consciousness and coma

1. Dr. Nishtha Jain
Senior resident
Department of neurology
GMC, kota.

2. Consciousness may be defined as a
state of awareness of self and
surroundings.

3. Reticular activating system
 found in the reticular formation in the core of the upper
brainstem.
 Inputs from every sensory system.
 Physiologically involved in sleep/wake regulation and
arousal/consciousness.

5. Coma is a state of complete
unresponsiveness to arousal in
which the patient lies with the eyes
closed.

11. Rapid Initial Examination
and Emergency Therapy
 to ensure that the comatose patient is medically and
neurologically stable.
 to rule out the need for immediate medical or surgical
intervention.

13. Emergency Treatment
 A baseline serum glucose level should be obtained
before glucose administration.
 Empirical use of supplemental oxygen, intravenous (IV)
thiamine (at least 100 mg), and IV 50% dextrose in water
(25 g).
 Naloxone hydrochloride IV- 0.4 to 2 mg if opiate overdose
is the suspected cause.

14. General Examination

17. Head and Neck Examination
 Laceration or edema of the scalp : head trauma.
 raccoon eyes refers to orbital ecchymosis : anterior
basal skull fracture.
 The Battle sign : hematoma overlying the mastoid,
originating from basilar skull fracture extending into the
mastoid portion of the temporal bone.

18.  Meningismus neck stiffness : infectious or carcinomatous
meningitis, subarachnoid hemorrhage, or central or
tonsillar herniation.
 Scars on the neck : endarterectomy, implying vascular
disease, or from thyroidectomy or parathyroidectomy,
suggesting concomitant hypothyroidism,
hypoparathyroidism, or both.
 Goiter : hypothyroidism or hyperthyroidism.

19. Systemic Examination
 Cardiac examination- arrythmias, cardiac murmurs
 Abdominal examination- abnormal bowel sounds,
organomegaly, masses, and ascites.

20. Neurological Examination
 state of consciousness,
 respiratory pattern,
 pupillary size and response to light,
 spontaneous and reflex eye movements,
 and skeletal muscle motor response.

23. Respiratory pattern

24. Pupil Size and Reactivity
 Thalamic lesions cause small, reactive pupils, often
referred to as diencephalic pupils.
 Similar pupillary findings are noted in many toxic-
metabolic conditions resulting in coma.
 Hypothalamic lesions or lesions elsewhere along the
sympathetic pathway : Horner syndrome.

25.  Midbrain lesions produce three types of pupillary
abnormality, depending on the lesion:
 Dorsal tectal lesions interrupt the pupillary light reflex,
resulting in midposition pupils, which are fixed to light but
react to near vision.
 Spontaneous fluctuations in size occur, and the
ciliospinal reflex is preserved.

26.  Nuclear midbrain lesions usually affect both sympathetic
and parasympathetic pathways, resulting in fixed,
irregular midposition pupils, which may be unequal.
 Lesions of the third nerve fascicle in the brainstem, or
after the nerve has exited the brainstem, cause wide
pupillary dilation unresponsive to light.

27.  Pontine lesions interrupt sympathetic pathways and
cause small, so-called pinpoint pupils which remain
reactive.
 Lesions above the thalamus and below the pons should
leave pupillary function intact, except for Horner
syndrome in medullary or cervical spinal cord lesions.

28. Ocular Motility
 Evaluation of ocular motility consists of
(1) observation of the resting position of the eyes,
including eye deviation;
(2) rotation of spontaneous eye movements; and
(3) testing of reflex ocular movements.

29. Abnormalities in Resting Position
 Unilateral third nerve palsy from either an intramedullary
midbrain lesion or extramedullary compression causes
the affected eye to be displaced downward and laterally.
 A sixth nerve palsy produces inward deviation.
 Isolated sixth nerve palsy, however, is a poor localizer.

30.  Conjugate lateral eye deviation : ipsilateral lesion in the
frontal eye fields, a lesion anywhere in the pathway from
the ipsilateral eye fields to the contralateral parapontine
reticular formation.
 Dysconjugate lateral eye movement : sixth nerve palsy
in the abducting eye, a third nerve palsy in the adducting
eye, or an internuclear ophthalmoplegia.
 An internuclear ophthalmoplegia may be differentiated
from a third nerve palsy by the preservation of vertical
eye movements.

31.  Downward deviation of the eyes : brainstem lesions
(most often from tectal compression); metabolic
disorders such as hepatic coma.
 Thalamic and subthalamic lesions produce downward
and inward deviation of the eyes : looking at the tip of the
nose.
 Skew deviation usually indicates a posterior fossa lesion
(brainstem or cerebellar).

32. Spontaneous Eye Movements
 Purposeful-appearing eye movements in a patient who
seems unresponsive : locked-in syndrome, catatonia,
pseudocoma, or PVS.
 When roving eye movements are present : brainstem is
relatively intact and coma is due to a metabolic or toxic
cause or bilateral lesions above the brainstem.

33.  Nystagmus occurring in comatose patients suggests an
irritative or epileptogenic supratentorial focus.
 An epileptogenic focus in one frontal eye field causes
contralateral conjugate eye deviation.
 An electroencephalogram (EEG) is required to ascertain
the presence of this condition.

34.  Ocular bobbing : rapid downward jerks of both eyes
followed by a slow return to the midposition.
 In the typical form, there is associated paralysis of both
reflex and spontaneous horizontal eye movements.
 Monocular or paretic bobbing occurs when a coexisting
ocular motor palsy alters the appearance of typical
bobbing.

35.  Atypical bobbing : ocular bobbing when lateral eye
movements are preserved.
 Typical ocular bobbing : specific but not pathognomonic
for acute pontine lesions.
 Atypical ocular bobbing occurs with anoxia and is
nonlocalizing.

36.  Ocular dipping, also known as inverse ocular bobbing :
spontaneous eye movements in which an initial slow
downward phase is followed by a relatively rapid return.
 associated with diffuse cerebral damage.
 Reverse ocular bobbing : slow initial downward phase
followed by a rapid return that carries the eyes past the
midposition into full upward gaze.
 Reverse ocular bobbing : nonlocalizing.

37.  Vertical nystagmus due to an abnormal pursuit or
vestibular system is slow deviation of the eyes from the
primary position, with a rapid (saccadic) immediate return
to the primary position.
 It is differentiated from bobbing by the absence of latency
between the corrective saccade and the next slow
deviation.

38.  Ocular-palatal myoclonus occurs after damage to the
lower brainstem involving the Guillain-Mollaret triangle,
which extends between the cerebellar dentate nucleus,
red nucleus, and inferior olive.
 Ocular flutter is back to- back saccades in the horizontal
plane, a manifestation of cerebellar disease.

39. Reflex Ocular Movements

41. Motor System
 Bilateral midbrain or pontine lesions responsible for
decerebrate posturing.
 Less commonly, deep metabolic encephalopathies or
bilateral supratentorial lesions involving the motor
pathways may produce a similar pattern.

42.  Decorticate posturing : much poorer localizing posture
result from lesions in many locations, although usually
above the brainstem.
 Decorticate posture is not as ominous a sign as
decerebrate posture, because the former occurs with
many relatively reversible lesions.

43.  Myoclonic jerking : anoxic encephalopathy or other
metabolic comas such as hepatic encephalopathy.
 Rhythmic myoclonus : a sign of brainstem injury.
 Tetany : hypocalcemia.
 Cerebellar fits : intermittent tonsillar herniation and
characterized by deterioration of level of arousal,
opisthotonos, respiratory rate slowing and irregularity,
and pupillary dilatation.

44. Coma and Brain Herniation
Supratentorial herniation
1. Uncal (transtentorial)
2. Central
3. Cingulate (subfalcine/transfalcine)
4. Transcalvarial
Infratentorial herniation
5. Upward (upward cerebellar or upward transtentorial)
6. Tonsillar (downward cerebellar)

46. Coma and Brain Herniation
 Classically, the uncal pattern includes early signs of third
nerve and midbrain compression.
 The pupil initially dilates as a result of third nerve
compression returns to the midposition with
midbrain compression that involves the sympathetic as
well as the parasympathetic tracts compression of
ipsilateral PCA compression of contralateral midbrain
and multiple haemorrhages in brainstem.

47.  Central pattern : mild impairment of consciousness, with
poor concentration, drowsiness, or unexpected agitation;
 small but reactive pupils;
 loss of the fast component of cold caloric testing;
 poor or absent reflex vertical gaze; and
 bilateral corticospinal tract signs, including increased
tone of the body ipsilateral to the hemispheric mass
lesion responsible for herniation.

49. Differentiating Toxic-Metabolic Coma
from Structural Coma
 Time course of the illness : structural lesions have more
abrupt onset, whereas metabolic or toxic causes are
slowly progressive.
 Focal features or notable asymmetry on neurological
examination : structural lesion. Toxic, metabolic, and
psychiatric diseases : symmetrical.

50.  Metabolic problems : milder alterations in arousal,
typically with waxing and waning of the behavioral state ,
acute structural lesions : same level of arousal or
progressively deteriorate.
 Deep, frequent respiration most commonly due to
metabolic abnormalities.

51.  Papilledema are almost pathognomonic of structural
lesions.
 Papilledema does not occur in metabolic diseases except
hypoparathyroidism, lead intoxication, and malignant
hypertension.
 The pupils usually are symmetrical in coma from toxic-
metabolic causes.

52.  Asymmetry in oculomotor function typically is a feature of
structural lesions.
 Roving eye movements with full excursion are most often
indicative of metabolic or toxic abnormalities.
 Muscle tone usually is symmetrical and normal or
decreased in metabolic coma.
 Structural lesions cause asymmetrical muscle tone.

53. Differentiating Psychiatric Coma
and Pseudocoma from Metabolic
or Structural Coma
 The malingering or hysterical patient often gives active
resistance to passive eye opening.
 It is nearly impossible for the psychiatric or malingering
patient to mimic the slow, gradual eyelid closure.
 Blinking also increases in psychiatric and malingering
patients but decreases in patients in true stupor.

54.  Passive eye opening in a sleeping person or a truly
comatose patient (if pupillary reflexes are spared) results
in pupillary dilation.
 Opening the eyes of an awake person produces
constriction.
 This principle may help differentiate coma from
pseudocoma.

55.  Roving eye movements cannot be mimicked and thus
also are a good sign of true coma.
 Finally, if during cold caloric testing, the eyes do not
tonically deviate to the side of the caloric instillation, and
the fast phases are preserved, stupor or true coma is
essentially ruled out.
 Moreover, cold caloric testing with the resultant vertigo
usually “awakens” psychiatric and malingering patients.

58. Electroencephalography
 Metabolic disorders : a decrease in the frequency of
background rhythms and the appearance of diffuse theta
activity.
 Hepatic encephalopathy : bilaterally synchronous and
symmetrical, medium- to high-amplitude, broad triphasic
waves, often with a frontal predominance.

59.  Herpes simplex encephalitis : unilateral or bilateral
periodic sharp waves with a temporal preponderance.
 The EEG also can help confirm a clinical impression of
catatonia, pseudocoma, the locked-in syndrome, PVS,
and brain death.

60. Prognosis
 Only about 15% of patients in nontraumatic coma make a
satisfactory recovery.
 Functional recovery is related to the cause of coma.
 Cerebrovascular disease including subarachnoid
hemorrhage : worst prognosis; coma from hypoxia-
ischemia : intermediate prognosis; coma due to hepatic
encephalopathy and other metabolic causes: best
ultimate outcome.

61.  Age does not appear to be predictive of recovery.
 The longer a coma lasts, the less likely the patient is to
regain independent functioning.
 Factors that adversely impact brain injury following
cardiac arrest include cerebral edema, pyrexia,
hyperglycemia, and seizures.

62.  Absence of pupillary light or corneal reflexes, and motor
response to noxious stimuli no greater than extension :
poor prognosis.
 Other poor prognostic signs : myoclonic status
epilepticus, bilateral absence of the N20 response from
the somatosensory cortex.

63. Referrences
 Bradley’s Neurology in Clinical Practice, sixth edition.
 The Acutely Comatose Patient: Clinical Approach and
Diagnosis. S. A Moore, E F. Wijdicks. Semin Neurol
2013;33:110–120.
 Emergency Neurological Life Support: Approach to the
Patient with Coma. J. S Huff, R D. Stevens, S D.
Weingart, W S. Smith. Neurocrit Care 2012.
 Management of the Patient with Diminished
Responsiveness. S Hocker, A. A. Rabinstein. Neurol Clin
30 (2012) 1–9.
 Evaluation and prognosis of coma. J. J Provencio.
Continuum Lifelong Learning Neurol 2009;15(3).