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NATESAN D
Consciousness
State of consciousness
Alert: Normal state of arousal Lethargy: responds-to verbal stimuli although slow and inappropriate. Stupor: the subject can be aroused only by vigorous and repeated noxious stimuli. Coma: unarousablely unresponsive.
Coma mimics
y Psychogenic unresponsiveness y Locked in syndrome y Akinetic mutism y Catatonia y Persistent vegetative state
Coma Pathophysiology
Coma Pathophysiology
y Coma implies dysfunction of: Ascending Reticular Activating System or Both hemi-cortices y Anatomically, this means central brainstem structures (bilaterally) from caudal medulla to rostral midbrain both hemispheres
Classifications
y Supratentorial lesions cause coma by either widespread bilateral disease, increased intracranial pressure, or herniation. y Infratentorial lesions involve the RAS, usually with associated brainstem signs y Metabolic coma causes diffuse hemispheric involvement and depression of RAS, usually without focal findings y Psychogenic
Plum and Posner, 1982
Supratentorial Lesions
y Epidural or Subdural
Pathophysiology
y Altered consciousness is based on
Increased intracranial Herniation Diffuse bilateral
pressure
lesions
Herniation syndromes
1. 2. 3. 4. 5. 6.
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
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
Breathing in coma
y Forebrain Post hyperventilation apnea Cheyne stoke respiration y Hypothalamus midbrain Central neurogenic hyperventilation
Breathing in coma
y Lower pontine tegmentum Apneustic breathing Cluster breathing Short cycle periodic breathing Ataxic breathing y Medulla Ataxic breathing Slow regular respiration Gasping (terminal)
Posture
y Cerebral
hemisphere
Decorticate posture Diagonal posture
y Diencephalon
supratentorial
y Upper brain stem Decerebrate posture y Pontine Abnormal ext arm Weak flexion leg y Medullary Flaccidity
PUPIL
Diencephalic (metabolic) Midbrain tectal Midbrain nuclear 3rd nerve Pontine Opiate Organophosphorus Atropine
Small reactive Midsize,fixed Irregular pear shaped Fixed widely dilated Pinpoint reactive Pinpoint Small Wide dilated
The pupils usually are symmetrical in coma from toxic-metabolic causes. Patients with metabolic or toxic encephalopathies often have small pupils with preserved reactivity. Exceptions
- methyl alcohol poisoning: dilated and unreactive pupils - Late toxic or metabolic coma(terminal asphyxia) the pupils dilate initially and then become fixed at midposition within 30 minutes
metabolic insult and usually is spared in coma from drug intoxication or metabolic causes, even when other brainstem reflexes are absent.
y Exceptions Hypothermia may fix pupils severe barbiturate intoxication may fix pupils neuromuscular blocking agents produce midposition or small pupils glutethimide and atropine dilate pupils
Infratentorial Lesions
y Cause coma by affecting reticular activating
system in pons y Brainstem nuclei and tracts usually involved with resultant focal brainstem findings
Infratentorial Lesions
Causes of Coma
y Basilar artery y
y y y
Differential Characteristics
y History of preceding brainstem dysfunction or
sudden onset of coma y Localizing brainstem signs precede or accompany onset of coma and always include oculovestibular abnormality y Cranial nerve palsies usually present y Bizarre respiratory patterns common, usually present at onset of coma
Plum and Posner, 1982
Ocular motility
metabolic coma
y Exceptions: rarely in phenobarbital or phenytoin intoxication .
frontal/pontine damage
Conjugate
Dysconjugance suggests
CN abn.
Moving
Roving, dipping, bobbing
Eye movement
y Metabolic Roving eye movement, Oculocephalic, Vestibuloocular y Supratentorial Contralateral conjugate palsy y Thalamus Upper turn down
y Midbrain Ipsilateral 3rd cranial nerve paresis y Pontine Ipsilateral 6th cranial nerve paresis Ipsilateral gaze palsy One and half syndrome Bilateral gaze palsy Ocular bobbing
Eye movements
y Oculocephalic reflex Eye response to head turning Proprioception from the neck triggers the pontine conjugate eye center
Eye movements
y Oculovestibular reflex Eye response to cold water on the tympanic membrane Horizontal semicircular canal stimulation triggers the pontine conjugate eye center
Caloric reflex
y Ensure TM integrity y Elevation of head to 30
degrees (so that lateral semicircular canal is vertical) y Instillation of up to 10 ml of ice water
Both ears, cold waterdownward gaze Both ears, warm waterupward gaze
ear
Metabolic Coma
Etiologies
y Respiratory
Hepatic
y Electrolyte
Toxins,
drugs
Metabolic Coma
Differentiating Features
y Confusion and stupor commonly precede motor y y y y
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
medications, or the setting in which they are found. y The response to initial emergency therapy may help differentiate metabolic or toxic causes of coma y Structural lesions have focal features or at least notable asymmetry on neurological examination. Toxic, metabolic, and psychiatric diseases are characterized by their symmetry
milder alterations in arousal, typically with waxing and waning of the behavioral state
y Patients with acute structural lesions tend to stay
of arousal
Causes of Coma
More than half of all cases of coma are due to metabolic brain dysfunction (Almost half of these are drug poisonings)
Causes of Coma
supratentorial (44/101 ICH) 65 subtentorial lesions (40/65 brainstem infarcts) 326 diffuse or metabolic brain dysfunction
149
drug intoxication
o Brief history & examination o I.V. line & sampling o Treat reversible causes of coma
supplemental oxygen intravenous thiamine (at least 100 mg) intravenous 50% dextrose in water (25 g) Naloxone hydrochloride intravenously, (0.4 to 2.0 mg) o Treatment of ICP until surgical intervention is possible. o Comprehensive history and secondary examination
Airway
y Intubate anyone who will let you y Any of the following are adequate criteria
o o o o o
GCS < 9 Airway not secure or open Breathing not adequate Any significant respiratory failure Uncertainty regarding direction or rate of mental status changes, particularly if constant observation not available (during CT scans, etc..)
Circulation
y Is patient in shock?
Check pulses, heart rate, blood pressure, perfusion Remember hypotension is late sign of shock Bradycardia and Hypertension can be sign of raised intracranial pressure.
Disability - Neurologic
y Glasgow coma scale Provides easily reproducible Allows rapid assessment and record of baseline neurologic status Allows physician to track neurologic changes over time and multiple examiners
y Verbal Response
Secondary Survey
y Do a quick general exam of the entire body to
identify acute life threatening conditions y Only very rarely is acute neurosurgical intervention appropriate before other acute life threatening injuries are stabilized
Neurologic Examination
Secondary Survey
Posner et al (2008), the key components of the
neurological examination of the comatose patient are:
y level of consciousness (GCS) y the pattern of breathing y size and reactivity of the pupils y eye movements and oculovestibular responses y motor responses (tone, reflexes and posturing)
ABNORMAL FINDINGS Symmetric tone and response (flexor or extensor) to pain Myoclonus (possible) Periodic cycling of breathing
Supratentorial mass Ipsilateral 3rd cranial nerve palsy with unilateral dilated compressing the fixed pupil and oculomotor paresis brain stem Contralateral homonymous hemianopia and absent blinking response to visual threat Contralateral hemiparesis Brain stem lesion Early abnormal pupillary and oculomotor signs Abnormal oculocephalic & oculovestibular reflex Asymmetrical motor responses Decorticate rigidity (usually due to an upper brain stem lesion) or decerebrate rigidity (usually due to a bilateral midbrain or pontine lesion) Hyperventilation (due to a midbrain or upper pontine lesion) Spontaneous, conjugate roving eye movements in mild coma Fixed eye position in deeper coma Abnormal oculovestibular reflex Decorticate and decerebrate rigidity or flaccidity
Toxic-metabolic dysfunction
1. Any evidence of brainstem abnormality 2. Any evidence of rostral caudal progression 3. Any focal deficits 4. Progression of motor exam from withdrawal to posturing
lesion less likely than metabolic cause y Mass lesion still possible, though - CT scan y Urgency of intubation less but should consider
Will patient deteriorate, particularly while out of constant observation (CT scanner)? Can patient protect airway?
Coma mimics
y Psychogenic unresponsiveness y Locked in syndrome y Akinetic mutism y Catatonia y Persistent vegetative state
Akinetic Mutism
y Silent, immobile but alert appearing y Usually due to lesion in bilateral mesial frontal lobes,
Locked-In Syndrome
y Infarction of basis pontis (all descending motor
fibers to body and face) y May spare eye-movements y Often spares eye-opening and vertical movements y EEG is normal or shows alpha activity
Catatonia
y Symptom complex associated with severe
Mutism with marked decrease in motor activity can also be seen in organic brain disease: encephalitis, toxic and drug-induced psychosis
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