Motor ability/response, verbal output/response, and eye opening

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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 dysfunctionCheyne-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 palsytentorial 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 midbrainabolish 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 opioidpin-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 posturingflexion 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


- 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 tentoriumpressure on ipsilateral third nerveCN 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

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