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Define consciouness

Total awareness of self and environment
-arousal: level of alertness, ability to interact with environment
-awareness (content): sum of cognitive mental functions, "know what's going on"


Describe consciousness and brain structures

Depends on arousal of cerebral cortex by brainstem ascending reticular activating system (ARAS)
-input from many sensory systems
-projects to hypothalamus, thalamus, cortex


What does impaired consciousness mean?

Diffuse or bilateral impairment of both cerebral hemispheres
Failure of brainstem ARAS


Define confusion

Attention deficit, orientation disturbed, stimuli misinterpreted


Define delirium

Disorientation, stimuli misinterpreted, hallucinations (visual)


Define obtundation

Mental blunting, increased sleep, arouses to mild stimuli (voice)


Define stupor

Arouses only to noxious stimuli and not environmental, only rudimentary awareness (purposeful motor responses)


Define coma

Unarousable, unresponsive, unaware


Describe persistent vegatative

no reproducible response to stimuli, eyes may be open, roving eye movements, BP/pulse stable


Describe akinetic mutism

Appears +arousal
(-) awareness
No spontaneous motor activity


Describe locked in state (Monte Cristo Syndrome)

Normal sensation/cognition but complete paralysis except for vertical eye movements


Describe psychogenic state

+/altered arousal
+/altered changing/inconsistent physical examination


What does assessment of comatose patient include?

General medical exam
Neurological exam
Laboratory evaluation
Diagnosis and treatment


Describe history of comatose pt

From family, EMTs, witnesses
How and when pt was found
Sudden or gradual onset
Prior illnesses (esp vascular) and medications
Any recent symptoms (fever, confusion)
History of substance abuse


Describe general exam of comatose pt

Vital signs (resp rate and pattern)
Breath odor
Signs of trauma: raccoon eyes, battle sign, CSF leak (otorrhea, rhinorrhea)
Neck stiffness: meningitis, SAH


Describe considerations for hyper/hypotension and hyper/hypothermia in comatose pt

Hypertension: pheochromocytoma, drugs (amphetamine, cocaine, phenyclidine), increased ICP, PRES

Hypotension: Addison's, sepsis, drugs (Beta-blocker, Ca chanel blocker, TCA's, Li, sedatives, organophosphates, opioids, methanol), progression to brain death

Hyperthermia: infection, heat stroke, drugs (amphetamines, TCA's cocaine, salicylates, neuroleptics), serotonin syndrome, central (pontine hemorrhages)

Hypothermia: hypothyroid, hypoglycemia, exposure, drugs (opioids, sedatives, barbiturates, phenothiazine, Et-OH)


Describe skin considerations in comatose pt

Diaphoresis: thyroid storm, decrease BS, drugs (sympathomimetics, cholinergics)
Dry: hypothyroid, drugs (anticholinergics, TCAs)
Acne: long term antiepileptic use
Butterfly rash: systemic lupus
Dark pigmentation: Addison's disease
Cold, puffy, yellowish: Myxedema coma
Edema: acute hepatic or renal failure
Purpura: meningococcal meningitis, TTP, DIC, vasculitis, aspirin OD
Rash: meningitis, viral encephalitis, rickettsia
Needle marks: Drug OD


Describe breath odor considerations in comatose pt

Dirty restroom: uremia
Fruity: ketoacidosis
Musty: hepatic failure
Onion: paraldehyde (rarely used anymore to treat seizures)
Garlic: organophosphates (insecticides, herbicides, sarin)


What is the purpose of neurological examination of comatose pt?

1. Determine location and nature of process that is causing impaired consciousness with emphasis on anatomic level of brain involvement (supratentorial, subtentorial, or diffuse)
2. Narrow differential possibilities


What broad category of lesions produce coma?

1. Large, pressure producing supratentorial mass lesions
-cause dysfunction in upper ARAS
-cause downward herniation of brain to compress ARAS
2. Infratnetorial mass lesions that involve brainstem
3. Diffuse or multifocal brain disease


Describe unilateral hemisphere (mass effect) supratentorial causes of coma

Intracerebral hemorrhage
Large MCA infarct
Subdural hematoma
Epidural hematoma
Brain abscess


Describe bilateral hemisphere supratentorial causes of coma

Subarachnoid hemorrhage
Multiple infarcts
Venous thrombosis
Cerebral edema
Acute hydrocephalus
Multiple metastases


What are subtentorial causes of coma?

Pontine hemorrhage
Basilar artery occlusion
Central pontine myelinolysis
Cerebellar hemorrhage/infarct
Cerebellar/brainstem neoplasm
Cerebellar abscess


What are diffuse causes of coma?

Hyperglycemia (nonketotic)
Acute hypothyroidism
Heptaic failure
Malignant hypertension
Drug intoxication
Drug withdrawal
Malignant neuroleptic syndrome
Seizures (esp status epilepticus)


What are the essential and nearly-essential elements of the neuro exam of comatose pt?

Pupillary responses
Corneal reflex
Extraocular movements
Cough/gag reflex
Motor responses
Respiratory pattern

Neck stiffness
Carotid auscultation
Funduscopic examination

All of these should be performed in stepwise manner


Describe pupillary responses

1. Sympathetic/parasympathetic balance determines size
-sympathetic path: hypothalamus->lower cervical cord->sympathetic chain->superior cervical ganlgion->up carotid a. To CN V(I), long ciliary nerve (dilator), Mueller's muscle
-parasympathetic path: upper midbrain (Edinger Westfall nucleus)->CNIII->ciliary ganglion->short ciliary nerve (constrictor)

2. Nuclei/tracts controlling pupils are anatomically adjacent to ARAS. Therefore, absent or unequal responses imply brainstem lesion


With anisocoria: which is the abnormal pupil?

Rule of thumb:
If it's the large pupil, it should fail to constrict to light.
If it's the small pupil, it should fail to dilate in dark


Describe the rules of thumb for pupillary responses

Enlarged on one side: parasympathetic dysfunction (usually CNIII)
Enlarged bilaterally: bilateral CNIII lesion, post ictal, barbiturate intox
Constricted: sympathetic dysfunction (hypothalamus, carotid)
Pinpoint: pontine lesion, opiates pilocarpine
-Three P's of pinpoint pupils: Pontine lesion, oPiates, Pilocarpine
Midposition and unreactive: sympathetic and parasympathetic (midbrain)


Interpretation of pupillary signs may be confused by what?

Atropine/scopolamine: dilated, fixed
Opiates: pinpoint, +/- reactive
Pilocarpine: pinpoint
Glutethimide: dilated, fixed, unequal
Hypothermia, anoxia, ischemia: possible dilated, fixed, unequal


Describe extraocular movements in neuro exam of comatose pt

Conjugate gaze depends on intact CN III, IV, and VI, their nuclei, and interconnections
Frontal gaze centers deviates eyes to opposite side
Pontine gaze centers deviate eyes to same side


Describe spontaneous roving extraocular movements

Conjugate: implies brainstem intact
Dysconjugate: implies brainstem lesion


Describe spontaneous conjugate deviation at rest of extraocular movements

Hemispheric lesion:
Destructive: toward lesion
Irritative: away from lesion

Brainstem lesion
Destructive: away from lesion


Describe the types of nystagmus and indicated lesions

Ping-pong (right-left deviation every few seconds): bihemispheric, midbrain

Convergence (slow abduction with rapid jerk back): mesencephalon

Retractory (retraction orbit): mesencephalon

Bobbing (rapid down, slow up): pons

Dipping (slow down, rapid up): bihemispheric


Describe oculocephalic maneuver (Doll's eyes)

Tests mid-pons
Used to assess CN III, IV, and VI

Passive horizontal head rotation: eyes move horizontally opposite
Passive vertical head rotation: eyes move vertically opposite

Be sure neck is stable
Overridden in alert patient


Describe Caloric (oculovestibular) reflex

Lower pons
Otoscopic exam: be sure canal clear and TM intact
Irrigate TM with cold (usually) or warm water

Cold water irrigation with intact brainstem causes:
Eyes to deviate to irrigated side if unilateral irrigation
Eyes to deviate downward if bilateral irrigation


Describe motor responses in neuro exam of comatose pt

Purposeful: follows commands, localizes pain

-decorticate: arms flexed, and legs extended (hemispheric)
-decerebrate: all extremities extended (brainstem)
-flaccid: pontomedullary or metabolic


Describe respiratory patterns in comatose pt

Cheynes-Strokes: hyperpnia regularly alternating with apnea (bilateral hemispheres or diencephalon). Seen in many disorders ranging from metabolic to structural

Central neurogenic hyperventilation: midbrain

Apneustic breathing: long inspiration followed by apnea (mid/low pons). Seen in structural lesions and anoxia, hypoglycemia, meningitis

Ataxic: completely irregular (medullary respiratory centers)


Describe supratentorial mass lesions

Initial signs usually focal
Neurological signs at any given time point to one anatomic location
Progression of signs is rostral to caudal
Motor signs are often asymmetric


Describe herniation syndromes

Caused by expanding supratentorial mass lesions
Effect is to displace brain tissue into adjacent intracranial compartments (so called rostral to caudal progression of herniation)


Describe uncal transtentorial herniation

Herniation of uncus under edge of tentorium, compressing CN III (ipsilateral dilated pupil, poor EOM, ptosis), then contralateral brainstem (ipsilateral hemiparesis), then respiratory abnormalities, posturing, fixed pupils, and death


Describe central transtentorial herniation

Herniation into foramen magnum leads to early coma, small pupils, normal EOMs, posturing and later bilateral fixed pupils, respiratory arrest, and death


Describe cingulate gyrus herniation

Herniates under falx


Describe subtentorial mass lesions

History: preceding brainstem dysfunction usual (disequilibrium, dysarthria, dysphagia, diplopia, vertigo) but may be sudden onset of coma

Localizing brainstem signs precede or accompany onset of coma and almost always include a form of oculovestibular abnormality

Cranial nerve palsies usually present

Bizarre respiratory patterns common


Characterize diffuse/metabolic coma

Confusion and stupor commonly precede motor signs
Motor signs are usually symmetrical
Pupillary reactions are usually preserved
Asterixis, myoclonus, tremor, seizures common
Acid-base imbalance with hyper or hypoventilation frequently seen
Level of consciousness may fluctuate


Describe global cerebral ischemia

Occurs whenever blood flow is inadequate to meet metabolic requirements (oxygen and glucose) of brain, as in cardiac or pulmonary arrest

Result is spectrum of disorders, ranging from reversible encephalopathies to brain death


Describe brief (

Commonly reversible encephalopathies, generally after 12 hours or less of stupor or coma
Anteograde and/or retrograde amnesia can occur
Recovery often occurs within 7-10 days but may be delayed by 1 month or longer


Describe prolonged ischemic episodes

Focal cerebral dysfunction
Patients are usually comatose for at least 12 hours and may have lasting focal or multifocal motor, sensory, and cognitive deficits


Describe persistent vegetative state

Awake but functionally decorticate and unaware of surroundings
Eye opening, eye movements, sleep-wake cycles, and brainstem and spinal reflexes may remain intact


What does the definition of brain death imply?

Complete cessation of brain function (including respirations but not heartbeat)


Describe irreversibility of brain death

Cause of coma should be known. Must be adequate to explain clinical picture and must be irreversible
Sedative intoxication, hypothermia (≤ 90F), neuromuscular blockade, and shock must be ruled out, since these conditions can produce a clinical picture that resembles brain death but are potentially reversible.


Describe cessation of brain function

Unresponsiveness: pt must be unresponsive to all sensory input, including pain and speech

Absent brainstem reflexes: including pupillary, corneal, oculocephalic, and oculovestibular reflexes. Respiratory response are absent at 8 to 10 minutes after pt's pCO2 is allowed to rise to 60 mm Hg, while oxygenation is maintained with 100% O2 (apnea test)


Describe persistence of brain death

Criteria for brain death must persist for an appropriate length of time
Six hours with a confirmatory isoelectric (flat) EEG, performed according to technical standards of AEES
Twelve hours without confirmatory isoelectric EEG
Twenty-four hours for anoxic brain injury without a confirmatory isoelectric EEG


Describe precautionary notes about brain death

State law may impose additional requirements such as
-qualification of examiner
-confirmation by second examiner

Ancillary tests (EEG, angiography, nuc med scan) are not required unless there is uncertainty about diagnosis or apnea test cannot be performed. However, some countries do require them.


Describe the initial steps for management of comatose patient

A: Insure pt airways (spontaneous, mouth piece, ETT)
B: insure breathing and adequate oxygenations (pulse oxy, O2, ABG)
C: Insure adequate ciruclation and control any active bleeding (BP, P)-IV line, arterial line, ECG
Stabilize neck, get C-spine films if trauma suspected
Quick history (seizure, meds, drug use, trauma)
Quick exam
EKG to monitor for arrhythmias
Give glucose (1 amp=25gms), thiamine (100 mg IM)
Give specific antidote (Narcan)
Adjust body temperature
Control agitation
Stop seizures if present


Describe laboratory evaluation of comatose pt

Venous blood: glucose, electrolytes (including calcium, phosphorus, magnesium), BUN/creatinine, osmolality, drug screen, liver functions, ammonia, coagulation studies, thyroid function, blood cultures
Arterial blood: pH, pO2, pCO2, HCO3, HbCO
Urine: UA, culture, drug screen
If febrile: blood cultures
If stiff neck: LP (after CT) with CSF for cell count, glucose, protein, gram stain, cultures (bacterial, viral, and fungal)


Describe diagnostic testing

Noncontrast head CT
-acute blood
-space occupying lesion

-xanothochromia (SAH)

+/- MRI
-posterior fossa
-early infarct

+/- EEG


What are specific interventions for comatose pt?

Reduce elevated intracranial pressure
-elevate head of bed
-Intubate and hyperventilate to PCO2 of 20 mm
-use mannitol for ischemic lesions
-use decadron for tumor, abscess, and perhaps cerebral hemorrhage
-Lasix 20-40 mg IV possibly

Treat seizures
-lorazepam 2 mg IV q10-15 min up to 10 mg total
-phenytoin 18 mg/kg load (about 1000 mgs) then 300 mg/day


Describe Glasgow Coma Scale 3-15

Eye opening:
Never: 1
To pain: 2
To verbal: 3
Spontaneous: 4

Best verbal response:
None: 1
Sounds: 2
Inapp words: 3
Disoriented; 4
Oriented: 5

Best motor response
None: 1
Extensor: 2
Flexor: 3
Withdrawal: 4
Localizes: 5
Obeys: 6

Sum and individual elements are important: eg GCS = 9, E2, V3, M5