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CONSCIOUSNESS SYSTEM
EUFEMIO E. SOBREVEGA,MD
FELLOW, PHIL. NEUROLOGICAL ASSN.
FELLOW, PHIL. PSYCHIATRIC ASSN.
LEARNING OBJECTIVES:
• Consciousness system:
– Definition
– Anatomy: Role of ARAS, Thalamus, Cerebrum
– Experiments by Morozzi and Magoun
– Brain waves, Neurotransmitters
– Evaluation of Stupor and Coma
– Pathophysiology and Etiologies of Coma
– Diagnostic Clues
CONSCIOUSNESS
• DEFINITION:
- AWARENESS OF SELF AND ENVIRONMENT.
- AWAKE, ALERT CONDITION.
- CAPABLE OF PERCEIVING INTERNAL AND
EXTERNAL ENVIRONMENT.
- RESPONDING IN AN APPROPRIATE
MANNER TO INPUT STIMULI.
CONSCIOUSNESS
2 ASPECTS CONSCIOUSNESS:
– 1. CONTENT –
– COGNITIVE MENTAL FUNCTIONS THAT REFLECT
THE ACTIVITY OF CORTEX.
– 2. AROUSAL AND WAKEFULNESS
– DEPENDENT ON THE ASCENDING RETICULAR
ACTIVATING SYSTEM.
STRUCTURE responsible for
CONSCIOUSNESS
ARAS: Ascending Reticular Activating System
Eye
R ETICULAR FORMATION
Input from touch,
pain, and temperature
receptors
Input from ears
The Brainstem
ANATOMY OF THE
CONSCIOUSNESS SYSTEM
• STRUCTURES IN THE SYSTEM ARE:
1. PORTIONS OF THE BRAINSTEM RETICULAR
FORMATION.
2. ASCENDING PROJECTIONAL SYSTEM
3. NON-SPECIFIC THALAMIC NUCLIE
4. DIFFUSE PROJECTIONS FROM THE NONSPECIFIC THALAMIC
NUCLIE TO THE CORTEX. *
5. WIDESPREAD AREAS OF CEREBRAL CORTEX
*FIRST FOUR COLLECTIVELY CALLED ARAS.
LATERAL VIEW OF THE BRAIN SHOWING COMPONENTS
OF THE CONSCIOUSNESS SYSTEM
ASCENDING RETICULAR
ACTIVATING SYSTEM (ARAS)
• RETICULAR FORMATION:
• COMPLEX AGGREGATE OF LARGE MULTIPOLAR AND SMALL
ROUND NEURONS AND THEIR AXONS, DIFFUSELY
DISTRIBUTED IN CLUSTERS THROUGHOUT THE
CENTRAL TEGMENTAL PORTIONS OF THE BRAINSTEM.
• EXTENDS FROM THE DECUSSATION OF THE PYRAMIDS IN
THE MEDULLA TO THE THALAMUS.
RETICULAR FORMATION:
• FUNCTIONAL DIVISION:
1. LATERAL RECEPTIVE AREA:
- RECEIVES COLLATERAL BRANCHES FROM
ASCENDING SENSORY PATHWAYS.
2. MEDIAL PROJECTIONAL AREA:
- FROM WHICH EFFERENT FIBERS ARISE.
AFFERENT PATHWAYS
AFFERENT PATHWAYS
1. FROM ASCENDING TRACTS OF BOTH SOMATIC AND VISCERAL
SENSORY SYSTEM.
2. FROM THE CORTEX: CORTICORETICULAR F.,
CORTICOBULBAR AND CORTICOSPINAL PATHWAYS.
3. CEREBELLUM, BASAL GANGLIA, THALAMUS,
HYPOTHALAMUS, BRAINSTEM RETICULAR FORMATION.
4. VISCERAL EFFERENTS FRO SPINAL CORD AND CRANIAL
NERVES.
ASCENDING PROJECTIONAL SYSTEM
ASCENDING PROJECTIONAL
SYSTEM
• PROJECTS DIFFUSELY TO:
1. HYPOTHALAMUS
2. NONSPECIFIC NUCLIE OF THE
THALAMUS
NUCLIE OF THE THALAMUS
1. SPECIFIC NUCLIE:
- ASSOCIATED WITH THE SENSORY AND MOTOR
SYSTEMS AND WHICH CONNECT TO THE LOCALIZED
AREAS OF CORTEX.
2. NONSPECIFIC NUCLIE:
- RECEIVE AFFERENTS FROM THE RETICULAR
FORMATION, THE CORTEX AND OTHER THALAMIC
NUCLIE AND PROJECT TO ALL AREAS OF THE CORTEX
VIA THE DIFFUSE THALAMIC PROJECTION SYSTEM.
Figure 9-10: The diencephalon
Thalamus
18
Thalamus
NONSPECIFIC NUCLIE OF THE
THALAMUS
NONSPECIFIC NUCLIE OF THE
THALAMUS
• COMPONENTS:
1. MIDLINE NUCLIE
LOCATED NEAR THE MASSA INTERMEDIA.
2. INTRALAMINAR NUCLIE
LOCATED ALONG THE INTERNAL MEDULLARY
LAMINA (A BAND) OF MYELINATED FIBERS SEPARATING
THE ANTERIOR, MEDIAL AND LATERAL THALAMIC
NUCLIE.
3. RETICULAR NUCLIE
LOCATED ON THE LATERAL MARGIN OF THE
THALAMUS.
DIFFUSE THALAMOCORTICAL PROJECTIONS OF
THE CONSCIOUSNESS SYSTEM.
CONSCIOUSNESS, SLEEP AND COMA
RAPHE NUCLIE;
SEROTONINERGIC
NON-REM SLEEP
LOCUS CERULEUS:
NORADRENERGIC
REM SLEEP
NEUROTRANSMITTERS, BRAINSTEM NUCLIE AND SLEEP
• Measures: EEG (electrophysiology)
• Measures: EEG (electrophysiology)
Brain Waves
• Normal brain function involves continuous
electrical activity
• An electroencephalogram (EEG) records this
activity
• Patterns of neuronal electrical activity recorded are
called brain waves
• Each person’s brain waves are unique
• Continuous train of peaks and troughs
• Wave frequency is expressed in Hertz (Hz)
EEG
Hans Berger (first
recorded human
EEG, 1928)
Different EEG-bands (by frequency)
•Delta (0.5-4 Hz) - sleep
•Theta (5-7 Hz) - drowsy
•Alpha (8-12 Hz) - relaxed (eyes closed)
•Beta (13-22 Hz) - active
•Gamma (23-30 Hz) - very active
Types of Brain Waves
• Alpha waves – regular and rhythmic, low-amplitude,
slow, synchronous waves indicating an “idling” brain
• Beta waves – rhythmic, more irregular waves
occurring during the awake and mentally alert state
• Theta waves – more irregular than alpha waves; common
in children but abnormal in adults
• Delta waves – high-amplitude waves seen in deep sleep
and when reticular activating system is damped
• Measures: EEG
Actively awake: beta and gamma
Passively awake: alpha
Drowsy: theta
Light slow save sleep
Deep slow save sleep
Types of Brain Waves
Figure 12.20b
Giuseppe Moruzzi and Horace Magoun (1949)
EXPERIMENT BY MORUZZI AND MAGOUN ON CATS:
BRAINSTEM TRANSECTIONS AT DIFFERENT LEVELS
SHOWING WAKEFULNESS, SLEEP AND COMATOSE STATES
Reticular Formation
Figure 12.19
EVALUATION OF PATIENTS
IN STUPOR AND COMA
PARAMETERS:
1. LEVEL OF CONSCIOUSNESS
2. RESPIRATORY PATTERN
3. PUPILLARY SIZE AND REACTION TO
LIGHT
4. OCULOCEPHALIC REFLEX (DOLL’S EYES)
5. MOTOR RESPONSES
EVALUATION OF PATIENTS
IN STUPOR AND COMA
PARAMETERS:
1. LEVEL OF CONSCIOUSNESS
• AWAKE
• DROWSY
• LETHARGIC
• STUPUROUS
• COMATOSE
* DESCRIBE STIMULUS GIVEN AND THE
RESPONSE OF THE PATIENT.
EVALUATION OF PATIENTS
IN STUPOR AND COMA
PARAMETERS:
2. RESPIRATORY PATTERN LEVEL
- CHEYNE-STOKES RESPIRATION DIENCEPHALIC/
DIFFUSE CEREBRAL
- CENTRAL NEUROGENIC HYPERVENTILLATION MIDBRAIN
- APNEUSTIC BREATHING PONS
- ATAXIC / CLUSTER BREATHING MEDULLA
RESPIRATORY PATTERNS IN STUPOR
AND COMA (rostral caudal progression)
EVALUATION OF PATIENTS
IN STUPOR AND COMA
PARAMETERS:
3. PUPILLARY SIZE AND REACTION TO
LIGHT
PUPILLARY LIGHT REFLEX
PUPILS IN COMATOSE PATIENTS
EVALUATION OF PATIENTS
IN STUPOR AND COMA
PARAMETERS:
4. OCULOCEPHALIC REFLEX
(DOLL’S EYES PHENOMENON)
- TESTS INTEGRITY OF THE BRAINSTEM*
OCULOCEPHALIC REFLEX
(DOLL’S EYES PHENOMENON)
EVALUATION OF PATIENTS
IN STUPOR AND COMA
PARAMETERS:
5. MOTOR RESPONSES:
- ABSENT
- PRESENT
- WEAK (PARESIS)
- ABNORMAL:
* DECEREBRATE RIGIDITY
* DECORTICATE RIGIDITY
• EVALUATION
OF STUPOR
AND COMA.
EVALUATION OF STUPOR AND COMA
EVALUATION OF STUPOR AND COMA
EVALUATION OF STUPOR AND COMA
DECORTICATE RIGIDITY
EVALUATION OF STUPOR AND COMA
DECEREBRATE RIGIDITY
The COMATOSE PATIENT:
NEUROPHYSIOLOGY
• Consciousness requires:
• An intact pontine reticular activating system
• An intact cerebral hemisphere, or at least
part of a hemisphere
• Coma requires dysfunction of either the:
• Brainstem ascending reticular activating
system (ARAS), or
• Bihemispheric cerebral dysfunction
PATHOPHYSIOLOGY OF COMA
• A conscious state depends on intact cerebral
hemispheres, interacting with the ARAS
in the brainstem , midbrain, hypothalamus
and hypothalamus.
• Lesions diffusely affecting the cerebral
hemispheres, or directly affecting the
ARAS cause impairment of conscious
level.
The Comatose Patient
Classifications
• Supratentorial lesions cause coma by either
widespread bilateral disease, increased intracranial
pressure, or herniation.
• Infratentorial lesions involve the RAS, usually with
associated brainstem signs
• Metabolic coma causes diffuse hemispheric
involvement and depression of RAS, usually without focal
findings
• Psychogenic
Plum and Posner, 1982
Supratentorial Mass Lesions
• Hematoma
• Neoplasm
• Abscess
• Contusion
• Vascular Disease
• Diffuse Axonal Damage
Supratentorial Mass Lesions
PATHOPHYSIOLOGY
• Altered consciousness is based on
• Increased intracranial pressure
• Herniation
• Diffuse bilateral lesions
Supratentorial Mass Lesions
Differential Characteristics
•Initiating signs usually of focal
cerebral dysfunction
•Signs of dysfunction progress rostral
to caudal
•Neurologic signs at any given time
point to one anatomic area -
diencephalon, midbrain,
brainstem
•Motor signs are often asymmetrical
Plum and Posner, 1982
Herniation Syndromes
•Central herniation
Rostral caudal progression of
respiratory, motor, and pupillary
findings
May not have other focal findings
•Uncal herniation
Rostral caudal progression
CN III dysfunction and contralateral
motor findings
Herniation syndromes
Infratentorial Lesions
• Cause coma by affecting reticular
activating system in brainstem
• Brainstem nuclei and tracts usually
involved with resultant focal brainstem
findings
Infratentorial Mass Lesions
Differential Characteristics
• History of preceding brainstem dysfunction
or sudden onset of coma
• Localizing brainstem signs precede or
accompany onset of coma and always
include oculovestibular abnormality
• Cranial nerve palsies usually present
• “Bizarre” respiratory patterns common,
usually present at onset of coma
Plum and Posner, 1982
Infratentorial Lesions
Causes of Coma
• Neoplasm
• Vascular accidents
• Trauma
• Cerebellar hemorrhage
• Demyelinating disease
• Central pontine myelinolysis (rapid
correction of hyponatremia)
Metabolic Coma
Differentiating Features
• Confusion and stupor commonly precede
motor signs
• Motor sings are usually symmetrical
• Pupillary reactions are usually preserved
• Asterixis, myoclonus, tremor, and seizures
are common
• Acid-base imbalance with hyper- or
hypoventilation is frequent
Plum and Posner, 1982
Metabolic Coma
Etiologies
• Respiratory
– Hypoxia
– Hypercarbia
• Electrolyte
– Hypoglycemia
– Hyponatremia
– Hypercalcemia
• Hepatic
encephalopathy
• Severe renal failure
• Infectious
– Meningitis
– Encephalitis
• Toxins, drugs
PATHOPHYSIOLOGY OF COMA
• DIFFUSE CEREBRAL DAMAGE:
– e.g. metabolic encephalopathy: hepatic or renal failure,
hypoglycemia, demyelinating disease
• SUPRATENTORIAL MASS causing
– transtentorial herniation and midbrain compression:
e.g. tumor, hematoma, abscess
• INFRATENTORIAL LESIONS:
– brainstem compression and direct brainstem involvement.
e.g. ischemia, hemorrhage, tumor
CAUSES OF COMA AND IMPAIRED
CONSCIOUS LEVEL
• INTRACRANIAL:
– TRAUMA: diffuse white matter injury;
hematoma- extradural, subdural, “burst lobe”
– NEOPLASTIC: primary vs metastatic
– VASCULAR: subarachnoid hemorrhage,
intracerebral hematoma, massive cerebral infarct,
brainstem ifarction or hemorrhage
– INFECTIOUS: meningitis, encephalitis, abscess
– OTHERS: epilepsy, hydrocephalus
CAUSES OF COMA AND IMPAIRED
CONSCIOUS LEVEL
• EXTRACRANIAL :
– METABOLIC/ENDOCRINE: renal, hepatic failure,
electrolyte imbalance, hypoglycemia, diabetic
ketoacidosis, adrenal crisis, hypothyrodism, etc.
– RESPIRATORY INSUFFICIENCY: hypoventillation,
diffusion deficiency, perefusion deficiency
– DECREASED CARDIAC OUTPUT: e.g. myocardial
infarction, arrhythmias, hypotensive drugs
– DRUGS/TOXINS: sedatives, opiates, antidepressants,
antipsychotics, anticonvulsants, anesthetics, alcohol,
carbon monoxide
PSYCHOGENIC CAUSES
• HYSTERIA
• CATATONIA (mutism with deceased
motor activity)
• FUGUE STATES
DIAGNOSTIC CLUES
• HISTORY POSSIBLE CAUSE
Head injury --------- ---------------- --Diffuse shearing injury or
intracranial hematoma
Previous head injury (eg 6 wks) ----Subdural hematoma
Sudden collapse ----------------------- Intracerebral/subarachnoid
hemorrhage
Limb twitching, incontinence ------- Epilepsy, post ictal state
Gradual development of symptoms -- Mass lesions, metabolic or
infective cause
DIAGNOSTIC CLUES
• HISTORY POSSIBLE CAUSE
Previous Illness
Diabetes ---------------- ----- Hypo/Hyperglycemia
Epilepsy ---------------------- Postictal state
Psychiatric Illness ----------- Drug overdose
Alcoholism/ Drug Abuse ---- Drug toxicity
Viral Infection ---------------- Encephalitis
Malignancy ------------------ Intracranial metastasis
Management of the Comatose Patient
Disability - Neurologic
• Glasgow coma scale
– Provides easily reproducible and somewhat
predictive basic neurologic exam
– This allows rapid assessment and record of
baseline neurologic status
– Allows physician to track neurologic changes
over time and multiple examiners
Glasgow Coma Scale
• Three components. Score derived by
adding the score for each component.
• Eye opening (4 points)
• Verbal response (5points)
• Best motor response (6 points)
Glasgow Coma Scale
• Eye opening
• 4 - spontaneous
• 3 - to speech
• 2 - to pain
• 1 - none
• Verbal Response
• 5 - oriented
• 4 - confused conversation
• 3 - inappropriate words
• 2 - incomprehensible sounds
• 1 - none
• Best Motor Response
• 6 - obeys
• 5 - localizes
• 4 - withdraws
• 3 - abnormal flexion
• 2 - abnormal
extension
• 1 - none
LEARNING OBJECTIVES:
• Consciousness system:
– Definition
– Anatomy: Role of ARAS, Thalamus, Cerebrum
– Experiments by Morozzi and Magoun
– Brain waves, Neurotransmitters
– Evaluation of Stupor and Coma
– Pathophysiology and Etiologies of Coma
– Diagnostic Clues
• end
Identify/ fill in the blank
• 1. RAS stands for ____ _____ ______.
Identify/ fill in the blank
• 1. RAS stands for ____ _____ ______.
• 2. The RAS is located in the ____ of the
brainstem.
Identify/ fill in the blank
• 1. RAS stands for ____ _____ ______.
• 2. The RAS is located in the ____ of the
brainstem.
• 3. The lowest portion of the RAS is located in
the junction of _____ level of the brainstem
and the cervical spinal cord.
• 4. The RAS will have connection with the
_____ nuclie of the thalamus. (Specific or
Non-specific?)
• 4. The RAS will have connection with the
_____ nuclie of the thalamus. (Specific or
Non-specific?)
• 5. The nuclie of the thalamus will send
impulses to the diffuse areas in the _____
cortex.
• 6. Transection of the brainstem at the midbrain
level will cause persistent ______. (sleep or
wakefulness.)
• 6. Transection of the brainstem at the midbrain
level will cause persistent ______. (sleep or
wakefulness.)
• 7.Transection of the midpontine level of the
brainstem will cause persistent _____. (sleep
or wakefulness.
• 8. Pinpoint pupils, apneustic breathing are
findings indicative of a lesion in what level of
the brainstem?
• 8. Pinpoint pupils, apneustic breathing are
findings indicative of a lesion in what level of
the brainstem?
• 9. Dilated irregular pupils, ataxic or cluster
breathing are findings indicative of a lesion in
what level of the brainstem?
• 10. Brain waves are measured by an ancillary
procedure called the ____.

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CONSCIOUSNESS-SYSTEM.ppt

  • 1. CONSCIOUSNESS SYSTEM EUFEMIO E. SOBREVEGA,MD FELLOW, PHIL. NEUROLOGICAL ASSN. FELLOW, PHIL. PSYCHIATRIC ASSN.
  • 2. LEARNING OBJECTIVES: • Consciousness system: – Definition – Anatomy: Role of ARAS, Thalamus, Cerebrum – Experiments by Morozzi and Magoun – Brain waves, Neurotransmitters – Evaluation of Stupor and Coma – Pathophysiology and Etiologies of Coma – Diagnostic Clues
  • 3. CONSCIOUSNESS • DEFINITION: - AWARENESS OF SELF AND ENVIRONMENT. - AWAKE, ALERT CONDITION. - CAPABLE OF PERCEIVING INTERNAL AND EXTERNAL ENVIRONMENT. - RESPONDING IN AN APPROPRIATE MANNER TO INPUT STIMULI.
  • 4. CONSCIOUSNESS 2 ASPECTS CONSCIOUSNESS: – 1. CONTENT – – COGNITIVE MENTAL FUNCTIONS THAT REFLECT THE ACTIVITY OF CORTEX. – 2. AROUSAL AND WAKEFULNESS – DEPENDENT ON THE ASCENDING RETICULAR ACTIVATING SYSTEM.
  • 5. STRUCTURE responsible for CONSCIOUSNESS ARAS: Ascending Reticular Activating System Eye R ETICULAR FORMATION Input from touch, pain, and temperature receptors Input from ears
  • 7. ANATOMY OF THE CONSCIOUSNESS SYSTEM • STRUCTURES IN THE SYSTEM ARE: 1. PORTIONS OF THE BRAINSTEM RETICULAR FORMATION. 2. ASCENDING PROJECTIONAL SYSTEM 3. NON-SPECIFIC THALAMIC NUCLIE 4. DIFFUSE PROJECTIONS FROM THE NONSPECIFIC THALAMIC NUCLIE TO THE CORTEX. * 5. WIDESPREAD AREAS OF CEREBRAL CORTEX *FIRST FOUR COLLECTIVELY CALLED ARAS.
  • 8. LATERAL VIEW OF THE BRAIN SHOWING COMPONENTS OF THE CONSCIOUSNESS SYSTEM
  • 9. ASCENDING RETICULAR ACTIVATING SYSTEM (ARAS) • RETICULAR FORMATION: • COMPLEX AGGREGATE OF LARGE MULTIPOLAR AND SMALL ROUND NEURONS AND THEIR AXONS, DIFFUSELY DISTRIBUTED IN CLUSTERS THROUGHOUT THE CENTRAL TEGMENTAL PORTIONS OF THE BRAINSTEM. • EXTENDS FROM THE DECUSSATION OF THE PYRAMIDS IN THE MEDULLA TO THE THALAMUS.
  • 10. RETICULAR FORMATION: • FUNCTIONAL DIVISION: 1. LATERAL RECEPTIVE AREA: - RECEIVES COLLATERAL BRANCHES FROM ASCENDING SENSORY PATHWAYS. 2. MEDIAL PROJECTIONAL AREA: - FROM WHICH EFFERENT FIBERS ARISE.
  • 12. AFFERENT PATHWAYS 1. FROM ASCENDING TRACTS OF BOTH SOMATIC AND VISCERAL SENSORY SYSTEM. 2. FROM THE CORTEX: CORTICORETICULAR F., CORTICOBULBAR AND CORTICOSPINAL PATHWAYS. 3. CEREBELLUM, BASAL GANGLIA, THALAMUS, HYPOTHALAMUS, BRAINSTEM RETICULAR FORMATION. 4. VISCERAL EFFERENTS FRO SPINAL CORD AND CRANIAL NERVES.
  • 14. ASCENDING PROJECTIONAL SYSTEM • PROJECTS DIFFUSELY TO: 1. HYPOTHALAMUS 2. NONSPECIFIC NUCLIE OF THE THALAMUS
  • 15. NUCLIE OF THE THALAMUS 1. SPECIFIC NUCLIE: - ASSOCIATED WITH THE SENSORY AND MOTOR SYSTEMS AND WHICH CONNECT TO THE LOCALIZED AREAS OF CORTEX. 2. NONSPECIFIC NUCLIE: - RECEIVE AFFERENTS FROM THE RETICULAR FORMATION, THE CORTEX AND OTHER THALAMIC NUCLIE AND PROJECT TO ALL AREAS OF THE CORTEX VIA THE DIFFUSE THALAMIC PROJECTION SYSTEM.
  • 16. Figure 9-10: The diencephalon
  • 19. NONSPECIFIC NUCLIE OF THE THALAMUS
  • 20. NONSPECIFIC NUCLIE OF THE THALAMUS • COMPONENTS: 1. MIDLINE NUCLIE LOCATED NEAR THE MASSA INTERMEDIA. 2. INTRALAMINAR NUCLIE LOCATED ALONG THE INTERNAL MEDULLARY LAMINA (A BAND) OF MYELINATED FIBERS SEPARATING THE ANTERIOR, MEDIAL AND LATERAL THALAMIC NUCLIE. 3. RETICULAR NUCLIE LOCATED ON THE LATERAL MARGIN OF THE THALAMUS.
  • 21. DIFFUSE THALAMOCORTICAL PROJECTIONS OF THE CONSCIOUSNESS SYSTEM.
  • 23. RAPHE NUCLIE; SEROTONINERGIC NON-REM SLEEP LOCUS CERULEUS: NORADRENERGIC REM SLEEP NEUROTRANSMITTERS, BRAINSTEM NUCLIE AND SLEEP
  • 24. • Measures: EEG (electrophysiology)
  • 25. • Measures: EEG (electrophysiology)
  • 26. Brain Waves • Normal brain function involves continuous electrical activity • An electroencephalogram (EEG) records this activity • Patterns of neuronal electrical activity recorded are called brain waves • Each person’s brain waves are unique • Continuous train of peaks and troughs • Wave frequency is expressed in Hertz (Hz)
  • 27. EEG Hans Berger (first recorded human EEG, 1928) Different EEG-bands (by frequency) •Delta (0.5-4 Hz) - sleep •Theta (5-7 Hz) - drowsy •Alpha (8-12 Hz) - relaxed (eyes closed) •Beta (13-22 Hz) - active •Gamma (23-30 Hz) - very active
  • 28. Types of Brain Waves • Alpha waves – regular and rhythmic, low-amplitude, slow, synchronous waves indicating an “idling” brain • Beta waves – rhythmic, more irregular waves occurring during the awake and mentally alert state • Theta waves – more irregular than alpha waves; common in children but abnormal in adults • Delta waves – high-amplitude waves seen in deep sleep and when reticular activating system is damped
  • 29. • Measures: EEG Actively awake: beta and gamma Passively awake: alpha Drowsy: theta Light slow save sleep Deep slow save sleep
  • 30. Types of Brain Waves Figure 12.20b
  • 31. Giuseppe Moruzzi and Horace Magoun (1949)
  • 32. EXPERIMENT BY MORUZZI AND MAGOUN ON CATS: BRAINSTEM TRANSECTIONS AT DIFFERENT LEVELS SHOWING WAKEFULNESS, SLEEP AND COMATOSE STATES
  • 33.
  • 35. EVALUATION OF PATIENTS IN STUPOR AND COMA PARAMETERS: 1. LEVEL OF CONSCIOUSNESS 2. RESPIRATORY PATTERN 3. PUPILLARY SIZE AND REACTION TO LIGHT 4. OCULOCEPHALIC REFLEX (DOLL’S EYES) 5. MOTOR RESPONSES
  • 36. EVALUATION OF PATIENTS IN STUPOR AND COMA PARAMETERS: 1. LEVEL OF CONSCIOUSNESS • AWAKE • DROWSY • LETHARGIC • STUPUROUS • COMATOSE * DESCRIBE STIMULUS GIVEN AND THE RESPONSE OF THE PATIENT.
  • 37. EVALUATION OF PATIENTS IN STUPOR AND COMA PARAMETERS: 2. RESPIRATORY PATTERN LEVEL - CHEYNE-STOKES RESPIRATION DIENCEPHALIC/ DIFFUSE CEREBRAL - CENTRAL NEUROGENIC HYPERVENTILLATION MIDBRAIN - APNEUSTIC BREATHING PONS - ATAXIC / CLUSTER BREATHING MEDULLA
  • 38. RESPIRATORY PATTERNS IN STUPOR AND COMA (rostral caudal progression)
  • 39. EVALUATION OF PATIENTS IN STUPOR AND COMA PARAMETERS: 3. PUPILLARY SIZE AND REACTION TO LIGHT
  • 41. PUPILS IN COMATOSE PATIENTS
  • 42. EVALUATION OF PATIENTS IN STUPOR AND COMA PARAMETERS: 4. OCULOCEPHALIC REFLEX (DOLL’S EYES PHENOMENON) - TESTS INTEGRITY OF THE BRAINSTEM*
  • 44. EVALUATION OF PATIENTS IN STUPOR AND COMA PARAMETERS: 5. MOTOR RESPONSES: - ABSENT - PRESENT - WEAK (PARESIS) - ABNORMAL: * DECEREBRATE RIGIDITY * DECORTICATE RIGIDITY
  • 48. EVALUATION OF STUPOR AND COMA DECORTICATE RIGIDITY
  • 49. EVALUATION OF STUPOR AND COMA DECEREBRATE RIGIDITY
  • 50. The COMATOSE PATIENT: NEUROPHYSIOLOGY • Consciousness requires: • An intact pontine reticular activating system • An intact cerebral hemisphere, or at least part of a hemisphere • Coma requires dysfunction of either the: • Brainstem ascending reticular activating system (ARAS), or • Bihemispheric cerebral dysfunction
  • 51. PATHOPHYSIOLOGY OF COMA • A conscious state depends on intact cerebral hemispheres, interacting with the ARAS in the brainstem , midbrain, hypothalamus and hypothalamus. • Lesions diffusely affecting the cerebral hemispheres, or directly affecting the ARAS cause impairment of conscious level.
  • 52. The Comatose Patient Classifications • Supratentorial lesions cause coma by either widespread bilateral disease, increased intracranial pressure, or herniation. • Infratentorial lesions involve the RAS, usually with associated brainstem signs • Metabolic coma causes diffuse hemispheric involvement and depression of RAS, usually without focal findings • Psychogenic Plum and Posner, 1982
  • 53. Supratentorial Mass Lesions • Hematoma • Neoplasm • Abscess • Contusion • Vascular Disease • Diffuse Axonal Damage
  • 54. Supratentorial Mass Lesions PATHOPHYSIOLOGY • Altered consciousness is based on • Increased intracranial pressure • Herniation • Diffuse bilateral lesions
  • 55. Supratentorial Mass Lesions Differential Characteristics •Initiating signs usually of focal cerebral dysfunction •Signs of dysfunction progress rostral to caudal •Neurologic signs at any given time point to one anatomic area - diencephalon, midbrain, brainstem •Motor signs are often asymmetrical Plum and Posner, 1982
  • 56. Herniation Syndromes •Central herniation Rostral caudal progression of respiratory, motor, and pupillary findings May not have other focal findings •Uncal herniation Rostral caudal progression CN III dysfunction and contralateral motor findings
  • 58. Infratentorial Lesions • Cause coma by affecting reticular activating system in brainstem • Brainstem nuclei and tracts usually involved with resultant focal brainstem findings
  • 59. Infratentorial Mass Lesions Differential Characteristics • History of preceding brainstem dysfunction or sudden onset of coma • Localizing brainstem signs precede or accompany onset of coma and always include oculovestibular abnormality • Cranial nerve palsies usually present • “Bizarre” respiratory patterns common, usually present at onset of coma Plum and Posner, 1982
  • 60. Infratentorial Lesions Causes of Coma • Neoplasm • Vascular accidents • Trauma • Cerebellar hemorrhage • Demyelinating disease • Central pontine myelinolysis (rapid correction of hyponatremia)
  • 61. Metabolic Coma Differentiating Features • Confusion and stupor commonly precede motor signs • Motor sings are usually symmetrical • Pupillary reactions are usually preserved • Asterixis, myoclonus, tremor, and seizures are common • Acid-base imbalance with hyper- or hypoventilation is frequent Plum and Posner, 1982
  • 62. Metabolic Coma Etiologies • Respiratory – Hypoxia – Hypercarbia • Electrolyte – Hypoglycemia – Hyponatremia – Hypercalcemia • Hepatic encephalopathy • Severe renal failure • Infectious – Meningitis – Encephalitis • Toxins, drugs
  • 63. PATHOPHYSIOLOGY OF COMA • DIFFUSE CEREBRAL DAMAGE: – e.g. metabolic encephalopathy: hepatic or renal failure, hypoglycemia, demyelinating disease • SUPRATENTORIAL MASS causing – transtentorial herniation and midbrain compression: e.g. tumor, hematoma, abscess • INFRATENTORIAL LESIONS: – brainstem compression and direct brainstem involvement. e.g. ischemia, hemorrhage, tumor
  • 64. CAUSES OF COMA AND IMPAIRED CONSCIOUS LEVEL • INTRACRANIAL: – TRAUMA: diffuse white matter injury; hematoma- extradural, subdural, “burst lobe” – NEOPLASTIC: primary vs metastatic – VASCULAR: subarachnoid hemorrhage, intracerebral hematoma, massive cerebral infarct, brainstem ifarction or hemorrhage – INFECTIOUS: meningitis, encephalitis, abscess – OTHERS: epilepsy, hydrocephalus
  • 65. CAUSES OF COMA AND IMPAIRED CONSCIOUS LEVEL • EXTRACRANIAL : – METABOLIC/ENDOCRINE: renal, hepatic failure, electrolyte imbalance, hypoglycemia, diabetic ketoacidosis, adrenal crisis, hypothyrodism, etc. – RESPIRATORY INSUFFICIENCY: hypoventillation, diffusion deficiency, perefusion deficiency – DECREASED CARDIAC OUTPUT: e.g. myocardial infarction, arrhythmias, hypotensive drugs – DRUGS/TOXINS: sedatives, opiates, antidepressants, antipsychotics, anticonvulsants, anesthetics, alcohol, carbon monoxide
  • 66. PSYCHOGENIC CAUSES • HYSTERIA • CATATONIA (mutism with deceased motor activity) • FUGUE STATES
  • 67. DIAGNOSTIC CLUES • HISTORY POSSIBLE CAUSE Head injury --------- ---------------- --Diffuse shearing injury or intracranial hematoma Previous head injury (eg 6 wks) ----Subdural hematoma Sudden collapse ----------------------- Intracerebral/subarachnoid hemorrhage Limb twitching, incontinence ------- Epilepsy, post ictal state Gradual development of symptoms -- Mass lesions, metabolic or infective cause
  • 68. DIAGNOSTIC CLUES • HISTORY POSSIBLE CAUSE Previous Illness Diabetes ---------------- ----- Hypo/Hyperglycemia Epilepsy ---------------------- Postictal state Psychiatric Illness ----------- Drug overdose Alcoholism/ Drug Abuse ---- Drug toxicity Viral Infection ---------------- Encephalitis Malignancy ------------------ Intracranial metastasis
  • 69. Management of the Comatose Patient Disability - Neurologic • Glasgow coma scale – Provides easily reproducible and somewhat predictive basic neurologic exam – This allows rapid assessment and record of baseline neurologic status – Allows physician to track neurologic changes over time and multiple examiners
  • 70. Glasgow Coma Scale • Three components. Score derived by adding the score for each component. • Eye opening (4 points) • Verbal response (5points) • Best motor response (6 points)
  • 71. Glasgow Coma Scale • Eye opening • 4 - spontaneous • 3 - to speech • 2 - to pain • 1 - none • Verbal Response • 5 - oriented • 4 - confused conversation • 3 - inappropriate words • 2 - incomprehensible sounds • 1 - none • Best Motor Response • 6 - obeys • 5 - localizes • 4 - withdraws • 3 - abnormal flexion • 2 - abnormal extension • 1 - none
  • 72. LEARNING OBJECTIVES: • Consciousness system: – Definition – Anatomy: Role of ARAS, Thalamus, Cerebrum – Experiments by Morozzi and Magoun – Brain waves, Neurotransmitters – Evaluation of Stupor and Coma – Pathophysiology and Etiologies of Coma – Diagnostic Clues
  • 74.
  • 75.
  • 76.
  • 77.
  • 78.
  • 79. Identify/ fill in the blank • 1. RAS stands for ____ _____ ______.
  • 80. Identify/ fill in the blank • 1. RAS stands for ____ _____ ______. • 2. The RAS is located in the ____ of the brainstem.
  • 81. Identify/ fill in the blank • 1. RAS stands for ____ _____ ______. • 2. The RAS is located in the ____ of the brainstem. • 3. The lowest portion of the RAS is located in the junction of _____ level of the brainstem and the cervical spinal cord.
  • 82. • 4. The RAS will have connection with the _____ nuclie of the thalamus. (Specific or Non-specific?)
  • 83. • 4. The RAS will have connection with the _____ nuclie of the thalamus. (Specific or Non-specific?) • 5. The nuclie of the thalamus will send impulses to the diffuse areas in the _____ cortex.
  • 84. • 6. Transection of the brainstem at the midbrain level will cause persistent ______. (sleep or wakefulness.)
  • 85. • 6. Transection of the brainstem at the midbrain level will cause persistent ______. (sleep or wakefulness.) • 7.Transection of the midpontine level of the brainstem will cause persistent _____. (sleep or wakefulness.
  • 86. • 8. Pinpoint pupils, apneustic breathing are findings indicative of a lesion in what level of the brainstem?
  • 87. • 8. Pinpoint pupils, apneustic breathing are findings indicative of a lesion in what level of the brainstem? • 9. Dilated irregular pupils, ataxic or cluster breathing are findings indicative of a lesion in what level of the brainstem?
  • 88. • 10. Brain waves are measured by an ancillary procedure called the ____.