coma

1. COMA
MUHAMMAD ABD ELMONEIM

2. DEFINING COMA
"unarousable unresponsiveness"
•Defined coma as a state of unresponsiveness in which the
patient lies with his eyes closed and cannot be aroused to
respond appropriately to stimuli even with vigorous Stimulation
•The patient may grimace in response to painful stimuli and limbs
may demonstrate stereotyped withdrawal responses, but the
patient does not make localized responses or discrete defensive
movements

3. • The terms stupor, lethargy, and obtundation refer to states
between alertness and coma
• An alteration in arousal represents an acute, life threatening
emergency, requiring prompt intervention for preservation of
life and brain function

4. ETIOLOGIES AND
PATHOPHYSIOLOGY
•The ascending reticular activating system (ARAS) is a network
of neurons originating in the tegmentum of the upper pons and
midbrain, believed to be integral to inducing and maintaining
alertness
•These neurons project to structures in the diencephalon,
including the thalamus and hypothalamus, and from there to the
cerebral cortex
•Alterations in alertness can be produced by focal lesions within
the upper brainstem by directly damaging the ARAS
•Injury to the cerebral hemispheres can also produce coma, but
in this case, the involvement is necessarily bilateral and diffuse,
or if unilateral, large enough to exert remote effects on the
contralateral hemisphere or brainstem

5. • Magnetic resonance imaging (MRI) studies have indicated that
coma in supratentorial mass lesions occurs both with lateral
forces on the contralateral hemisphere and with downward,
brainstem compression
• Lesions below the level of the pons do not normally result in
coma
• Drugs and metabolic disease produce coma by a depression of
both cortex and ascending reticular activating system function

8. • Anatomically, dysfunction of one of the following three areas of
the brain can cause coma:
• The brainstem reticular activating system (RAS)
• Bilateral frontal lobes
• Bilateral temporal lobes
are all sufficient to cause coma

9. Assessment of coma
•Coma is an acute, life threatening situation. Evaluation must be
swift, comprehensive, and undertaken while urgent steps are
taken to minimize further neurological damage
•Emergency management should include:
• Resuscitation with support of cardiovascular and
respiratory system
• Correction of immediate metabolic upset, notably control of
blood glucose and thiamine if indicated; control of seizures
and body temperature; any specific treatments—for
example, naloxone for opiate overdose

10. Assessment of coma
• History—through friend, family or emergency medical
personnel
• General physical examination
• Neurological assessment—to define the nature of coma
• where is the lesion responsible for coma?
• what is its nature?
• what is it doing?

11. Assessment of coma
• Neurological diagnosis is based on history, thoughtful
examination, and the appropriate choice of investigations
• This is essential, as there is little point in performing a cranial
computed tomographic (CT) scan in a patient in
hypoglycaemic coma where urgent correction of the metabolic
disorder is paramount and any delay—for example, waiting for
a scan—is unacceptable

12. Assessment of coma
• The approach to clinical evaluation is used to categorise coma
into:
• Coma without focal signs or meningism. This is the most
common form of coma and results from anoxic-ischaemic,
metabolic, toxic, and drug induced insults, infections, and
post ictal states
• Coma without focal signs with meningism. This results from
subarachnoid haemorrhage, meningitis, and
meningoencephalitis
• Coma with focal signs. This results from intracranial
haemorrhage, infarction, tumour or abscess

13. Assessment of coma
Keep in mind
•Multifocal structural pathology, such as venous sinus
thrombosis, bilateral subdural haematomas, vasculitis or
meningitis, can present with coma without focal signs or
meningism and so mimic toxic or metabolic pathologies
•Conversely, any toxic/metabolic cause for coma may be
associated with focal findings—for example, hypoglycaemic or
hepatic encephalopathy
•Also focal signs may be the consequence of pre-existing
structural disease; in the septicaemic patient with a previous
lacunar infarct, for example, the focal neurology may be
mistakenly accepted as signs of the current illness

14. Assessment of coma
NEUROLOGIC EXAMINATION
•Level of consciousness
•Motor responses
•Brainstem reflexes:
• Pupillary light
• Ocular motility
• Corneal reflexes

15. Assessment of coma
Level of consciousness
•Arousability is assessed by noise (eg, shouting in the ear) and
somatosensory stimulation
•Pressing on the supraorbital nerve (medial aspect of the
supraorbital ridge) or the angle of the jaw, or squeezing the
trapezius, may have a higher yield than the more commonly used
sternal rub and nailed pressure
•Important responses include vocalization, eye opening, and limb
movement

17. Assessment of coma
Motor examination
•Muscle tone, spontaneous and elicited movements and reflexes
•Asymmetries of these often indicate a hemiplegia of the non-
moving side, implying a lesion affecting the opposite cerebral
hemisphere or upper brainstem
•Purposeful movements include crossing the midline,
approaching the stimulus, pushing the examiner's hand away or
actively withdrawing from the stimulus

18. Assessment of coma
• Decorticate posturing consists of upper-extremity adduction
and flexion at the elbows, wrists, and fingers, together with
lower-extremity extension, which includes extension and
adduction at the hip, extension at the knee, and plantar flexion
and inversion at the ankle . This occurs with dysfunction at the
cerebral cortical level or below and may reflect a "release" of
other spinal pathways
• Decerebrate posturing consists of upper-extremity extension,
adduction, and pronation together with lower-extremity
extension and traditionally implies dysfunction below the red
nucleus, allowing the vestibulospinal tract to predominate

19. Motor response to pain. (A) Left hemisphere lesion. The
two figures illustrate
localisation of pain with the left
hand and flexion (left hand
figure) or extension (right hand
figure) on the right
(B) Subcortical: unilateral left sided
lesion exerting a variable
contralateral effect. The figures
illustrate flexion to pain with the left
hand with either extension (right
hand figure) or flexion with the right
and hyperextension in both lower
limbs
(C) Midbrain upper pontine: a
bilateral upper and lower limb
extension response
(D) Lower pontine/medullary: a
bilateral extensor upper limb posture
with either flaccidity or minimal
diminished flexor response in lower
limbs

20. Assessment of coma
Brainstem reflexes
Pupils
•In transtentorial herniation, after initial dilation and loss of light
reactivity, pupils become somewhat reduced in size (4 to 5 mm)
and remain unreactive; they are called midposition and fixed
•Pupil size and symmetry should be noted as well. Pupils are
normally between 3 to 7 mm in diameter and equal, although
about 20 percent of normal individuals have up to 1 mm
difference in pupillary size. Typically, the pupils are spared in
metabolic and toxic conditions, except in certain toxic
syndromes, which are associated with either miosis or mydriasis
•In severe sedative drug overdose or in hypothermia, the pupils
are midposition and fixed; this syndrome can mimic brain death
•Lesions in the pontine tegmentum, which selectively disrupt
sympathetic outflow, can produce very small (<1 to 2 mm) pupils
in which a light response is barely perceptible, so-called pontine
pupils. Opiate overdose can also produce this sign

21. Assessment of coma

22. Assessment of coma
(A) Cingulate herniation
(B) Uncal herniation
(C) Tonsillar herniation

24. • Lesions above the thalamus and below the pons preserve
pupillary reactions

25. Eye movements
•Ocular pathways run from the mid brain to the pons, thus normal
reflex eye movements imply that the pontomedullary junction to
the level of the ocular motor nucleus in the mid brain is intact
•In the comatose patient, bilateral conjugate roving eye
movements that appear full indicate an intact brainstem and
further reflex testing is not required
•In addition the oculomotor nerve is susceptible to compression
in tentorial herniation

26. Oculocephalic and caloric response
This reflex is usually suppressed
(and therefore not tested) in
conscious patients
If nystagmus occurs, the patient
is awake and not truly in coma;
this can be a useful confirmatory
test for psychogenic
unresponsiveness

27. Corneal reflex
The reflex can be suppressed acutely contralateral to a large,
acute cerebral lesion, and also with intrinsic brainstem lesions.
Loss of the corneal reflex is also an index of the depth of
metabolic or toxic coma; bilaterally brisk corneal reflexes
suggest the patient is only mildly narcotized. Absent corneal
reflexes 24 hours after cardiac arrest is usually, but not
invariably, an indication of poor prognosis (assuming the patient
has not been sedated). Corneal reflexes may also be reduced or
absent at baseline in elderly or diabetic patients

30. SUMMARY AND
RECOMMENDATIONS
•Stupor and coma are alterations in arousal; these are neurologic
emergencies
•Causes of coma are diverse and include structural brain disease
and systemic disease. Cerebrovascular disease, trauma,
metabolic derangements, and intoxications are the most common
etiologies
•A complete history and physical examination can provide valuable
clues as to the underlying etiology
•The neurologic examination in coma patients includes assessment
of arousal, motor examination, and cranial nerve reflexes.
Important findings are abnormal reflexes that indicate dysfunction
in specific regions of the brainstem, or a consistent asymmetry
between right- and left-sided responses, which indicates structural
brain pathology as a cause
•Evaluation and early therapeutic interventions should proceed
promptly, even simultaneously. An algorithm for urgent evaluation

31. References
•Stupor and coma in adults
• Author
G Bryan Young, MD, FRCPC
• Section Editors
Michael J Aminoff, MD, DSc
Robert S Hockberger, MD, FACEP
• Deputy Editor
Janet L Wilterdink, MD