1. Glasgow Coma Scale – describes level of consciousness in a patient
- depends on physical examination of three domains: motor ability/response, verbal
output/response, and eye opening
- scores range from 3-15; Coma defines with score of 8 or less
2. Progression of Coma
- expanding intracranial lesion produces a pattern of worsening neurological function of
deepening coma
- signs of deepening coma can be used to assess the need for acute medical or surgical
intervention
- depth of coma can be monitored by close monitoring of the respiratory pattern, eye findings,
and motor examination
- progression of a coma reflects dysfunction of brain structures in a rostral to caudal fashion,
ultimately ending with dysfunction of medulla
Respiratory patterns
- hemispheric dysfunction  Cheyne-Stokes breathing, which is a cyclical breathing pattern
in which the depth of respiration varies in a smooth wave-like fashion with a periodicity of 1
or 2 minutes
- as coma deepens there may be a central hyperventilation pattern in which the depth and
frequency of respiration is abnormally high without variation; common cause is pulmonary
pathology or metabolic acidosis
- further deterioration  apneustic breathing pattern in which there is a deep breath which is
held for a prolonged period
- further deterioration  chaotic breathing pattern, ultimately leading to failure of the
respiratory drive (agonal)
Eye findings
- presence of partial or complete unilateral CNII palsy  tentorial herniation
- mid-position fixed pupils  midbrain involvement
- large, fixed pupils  tectal involvement
- pin-point pupils  pontine process
- pupillary light reflex depends on an arc that passes through the superior colliculi and then
into the Edinger-Westphal nucleus; lesions in tectum or midbrain  abolish pupillary
constrictor response to light  large, fixed pupils
- lesion in the pons (w/ sparing of midbrain structures)  interfere with descending
sympathetic pathways originating in hypothalamus  alters balance between sympathetic
and parasympathetic system leading to pupillary constrictions (Horner’s)
- overdose of opioid  pin-point pupils (distinguish by administering opioid antagonist)
Motor findings
- as descending CST influences are lost  postural reflexes generated in brainstem become
disinhibited
- emergence of reflexes is called posturing (abnormal tone in limbs)
- posturing reflexes provoked by noxious stimulation, but can also occur spontaneously
- misinterpreted as seizure
- rostral brainstem intact  decorticate posturing  flexion of arms and extension of legs;
reticulospinal (upper extremity flexing) and rubrospinal tracts
- extension of lower extremities driven by driven by disinhibited output of vestibular nuclei
while flexion of the upper extremities is driven by the reticulospinal tract
- as coma deepens  extension of upper and lower extremities with internal rotation of
arms; due to loss of descending influences from upper medulla and reflect disinhibited output
of the vestibular nuclei (vestibulospinal tract, decerebrate)
- finally, as coma progresses to the point where the vestibulospinal outflow if impaired 
limbs become flaccid
3. Sleep
- patients can be aroused from sleep
- active brain state with a complicated architecture and different stages, each of which has its
own EEG pattern
- little or no diminution in cerebral blood flow
Coma
- a sleep-like state from which a person cannot be aroused
- decreasing level of consciousness
- EEG pattern in coma does not have stages (as in sleep) and is characterized by abnormally
slow frequencies and abnormally low voltages
- abnormal decrease in blood flow to the brain
Brain Death
- no brain activity including most basic brainstem reflex functions
To be declared brain dead:
- no brainstem reflexes present, including pupillary light reflex, corneal reflexes, and
vestibuloocular reflex
- apnea in face of a high CO2 level; if medulla is intact, high concentration of carbon dioxide
will trigger an automatic breathing response
- electrical silence on EEG
- absence of blood flow
- absence of condition which can stimulate brain death, such as presence of CNS depressant
drugs, reversible metabolic lesions, or hypothermia
Persistent Vegetative State
- irreversible damage that does not lead to death
- return of sleep/wake cycles
- eyes may open and fixate
- brainstem behaviors like yawning, crying, grimacing, and grasping return
- level of consciousness improves, but content of consciousness does not improve
- absence of learning, meaningful communication, and purposeful movement
- cortical function has been permanently disrupted
4. Transtentorial herniation
- rostral portion of ascending reticular activating system located in midbrain and
diencephalon are critical for maintaining consciousness
- lesion in one of the cerebral hemispheres depresses level of consciousness by putting
pressure on the brainstem
- herniation of brain substance (uncus of temporal lobe) under the tentorium cerebelli
- transtentorial herniation occurs when the uncus of the temporal lobe is forced under the
tentorium  pressure on ipsilateral third nerve  CN III palsy
- further pressure on the brainstem then impinges on the ascending reticular activating
system leading a depressed level of consciousness
- as brainstem is shifted toward contralateral side  cerebral peduncles forced against
opposite edge of the tentorium leading to a hemiparesis that is ipsilateral to the side of the
lesion
Other cause of coma
- bilateral hemispheric process
- sub-falcine herniation occurs when an expanding cerebral hemisphere is forced under the
falx cerebri, putting pressure on the opposite hemisphere  leads to bihemispheric
dysfunction and coma