12.1. General information
Consciousness has two components: arousal and content. Impairment of arousal can vary from mild (drowsiness or somnolence), to obtundation, to stupor to coma. Coma is the severest impairment of arousal, and is defined as the inability to obey commands, speak, or open the eyes to pain.
The Glasgow Coma Scale (GCS) is shown in Table 12-1 (note: the scale is used to assess level of consciousness and is not designed for following neurologic deficits). Some centers record a “T” next to the total score for patients whose verbal axis cannot be assessed because of intubation2. 90% of patients with GCS ≤ 8 and none with GCS ≥ 9 meet the above definition of coma. Thus, GCS ≤ 8 is a generally accepted operational definition of coma.
A scale for use in children is shown in Table 12-23.
Coma results from one or more of the following:
• dysfunction of high brainstem (central upper pons) or midbrain
• bilateral diencephalic dysfunction
• diffuse lesions in both cerebral hemispheres (cortical or subcortical white matter)
POSTURING
The following terms are inaccurate in the implication of the location of the lesion. Decorticate posturing implies a more rostral lesion and prognosis may be better.
Decorticate posturing: Classically attributed to disinhibition by removal of corticospinal pathways above the midbrain.
Overview: abnormal flexion in UE and extension in LE.
Detail: slow flexion of arm, wrist and fingers with adduction in the UE. Extension, internal rotation, plantarflexion in LE.
Decerebrate posturing: Classically attributed to disinhibition of vestibulospinal tract (more caudal) and pontine reticular formation (RF) by removing inhibition of medullary RF (transection at intercollicular level, between vestibular and red nuclei).
Overview: abnormal extension in UE and LE.
Detail: opisthotonos (head and trunk extended), teeth clenched, arms extended, adducted and hyperpronated (internally rotated), wrists flexed, fingers flexed. Legs extended and internally rotated, feet plantarflexed and inverted, toes plantarflexed.
ETIOLOGIES OF COMA
TOXIC/METABOLIC CAUSES OF COMA
1. electrolyte imbalance: especially hypo- or hypernatremia, hypercalcemia, renal failure with elevated BUN & creatinine, liver failure with elevated ammonia
2. endocrine: hypoglycemia, nonketotic hyperosmolar state, DKA (diabetic ketoacidosis, AKA diabetic coma), myxedema coma, Addisonian crisis (hypoadrenalism)
3. vascular: vasculitis, DIC, hypertensive encephalopathy (see page 73)
4. toxic: EtOH, drug overdose (including narcotics, iatrogenic polypharmacy, barbiturates), lead intoxication, carbon monoxide (CO) poisoning, cyclosporine (causes an encephalopathy that shows white-matter changes on MRI that is often reversible with discontinuation of the drug)
5. infectious/inflammatory: meningitis, encephalitis, sepsis, lupus cerebritis, neurosarcoidosis (see page 71), toxic-shock syndrome
6. neoplastic: leptomeningeal carcinomatosis, rupture of neoplastic cyst
7. nutritional: Wernicke’s encephalopathy, vitamin B12 deficiency
8. inherited metabolic disorders: porphyria, lactic acidosis
9. organ failure: uremia, hypoxemia, hepatic encephalopathy, Reye’s syndrome, anoxic encephalopathy (e.g. post-resuscitation from cardiac arrest), CO2 narcosis
10. epileptic: status epilepticus (including non-convulsive status), post-ictal state (especially with unobserved seizure)
STRUCTURAL CAUSES OF COMA
1. vascular:
A. bilateral cortical or subcortical infarcts (e.g. with cardioembolism due to SBE, mitral stenosis, A-fib, mural thrombus…)
B. occlusion of vessel supplying both cerebral hemispheres (e.g. severe bilateral carotid stenosis)
C. bilateral diencephalic infarcts: well described syndrome. May be due to occlusion of a thalamo-perforator supplying both medial thalamic areas or with “top-of-the-basilar” occlusion. Initially resembles metabolic coma (including diffuse slowing on EEG), patient eventually arouses with apathy, memory loss, vertical gaze paresis
2. infectious: abscess with significant mass effect, subdural empyema, herpes simplex encephalitis
3. trauma: hemorrhagic contusions, edema, hematoma (see below)
4. neoplastic: primary or metastatic
5. herniation from mass effect: presumably brainstem compression causes dysfunction of reticular activating system or mass in one hemisphere causing compression of the other results in bilateral hemisphere dysfunction
6. increased intracranial pressure: reduces CBF
7. acute lateral shift (midline shift) of the brain: e.g. due hematoma (subdural or epidural): see Table 12-3
Table 12-3 Effect of lateral shift on level of consciousness4
|
Amount of midline shift |
Level of consciousness |
|
0-3 mm |
alert |
|
3-4 mm |
drowsy |
|
6-8.5 mm |
stuporous |
|
8-13 mm |
comatose |
PSEUDOCOMA
Differential diagnosis:
1. locked-in syndrome: ventral pontine infarction
2. psychiatric: catatonia, conversion reaction
3. neuromuscular weakness: myasthenia gravis, Guillain-Barré
12.2. Approach to the comatose patient
The following covers nontraumatic coma (see Head trauma, page 850 for that topic).
Initial evaluation: includes measures to protect brain (by providing CBF, O2, and glucose), assesses upper brainstem (Cr. N. VIII), and rapidly identifies surgical emergencies. Keep “pseudocoma” as a possible etiology in back of mind.
APPROACH TO COMATOSE PATIENT, OUTLINE
1. cardiovascular stabilization: establish airway, check circulation (heartbeat, BP, carotid pulse), CPR if necessary
2. obtain blood for tests
A. STAT: electrolytes (especially Na, glucose, BUN), CBC + diff, ABG
B. others as appropriate: toxicology screen (serum & urine), calcium, ammonia, antiepileptic drug (AED) levels (if patient is taking AEDs)
3. administer emergency supportive medications
A. glucose: at least 25 ml of D50 IVP. Due to potentially harmful effect of glucose in global ischemia, if possible check fingerstick glucose first, otherwise glucose is given without exception, unless it is known with certainty that serum glucose is normal
B. naloxone (Narcan®): in case of narcotic overdose. 1 amp (0.4 mg) IVP
C. flumazenil (Romazicon®): in case of benzodiazepine overdose (see page 52). Start with 0.2 mg IV over 30 seconds, wait 30 secs, then give 0.3 mg over 30 secs at 1 minute intervals up to 3 mg or until patient arouses
D. thiamine: 50-100 mg IVP (3% of Wernicke’s present with coma)
4. core neuro exam (assesses midbrain/upper pons, allows emergency measures to be instituted rapidly, more thorough evaluation possible once stabilized): → (see Core neuro exam below)
5. if herniation syndrome or signs of expanding p-fossa lesion with brainstem compression (see Table 12-4): initiate measures to lower ICP (see Treatment measures for elevated ICP, page 876), then get a CT scan if patient begins improving, otherwise emergency surgery (see page 1021). ✖ Do NOT do LP
Table 12-4 Signs of herniation syndrome or posterior fossa lesion
|
HERNIATION SYNDROMES |
SIGNS OF P-FOSSA LESION |
|
(also see Herniation syndromes, page 284) |
(also see Posterior fossa (infratentorial) tumors, page 590) |
|
• unilateral sensory or motor deficit • progressive obtundation → coma • unilateral 3rd nerve palsy • decorticate or decerebrate posturing (especially if unilateral) |
• initial symptoms of diplopia, vertigo, bilateral limb weakness, ataxia, occipital H/A • rapid onset of deterioration/coma • bilateral motor signs at onset • miosis • absent calorics to horizontal movement, possibly with preserved vertical movements • ocular bobbing • ophthalmoplegia • multiple cranial nerve abnormalities with long tract signs • apneustic, cluster or ataxic respirations |
6. if meningitis suspected (altered mental status + fever, meningeal signs…)
A. if no indication of herniation, p-fossa mass (see Table 12-4), focal deficit indicating mass effect or papilledema: perform LP, start antibiotics immediately (do not wait for CSF results) (see Meningitis, page 343)
B. if evidence of possible mass effect, coagulopathy or herniation, CT to R/O mass. If significant delay anticipated, consider empiric antibiotics or careful LP with small gauge needle (≤ 22 Ga.), measure opening pressure (OP), remove only a small amount of CSF if OP high, replace CSF if patient deteriorates (LP in this setting may be risky, see Lumbar puncture, page 201).
7. treat generalized seizures if present. If status epilepticus is suspected, treat as indicated on page 404 (obtain emergency EEG if available)
8. treat metabolic abnormalities
A. restore acid-base balance
B. restore electrolyte imbalance
C. maintain body temperature
9. obtain as complete history as possible once stabilized
10. administer specific therapies
CORE NEURO EXAM (FOR COMA)
A. respiratory rate and pattern: the most common disorder in impaired consciousness
1. Cheyne-Stokes: breathing gradually crescendos in amplitude and then trails off, followed by an expiratory pause, and then the pattern repeats. Hyperpneic phase is usually longer than apneic. Usually seen with diencephalic lesions or bilateral cerebral hemisphere dysfunction (non-specific), e.g. early increased ICP or metabolic abnormality. Results from an increased ventilatory response to CO2
2. hyperventilation: usually in response to hypoxemia, metabolic acidosis, aspiration, or pulmonary edema. True central neurogenic hyperventilation is rare, and usually results from dysfunction within the pons. If no other brainstem signs are present, may suggest psychiatric disorder
3. cluster breathing: periods of rapid irregular breathing separated by apneic spells, may appear similar to Cheyne-Stokes, may merge with various patterns of gasping respirations. High medulla or lower pons lesion. Often an ominous sign
4. apneustic (rare): a pause at full inspiration. Indicates pontine lesion, e.g. with basilar artery occlusion
5. ataxic (Biot’s breathing): no pattern in rate or depth of respirations. Seen with medullary lesion. Usually preterminal
B. pupil (size in mm) in ambient light, and in reaction to direct/consensual light
1. equal and reactive pupils indicates toxic/metabolic cause with few exceptions (see below) (may have hippus). The light reflex is the most useful sign in distinguishing metabolic from structural coma
A. the only metabolic causes of fixed/dilated pupil: glutethimide toxicity, anoxic encephalopathy, anticholinergics (including topically applied atropine), occasionally with botulism toxin poisoning
B. narcotics cause small pupils (miosis) with a small range of constriction and sluggish reaction to light (in severe overdose, the pupils may be so small that a magnifying glass may be needed to see reaction)
2. unequal (note: an afferent pupillary defect does not produce anisocoria (see Alterations in pupillary diameter, page 831)):
A. fixed and dilated pupil: usually due to oculomotor palsy. Possible herniation, especially if larger pupil associated with ipsilateral 3rd nerve EOM palsy (eye deviated “down and out”)
B. possible Horner’s syndrome: consider carotid occlusion/dissection
3. bilateral pupil abnormalities
A. pinpoint with minute reaction that can be detected with magnifying glass5: pontine lesion (sympathetic input is lost; parasympathetics emerge at Edinger-Westphal nucleus and are unopposed)
B. bilateral fixed and dilated (7-10 mm): subtotal damage to medulla or immeinspiration diate post-anoxia or hypothermia (core temperature < 90° F (32.2° C))
C. midposition (4-6 mm) and fixed: more extensive midbrain lesion, presumably due to interruption of sympathetics and parasympathetics
C. extraocular muscle function
1. deviations of ocular axes at rest
A. bilateral conjugate deviation:
1. frontal lobe lesion (frontal center for contralateral gaze): looks toward side of destructive lesion (away from hemiparesis). Looks away from side of seizure focus (looks at jerking side), may be status epilepticus. Reflex eye movements (see below) are normal
2. pontine lesion: eyes look away from lesion and towards hemiparesis; calorics impaired on side of lesion
3. “wrong way gaze”: medial thalamic hemorrhage. Eyes look away from lesion and towards hemiparesis (an exception to the axiom that the eyes look towards a destructive supratentorial lesion)5
4. downward deviation: may be associated with unreactive pupils (Parinaud’s syndrome, see page 114). Etiologies: thalamic or mid-brain pretectal lesions, metabolic coma (especially barbiturates), may follow a seizure
B. unilateral outward deviation on side of larger pupil (III palsy): uncal herniation
C. unilateral inward deviation: VI (abducens) nerve
D. skew deviation
1. III or IV nerve/nucleus lesion
2. infratentorial lesion (frequently dorsal midbrain)
2. spontaneous eye movements
A. “windshield wiper eyes”: random roving conjugate eye movements. Non-localizing. Indicates an intact III nucleus and medial longitudinal fasciculus
B. periodic alternating gaze, AKA “ping-pong gaze”: eyes deviate side to side with frequency of ≈ 3-5 per second (pausing 2-3 secs in each direction). Usually indicates bilateral cerebral dysfunction
C. ocular bobbing: repetitive rapid vertical deviation downward with slow return to neutral position. Pontine lesion (see page 838)
3. internuclear ophthalmoplegia (INO): due to lesion in medial longitudinal fasciculus (MLF) (fibers crossing to contralateral III nucleus are interrupted). Eye ipsilateral to MLF lesion does not adduct on spontaneous eye movement or in response to reflex maneuvers (e.g. calorics) (see page 834)
4. reflex eye movements (maneuvers to test brainstem)
A. oculovestibular reflexA, AKA ice water calorics: first rule-out TM perforation and occlusion of the EAC by cerumen. Elevate the HOB 30°B, irrigate one ear with 60-100 ml of ice waterC. NB: response is inhibited by neuromuscular blocking agents (NMBA)
1. a comatose patient with an intact brainstem will have tonic conjugate eye deviation to side of cold stimulus which may be delayed up to one minute or more. There will be no fast component (nystagmus) (the cortical component) even if the brainstem is intact (NB: oculocephalic reflexD (doll’s eyes) provides similar information as oculovestibular reflexE, but poses a greater risk to the spinal cord if C-spine not cleared)
2. no response: symmetrical, could be specific toxin (e.g. neuromuscular block or barbiturates), metabolic cause, brain death or possibly massive infratentorial lesion
3. asymmetric: infratentorial lesion, especially if response inconsistent with 3rd nerve palsy (herniation). Usually maintained in toxic/metabolic coma
4. nystagmus without tonic deviation (i.e. eyes remain in primary position) virtually diagnostic of psychogenic coma
5. contralateral eye fails to adduct: INO (MLF lesion)
B. optokinetic nystagmus presence strongly suggests psychogenic coma
D. motor: muscle tone and reflexes, response to pain, Babinski (note asymmetries)
1. appropriate: implies corticospinal tracts and cortex intact
2. asymmetric: supratentorial lesion (tone usually increased), unlikely in metabolic
3. inconsistent/variable: seizures, psychiatric
4. symmetric: metabolic (usually decreased). Asterixis, tremor, myoclonus may be present in metabolic coma
5. hyporeflexia: consider myxedema coma, especially in patient presenting weeks after transsphenoidal surgery
6. patterns
A. decorticate posturing: arms flex, legs extend: large cortical or subcortical lesion
B. decerebrate posturing: arms and legs extend: brainstem injury at or below lower midbrain
C. arms flexed, legs flaccid: pontine tegmentum
D. arms flaccid, legs appropriate (“man-in-the-barrel syndrome”): anoxic injury (poor prognosis)
E. ciliospinal reflexes (pupillary dilatation to noxious cutaneous stimuli): tests integrity of sympathetic pathways
1. bilaterally present: metabolic
2. unilaterally present: possible 3rd nerve lesion (herniation) if on side of larger pupil. Possible pre-existing Horner’s syndrome if on side of smaller pupil
3. bilaterally absent: usually not helpful
A. oculovestibular reflexes (calorics): the anticipated response is commonly misunderstood. In a normal awake patient there is slow deviation towards the side of the cold stimulus with nystagmus (which is named for the rapid, cortical phase) in the opposite direction (hence the mnemonic “COWS” (cold-opposite, warm-same)). Nystagmus will be absent in the comatose patient
B. HOB at 30° places the horizontal semicircular canal (SCC) vertically for maximal response6 (p 56)
C. cold water → downward endolymphatic currents, away from the ampulla of the horizontal SCC6 (p 57)
D. oculocephalic reflex (“doll’s eyes” or “doll’s head”): do not perform if there is any uncertainty about cervical-spine stability. In an awake patient, the eyes will either move with the head, or, if the movement is slow enough and the patient is fixating on an object, there will be contraversive conjugate eye movement7 (c.f. oculovestibular reflex which does not depend on patient’s level of cooperation). In a comatose patient with an intact brainstem & cranial nerves, there will also be contraversive conjugate eye movement (a positive doll’s eyes response)
E. oculovestibular reflexes are absent but oculocephalic are maintained only when vestibular inputs are interrupted, e.g. streptomycin toxicity of labyrinths or bilateral vestibular schwannomas
12.3. Herniation syndromes
Classic teaching has been that shifts in brain tissue (e.g. caused by masses or increased intracranial pressure) through rigid openings in the skull (herniation) compress other structures of the CNS producing the observed symptoms. This view has been challenged8, with the hypothesis that herniation may be an epiphenomenon that occurs late in the process and is not actually the cause of the observations. However, herniation models still serve as useful approximations.
The five most common herniation syndromes are:
1. central (transtentorial) herniation (see page 285) } supratentorial herniation
2. uncal herniation (see page 286) } supratentorial herniation
3. cingulate herniation: cingulate gyrus herniates under falx (AKA subfalcine herniation). Usually asymptomatic unless ACA kinks and occludes causing bifrontal infarction. Usually warns of impending transtentorial herniation
4. upward cerebellar (see below) } infratentorial herniation
5. tonsillar herniation (see below) } infratentorial herniation
COMA FROM SUPRATENTORIAL MASS6
Central and uncal herniation each causes a different form of rostral-caudal deterioration. Central herniation results in sequential failure of: diencephalon, midbrain, pons, medulla (see page 285). For uncal herniation, see page 286. “Classic” signs of increased ICP (HTN, bradycardia, altered respiratory pattern) usually seen with p-fossa lesions may be absent in slowly developing supratentorial masses.
Distinction between central and uncal herniation is difficult when dysfunction reaches the midbrain level or below. Predicting the location of the lesion based on the herniation syndrome is unreliable.
Clinical characteristics differentiating uncal from central herniation
• decreased consciousness occurs early in central herniation, late in uncal
• uncal herniation syndrome rarely gives rise to decorticate posturing
Differential diagnosis of supratentorial etiologies
1. vascular: CVA, intracerebral hemorrhage, SAH
2. inflammatory: cerebral abscess, subdural empyema, herpes simplex encephalitis
3. neoplastic: primary or metastatic
4. traumatic: epidural or subdural hematoma, depressed skull fracture
COMA FROM INFRATENTORIAL MASS
NB: it is essential to identify patients with primary posterior fossa lesions (see Table 12-4, page 281) as they may require emergent surgical intervention (see page 1021).
Etiologies of infratentorial mass
1. vascular: brainstem infarction (including basilar artery occlusion), cerebellar infarction or hematoma
2. inflammatory: cerebellar abscess, central pontine myelinolysis, brainstem encephalitis
3. neoplasms: primary or metastatic
4. traumatic: epidural or subdural hematoma
HYDROCEPHALUS
Infratentorial masses can produce obstructive hydrocephalus by compressing the Sylvian aqueduct and/or 4th ventricle (see page 586).
UPWARD CEREBELLAR HERNIATION
Occasionally seen with p-fossa masses, may be exacerbated by ventriculostomy. Cerebellar vermis ascends above tentorium, compressing the midbrain, and possibly occluding SCAs → cerebellar infarction. May compress sylvian aqueduct → hydrocephalus.
TONSILLAR HERNIATION
Cerebellar tonsils “cone” through foramen magnum, compressing medulla → respiratory arrest. Usually rapidly fatal.
Occurs with either supra- or infratentorial masses or with elevated ICP. May be precipitated by LP. In many cases, there may simply be pressure on the brainstem without actual herniation9. There are also cases with significant cerebellar herniation through the foramen magnum with the patient remaining alert8.
12.3.1. Central herniation
AKA transtentorial herniation AKA tentorial herniation. Usually more chronic than uncal herniation, e.g. due to tumor, especially of frontal, parietal or occipital lobes.
The diencephalon is gradually forced through the tentorial incisura. The pituitary stalk may be sheared, resulting in diabetes insipidus. PCAs may be trapped along the open edge of the incisura, and may occlude producing cortical blindness (see Blindness from hydrocephalus, page 335). The brainstem suffers ischemia from compression and shearing of perforating arteries from basilar artery → hemorrhages within the brainstem (Duret hemorrhages).
CT or plain x-ray criteria
Downward displacement of the pineal gland may be demonstrated10. Perimesencephalic cisterns are compressed.
DIENCEPHALIC STAGE
Early. May be due to diffuse bilateral hemisphere dysfunction (e.g. from decreased blood flow from increased ICP) or (more likely) from bilateral diencephalic dysfunction due to downward displacement. This stage warns of impending (irreversible) midbrain damage but is frequently reversible if the cause is treated.
|
Consciousness |
Altered alertness is first sign; usually lethargy, agitation in some. Later: stupor → coma. |
|
Respiration |
Sighs, yawns, occasional pauses. Later: Cheyne-Stokes. |
|
Pupils |
Small (1 - 3 mm), small range of contraction. |
|
Oculomotor |
Conjugate or slightly divergent roving eyes; if conjugate then brainstem intact. Usually positive DOLL’S EYES and conjugate ipsilateral response to cold water calorics (CWC). Impaired up-gaze due to compression of superior colliculi and diencephalic pretectum (Parinaud’s syndrome see page 114) |
|
Motor |
Early: appropriate response to noxious stimuli, bilateral Babinski, gegenhalten (paratonic resistance). If previously hemiparetic contralateral to lesion: may worsen. Later: motionlessness & grasp reflexes, then DECORTICATE (initially contralateral to lesion in most cases). |
MIDBRAIN - UPPER PONS STAGE
When midbrain signs fully developed (in adults), prognosis is very poor (extreme ischemia of midbrain). Fewer than 5% of cases will have a good recovery if treatment is successfully undertaken at this stage.
|
Respiration |
Cheyne-Stokes → sustained tachypnea. |
|
Pupils |
Moderately dilated midposition (3-5 mm), fixed*. |
|
Oculomotor |
Doll’s eyes & CWC impaired, may be dysconjugate. MLF lesion → internuclear ophthalmoplegia (when doll’s or CWC elicited and dysconjugate, medially moving eye moves less than laterally moving eye). |
|
Motor |
Decorticate → bilaterally DECEREBRATE (occasionally spontaneously). |
* in pontine hemorrhage pinpoint pupils appear because the loss of sympathetics leaves the parasympathetics unopposed, whereas in herniation, the parasympathetics are usually lost, too (3rd nerve injury)
LOWER PONS - UPPER MEDULLARY STAGE
|
Respiration |
Regular, shallow and rapid (20-40/min). |
|
Pupils |
Midposition (3-5 mm), fixed. |
|
Oculomotor |
Doll’s eyes and CWC unelicitable. |
|
Motor |
Flaccid. Bilateral Babinski. Occasionally LE flexion to pain. |
MEDULLARY STAGE (TERMINAL STAGE)
|
Respiration |
Slow, irregular rate and depth, sighs/gasps. Occasionally hyperpnea alternating with apnea |
|
Pupils |
Dilate widely with hypoxia. |
OUTCOME AFTER CENTRAL HERNIATION
In a series of 153 patients with signs of central herniation (altered level of consciousness, anisocoria or fixed pupils, abnormal motor findings) 9% had good recovery, 18% had functional outcome, 10% were severely disabled, and 60% died11.
Factors associated with a better result were young age (especially age ≤ 17 yrs), anisocoria with deteriorating Glasgow Coma Score and nonflaccid motor function. Factors associated with poor outcome were bilaterally fixed pupils, with only 3.5% of these patients having a functional recovery.
12.3.2. Uncal herniation
Usually occurs in rapidly expanding traumatic hematomas, frequently in the lateral middle-fossa or temporal lobe pushing medial uncus and hippocampal gyrus over edge of tentorium, entrapping third nerve and directly compressing midbrain. PCA may be occluded (as with central herniation). For CT criteria see below.
Impaired consciousness is NOT a reliable early sign. Earliest consistent sign: unilaterally dilating pupil. However, it is unlikely that a patient undergoing early uncal herniation would be completely neurologically intact except for anisocoria (do not dismiss confusion, agitation, etc.). Once brainstem findings appear, deterioration may be rapid (deep coma may occur within hours).
CT criteria12
Tentorial incisura surrounds interpeduncular and pre-pontine cisterns and brainstem. There is great interpersonal variability in the amount of space in the incisura.
Impending uncal or hippocampal herniation may be indicated by encroachment on lateral aspect of suprasellar cistern → flattening of normal pentagonal shape. Once herniation occurs CT may show: brainstem displacement and flattening, compression of contralateral cerebral peduncle, midbrain rotation with slight increase of ipsilateral subarachnoid space. Also, contralateral hydrocephalus may occur13.
Obliteration of parasellar and interpeduncular cisterns occurs as uncus and/or hippocampus are forced through hiatus. Brainstem compression → AP elongation. Since dural structures enhance with IV contrast, this may be used to help delineate tentorial margins when necessary.
EARLY THIRD NERVE STAGE
(NOT A BRAINSTEM FINDING, DUE TO 3RD NERVE COMPRESSION)
|
Pupils |
Unilaterally dilating pupil (may be sluggish); 85% ipsilateral to lesion14 |
|
Oculomotor |
Doll’s = normal or dysconjugate. CWC = slow ipsilateral deviation, impaired nystagmus, may be dysconjugate if external oculomotor ophthalmoplegia (EOO). |
|
Respirations |
Normal. |
|
Motor |
Appropriate response to nociceptive stimulus. Contralateral Babinski. |
LATE THIRD NERVE STAGE
Midbrain dysfunction occurs almost immediately after symptoms extend beyond those due to focal cerebral lesion (i.e. may skip diencephalic stage, due to lateral pressure on midbrain). Treatment delays may result in irreversible damage.
|
Pupils |
Pupil fully dilates. |
|
Oculomotor |
Once pupil blown, then external oculomotor ophthalmoplegia (EOO). |
|
Consciousness |
Once EOO, stuporous → comatose. |
|
Respirations |
Sustained hyperventilation, rarely Cheyne-Stokes. |
|
Motor |
Usually produces contralateral weakness. However, the contralateral cerebral peduncle may be compressed against the tentorial edge causing ipsilateral hemiplegia (Kernohan’s phenomenon, a false localizing sign). Then bilateral decerebration (decortication unusual). |
MIDBRAIN - UPPER PONS STAGE
|
Pupils |
Contralateral pupil fixes in midposition or full dilation. Eventually, both midposition (5-6 mm) and fixed. |
|
Oculomotor |
Impaired or absent. |
|
Respirations |
Sustained hyperpnea. |
|
Motor |
Bilateral decerebrate rigidity. |
From this point onward, the uncal syndrome is indistinguishable from central herniation (see above).
12.4. Hypoxic coma
Anoxic encephalopathy may be due to anoxemic anoxia (drop in pO2) or anemic anoxia (following exsanguination or cardiac arrest). Myoclonus is common.
Vulnerable cells:
1. cerebral grey matter: lesions predominate in 3rd cortical layer (white matter is usually better preserved due to lower O2 requirements)
2. Ammon’s horn is also vulnerable
3. in the basal ganglia (BG):
Table 12-5 Patients with BEST chance of regaining independence*
|
Time of exam |
Finding |
|
< 6 hrs from onset |
(pupillary light reflex present) |
|
1 day |
(GCS-motor > 3) |
|
3 days |
(GCS-motor > 3) |
|
1 week |
GCS-motor = 6 |
|
2 weeks |
oculocephalic WNL |
A. anoxemic anoxia severely affects globus pallidus
B. anemic anoxia affects the caudate nucleus and putamen
4. in the cerebellum: Purkinje cells, dentate nuclei, and inferior olives are affected
Multivariate analysis yields out-come prognosticators shown in Table 12-5 and Table 12-6. NB: this analysis applies only to hypoxic-ischemic coma15. More recent studies confirm the poor prognosis of unreactive pupils and lack of motor response to pain16; if either of these findings are seen within a few hours after cardiac arrest there is an 80% risk of death or permanent vegetative state, and if present at 3 days these this rate rose to 100%.
Glucocorticoids (steroids) have been shown to have no beneficial effect on survival rate or neurological recovery rate after cardiac arrest17.
Table 12-6 Patients with virtually NO chance of regaining independence*
|
Time of exam |
Finding |
|
< 6 hrs |
no pupillary light reflex |
|
1 day |
(GCS-motor < 4) |
|
3 days |
GCS-motor < 4 |
|
1 week |
(GCS-motor < 6) |
|
2 week |
(oculocephalic not WNL) |
* abbreviations: WNL = within normal limits, GCS = Glasgow Coma Scale (“GCS-motor” refers to the motor score…); EOM = extraocular muscle;
12.5. References
1. Teasdale G, Jennett B: Assessment of coma and impaired consciousness: A practical scale. Lancet 2: 81-4, 1974.
2. Valadka A B, Narayan R K: Emergency room management of the head-injured patient. In Neurotrauma, Narayan R K, Wilberger J E, and Povlishock J T, (eds.). McGraw-Hill, New York, 1996: pp 119-35.
3. Hahn Y S, Chyung C, Barthel M J, et al.: Head injuries in children under 36 months of age: Demography and outcome. Childs Nerv Syst 4: 34-40, 1988.
4. Ropper A H: Lateral displacement of the brain and level of consciousness in patients with an acute hemispheral mass. N Engl J Med 314: 953-8, 1986.
5. Fisher C M: Some neuro-ophthalmological observations. J Neurol Neurosurg Psychiatry 30: 383-92, 1967.
6. Plum F, Posner J B: In The diagnosis of stupor and coma. F A Davis, Philadelphia, 3rd ed., 1980: pp 87-130.
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