemic infections: pneumonia, peritonitis, typhoid fever,
malaria, septicemia, Waterhouse- Friderichsen syndrome

65. Classification of Coma
D. Circulatory collapse (shock) from any cause
E. Postseizure states
F. Hypertensive encephalopathy and eclampsia
G. Hyperthermia and hypothermia
H. Concussion
I. Acute hydrocephalus

66. Classification of Coma
2. Diseases that cause meningeal irritation and an excess of white
blood cells (WBCs) or red blood cells (RBCs) in the CSF, usually without
focal or lateralizing cerebral or brainstem signs
A. Subarachnoid hemorrhage from ruptured aneurysm, arteriovenous
malformation, and cerebral trauma.
B. Acute bacterial meningitis
C. Viral meningoencephalitis
D. Neoplastic meningeal infiltration
E. Parasitic meningitis
F. Pituitary apoplexy

67. Classification of Coma
3. Diseases that cause focal brainstem or lateralizing cerebral signs, with or
without changes in the CSF.
A. Hemispheral hemorrhage or massive cerebral infarction
B. Brainstem infarction caused by basilar artery thrombosis or embolism
C. Brain abscess, subdural empyema, herpes encephalitis
D. Epidural and subdural hemorrhage and brain contusion
E. Brain tumor
F. Cerebellar and pontine hemorrhage
G. Multiple focal cerebral lesions that cumulate to cause generalized brain
dysfunction: multiple embolic infarction caused by bacterial endocarditis,
TTP, sagittal sinus thrombosis, diffuse fat embolism.

71. Thank you