ABSTRACT
I. PRINCIPLES OF COMA AND DELIRIUM (SEE CHAPTER 7, PART A)
A. Consciousness: definition and anatomy 1. Consciousness
a. Consists of arousal (ability to interact with external environment, wakefulness) and awareness of content (ability to perceive and understand content)
b. States of consciousness are defined in Table 10-1 2. Anatomical structures involved in consciousness
a. As noted above, consciousness is defined by arousal and awareness of content, thus certain parts of the brain are involved in these activities
b. Arousal is predominantly a function of the ascending reticular activating system (ARAS) 1) ARAS cell bodies are in pons and midbrain and the
axons ascend in the central tegmental tract 2) ARAS receives collaterals from somatic and special
sensory systems 3) ARAS projects to the reticular nucleus of thalamus
and to hypothalamus (which projects to limbic cortex and basal forebrain)
4) In addition, the midline raphe nuclei and locus ceruleus project diffusely to cerebral cortex
c. Awareness of content is a direct function of the cerebral hemispheres and the projections to them from thalamus, hypothalamus, brainstem
d. The anatomical structures of the ARAS and their
connections are noted in Figure 10-1 and Table 10-2 (for additional details on anatomical structures involved in consciousness and attention, see Chapter 7)
e. Change in consciousness may be due to diffuse, multifocal, or strategic lesions
Three Anatomical Areas to Alter Level of Consciousness
Reticular formation (upper midbrain)
Bilateral diencephalon (thalamus)
Bilateral cerebral hemisphere
1) Toxic-metabolic causes affect cerebral hemispheres and brainstem in diffuse manner
2) Unilateral supratentorial lesions with mass effect toward opposite hemisphere or with central herniation may result in reduced level of consciousness, as may multifocal supratentorial lesions
3) Diencephalic lesions (usually bilateral) may result in reduced levels of consciousness
4) Infratentorial lesions involving ARAS may result in reduced levels of consciousness
B. Clinical Approach to Coma 1. Differential diagnosis is listed in Table 10-3 2. Clinical history
a. Obtain information from witnesses about onset and course, medical history, and medications
b. Specifically obtain information about recent injury or trauma, seizure-like activity, recent symptoms (including fever, previous medical problems)
3. Examination: used to localize the problem and determine prognosis (Fig. 10-2) a. General examination
1) Look for signs of trauma (Battle’s sign, i.e., bruising of
Table 10-1. Levels of Consciousness
State Description
Table 10-2. Structures Involved in Consciousness and Their Connections
Structure Description Input Output
mastoid), cerebrospinal fluid (CSF) leak 2) Evidence of seizure activity: tongue biting, urinary
incontinence b. Level of consciousness
1) See Table 10-1 2) Glasgow Coma Scale (GCS) score is commonly used
c. Respiratory 1) Respiratory pattern should be observed, may provide
localization information (Fig. 10-2) 2) Many patients require mechanical ventilation, obscur-
ing ability to observe these patterns d. Eyes
1) Oculocephalic (doll’s eyes) a) Remember to rule out cervical spine injury before
performing this maneuver b) Rotate head from side to side or vertically
i) In normal functioning brainstem, eyes move opposite the head movement and are conjugate
ii) Normal function implies that cranial nerves (CNs) III and VI (horizontal) or CNs III and IV (vertical) are intact in pons and midbrain, also the medial longitudinal fasciculus that connects CNs III and VI
2) Caloric testing a) Be sure tympanic membrane is intact and head of
bed is at 30 degrees b) Instill cold water in ear c) If brainstem is intact, tonic deviation of eyes
toward cold ear (this also assesses CNs III and VI, medial longitudinal fasciculus, and vestibular input [CN VIII])
3) Pupils: observe size and reactivity (for pupillary pathways, see Chapter 3) a) Midposition, fixed pupils: rule out trauma, eye
drops, medications (atropine) or poisoning as cause of fixed pupils
Table 10-3. Differential Diagnosis of Coma
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i) Often a result of diffuse midbrain lesion or midbrain damage from transtentorial herniation
ii) Sympathetic tone and parasympathetic tone are impaired, causing midposition pupils
iii) Efferent path of light reflex is impaired, so pupils are unreactive
b) Pinpoint pupils: rule out toxins and medications (narcotics) as cause i) Typically found with pontine lesion ii) Bilateral impairment of sympathetic nerves pro-
duces pinpoint pupils because of unopposed tonic parasympathetics (CN III)
iii) May also have small pupils from lesions in upper brainstem (above red nucleus) and diencephalic region because of impaired sympathetic outflow from hypothalamus
c) Fixed, dilated pupils: rule out toxins and metabolic dysfunction (e.g., hypothermia, barbiturates); can be related also to extensive medullary lesion
d) Unequal pupil size: consider Horner’s syndrome (sympathetic dysfunction) vs. CN III nerve palsy (see Chapter 3)
e) Poor pupil reactivity: consider if the lesion is afferent (CN II), efferent (CN III), or in midbrain tectum
4) Gaze preference a) Horizontal gaze preference may occur at level of
frontal cortex or in pons b) Gaze preference at level of pons can affect medial
longitudinal fasciculus and CN VI or nucleus of CN VI
i) Patients look toward the side of hemiparesis if there is concomitant corticospinal tract damage
ii) Oculocephalic maneuver will not overcome gaze preference
c) Gaze preference at the level of the frontal cortex is result of frontal eye field being affected i) Patients look away from side of hemiparesis if
the corticospinal tract is also involved ii) Oculocephalic maneuver will overcome gaze
preference (i.e., patient’s eyes will cross midline with oculocephalic maneuver)
5) Spontaneous eye movements a) Skew deviation: may localize to midbrain (CNs
III and IV) b) Periodic alternating gaze: eyes deviate side to side;
may be related to bilateral cerebral hemisphere dysfunction
c) Ocular bobbing: may localize to pons e. Motor response to stimulus
1) Rubrospinal tracts beginning in midbrain project to ventral horn cells of contralateral flexors of upper extremities
2) Pontine reticulospinal tracts and medullary vestibulospinal tracts (both excitatory) project to ventral horn cells of extensors of extremities
3) Corticospinal tract projects to extremities to control fine motor movements, and varying influences of corticospinal and extrapyramidal tracts result in normal tone
4) Decorticate posturing, i.e., flexion of upper extremities, extension of lower extremities: the lesion is above the red nucleus and cortical influence is impaired (Fig. 10-2)
5) Decerebrate posturing, i.e., extension of all four extremities: the lesion is below the red nucleus and above the vestibular nuclei (Fig. 10-2)
6) Lesions below the vestibular nuclei may result in absent movement of the extremities because of disruption of projections from vestibular and pontine reticular nuclei that provide extensor tone; the medullary reticulospinal tract remains intact and is inhibitory to motor neurons controlling extensors of the extremities
C. Clinical Management of Comatose Patients (Table 10-4)
D. Brain Death 1. Definition: cessation of all brain and brainstem
function
Glasgow Coma Scale Points Best eye Best verbal Best motor
6 --- --- Obeys commands
5 --- Oriented Localizes pain
4 Sponta-Confused Withdraws in
neous response to pain
3 To speech Inappropriate Flexion
(decorticate)
2 To pain Incompre-Extension
hensible (decerebrate)
1 None None None
2. Criteria for brain death vary among countries 3. Only consider applying the following criteria after
ruling out possible confounding conditions: severe metabolic disturbances, drug intoxication (sedatives, barbiturates, etc.), poisoning, neuromuscular blocking agents, severe hypothermia (temperature <32°C), hypotension
4. Criteria include a. Coma b. Absence of motor responses
1) These include absence of response to deep central
pain and absence of decorticate or decerebrate posturing
2) Spinal cord-mediated reflexes are compatible with brain death, including flexor plantar response, rapid flexion of arms, raising one or all limbs off the bed and sitting up (“Lazarus sign”), or jerking of one limb or multifocal spinal myoclonus
c. Absence of pupillary responses to light; pupils at midposition
d. Absence of corneal reflexes e. Absence of gag reflex f. Absence of cough with tracheal suctioning g. Absence of sucking and rooting reflexes h. Absence of respiratory drive (apnea) at PaCO2 60 mm
Hg or at 20 mm Hg above normal baseline pressure 1) Apnea test is important component of evaluation of
patient for brain death 2) Subject should fulfill all above criteria before apnea
test is considered 3) Additional prerequisites for the test: positive fluid
balance, absence of hypothermia (core temperature >32.2°C), systolic blood pressure >90 mm Hg, arterial PaCO2 ≥40 mm Hg, arterial PaO2 ≥200 mm Hg
4) Apnea: the lack of any spontaneous respirations after discontinuation of the ventilator
5) Positive apnea test (apnea related to brain death): PaCO2 level is more than 60 mm Hg without respirations
6) Patients with chronic hypercapnea (CO2 retainers, e.g., patients with chronic obstructive pulmonary disease) have higher PaCO2 levels at baseline: apnea test may be unreliable and a confirmatory test should be considered
7) PaCO2 level increases 3 to 6 mm Hg per minute and 6 to 8 minutes may be needed to reach target level of 60 mm Hg; this may be facilitated if apnea test is started at baseline of 40 mm Hg
8) Because severe hypoxemia predisposes patient to cardiac arrhythmias and must be avoided, ventilate for 15 minutes with 100% oxygen before the test and through a catheter placed at the level of the carina during testing
9) Baseline arterial blood gases should be measured and repeated at regular intervals until the criterion for positive apnea test is met
i. Interval between two evaluations according to age 1) Term to 2 months old: 48 hours 2) >2 months to 1 year old: 24 hours 3) >1 year but <18 years old: 12 hours 4) ≥18 years old: first exam may be used (according to
Table 10-4. Clinical Management of Comatose Patients
some authorities) with overwhelming clinical evidence of brain death
j. Confirmatory test 1) Term to 2 months old: 2 confirmatory tests 2) >2 months to 1 year old: 1 confirmatory test 3) >1 year but <18 years old: optional 4) ≥18 years old: optional
k. Optional confirmatory tests: electroencephalography (EEG), cerebral angiography, transcranial Doppler, nuclear studies
E. Clinical Approach to Delirium 1. Definition: fluctuating alteration of consciousness and
cognition due to general medical condition 2. Predisposing factors
a. Elderly b. Dementia c. Metabolic disturbances d. Visual or auditory impairment
3. Causes a. Many of same factors that result in coma may result in
delirium, but delirium more commonly is due to toxicmetabolic mechanisms
b. Other common causes: medications, withdrawal syndromes, systemic infections, surgery, electrolyte fluctuations, hypoxemia (see Chapter 7)
4. Management a. Identify precipitating factors b. Adjust environment to improve sleep-wake cycle, reduce
noxious stimuli, reduce noise c. Medications if needed may include neuroleptics
A. Pathophysiology 1. ICH results in shear force through brain parenchyma 2. Imaging studies show rebleeding may occur within first
12 hours after onset of symptoms 3. Edema (both vasogenic and cytotoxic) occurs and may
cause clinical deterioration, generally between 24 and 72 hours
B. Differential Diagnosis: varies according to site (Table 10-5)
1. Hypertensive hemorrhages usually occur in deep locations, in following order of decreasing prevalence: a. Basal ganglia (Fig. 10-3) b. Subcortical white matter
c. Cerebellum d. Thalamus e. Pons
2. Amyloid angiopathy a. Common cause of lobar intraparenchymal hemorrhages
in elderly (generally >65 years) b. Congophilic (amyloid) material is deposited in small
blood vessels of brain and meninges and may result in hemorrhage
c. This amyloid is similar to that deposited in Alzheimertype plaques (Fig. 10-4)
d. High risk of hemorrhage recurrence, especially if the patient carries APOE ε2 or ε4 allele
C. Clinical Presentation 1. Focal neurologic deficits 2. Headache 3. Nausea, vomiting 4. Alteration in level of consciousness
D. Diagnostic Evaluation 1. Computed tomography (CT) of head: hyperdensity
consistent with blood 2. Magnetic resonance imaging (MRI)
a. May be useful to rule out underlying structural abnormality such as arteriovenous malformation or tumor
b. Gradient echo sequences may demonstrate silent microhemorrhages in patients with amyloid angiopathy or those with cavernous malformations
c. Can be used to determine approximate timing of hemorrhage (Fig. 10-5, Table 10-6)
3. Angiography: may be required to rule out aneurysm or arteriovenous malformation, especially in lobar-related hemorrhages
E. Management 1. Supportive measures 2. Blood pressure: should maintain mean arterial pressure
less than 120 to 130 mm Hg 3. Mechanical ventilation: may be required, especially in
comatose patients 4. Corticosteroids (methylprednisolone, dexamethasone):
clinical trials have not shown benefit 5. Surgical options: several randomized clinical trials eval-
uated surgical evacuation of hemorrhage vs. supportive care-mixed results but majority showed no difference in surgery vs. supportive care; one trial showed that surgery could improve mortality but not morbidity; ongoing studies are evaluating whether early surgery may help
6. Recombinant factor VIIa a. Early treatment with recombinant factor VIIa after onset
of ICH limits growth of the hematoma, reduces mortality, and improves functional outcomes
b. Increased risk of thromboembolic complications
F. Outcome 1. Most consistent and sensitive predictors of outcome:
size (volume) of hemorrhage and initial GCS score 2. Possible additional predictors: deep location, intraven-
tricular extension, time to presentation 3. Volume more than 60 mL or GCS score less than 8 (or
both) predicts poor outcome
A. Pathophysiology 1. SAH: extravasated blood in subarachnoid space
a. Dural innervation is the substrate for pain b. Patients may have altered levels of consciousness, nausea,
and vomiting with hydrocephalus 2. Most common cause of all SAHs: trauma 3. Most common cause of nontraumatic SAHs: aneurysm
rupture
B. Presentation 1. Thunderclap headache or “the worst headache of my
life” 2. Nausea, vomiting 3. Meningismus 4. Patient may have altered level of consciousness 5. May have focal neurologic symptoms if ICH present in
addition to SAH 6. Ocular hemorrhage
a. Subhyaloid hemorrhage b. Retinal hemorrhage c. Vitreal hemorrhage (Terson’s syndrome)
C. Diagnosis 1. Complaint of a thunderclap headache should alert cli-
nician to diagnosis of SAH 2. Head CT without contrast
a. 92% of patients scanned within 24 hours after symptom
Table 10-5. Differential Diagnosis of Intraparenchymal Cerebral Hemorrhage
Table 10-6. Magnetic Resonance Imaging Characteristics of Intraparenchymal Cerebral Hemorrhage
T1 signal T2 signal
Stage Timing Central* Peripheral† Central* Peripheral†
onset show blood (hyperdensity) in subarachnoid spaces (Fig. 10-6 A)
b. CT findings “normalize” in up to 10% of patients by day 3 and in 50% by day 7
c. Note: if CT is negative but SAH is strongly suspected clinically, perform lumbar puncture if not otherwise contraindicated
d. Note: look closely in interpeduncular region for subtle
blood that may represent perimesencephalic SAH (Fig. 10-6 B), which has a more benign prognosis and is not usually associated with aneurysm rupture
3. Lumbar puncture a. Perform following tests on CSF: opening pressure,
leukocyte count, erythrocyte count in tubes 1 and 4, protein, glucose, Gram’s stain, xanthochromia
b. Distinguishing traumatic tap from SAH 1) If traumatic tap: erythrocyte count should decrease
from tube 1 to tube 4 2) Xanthochromia: should be evident with SAH but not
traumatic tap if symptoms started at least 6 hours earlier a) Xanthochromia: yellow tinge to CSF noted after
CSF is centrifuged b) It results from breakdown products of erythrocytes
and may be present if ictus was at least 6 hours before CSF examination
c) Thus, CSF examination performed less than 6 hours after onset may yield false-negative results because insufficient time has lapsed for erythrocytes to break down and form xanthochromia
d) For the same reason, xanthochromia is usually not
observed in traumatic tap e) Positive xanthochromia may also be seen when
CSF protein is very high or patient has hyperbilirubinemia
c. Note on CSF 1) For every 750 to 1,000 erythrocytes, 1 leukocyte 2) For every 1,000 erythrocytes, 1 mg/dL of protein
4. Angiography is necessary if nontraumatic SAH is expected a. Angiography can help detect the presence and morphol-
ogy of aneurysm and related abnormality b. Conventional angiography is superior to magnetic reso-
nance angiography (MRA) or CT angiography in this situation
c. Most common cause of nontraumatic SAH: saccular or berry aneurysms
d. Ruptured aneurysms are commonly smaller than 10 mm in diameter
e. Giant aneurysm, saccular aneurysm more than 25 mm in diameter may also rupture (Fig. 10-7); angiography is helpful in determining size, morphology, and relation of aneurysm to other blood vessels
D. Differential Diagnosis 1. Differential diagnosis of thunderclap headache (see
Chapter 18) 2. Differential diagnosis of SAH is listed in Table 10-7
E. Management of SAH 1. Aims: to support patient and prevent complications 2. Complications
a. Rebleeding 1) Timing: early 2) Risk: 4% in first 24 hours, 1% daily thereafter for
first 2 weeks 3) Treatment: endovascular coiling vs. surgical clipping
b. Hydrocephalus
1) Timing: early 2) Risk: 20% to 25% of patients develop hydrocephalus 3) Treatment: external ventricular drain or ventriculo-
peritoneal shunt c. Vasospasm
1) Timing: 4 to 14 days 2) Risk: up to 50% of patients have asymptomatic
vasospasm, 15% to 20% develop infarctions 3) Monitor: can be detected with transcranial Doppler
ultrasonography, angiography 4) Medical treatment
a) Augment blood pressure b) Increase volume status c) Nimodipine: reduces cerebral infarction rate due
to vasospasm but does not affect incidence of vasospasm
d) Endovascular treatment: angioplasty or intraarterial papaverine
d. Cardiovascular complications 1) Electrocardiographic changes (U waves) 2) Arrhythmia 3) Myocardial stunning (possibly due to catecholamine
surge) e. Seizures
1) Occur in 10% to 20% of patients 2) More common if associated intracerebral hemorrhage 3) Controversy about need for prophylactic antiepileptic
use, but treatment definitely indicated when seizure occurs
f. Pulmonary edema: neurogenic pulmonary edema may occur but is rare
g. Hyponatremia 1) Occurs in 10% to 30% of patients typically 2 to 10
days after symptom onset 2) May be secondary to cerebral salt-wasting syndrome
F. Outcome of SAH 1. Mortality rate: approximately 30% 2. For patients who arrive at hospital with SAH, initial
World Federation of Neurosurgeons (WFNS) grade and GCS score are used to determine outcome
3. Other factors that may contribute: age, amount of blood by CT (Fisher grade), seizures
4. Poor-grade SAH (WFNS grade 4-5): poor outcome if patient does not improve any grade within first 48 hours despite supportive treatment and ventriculostomy when needed
A. Epidemiology 1. Approximately 3% to 5% of U.S. general population
harbors an unruptured intracranial aneurysm 2. U.S. annual incidence of SAH: 30,000 3. This statistic suggests not all unruptured intracranial
aneurysms found incidentally will rupture 4. Location
a. More than 90% of aneurysms: anterior circulation (anterior communicating and posterior communicating arteries are most common)
b. 5% to 10%: posterior circulation c. Multiple aneurysms: 20% to 30% of patients
B. Causes 1. Risk factors for aneurysm formation
a. Female sex b. Hypertension c. Smoking d. Cocaine and/or methamphetamine use e. Certain connective tissue diseases (see below) f. Family history of two or more first-degree relatives
2. Good population-based data indicate polycystic kidney disease is associated with intracranial aneurysm formation
3. Case report and case series data suggest the following may predispose to intracranial aneurysm formation: a. Aortic coarctation
Table 10-7. Etiologies of Subarachnoid Hemorrhage
World Federation of Neurosurgeons Grading Scale for Subarachnoid Hemorrhage
Glasgow Coma Grade Focal deficit Scale score
1 Absent 15
2 Absent 13-14
3 Present 13-14
4 May/may not 7-12 be present
5 May/may not 3-6 be present
b. Pseudoxanthoma elasticum c. Ehlers-Danlos syndrome type IV d. Marfan syndrome e. Neurofibromatosis
C. Clinical Presentation 1. Unruptured intracranial aneurysms may present with
symptoms that are related to the aneurysm or the aneurysm may be noted incidentally when cerebral imaging study is performed for symptoms unrelated to aneurysm
2. Symptoms may include a. Compression
1) Unruptured intracranial aneurysms may compress nearby structures
2) Posterior communicating artery aneurysms often produce ipsilateral CN III palsy
b. Ischemic stroke: unruptured intracranial aneurysms may thrombose, producing thromboembolic stroke
3. Diagnosis a. Occasionally large aneurysms may be detected on unen-
hanced CT 1) Aneurysm often appears as slightly hyperdense well-
circumscribed structure 2) Occasionally, aneurysm wall may appear calcified
b. Diagnosis can be made with noninvasive studies such as MRA or CT angiography
c. Further characterization of the aneurysm may require conventional angiography, especially if endovascular coiling or surgical intervention is considered
4. Natural history a. Debated b. International Study of Unruptured Intracranial
Aneurysms (ISUIA) provides data from selected population on the natural history of these aneurysms 1) Predictors of future rupture: posterior circulation
aneurysm (including posterior communicating artery aneurysm), increasing size, and previous SAH from separate aneurysm (Table 10-8)
2) Patients with an anterior circulation aneurysm smaller than 7 mm and no previous history of SAH: very low risk of future rupture
5. Treatment a. Options: observation, surgical clipping, endovascular
coiling b. Treatment is based on
1) Patient age 2) Natural history of aneurysm in individual patient 3) Risk of coiling vs. open surgery based on angioarchi-
tecture of aneurysm
A. Infectious Aneurysms 1. Epidemiology
a. 3% of all intracranial aneurysms b. 2% to 12% of all patients with infectious endocarditis
2. Pathogenesis a. Aneurysm dilatation may result from
1) Direct infection of intima and inflammation of muscularis from septic emboli
2) Septic emboli to vasa vasorum, causing destruction of adventitia and muscularis
b. May occur within 7 to 10 days after initial infection c. Etiology
1) Majority of infectious intracranial aneurysms due to bacterial sources
2) Infectious endocarditis is most common source for septic emboli, but contiguous spread from parameningeal infection or seeding from remote site may also produce arteritis and aneurysm
3) Fungal intracranial aneurysms are more commonly due to contiguous spread but are exceedingly rare and
Table 10-8. Five-Year Cumulative Rupture Rates of Unruptured Intracranial Aneurysms
Diameter, mm
<7
Location Group 1* Group 2† 7-12 13-24 ≥25
usually in immunocompromised patients 4) Organisms
a) Streptococcus (most common) b) Staphylococcus aureus c) Enterococcus d) Aspergillus (rare) e) Phycomycetes (rare)
3. Clinical presentation a. Incidental b. Headache
1) Neurologic deficit in setting of endocarditis or fever 2) Seizures
4. Natural history a. Exact risk of rupture of infectious aneurysms: not
known because of their rarity b. Rupture usually occurs early after disease onset; may be
the clue leading to diagnosis of endocarditis 5. Diagnosis
a. MRI of head may suggest aneurysm, but conventional angiography is best to make the diagnosis
b. Aneurysms often are distal in arterial tree, so currently MRA is sometimes unreliable in making the diagnosis (Fig. 10-8)
6. Treatment
a. Targeted antibiotic treatment and surgery in selected patients
b. Surgery is considered for 1) Ruptured aneurysm 2) Life-threatening mass effect of aneurysm 3) Evidence of enlargement 4) Easily accessible single aneurysms
B. Fusiform Aneurysms 1. Epidemiology
a. Uncommon b. Estimated prevalence by autopsy studies: 0.05%
2. Pathogenesis a. Risk factors for development of this aneurysm type:
smoking, hypertension, male sex, age b. Concomitant pathology in other vessels is common,
with high incidence of abdominal aortic aneurysms c. More common in posterior than anterior circulation
3. Radiographic diagnosis a. Dilatation of arterial segment(s) 1.5 times normal size
without a definable neck; may also be tortuous and/or elongated
b. Best defined by both cross-sectional imaging and angiography (Fig. 10-9)
4. Clinical presentation a. Typically in patients older than 60 years b. Asymptomatic c. SAH d. Mass effect (compression) e. Ischemia (thrombosed aneurysm with thromboemboli)
5. Natural history a. Risk of hemorrhage: reportedly rare, but may be as high
as 2.3% annually in posterior circulation if there is enlargement of entire basilar artery with a superimposed aneurysmal segment
b. Risk of ischemia: may be as high as 5% to 6% annually for posterior circulation aneurysms
c. Mortality: median survival with posterior circulation fusiform aneurysms is approximately 7 to 8 years
d. Most common cause of death: cerebral ischemia 6. Treatment
a. Treatment options are limited b. In selected patients, vessel may be sacrificed or feeding
vessel may be occluded to reduce flow to the parent vessel; this may reduce chance of aneurysm enlarging (but this has not been proved definitively)
C. Dissecting Aneurysms 1. Pathogenesis
a. False aneurysms resulting from intimal tear and intramural hemorrhage
b. Most commonly are extracranial; may be saccular or fusiform
c. Angiography or MRA may help distinguish between dissecting and typical acquired aneurysms 1) This distinction is not always possible 2) Suggestive features: evidence of false lumen, intimal
flap, retention of contrast in lumen or tapering of artery at proximal end of the aneurysm
2. Etiology a. Trauma b. Atherosclerosis c. Fibromuscular dysplasia d. Infection e. Arteritis
3. Clinical presentation a. Cerebral infarction or transient ischemic attack b. Extracranial dissecting aneurysms rarely rupture; because
their extradural location eliminates concern about SAH, treatment is typically aimed at preventing further ischemia
c. Intracranial dissecting aneurysms 1) May present with ischemia 2) Are intradural, thus substantial risk of SAH 3) Over half of patients experience rebleeding after initial
hemorrhage, with substantial increase in morbidity 4. Treatment: surgical vs. endovascular repair depending
on location and size
D. Neoplastic Aneurysms 1. Exceedingly rare 2. Have been described in association with many types
of primary and metastatic brain tumors 3. Tumor emboli infiltrate and weaken vessel wall and
may result in aneurysm formation 4. Typically located distally; may be saccular or fusiform
in shape
A. Intracranial Pressure (ICP) 1. Physiology
a. The skull is a fixed structure not allowing expansion b. Intracranial volume (~1,900 cm3) consists of three
compartments: brain (80%), blood (10%), CSF (10%) c. Monroe-Kellie doctrine: if the volume of one of these
compartments increases, the volume of another must decrease to maintain normal ICP (0-20 mm Hg)
d. First measures in preventing increasing ICP: generally CSF is shifted to spinal subarachnoid space and arterial and venous structures collapse, reducing blood volume
e. If these measures are not effective, the brain may begin to herniate because of increasing ICP, or if ICP increases above mean arterial pressure, then cerebral perfusion pressure will drop and ischemia result
f. Autoregulation 1) Changes in cerebral perfusion pressure between 60
and 160 mm Hg do not alter cerebral blood flow because of autoregulation a) Above or below these pressures, flow is related to
pressure (Fig. 10-10) b) In patients with long-standing hypertension, the
entire curve is shifted to the right; therefore, it is important not to aggressively treat blood pressure to levels that can decrease cerebral blood flow
c) The shift in autoregulation is an important adaptive mechanism against large increases in blood pressure that may otherwise cause hypertensive encephalopathy
2) Autoregulation may become impaired, resulting in pressure-dependent flow if brain injury occurs, with the brain becoming more susceptible to ischemia
2. Causes of raised ICP (Table 10-9) a. Space-occupying mass, for example, brain tumor, abscess b. Brain edema
1) Cytotoxic: fluid accumulation within cells 2) Vasogenic: proteinaceous fluid leaks into extracellular
space from capillaries
Relation Between Cerebral Perfusion Pressure and Intracranial Pressure
Formula Normal
3) Interstitial: CSF pushed into extracellular space in periventricular white matter in hydrocephalus
c. Hydrocephalus: increased CSF from 1) Overproduction: rare, choroid plexus papilloma 2) Ventricular obstruction: obstructive hydrocephalus
3) Arachnoid granule obstruction: nonobstructive, communicating hydrocephalus
d. Venous thrombosis: impairs CSF reabsorption 3. Diagnosis: clinical signs
a. Headache b. Vomiting c. Papilledema d. Herniation syndromes (see below) e. Hypertension and bradycardia f. Transient visual obscurations g. False localizing CN VI palsy
4. Indications for ICP monitoring a. GCS score less than 8 b. Severe head trauma c. ICP waveforms
1) Plateau (A) waves a) Sudden surges in ICP to 50 to 80 mm Hg lasting 5
to 20 minutes
b) Presence of A waves suggests failing compliance of the brain to ICP and risk for ischemia
2) B waves: smaller surges in ICP to 20 mm Hg for 1 to 2 minutes
5. Management (Table 10-10) a. Measures to reduce intracranial pressure are aimed at
reducing volume of CSF, brain, or blood (or combination)
b. Specific measure for reducing intracranial pressure: depends on the abnormality
6. Herniation syndromes: supratentorial (Fig. 10-11) a. Subfalcine
1) Herniation of brain tissue under falx cerebri 2) Generally occurs with unilateral space-occupying
mass in a cerebral hemisphere b. Central (diencephalic)
1) Diencephalon is displaced downward through tentorium cerebelli, resulting in rostrocaudal
Table 10-10. Management of Increased Intracranial Pressure
Measure Compartment Recommended
Table 10-9. Etiologies of Increased Intracranial Pressure
deterioration of sequential brainstem structures 2) May result in Duret’s hemorrhages of brainstem (Fig.
