Copy of COMA cNS lecture for under gra.ppt

Copy of COMA cNS

1. COMA

2. •Anatomical aspect
•A conscious individual is
•1-Aware of himself and his environment
•2- Capable of responding to various stimuli
in a proper way
• The sensory stimuli reach the cerebral
cortex and enter consciousness by means of
•1)-Ascending leminscal tracts concerned
with specific modalities of sensations e.g.
tactile, visual, auditory

3. •2)-The ascending reticular activating
system (RAS)
Anatomy
•-It is situated in the brainstem-merges into
the thalamic centers
•-Receives collateral branches from all
ascending sensory pathways
•- Projects diffusely to the cerebral cortex of
both sides

4. •-RAS is a physiologic system consists of
neurons located bilaterally in the medial
tegmental gray matter of the brain stem
that extends from the medulla to the
diencephalons (the important part extends
from the rostral pons to the caudal
diencephalons)

5. Physiology
•1-It has arousal effect on the cerebral
cortex
•2-A motor downstream effect both
facilitatory and inhibitory upon the spinal
cord
•3- It has regulatory control on autonomic or
vegetative activities

6. Physiological aspect
•-Awareness and thinking are dependent
on
•1- Integrated and organized thoughts
•2- Subjective experiences
•3- Emotions
•4- Mental processes
each of which resides to some extent in
anatomically defined regions of the brain

7. • -STATES OF REDUCED ALERTNESS

8. CONFUSION
•is the inability to maintain a coherent
sequence of thoughts accompanied by
inattention and disorientation i.e. is a
disorder of the content of consciousness

9. •THE CONFUSIONAL STATE
•Confusion is a behavioral state of reduced
mental clarity in which
•-Inattention and disorientation are the main
early signs
•-with worsening there is deterioration in
memory, perception, comprehension,
problem solving language function and
various aspects of emotional behavior

10. This global cortical dysfunction is
expected in
1- The metabolic diseases
2-Pharmacologic agents
that are the most common sources of
acute confusional state
CONFUSION+DROWSINESS

(ENCEPHALOPATHY)

11. Confusion may be accompanied by
1- Illusion (misperception), or
2- Hallucination (spontaneous endogenous
perception)
-Psychiatrists use the term DELIRIUM instead
of CONFUSION

-While neurologists prefer to reserve it as a
description for an agitated, and confused
patient

12. Drowsiness
• is a disorder that simulates light sleep
from which the patient can be easily
aroused by touch, or noise and can
maintain alertness for some time

13. Stupor
• is a state in which the patient can be
awakened only by vigorous stimuli, and an
effort to avoid uncomfortable stimuli is
displayed
•--Both types show some degree of mental
confusion in form of incorrect verbal
response or slow or even absent

14. COMA
• in which the patient can not be aroused
by stimulation and no purposeful attempt
is made to avoid painful stimuli
•--So the description of the behavioral state
and response evoked by various stimuli
are important

15. Dementia
• is due to permanent degeneration of
mind and is characterized by intellectual,
affect, and behavior changes

16. COMA LIKE SYNDROMES AND RELATED
STATES
COMA
•is characterized by complete
unarousability
VEGETATIVE state
• patients who were earlier comatose but
whose eyelids have after a time opened
giving the appearance of wakefulness

17. - There may be yawning, and random limb
and head movements
- There is an absolute absence of response
to commands
-and inability to communicate
-Absent response to visual stimuli

18. - +ve Babinski signs
- Decerebrate or decorticate limb posturing
-Autonomic nervous system functions are
preserved
- It results from global damage to the
cerebral cortex

19. AKINETIC MUTISM
• Refers to a partially or fully awake patient
who when unstimulated remains immobile
and silent
•Hydrocephalus, mass in the region of3rd
ventricle, or frontal lobes, or
periaqueductal or low diencephalic regions

20. ABULIA
•Is a mild form of a kinetic mutism in which
the patient is hypo kinetic and slow to
response but generally gives correct
answers
•It is typical to halt while reciting numbers
or sequential calculations with delay to
resume correctly

21. The locked in state
•Is a pseudo coma in which patients are
awake but have no means of producing
speech or limb, face or pharyngeal
movements
•It is due to INFARCTION OF VENTRAL
PONS, while RAS arousal system ,vertical
eye movements and lid elevation remain
unimpaired.

22. D.D.
•Similar condition may occur as a result of
total paralysis of limb, ocular, and
oropharyngeal as in case of acute G B
syndrome
•unlike brain stem stroke vertical eye
movement is not spared

23. Certain psychiatric states can mimic
coma by producing unresponsiveness
CATATONIA
• Is a hypo mobile syndrome
• the patient appear awake with eyes open
but make no voluntary or responsive
movements
•-but they blink spontaneously
•-may have waxy flexibility
•-on recovery may have some memory of
events

24. Hysterical
•voluntary attempts to appear comatose,
eyelid elevation is actively resisted,
blinking occurs, and the eyes move
concomitantly with head rotation

25. ANATOMIC CORRELATIONS OF
CONSCIOUSNESS
•A normal level of consciousness
depends upon
•-activation of the cerebral hemispheres
by brainstem RAS
•-both of them and its connections must
be preserved
•So the principle causes of coma are

26. •1) Widespread damage of both
hemispheres
•2) Suppression of cerebral function by
extrinsic drugs toxins or hypoxia or by
internal metabolic derangements
• 3) Brainstem lesions that cause
proximal damage to the RAS

27. •4) Transtentorial herniation →brainstem
dysfunction (transfalcial i.e. displacement
of cingulated gyrus or medial temporal
lobe displacement or cerebellar tonsils or
uncal herniation

28. •or impaction of the anterior medial
temporal gyrus into anterior portion of the
tentorial opening causing compression
of3rd nerve with papillary dilatation
•5) Coma may be due to midbrain
compression by parahippocampal gyrus

29. •6) Central herniation
•upper diencephalic or thalamic herniation
→meiotic pupil and drowsiness
•7) The compression will affect
•1st midbrain, pons and finally the medulla
with its clinical data

30. PATHOPHYSIOLOGY OF COMA
AND CONFUSION
•1
)
Coma of metabolic origin is produced
by interruption of energy substrate delivery
or by alteration of the neurophysiologic
responses of neuronal membranes

31. •2)These metabolic abnormalities can
cause widespread neuronal dysfunction in
the cortex that reduces all aspects of
mentation and results in an acute
confusional state i.e. metabolic
encephalopathy

32. • -CBF is 75mL/100g/min in gray zone and
30mL/100g/min in white one i.e. mean
55mL/100g/min
•-Oxygen consumption is 3.5 mL/100g/min
- Glucose is 5mg/100g/min
• 3
)
Brain stores of glucose provide
energy for approximately 2 min after blood
flow is interrupted and consciousness is
lost within 8-10 s

33. •4) Hypoxia exhausts glucose more rapidly
•5
)
CBF
•At 25mL→slow EEG
•At 15mL →brain electrical activity ceases
At 10 mL → irreversible brain damage
(rapidity and duration are important
factors)

34. •6) Hypernatremia
•-Hyperosmolarity (serum osmolarity
above 350mosmol/L)
•-Hypercapnia (due to Pco2 retention)
•-Hypercalcemia
•-Hypothyroidism, VitB12 deficiency and
hypothermia

35. •- Hepatic or renal encephalopathy is
reversible and it may be due to
•-impaired energy supplies
•-change ion fluxes across neuronal
membranes and
•-neurotransmitter abnormalities

36. -Hyponatremia
-below 125mmol/L → acute or sub acute
confusion
-while its level below115mmol/L → coma
and convulsion

37. APPROACH TO THE PATIENT
HISTORY
•1-The circumstances and temporal profile of
onset
•2-The precise details of preceding
neurological symptoms
•3-The use of drugs
•4- History of liver, kidney or other medical
disease
•5-Evaluation from relatives and ambulance
attendants

38. EXAMINATION
•1-The temperature (systemic infection,
meningitis, encephalitis or lesion that has
disturbed the temperature center)
•-If it is high with dry skin (heat stroke or
anticholinergic drug intoxication)
•-If it is low (environmental, alcohol, barbiturate,
hypoglycemia hypothyroidism )
•-If it is below31c,it may be the cause

39. •2-Abnormal respiratory patterns→
brainstem lesion
•3-A change of pulse combined with
hyperventilation and hypertension →↑ICT
•4-Marked hypertension (encephalopathy,
Hge, hydrocephalus, after head trauma)

40. • -Hypotension (MI, Hge, septicemia,
addisonian crisis, alcohol intoxication
•5-Fundoscopic examination
•6-Generalized cutaneous petechiae

41. NEUROLOGIC ASSESSMENT
An exact description of spontaneous and
elicited movements is of great value in
establishing the level of neurological
dysfunction
Inspection
The patient state
Respiration
Spontaneous movements

42. •Posture
•1-Decorticate (flexion of elbows, wrists
and arm supination) suggests severe
bilateral damage in the hemispheres
above the midbrain
•2-Decerebrate (extension of the elbows
and wrists with pronation) suggests
damage to the corticospinal tracts in the
midbrain or caudal diencephalons

43. •3-Arm extension with minimal leg flexion
or flaccid legs →low pons lesion
•4-Acute lesions of any type cause limb
extension regardless the site, and all
extensor postures become flexion with
time

44. 5-Metabolic coma produce decerebrate
rigidity, and may associated with multifocal
myoclonus, and bilateral asterixis
Elicited movements
1-Spokin voice
2-Noxious stimuli denotes an intact
corticospinal system

45. Brainstem reflexes
Are a key to localization of the lesion in coma ,
because
1 -coma associated with normal brainstem
function indicates widespread and bilateral
hemispheral disease
2-Brainstem reflexes are
1 -pupillary light responses
2 -eye movements both spontaneous and elicited
3 -respiratory pattern

46. 1 -pupillary light responses
-Light reaction in pupils smaller than 2mm
is difficult

-Symmetrically reactive round pupils
(2.5-5mm
)
in diameter usually exclude
midbrain damage

47. -One enlarged unreactive pupil(≥5mm)
results either from intrinsic MB lesion on
the same side or effect of mass on other
side
•-Bilateral dilated unreactive pupils
means severe MB damage, or herniation
or drugs

48. •-Bilateral small reactive but not pinpoint
pupil(1-2.5mm)
• metabolic encephalopathy
•-Smaller than(1mm) and reactive
• pontine Hge
•-Unilateral small pupil
Horner" syndrome with ipsilateral large
cerebral Hge
•-Lid tone i.e. resistance to opening and
speed of closure

49. Eye movements
-Inspection
the resting position and spontaneous
movements
1 -Horizontal divergence of the eyes at
rest is observed in drowsiness
2 -An adducted eye at rest 6th nerve
lesion, if it is bilateral →↑ICT

50. •3-An abducted eye →3rd nerve lesion
•
•4-vertical separation of the ocular axes or
skew deviation →pontine or cerebellar
lesions
•4-Spontaneous eye movements in coma
take the form of conjugate horizontal
roving

51. •- Ocular bobbing (a brisk downward
and slow upward movement with loss of
horizontal one ) → bilateral pontine
damage

52. •-Ocular dipping (slow arrhythmic
downward movement with faster upward
one and preserved horizontal one
→diffuse damage to cerebral cortex
•-The eyes may turn down and inward in
thalamic and upper midbrain lesions

53. Incomplete adduction of the eye
indicates 3rd nerve or MLF lesions
(internal ophthalmoplegia)
1-3rd nerve is associated by an enlarged
pupil, and horizontal ocular divergence
at rest
2-While MLF lesions are unrelated to
papillary function and leave the globe in
the 1ry position

54. Doll's-eye responses
•-Are reflex movements tested by moving
the head from side to side or vertically,
first slowly then briskly
•-eye movements are evoked in the
opposite direction to the head
movements, it is generated by labyrinths
and cervical proprioceptors

55. •They are normally suppressed by visual
fixation mediated by the cerebral
hemispheres in awake patients
•- but appear as the hemispheres become
suppressed or inactive

56. •-Conjugate movements demonstrate the
integrity of
•1- pathways extending from the high
cervical spinal cord and medulla

•2- vestibular and proprioceptive input

57. •-In coma resulting from bihemispheral
disease or metabolic or drug depression,
the eyes move easily or loosely from side
to side in a direction opposite to the
direction of head turning
•-it is a reflection of disinhibition of
brainstem reflexes by damaged cerebral
hemispheres

58. •-Thus full and conjugate eye movements
that are induced by oculo -cephalic
maneuver demonstrate the intactness of
large segment of brainstem and virtually
exclude a primary lesion of the brainstem
as the cause of coma

59. •-Caloric stimulation
•(oculovestibular response)→ tonic
deviation of both eyes to the side of
cool-water irrigation
•(means intact brainstem reflexes)
•-In hysterical coma there is an obligate
rapid corrective movements away from
the side of tonic deviation
•(absence of this nystagmus -like quick
phase means cerebral damage)

60. Drugs
•-Phenytoin, tricyclic antidepressants and
barbiturates, alcohol, N-M blockers
• -The presence of
•1- normal light reaction
•2-normal papillary size
•will distinguish most drug induced coma from
brainstem lesions
•-Small (1-3mm) and nonreactive pupils
(barbiturate or hydrocephalus)
•- CORNEAL REFLEXES are rarely useful alone

61. RESPIRATION
•- respiratory patterns of no localizing
value
•-Shallow and slow →metabolic or drug
induced
•-Rapid and deep →metabolic acidosis
•-Cheyne -Stokes →mild bihemispheral
damage or metabolic one and commonly
accompanies light coma

62. •- gasping reflect bilateral lower brainstem
damage and is terminal one
•-In brain-dead patients, shallow
respiratory- like movements with irregular
non-repetitive back arching may be
produced by hypoxia and are generated
by the surviving cervical spinal cord and
lower medulla

63. Laboratory examination
•1-Chemical blood determinations
•2-CT &MRI
•3-EEG is useful in metabolic or drug
induced confusional states but is rarely
diagnostic in coma
•4-The amount of background slowing of
the EEG is useful guide of severity of
diffuse encephalopathy

64. •5-Predominant high-voltage slowing (delta
waves) in the frontal regions is typical of
metabolic coma
•6-Widespread fast (beta) activity
implicates the effects of sedative drugs

65. •7-Alpha coma
•results from either high pontine or diffuse
cortical damage, and its EEG pattern is
widespread invariant activity resembling
the normal alpha rhythm of waking but
unresponsive to environmental stimuli

66. •8-Coma due to persistent epileptic
discharges that are not clinically
manifested may be revealed by EEG
•9-Normal alpha activity on EEG may alert
the clinician to the locked-in syndrome or a
hysterical case
•10-Lumber puncture for diagnosis of
meningitis or encephalitis

67. Brain death
•Definition
•Is a state of total cessation of cerebral
blood flow and global infarction of the
brain, while the respiration is maintained
by artificial support and the heart
continues to function

68. •Diagnosis
•1-Widespread cortical destruction shown
by deep coma
•2-Global brainstem damage demonstrated
by absent pupillary light reaction, and
absent both oculo -vestibular and corneal
reflexes
•3-Medullary destruction indicated by
complete apnea

69. •4-The pulse is invariant and unresponsive
to atropine
•5-The pupils need not be enlarged but
should not be constricted
•6-Absence of deep tendon reflexes is not
required because the spinal cord may
remain functioning

70. •7-Some period of observation 6-24h is
desirable during which this state is shown
to be sustained
•8-Apnea proved by highPco2, with
removal of the respirator and use tracheal
cannula Co2 increases 2-3mmHg/min and
may reach 50-60mmHg
•9-An isoelectric EEG is a confirmatory test

71. •10-Radionuclide scanning, cerebral angiography
and transcranial Doppler may be used to
demonstrate the absence of cerebral blood flow
•D.D.
•1-Large posterior fossa lesions that compress
the brainstem
•2-CNS-depressant drugs
•3-profound hypothermia
•All can simulate brain death

72. Normal brainstem reflexes, with no
lateralization
A-Bilateral hemispheral dysfunction without
mass
-Drugs, Endogenous metabolic
encephalopathy, shock, HPT
encephalopathy, meningitis, encephalitis,
epilepsy, Reye' syndrome, SA Hge, and
hysterical coma

73. •B-Anatomic lesions of hemisphere
Hydrocephalus, bilateral subdural
hematoma, or head trauma, SAHge, acute
disseminated encephalomyelitis

74. Normal brainstem reflexes with lateralizing
signs
A-Unilateral mass lesion
•Hge, infarction, encephalitis, subdural
hematoma, tumor, abscess, vasculitis with
multiple infarction, metabolic
encephalopathy on top of focal lesion, and
pituitary apoplexy

75. •B-Diffuse hemispheral dysfunction with
asymmetric signs
•-Metabolic encephalopathy, thrombotic
thrombocytopenic purpura, and epilepsy
with focal seizures

76. Multiple brainstem abnormalities
•A-Anatomic lesion of brainstem
•Hge, tumor, abscess, cerebellar infarction
with brainstem compression, mass in
hemisphere with brainstem compression,
demyelination
•B-Brainstem dysfunction without mass
•Basilar artery thrombosis, severe drug
overdose, brainstem encephalitis basilar
artery migraine

77. Prognosis
•1-Glasgow coma scale has a predictive value
in cases of brain trauma e.g.
•
•95% death rate in patients whose pupillary
reaction or reflex eye movement are absent 6h
after onset of coma
•91% death rate if the pupils are unreactive at
24h

78. •2-The prognosis of non traumatic coma is
difficult because of the heterogeneity of
contributing diseases e.g. metabolic coma
generally has more favorable prognosis
•3-Unfavorable signs in the first hours after
admission are the following

79. •- one day after onset of coma, the
absence of any two of pupillary reaction,
corneal reflex
•absence of eye opening and muscle tone
predict death
• at 3 days strengthen the prediction

80. •3-Bilateral absence of cortical somato-
sensory evoked potentials is associated
with death or a vegetative state
•4-The prognosis for regaining full mental
state once the vegetative state has
supervened is almost nil

81. Old classification
StateLethargy
&Drowsn
ess
StuporSemi-
coma
Coma
Conscio
usness
ImpairedImpairedLostLost
Resp to
ex
stimuli
Verb
resp
+ve to
verbal
stim
Verb-
resp
+ve to
vigorous
stim
-ve verb
resp&+v
e reflex
resp to
pain
-ve verb
or reflex
resp to
pain

82. Glasgow coma scale
Eye openSpontane
ous
(4)
+ve resp
to speech
(3)
+ve resp
to pain
(2)
None
(1)
Verb respOriented
(5)
Confused
(4)
+ve
words,
-ve senten
(3)
+Ve
sounds,-
ve words
(2)
None
(1)
Motor
resp
Obeys
orders
(5)
Local to
pain
(4)
Flexes to
pain
(3)
Extends
to pain
(2)
None
(1)