1. Neurosurgical Aspects of
Central Nervous System
Infections
Jason A. Heth, MD
Infections of the central nervous system (CNS) can
be severe, life changing, and potentially fatal. Neuro-
surgeonsplayacrucialroleinthetreatmentofcertain
CNS infections. Imaging is important for appropriate
diagnosis, lesion localization, identification of sur-
gicalcandidates,andperformanceofsurgicalproce-
dures. High-quality imaging is therefore crucial to the
neurosurgeon. The knowledge of how neurologic
imaging is used by the neurosurgeon may be helpful
to the interpreting neuroradiologist. This article
reviews the most common CNS infections neuro-
surgeons encounter. Pathogenesis; microbiology;
surgical indications; treatment, including surgical
procedures; and prognosis are discussed.
INTRACEREBRAL ABSCESS
Brain abscess has been one of the most feared
CNS infections. This fear arose from the initial
poor outcomes and from the rapid neurologic
deterioration that can occur. Although rapid dete-
rioration can still occur, the overall outcomes have
improved because of improved antibiotics and
imaging, which minimize the delay in diagnosis
and treatment.
The brain parenchyma is not prone to paren-
chymal abscess formation, whereas other events
and risk factors are required to set the stage for
abscess formation. Inoculation can occur from
direct implantation (such as a bullet entering the
brain or after neurosurgery) or contiguous spread
(such as from adjacent sinusitis or mastoiditis).1,2
Most commonly, however, infection elsewhere
spreads hematogenously to the CNS.3
A classic
example is bacterial endocarditis with septic
emboli to the brain resulting in cerebral abscess
formation.4,5
Other common primary sites include
dental abscesses,6
cutaneous abscesses, urinary
tract infection, pulmonary infection, and soft tissue
infection.3
Department of Neurosurgery, University of Michigan, 1500 East Medical Center Drive, Ann Arbor, MI 48103-5338,
USA
E-mail address: jheth@umich.edu
KEYWORDS
Cerebral abscess Meningitis Subdural empyema Encephalitis CNS infection
KEY POINTS
Intracerebral abscesses can rapidly cause severe neurologic deficits or death and require prompt
evaluation, imaging, and treatment.
Subdural empyema is an uncommon but potentially life-threatening infection that typically requires
prompt surgical decompression, culturing, and antibiotics.
The organisms causing meningitis vary by the age of presentation and require prompt treatment
with differing antibiotics.
Herpes simplex encephalitis requires very rapid recognition, diagnosis, and antiviral treatment to
prevent severe neurologic deficits or death.
Spinal diskitis and spinal epidural abscess are uncommonly a threat to life but may cause para-
plegia or quadriplegia without expeditious evaluation, imaging, and treatment.
Neuroimag Clin N Am 22 (2012) 791–799
doi:10.1016/j.nic.2012.05.005
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2. Several conditions can predispose to cerebral
abscess formation. Systemic immunosuppression
is frequently involved. Immunosuppression can
occur because of intentional immunosuppression
(eg, to prevent organ transplant rejection),
immune system destruction (eg, with human
immunodeficiency virus [HIV] and AIDS), or other
medications that affect the immune system (eg,
corticosteroids and chemotherapy agents). Pulmo-
nary arteriovenous malformations, with or without
Osler-Weber-Rendu syndrome,7,8
and congenital
cyanotic heart malformations9,10
are also thought
to be risk factors.
Abscess development occurs in a 3-step
process.11
The early cerebritis phase is marked
by an area of poorly demarcated inflammation.
The late cerebritis phase is marked by the migra-
tion of fibroblasts, which start depositing reticulin.
In addition, necrosis begins to appear centrally.
The early capsule (abscess) stage is marked by
the migration of additional fibroblasts and genera-
tion of more reticulin in an attempt to wall off an
increasing amount of central necrosis. The late
capsule stage is marked by a mature collagen
capsule surrounding the central necrotic zone.
The microbiology typically reflects the patho-
gens from the primary site that seeded the CNS.
Therefore, gram-positive cocci (GPC) predomi-
nate after intravascular infection. Infections begin-
ning from the urinary tract are more frequently
gram-negative rods (GNR). Postsurgical and
penetrating injuries typically result in skin-related
pathogens—mostly GPC. Abscesses resulting
from contiguous sinus spread often may harbor
more anaerobic organisms,3
whereas dental
abscesses give rise to polymicrobial or anaerobic
cerebral abscess pathogens.
Patients present with a myriad of possible symp-
toms. The most common symptoms are headache,
fever, nausea and vomiting, focal neurologic defi-
cits, abnormal sensorium, and decreased level of
consciousness.
Treatment of brain abscess requires accurate
microbiological diagnosis and appropriate antibi-
otic therapy. If a patient is not neurologically
deteriorating, has no or minimal deficits; and if
a microbiological diagnosis can be obtained from
another location, antibiotic therapy may be
prescribed without a neurosurgical procedure.
This strategy does require high quality diagnostic
imaging to characterize the lesions initially and
during follow-up. If the lesions respond to antibi-
otics by decreasing in size and ultimately resolu-
tion, then no neurosurgical procedures are
required. If the lesions grow, then biopsy and
drainage may be required. Stereotactic biopsy
and needle drainage is required when abscess is
strongly suspected but no primary sites can be
identified to culture and when there is a large
lesion or lesions causing mass effect and signifi-
cant neurologic deficits. Craniotomy for resection
of abscess is another surgical alternative if needle
drainage is not successful.
The prognosis is related to the initial presentation,
response to antibiotic therapy, and any systemic
conditions or risk factors that may hinder innate
immunologic attempts to clear the infection. Recent
mortality ranges from 5 to 50.3,12–14
Patients with no
risk factors and stereotactic aspiration had 5%
mortality whereas those with several risk factors
had 50% mortality.12
Negative prognostic factors
include worse functional status at presentation,
immunocompromise,12
and older age.3
SUBDURAL EMPYEMA
Subdural empyema (SDE) is a very serious but
uncommon CNS infection. An empyema is a local-
ized purulent infection in an actual cavity or
a potential space. In SDE, the empyema occurs
in the subdural space. Several mechanisms
explain the development of SDE. SDE can occur
as a complication of meningitis,15
after crani-
otomy,16,17
and as a result of extension of para-
nasal sinus infections1,18
or otitis media.
Patients with SDE present with headache, signif-
icant neurologic deficits, seizures, decreased level
of consciousness, and fever. Empyema can
compress the brain focally to cause focal deficits.
SDE can cause significant inflammation in the
subjacent cortex to cause seizures. If the mass
effect, inflammation, and edema are significant
enough, midline shift, herniation, and global decline
can occur.
Therangeofmicrobiologicaldiagnosesisdifferent
from that of intracerebral abscess and meningitis
because of the direct extension from the paranasal
sinuses or mastoid. Gram-negative organisms are
Intracerebral abscesses can rapidly cause severe
neurologic deficits or death and require prompt
evaluation, imaging, and treatment.
Subdural empyema is an uncommon but poten-
tially life-threatening infection that typically
requires prompt surgical decompression,
culturing, and antibiotics.
Heth792

3. frequently reported to predominate.19,20
In contrast,
cultures from postsurgical SDE usually are domi-
nated by gram-positive species.16,17,21
Surgical treatment must address 3 issues. The
first issue is accurate microbiological diagnosis.
On occasion this may be obtained from a primary
site such as the paranasal sinuses or mastoid. If
no other active site is identified, neurosurgical inter-
vention is required. The second issue is CNS mass
effect. Mass effect, midline shift, and parenchymal
displacement typically call for surgical intervention.
Very significant mass effect and cerebral edema
may require craniotomy or craniectomy for decom-
pression and debridement. The third and final issue
is the possibility of surgical treatment for purulent
loculations that may be too large for antibiotics
alone to treat. In such situations, it may be possible
to culture, aspirate purulent material, and irrigate
the subdural space with antibiotic solution through
burr holes.
The prognosis is guarded with SDE. These
patients are very ill, both systemically and neurolog-
ically. They require close multidisciplinary manage-
ment among the neurosurgical, infectious disease,
and critical care teams. Tsai and colleagues21
re-
ported 11 of 15 patients having good outcomes
(normal to moderate disability) and 4 of 15 patients
having poor outcomes (severe disability to death).
Hlavin and colleagues19
reported a mortality rate of
18.5% and an additional 18.5% survived withneuro-
logic morbidity. They also found advanced age and
more significant encephalopathy at presentation to
portend a worse prognosis as well.
MENINGITIS
Meningitis is one of the most common CNS infec-
tions, with an incidence of 3.67 to 12.5/100,000
patients.22,23
Meningitis is an infection of the cere-
brospinal fluid (CSF) and the meningeal layer
surrounding the brain. The infection can involve
the cerebral ventricles to cause ventriculitis.
Meningitis is most frequently treated by neurol-
ogists, pediatricians, and infectious disease
specialists. However, it is crucial for all physicians
to understand and recognize meningitis because
meningitis is generally very treatable when
promptly diagnosed and treated, whereas menin-
gitis can be devastating if diagnosis and treatment
are delayed.
Meningitis presents most commonly with head-
ache, fever, and nuchal rigidity. Other symptoms
include seizures and cranial nerve deficits. Loss
of consciousness can occur from seizures, inflam-
mation and cerebral edema, or hydrocephalus.
Herniation can occur and cause coma and death.
The pathogenesis and range of responsible
microbes differ with age groups. Neonatal menin-
gitis occurs due to exposure to pathogens during
delivery, particularly with vaginal delivery.24
Patho-
gensinclude Escherichiacoli,groupBstreptococci,
and Listeria. Children aged 3 months to 5 years are
predominantly affected by Streptococcus pneumo-
niae and Neisseria meningitidis (meningococcus).
Pneumococcus is a colonizer of the nasopharynx
that is transmitted via respiratory droplets and
secretions. From the nasopharynx, it can spread
to cause meningitis. A 7-valent pneumococcal
vaccine was licensed for use in the United States
which resulted in a decrease in childhood pneumo-
coccal meningitis incidence and mortality.15
Menin-
gococci are gram-negative commensal bacteria
that colonize the nasopharynx. Transmission also
occurs through respiratory droplets and secretions.
Once colonization has occurred, meningococci
can then progress to meningitis, which has a very
fulminant and rapid course. This fact makes vacci-
nation strategies much more attractive to prevent
meningococcal meningitis.25
A quadrivalent menin-
gococcal vaccine was licensed for use in 2005, and
monitoring is ongoing to assess the decrease in
meningococcal meningitis incidence. Haemophilus
influenzae type b previously was an important
species in this age group; however, routine child-
hood immunization (Hib) begun in the early 1990’s
has reduced the incidence of H influenzae menin-
gitis nearly to 0. Patients aged 5 years–50 years
continue to experience meningitis caused predom-
inantly by S pneumoniae and meningococci.24
Spread is facilitated among people living in close
quarters, such as dormitories. Patients older than
50 years experience S pneumoniae and meningo-
coccal infections; however, Listeria and gram-
negative entericorganisms can also be causative.24
The treatment of meningitis requires prompt
diagnosis and antibiotic administration. If there is
any suspicion about the possible presence of
meningitis, especially if a patient is experiencing
significant symptoms, a first dose of broad-
spectrum antibiotics should be given. The mainstay
of diagnosis is the lumbar puncture (LP). Gram’s
stain and cell count with differential, total protein,
and glucose are recommended. Again, antibiotic
administration is begun without waiting for these
results if concern of meningitis is present.
Neurosurgical intervention is required if hydro-
cephalus is present. In the setting of meningitis,
The organisms causing meningitis vary by the
age of presentation and require prompt treat-
ment with differing antibiotics.
Central Nervous System Infections 793

4. a ventriculostomy would be placed for ventricular
drainage while the infection is treated. Once
treated, it may be possible to wean the drainage if
the normal CSF outflow can resume. If the normal
CSF outflow does not re-establish itself, ventriculo-
peritoneal shunt placement is likely required.
Heroic measures such as craniectomies, either
supratentorially or in the posterior fossa in the
case of trans-foramen magnum herniation are
sometimes recommended in severe cases.26,27
These procedures are more likely to be considered
when the deterioration has been very abrupt,
observed, brought rapidly to medical attention,
and the patient is already in the hospital so that
surgery can be rapidly undertaken. When rapid
devastating deficits develop before the patient
presents in hospital, the time involved in transport,
evaluation, transport to operating room, set-up,
and start, even when rapidly undertaken, rarely
occurs quickly enough to reverse neurologic
devastation.
Prognosis for patients with meningitis is variable.
Rapid diagnosis and initiation of antibiotics is
crucial to improving outcomes; Køster-Rasmussen
and colleagues28
demonstrated a 30% increase in
odds of unfavorable outcome per hour of delay
before antibiotic administration. Recent mortality
ranges from 13% to 18.7%.13,22
Neonates, the
elderly, the immunocompromised, and those
presenting with significant neurologic deficits
suffer higher mortality rates. Major morbidities
occurred in 12.8% of cases and minor morbidities
occurred in 8.6% of cases.29
The most common
morbidities were hearing loss (33.6%), seizures
(12.6%), and motor deficits (11.6%).29
VIRAL, FUNGAL, AND PARASITIC INFECTIONS
Viral and fungal infections can also cause very
significant neurologic dysfunction and imaging
abnormalities. Antiviral and antifungal agents are
the main treatments for these infections; however,
neurosurgical treatment is also sometimes
required. Such infections include herpes encepha-
litis (HSE), viral encephalitis, toxoplasmosis, and
neurocysticercosis.
HSE
Herpes encephalitis (HSE) is a very serious condi-
tion, which is the most common and likely most
severe viral encephalitis and therefore will be dis-
cussed separately. The herpes virus reactivates
and generates a very significant inflammatory
reaction that occurs predominantly in the temporal
lobes. Viral reactivation sets off a chain of events
resulting in necrosis (frequently hemorrhagic) in
the temporal lobes. Although a high percentage
of the population harbors the herpes virus, HSE
is uncommon, occurring in approximately 1 in
250,000 to 500,000 patients per year.30
Patients may present with altered mentation,
decreasing consciousness, focal neurologic find-
ings, headache, seizures, and fever. HSE occurs
in all age ranges.30
Effective treatment of HSE depends on rapid
recognition and treatment. The presentation,
physical examination, imaging, and laboratory
results from peripheral blood typically suggest
the diagnosis to begin intravenous acyclovir. Early
administration of antiviral medication is crucial in
halting the process. LP may also be recommended
as long as the basal cisterns are patent, and the
risk of herniation after LP is thus minimized. CSF
is examined to rule out bacterial infection. CSF
analysis typically demonstrates a cellular pleocy-
tosis and high protein with normal glucose values.
Detection of HSV DNA by polymerase chain reac-
tion (PCR) has a sensitivity of 94% and a specificity
of 98%31
and is now the gold standard of clinical
diagnosis of HSV encephalitis.
The primary treatment is the rapid use of
acyclovir as first-line therapy.32
Seizures are
aggressively treated. Attentive supportive care is
provided. Surgical intervention is rarely undertaken
with the possible exception of fulminant HSE with
significant mass effect on the brainstem. In this
setting, craniectomy may be considered.33,34
The prognosis for HSE depends on early diag-
nosis. Without effective treatment, mortality rate
is greater than 70% with only 9% of survivors
returning to normal function30
With acyclovir, the
6-month mortality is 19%.30
The rate of return to
normal function in the setting of acyclovir treat-
ment is 38%.30
Viral Encephalitis
Viral encephalitis is a diffuse viral infection, particu-
larly of the cerebrum and cortex. Patients with viral
encephalitis present with a range of symptoms,
including headaches, behavioral changes, fever,
seizures, and altered sensorium.32,35
Viral patho-
gens include Varicella; Enteroviruses; Measles;
Rubella; Mumps; arthropod-borne viruses, such
as West Nile Virus and Japanese encephalitis;
rabies; and human herpes virus 6 amongst many
others.36
Diagnosis typically, includes history,
Herpes simplex encephalitis requires very rapid
recognition, diagnosis, and antiviral treatment
to prevent severe neurologic deficits or death.
Heth794

5. physical examination, laboratory studies, imaging,
and LP. LP is notable for lack of bacterial growth,
normal glucose, high protein, and possibly a high
white blood cell count. Frequently, CSF leukocy-
tosis shows a predominance of lymphocytes.
CSF from LP can also be subjected to PCR testing
to assay for herpes simplex virus (HSV), Varicella
zoster virus (VZV), human herpes virus (HHV) 6
and 7, cytomegalovirus (CMV), Epstein-Barr virus
(EBV), enteroviruses, and HIV amongst others.32
Serologic testing for antibodies to HSV, VZV,
CMV, HHV6 and HHV7, EBV, HIV, influenza A and
B, respiratory syncytial virus, rotavirus, coxsackie
B5 and parainfluenza 1 viruses32
is also available.
The minimum treatment of viral encephalitis is
attentive supportive care. Seizures are aggres-
sively treated. Depending on the causative agent,
antiviral therapy may be available. For VZV,
acyclovir may also be used. Foscarnet or ganciclo-
vir can be used for HHV6. Ganciclovir, foscarnet,
cidofovir can be tried for CMV. Corticosteroid
treatment is controversial and no definitive
recommendations are made for their use in viral
encephalitis.
The prognosis is generally variable and depends
on the patient’s age, systemic condition, and the
causative virus. In adults, West Nile Virus encepha-
litis resulted in death in 13% of cases and 38% dis-
charged to a long-term care facility.37
Wong and
Yeung38
reported mortality of 28%. Of the survi-
vors, 24% had neurologic sequelae. Wang and
colleagues39
reported 26% mortality in culture-
proven enterovirus cases. As these representative
reports demonstrate, mortality and morbidity rates
can be considerable for viral encephalitis.
Toxoplasmosis
Toxoplasma gondii is an obligate intracellular para-
site that is the causative agent of CNS toxoplas-
mosis. T gondii is typically acquired by ingestion
of oocysts from contaminated soil or food, or
bradyzoites in undercooked meat.40
In im-
munocompetent adults, the parasites is typically
controlled; however, it can reactivate in the setting
of immunosuppression. Two populations may be
affected by this parasite: neonates and the immu-
nosuppressed patients (particularly patients with
AIDS and transplant patients).41,42
Risk factors
for acquiring T gondii include working with meat;
having 3 or more cats; eating locally produced
cured, dried, or smoked meat; eating rare lamb
or raw ground beef; and drinking unpasteurized
goat’s milk.43
Neonates may be infected by in ute-
ro transplacental transmission of the parasite,
which can cause fetal death, CNS calcifications,
chorioretinitis, and hydrocephalus. Adult patients
again may present with varying symptoms and
signs, including headache, fever, seizures, focal
neurologic deficits, and more severely diminished
sensorium. PCR and quantitative real time PCR
can also be done for the DNA of Toxoplasma in
the CSF with sensitivity of 79% to 100% and spec-
ificity of 92% to 97%.44,45
In some occasions,
when all attempts at diagnosis have failed, stereo-
tactic biopsy of a representative lesion can be
performed. This procedure has been an issue in
the management of patients with AIDS with
abnormal ring-enhancing lesions. The differential
diagnosis in this setting includes lymphoma. One
strategy to obtain the diagnosis is to treat for
toxoplasmosis and assess the response.46,47
A
positive response favors a toxoplasmosis diag-
nosis whereas no response still leaves a diagnostic
dilemma that may require surgical biopsy to
resolve.
Toxoplasmosis is treated with antitoxoplasmo-
sis agents. The prognosis is good if treatment is
started expeditiously and the immunosuppression
can be minimized.
Neurocysticercosis
Neurocysticercosis is a parasitic disease caused
by Taenia solium. Humans are the definitive hosts
in whom the parasite develops into an adult tape-
worm, reproduces, and sheds eggs. The eggs can
then be ingested by several intermediate hosts.
Pigs are the prototypical intermediate host. The
cysticerci lodge in the skeletal muscle of pigs; if
the meat from infected pigs is not cooked appro-
priately, the cysts from the ingested meat allow
the parasite to complete its life cycle by devel-
oping into adult tapeworms,48
resulting in taeni-
asis. When a human ingests the parasite eggs,
they treat the human host as an intermediate
host. The eggs hatch and migrate throughout the
body to lodge and develop into cystic larval forms.
These cysts can occur in the skeletal muscle,
brain, eye, and subcutaneous tissue.49,50
Neuro-
cysticercosis is endemic in the developing world
and is a leading cause of epilepsy worldwide.49
Patients with neurocysticercosis may present in
different manners based on lesion location. Symp-
toms depend on cyst location, the number of
cysts, and the degree of immune response to the
disease.49
Cysts can occur in the brain paren-
chyma, the ventricular system, the subarachnoid
space, and the spinal cord. Seizures can occur
when cysts cause cortical dysfunction. Hydro-
cephalus can be caused by cysts occluding the
CSF outflow pathways and can be symptomatic
with headaches, somnolence, or loss of con-
sciousness. Focal neurologic deficits can arise
Central Nervous System Infections 795

6. from loss of function caused by a cortical or spinal
cyst. Patients may also present with dementia.51
The clinical setting and imaging can strongly
suggest the diagnosis. Serologic testing on CSF
and peripheral blood are very specific and quite
sensitive for T solium infection.49,50
Diagnostic
biopsy may be obtained from cysts in other loca-
tions, such as skeletal muscle. Patients in whom
these evaluations cannot solidify the diagnosis,
a diagnostic CNS biopsy may be required.
Treatment is directed at the presenting symp-
toms as well as the parasite itself. Seizures are
aggressively treated. Seizure control is very high
with appropriate anticonvulsant management
although lifelong anticonvulsants may be required.
Hydrocephalus must be aggressively treated.
Endoscopic treatment can include cyst removal,
third ventriculostomy, and septum pellucidum
fenestration.52,53
If endoscopic treatment fails or
is not an option, shunt placement can be per-
formed although there is a concern for high rate
of failure with neurocysticercosis. If a cyst is large
and causing mass effect and neurologic deficits,
a cyst resection could be considered. Cysticidal
treatment is recommended to treat the parasites
themselves.
The prognosis depends on the manner of
presentation. Seizures can be readily controlled
with good outcomes. Hydrocephalus can also be
effectively treated. Intracranial hypertension re-
sulting from mass effect from the cysts or from
an aggressive immune response to the cysts can
be life threatening.
SPINAL DISKITIS AND SPINAL EPIDURAL
ABSCESS
Vertebral diskitis and spinal epidural abscess (SEA)
are CNS infections that can affect the spine and
spinal cord. They are discussed here, because
they are readily treated with good outcomes if
promptly recognized and treated. If not promptly
recognized and treated, they can cause rapid onset
paraplegia and quadriplegia. Diskitis and SEA
occur through similar mechanisms. Diskitis can
also occur through direct inoculation (even with
proper antisepsis), such as LP, diskogram, surgical
exposure, and epidural anesthesia.The disk space
can be seeded from a primary infection elsewhere,
such as a soft tissue infection or endocarditis.
SEA can arise from untreated diskitis as well as
direct exposure54,55
as previously mentioned. In
one report, as many as 52.6% of SEA cases were
associated with neurosurgical procedures or spinal
blocks.56
SEA can also occur from contiguous
spread. An example is cervical soft tissue abscess
that erodes into the cervical spinal canal.
The main complaint of patients with diskitis is
pain appropriate to the spinal level. Diskitis is
a very painful condition and responds poorly to
first-line medications used to treat degenerative
spine disease. Fever can also occur.56,57
Diskitis
in the lumbosacral region can cause radicular
symptoms with leg pain and radicular deficits.
Stenosis can also occur and cause leg pain that
worsens with ambulation. Diskitis in the cervical
and thoracic regions can cause radicular symp-
toms, but most importantly cervicothoracic diskitis
can cause spinal cord compression, myelopathy,
and quadriparesis/plegia or paraparesis/plegia,
respectively. Incontinence can also occur.57
Risk factors for diskitis and SEA are similar to
previousinfectiousconditionsdiscussedandinclude
diabetes mellitus, end-stage renal disease, endocar-
ditis, immunosuppression, hepatic cirrhosis, and
illicit intravenous drug use.57,58
Patients with SEA also can have pain55
although it
is not as uniformly and exquisitely painful as diskitis.
The same range of neurologic deficits can occur.
The microbiological species involved vary.56,57
Staphylococci are the species most commonly iso-
lated.56–58
If seeding occurs from a primary site, the
microbiology of the primary site will dictate the
diagnosis. Direct spread from cervical, abdominal,
or pelvic abscess increases the possibility of GNR,
anaerobic, and polymicrobial infections. Individ-
uals in whom diskitis and SEA occur from direct
manipulation, skin flora and GPC dominate. Fungal
and candidal diskitis can also occur.59
Diagnosis and treatment of diskitis and SEA
must address 3 issues. The first issue is microbio-
logical diagnosis, which allows prescription of
maximally effective antibiotics.Diagnosis from
a primary site may be possible. With diskitis,
computed tomography–guided needle biopsy
yields the diagnosis in 90% of cases.59
In some
cases, open biopsy may be required if all other
diagnostic attempts have failed. The second issue
that must be addressed is neural compression. In
spinal cord compression with cervical or thoracic
myelopathy, emergent decompression is indi-
cated and usually requires laminectomy. If cauda
equina symptoms develop from lumbar diskitis or
SEA, emergent decompression, usually laminec-
tomy, is required. In cases of radicular symptoms
only, nerve root decompression may be consid-
ered. The third issue that must be considered is
Spinal diskitis and spinal epidural abscess are
uncommonly a threat to life but may cause
paraplegia or quadriplegia without expeditious
evaluation, imaging, and treatment.
Heth796

7. spinal stability. If the infection has destroyed crit-
ical spinal elements, then spinal stabilization may
be also be required.
The prognosis for diskitis is generally good if
promptly diagnosed and the treatment is rapidly
begun. Eighty percent of cases can experience
a good outcome.59
Mortality is uncommon and
depends more on systemic infection. Similarly,
prompt diagnosis is important to overall prognosis
in SEA.56
The prognosis in SEA has been variable in
the literature. One group reported 10 of 21 cases
deteriorating,58
whereas another reported 67% to
75% of patients improving after treatment57
and
5% worsening neurologically. Mortality rate in
SEA can be up to 23% and can occur secondary
to systemic sepsis or resulting from systemic
conditions that predispose to SEA, such as end-
stage renal disease.57
SUMMARY
CNS infections are very serious conditions, which
cause rapidly progressive symptoms and loss of
function. Rapid deterioration can also lead to
death, which is particularly true of cerebral
abscess, SDE, meningitis, and herpes simplex
encephalitis. Although perhaps not as frequently
life threatening, diskitis and SEA can cause rapid
onset of very severe neurologic deficits. In all of
these conditions, rapid diagnosis and treatment is
crucial. Imaging is important for appropriate locali-
zation, diagnosis, and surveillance once treatment
has begun. Viral encephalitis, toxoplasmosis, and
neurocysticercosis can also cause a myriad of
symptoms and disability. Again, imaging plays
a crucial role in diagnosis and in treatment of these
conditions as well.
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