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coma :-
defined as a state of unconsciousness
in which the eyes are closed and sleep–
wake cycles absent
Causes of Coma
• To cause coma state, must either:
– 1. produce bilateral dysfunction of cerebral hemispheres
– 2. damage/depress physiologic activating mechanisms
• Lie along central core of upper brainstem and
diencephalon
– 3. metabolically or physiologically damage or depress
brain globally
Coma Examination
• Vitals
• Assess level of consciousness
– Glasgow coma scale – quick; developed for head trauma
• Pattern of breathing
• Size/reactivity of pupils
– Fundoscopic examination
• Eye movements and oculovestibular response
• Brainstem reflexes
• Skeletal motor responses
– spontaneous/withdrawal/patterned
– DTR's
– babinski
Neural basis of consciousness
Consciousness cannot be readily
defined in terms of anything else
A state of awareness of self and
surrounding
Pathophysiology
 Almost all instances of diminished
alertness can be traced to:
 widespread abnormalities of the cerebral
hemispheres
 reduced activity of a special
thalamocortical alerting system termed the
reticular activating system (RAS).
 The proper functioning of this system, its
ascending projections to the cortex, and
the cortex itself are required to maintain
alertness and coherence of thought.
Cont…
The ascending RAS,
from the lower border
of the pons to the
ventromedial
thalamus
The cells of origin of
this system occupy a
paramedian area in
the brainstem
Cont…
 It follows that the principal causes of coma are:
(1) lesions that damage the RAS in the upper midbrain or
its projections
(2) destruction of large portions of both cerebral
hemispheres
(3) suppression of reticulocerebral function by drugs,
toxins, or metabolic derangements such as
hypoglycemia, anoxia, uremia, and hepatic failure
Coma Due to Metabolic
Disorders
 Interruption of the delivery of energy substrates
(e.g., hypoxia, ischemia, hypoglycemia)
 Alteration of neuronal excitability (drug and alcohol
intoxication, anesthesia, and epilepsy)
 Unlike hypoxia-ischemia, which causes neuronal
destruction, most metabolic disorders such as
hypoglycemia,hyponatremia,hyperosmolarity,
hypercapnia, hypercalcemia, and hepatic and renal
failure : - impaired energy supplies,
-changes in ion fluxes across neuronal
membranes, and
-neurotransmitter abnormalities.
 Glasgow Coma Scale or GCS is a
neurological scale that aims to give a reliable,
objective way of recording the conscious state
of a person for initial as well as subsequent
assessment.
Glasgow Coma Scale
 The test measures the motor response, verbal response
and eye opening response with these values
I. Motor Response

6 - Obeys commands fully
5 - Localizes to noxious stimuli
4 - Withdraws from noxious stimuli
3 - Abnormal flexion, i.e. decorticate posturing
2 - Extensor response, i.e. decerebrate
posturing
1 - No response
II. Verbal Response

5 - Alert and Oriented
4 - Confused, yet coherent, speech
3 - Inappropriate words and jumbled phrases
consisting of words
2 - Incomprehensible sounds
1 - No sounds
III. Eye Opening

4 - Spontaneous eye opening
3 - Eyes open to speech
2 - Eyes open to pain
1 - No eye opening
Mild (13-15):
 More in-depth discussion on the Mild TBI
Symptoms page.
Moderate Disability (9-12):
 Loss of consciousness greater than 30
minutes
 Physical or cognitive impairments which may
or may not resolve
 Benefit from Rehabilitation
Vegetative State (Less Than 3):
 Sleep wake cycles
 Arousal, but no interaction with environment
 No localized response to pain
Persistent Vegetative State:
 Vegetative state lasting longer than one
month
Brain Death:
 No brain function
 Specific criteria needed for making this
diagnosis
Injury to specific areas of the
brain will cause certain
symptoms.
 For example, injury to the frontal lobes will cause
loss of higher cognitive functions, such as loss of
inhibitions leading to inappropriate social
behavior. Injury to the cerebellum will cause loss
of coordination and balance. The brainstem
controls things like breathing and heart rate, as
well as arousal. An injury to this area could inhibit
any of these processes.
References
1. Posner, Jerome; Spaer, Clifford; Schiff, Nicholas; Plum, Fred. 2007. Plum and
Posner's Diagnosis of Stupor and Coma.. 4th ed. New York: Oxford Press.
2. Nakagawa TA, Ashwal S, Mathur M, Mysore MR, Bruce D, Conway EE Jr,
Duthie SE, Hamrick S, Harrison R, Kline AM, Lebovitz DJ, Madden MA,
Montgomery VL, Perlman JM, Rollins N, Shemie SD, Vohra A, Williams-
Phillips JA, Society of Critical Care Medicine, Section on Critical Care and
Section on Neurology of the American Academy of Pediatrics, Child
Neurology Society. Guidelines for the determination of brain death in infants
and children: an update of the 1987 Task Force recommendations. Crit
Care Med. 2011 Sep;39(9):2139-55. [91 references]
1. Nelson text book of pediatrics 19th ed.
2. Up to date 21.2
3. Harrison 19th ed.
4. Kumar and clark med
5. ceil
THANK YOU

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Clinical path phys(neurologic coma)

  • 1.
  • 2. coma :- defined as a state of unconsciousness in which the eyes are closed and sleep– wake cycles absent
  • 3. Causes of Coma • To cause coma state, must either: – 1. produce bilateral dysfunction of cerebral hemispheres – 2. damage/depress physiologic activating mechanisms • Lie along central core of upper brainstem and diencephalon – 3. metabolically or physiologically damage or depress brain globally
  • 4. Coma Examination • Vitals • Assess level of consciousness – Glasgow coma scale – quick; developed for head trauma • Pattern of breathing • Size/reactivity of pupils – Fundoscopic examination • Eye movements and oculovestibular response • Brainstem reflexes • Skeletal motor responses – spontaneous/withdrawal/patterned – DTR's – babinski
  • 5. Neural basis of consciousness Consciousness cannot be readily defined in terms of anything else A state of awareness of self and surrounding
  • 6. Pathophysiology  Almost all instances of diminished alertness can be traced to:  widespread abnormalities of the cerebral hemispheres  reduced activity of a special thalamocortical alerting system termed the reticular activating system (RAS).  The proper functioning of this system, its ascending projections to the cortex, and the cortex itself are required to maintain alertness and coherence of thought.
  • 7. Cont… The ascending RAS, from the lower border of the pons to the ventromedial thalamus The cells of origin of this system occupy a paramedian area in the brainstem
  • 8. Cont…  It follows that the principal causes of coma are: (1) lesions that damage the RAS in the upper midbrain or its projections (2) destruction of large portions of both cerebral hemispheres (3) suppression of reticulocerebral function by drugs, toxins, or metabolic derangements such as hypoglycemia, anoxia, uremia, and hepatic failure
  • 9. Coma Due to Metabolic Disorders  Interruption of the delivery of energy substrates (e.g., hypoxia, ischemia, hypoglycemia)  Alteration of neuronal excitability (drug and alcohol intoxication, anesthesia, and epilepsy)  Unlike hypoxia-ischemia, which causes neuronal destruction, most metabolic disorders such as hypoglycemia,hyponatremia,hyperosmolarity, hypercapnia, hypercalcemia, and hepatic and renal failure : - impaired energy supplies, -changes in ion fluxes across neuronal membranes, and -neurotransmitter abnormalities.
  • 10.  Glasgow Coma Scale or GCS is a neurological scale that aims to give a reliable, objective way of recording the conscious state of a person for initial as well as subsequent assessment.
  • 11. Glasgow Coma Scale  The test measures the motor response, verbal response and eye opening response with these values
  • 12. I. Motor Response  6 - Obeys commands fully 5 - Localizes to noxious stimuli 4 - Withdraws from noxious stimuli 3 - Abnormal flexion, i.e. decorticate posturing 2 - Extensor response, i.e. decerebrate posturing 1 - No response
  • 13. II. Verbal Response  5 - Alert and Oriented 4 - Confused, yet coherent, speech 3 - Inappropriate words and jumbled phrases consisting of words 2 - Incomprehensible sounds 1 - No sounds
  • 14. III. Eye Opening  4 - Spontaneous eye opening 3 - Eyes open to speech 2 - Eyes open to pain 1 - No eye opening
  • 15. Mild (13-15):  More in-depth discussion on the Mild TBI Symptoms page.
  • 16. Moderate Disability (9-12):  Loss of consciousness greater than 30 minutes  Physical or cognitive impairments which may or may not resolve  Benefit from Rehabilitation
  • 17. Vegetative State (Less Than 3):  Sleep wake cycles  Arousal, but no interaction with environment  No localized response to pain
  • 18. Persistent Vegetative State:  Vegetative state lasting longer than one month
  • 19. Brain Death:  No brain function  Specific criteria needed for making this diagnosis
  • 20. Injury to specific areas of the brain will cause certain symptoms.  For example, injury to the frontal lobes will cause loss of higher cognitive functions, such as loss of inhibitions leading to inappropriate social behavior. Injury to the cerebellum will cause loss of coordination and balance. The brainstem controls things like breathing and heart rate, as well as arousal. An injury to this area could inhibit any of these processes.
  • 21. References 1. Posner, Jerome; Spaer, Clifford; Schiff, Nicholas; Plum, Fred. 2007. Plum and Posner's Diagnosis of Stupor and Coma.. 4th ed. New York: Oxford Press. 2. Nakagawa TA, Ashwal S, Mathur M, Mysore MR, Bruce D, Conway EE Jr, Duthie SE, Hamrick S, Harrison R, Kline AM, Lebovitz DJ, Madden MA, Montgomery VL, Perlman JM, Rollins N, Shemie SD, Vohra A, Williams- Phillips JA, Society of Critical Care Medicine, Section on Critical Care and Section on Neurology of the American Academy of Pediatrics, Child Neurology Society. Guidelines for the determination of brain death in infants and children: an update of the 1987 Task Force recommendations. Crit Care Med. 2011 Sep;39(9):2139-55. [91 references] 1. Nelson text book of pediatrics 19th ed. 2. Up to date 21.2 3. Harrison 19th ed. 4. Kumar and clark med 5. ceil