CHAPTER

26

Infectious Processes

Affecting the

Nervous System

Ross H. Miller

Infections involving the intracranial and intraspinal spaces
are caused by microorganisms. These organisms reach the
central nervous system (CNS) via the bloodstream and/or
invade the spaces directly following penetrating wounds or

surgery. Infections may enter the skull by direct extension

from the mastoid air cells (to the temporal area) or paranasal
sinuses (frontal area) of the intracranial cavity.' A congenital
dermal sinus may become infected and the infection extend
into the intracranial and intraspinal spaces.

Infections become disseminated by the cerebrospinal fluid

(CSF) once the organisms reach the CSP. Treatment of
infections of the CNS involves: (1) identification of the
organism and its source, (2) selection of appropriate antimi-
crobials (see Table 26-1),

2

(3) removal of any collection of

purulent material (abscesses, empyema), (4) treatment of the

sources of the infection, and (5) control of any complications
that may occur as a result of infection.

GENERALIZED INFECTIONS OF THE

NERVOUS SYSTEM

MENINGITIS

Bacterial infections When an infectious process in-

vades the leptomeninges, headache, fever, and stiff neck
indicate irritation of the structures. Organisms responsible
for meningitis vary with the age of the patient. Escherichia
coli, fi-hemolytic streptococci, and Haemophilus influenzae
are most common in pediatric patients. Streptococcus pneu-

moniae and Neisseria meningitidis are more common in

adult patients. Fungi and Mycobacterium tuberculosis pro-
duce chronic meningitis.

Headache, fever, sensitivity to light, nausea, and vomiting

are the most common symptoms of meningitis. Seizures may

occur with cortical irritation by the inflammatory process.
Invasion of the brain by the infection will produce focal
neurological defects. Cranial nerve palsies occur with exu-
dates over the base of the brain and are more common in
chronic meningitis caused by tuberculosis or fungi.

3

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4

Upon

examination, the patient may be irritable and drowsy, and
the neck will be stiff. Papilledema may be present.

Examination of CSF will confirm the diagnosis of menin-

gitis in most patients. A lumbar puncture (LP) should be
postponed when papilledema is present. Hemiation of a
temporal lobe into the tentorial notch or hemiation of the
cerebellar tonsils into the foramen magnum may occur with
release of CSF from the lumbar area. It is important to
obtain a computerized tomogram (CT) or magnetic reso-
nance image (MRI) to rule out a mass lesion as a cause for
the papilledema before a decision is made to perform an LP.

Meningitis is confirmed if the CSF contains large num-

bers of polymorphonuclear or mononuclear cells. CSF glu-
cose is decreased in pyogenic infections; CSF protein, as
well as pressure, is elevated.

The organism is usually identified in the CSF by direct

smear and culture. Following its identification, its sensitivity
to antibiotics is determined and the appropriate antibiotic

prescribed.

2

In some cases, it may be necessary to place

antibiotics directly into the CSF if they do not effectively
cross the blood-brain barrier. Some antibiotics (e.g., penicil-
lin) may produce convulsions when introduced in large
concentrations in the CSF, and this should be avoided.

5

Fungal Infections Fungal infections are usually treated

with amphotericin B.

3

Intraventricular catheters may be used

to place antibiotics directly into the ventricles. Prolonged
therapy can be obtained by attaching a reservoir to the
catheter, enabling the physician to repeat treatments without
repeated ventricular puncture. In selected patients, a lumbar

subarachnoid catheter may be used for repeated injections of

antibiotics into the lumbar CSF.

505

506 CHAPTER 26

Table 26-1

INFECTIONS OF THE CENTRAL

NERVOUS SYSTEM AND THEIR

TREATMENT

Diagnosis is confirmed by culturing this mycotic organism
from CSF, its presence confirmed by India ink preparation,

in addition to positive cryptococcal antigen and antibody

tests. Treatment of cryptococcal infection is with amphoteri-
cin B, 5-fluorouracil, and ketoconazole.

3

Antimicrobial Agent

Causative Bacteria

A. Staphylococcus aureus

Oxycillin
Nafcillin
Cefazolin

Vancomycin
Amoxicillin
Clindomycin

Penicillin G

I. Streptococcus

Penicillin V
Amoxicillin
Cefazolin
Erythromycin
Chloramphenicol

Erythromycin
Penicillin G
Amoxicillin

C. Pneumococcus

Cefuroxamine

D. H, influenza

Ampicillin
Cefotaxime
Chloramphenicol
Ceftriaxone

Gentamicin
Amikacin
Imipenem-cilastatin
Ceftazidime + amino

glycoside

E. Pseudomonas aeruginosa

Gentamicin
Amikacin

f. E. coli

»

Streptomycin
Isoniazid
Rifampin
Ethambutol

G> Mycobacterium tuberculosis

H. Viral Infection

Herpes

AIDS
Influenza A

Amantadine
Vidarabine
Acylovir (most often used)
Ribavirin
Zidovudine (AIDS)

I. Fungal Infections

Cryptococcus neoformans

Histoplasma capsulatum
Coccidioides immitis

Aspvrs'illus fumigatus

Amphotericin B

Flucytosin
Ketoconazole
Mieonazole

Cryptococcosis Cryptococcus neoformans is a wide-

spread mycotic infection of the CNS, most often seen in

immunosuppressed patients with AIDS. It may invade the
meninges or present with symptoms of diffuse encephalitis.
Cryptococcus causes severe thickening of the meninges,
followed by hydrocephalus and cranial nerve dysfunction.

ACQUIRED IMMUNODEFICIENCY SYNDROME
(AIDS)

The proliferation of AIDS in the population is reaching
disastrous proportions.

6

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7

A wide variety of central and pe-

ripheral nervous system abnormalities occurs during the
course of HIV infection.

Direct infiltration of the nervous system is common in

patients with HIV. The infection produces clinical manifes-
tations that include AIDS dementia complex (ADC), sec-
ondary meningoencephalitis, and peripheral mono- and poly-
neuropathies, including peripheral facial nerve palsy and
brachial plexopathy. A Guillain-Barre syndrome and myelo-
pathy may develop.

Examination of CSF in patients with HIV infection shows

mononuclear pleocytosis with elevation of CSF protein but
normal levels of glucose. The HIV is detected by culture and
anti-HIV specific antibody can be demonstrated in the CSF.
CSF findings may subside if the patient becomes asympto-
matic.

AIDS Dementia Complex This is the most frequent

clinical feature of the CNS in a patient with AIDS. Patho-
logical abnormalities are found mainly in the basal ganglia
and hypothalamus, with mononuclear cell infiltrates. Reac-
tive gliosis, atrophy of white matter, loss of myelin, and
brain cell vacuolation also occur. HIV can be detected in the
affected brain tissue.

Principal symptoms of ADC include impairment of mem-

ory, concentration, and intellectual performance. Motor re-
sponses are delayed and there is decreased response to
verbal and visual stimuli. Patients with ADC progress to
total immobility, mutism, and loss of sphincter control.

Electroencephalography (EEG) may show diffuse slow-

ing. Brain CT is normal in the early stages of ADC, while
MRI shows multifocal areas of increased signal in the white
matter, basal ganglia, and thalamus on T2-weighted images.

HIV Myelopathy Changes in spinal cord function may

or may not occur in patients with ADC. Vacuolation of the

posterior and lateral columns of the spinal cord occur. Pa-
tients

with myelopathy will present with ataxia, spasticity,

and weakness of the lower extremities, as well as hypore-
flexia, paraparesis, and sphincter dysfunction.

CT and MRI may be helpful in the diagnosis of AIDS

myelopathy, but in patients with AIDS the diagnosis is made
primarily by exclusion of other lesions which could cause
the presenting symptoms: e.g., vitamin B^ deficiency, spinal
cord tumor, multiple sclerosis.

Acute transverse myelitis may be secondary to lymphoma

INFECTIOUS PROCESSES AFFECTING THE NERVOUS SYSTEM 507

or herpes zoster, but it can also be due to direct infection of
neurons in the spinal cord by HIV.

Peripheral Neuropathy Distal sensory neuropathy

occurs during the early stages of HIV infection. Initial
symptoms include paresthesias of the hands and/or feet,
pain, and progression to muscle weakness. All abnormalities
are more frequent in the lower extremities, but slow progres-
sion may reach the girdle muscles and muscles supplied by
the sacral or brachial plexus.

Nerve conduction velocities, EMG, and sural nerve biopsy

show abnormalities consistent with axonal neuropathy with
secondary demyelinization.

Treatment with antidepressants, salicylates, anticonvul-

sants, and analgesics may relieve some of the symptoms.
Specific treatment of HIV infection of the CNS is still in the

early stages of development.

8

Zidovudine may help reverse

or halt progression of some neurological symptoms. Side
effects of zidovudine may be confused with progression of
the disease, and patients who respond to therapy may have
significant exacerbation of their symptoms if medications
are discontinued.

Other Manifestations of HIV Other diseases of the

meninges and CNS may accompany HIV. Patients with
diffuse neurological dysfunctions have neurological symp-
toms that present with fever, headache, nausea, and vomiting
secondary to an associated infection of the CNS. Diseases
presenting with focal neurological defects include: single or
multiple brain abscesses, herpes encephalitis, fungal infec-
tions, and malignancies. Lymphoma of the brain is the most
commonly associated tumor with HIV.

Acute vascular events have been described in patients

with AIDS; these may be caused by necrotizing vasculitis
due to secondary bacterial,

9

.

10

fungal,

6

or viral

8

infection.

Progressive multifocal leukoencephalopathy (PMLE) may

occur because of papovavirus infection of the brain. Focal

signs associated with PMLE depend on the area of the brain
affected by the changes in the site of greatest involvement.

Meningeal diseases associated with AIDS usually are sub-

acute or chronic in course. Headache and fever are early
symptoms, followed by slow development of focal and dif-
fuse signs.

The diagnosis of CNS dysfunction as a result of HIV may

be difficult. Awareness or suspicion of HIV is the most
important indicator.

7

Neurological examination of the patient reveals diffuse

and focal changes caused by lesions of the nervous system
and it provides a baseline for future reference to assess the
effectiveness of treatment and progression of disease.

CT and MRI aid in the diagnosis of patients with AIDS.

Lesions seen on CT and MRI may be similar to those in
patients who do not have HIV, but infections are often more
severe because of AIDS.

Guillain-Barre syndrome can occur at any time in the

course of AIDS. Treatment with corticosteroids will often

aggravate symptoms, due to their added immunosuppressive
effect.

Cytomegalovirus will produce a cauda equina syndrome

with flaccid paralysis, absent reflexes, and loss of bladder
and bowel control.

Brachial and sacral plexopathies arise during the acute

phases of the disease. They may resolve spontaneously,
although recurrence of symptoms develops with disease pro-
gression, in spite of treatment with azidothymidine (zidovu-
dine).

The localization and extent of the neuromuscular disease

associated with HIV infection requires a thorough neurologi-
cal examination, CT and MRI of the spinal cord, EMG, CSF
analysis, nerve and muscle biopsies.

The diagnosis of AIDS and associated diseases of the

CNS requires awareness on the part of the physician that
AIDS may be present in any patient with symptoms of
infection in the CNS and peripheral nerves. Recognition of

the potential for HIV is mandatory to protect the patient as
well as those involved in the treatment of that patient.

7

LOCALIZED BACTERIAL INFECTIONS

Subgaleal abscess usually occurs secondary to scalp

trauma.

10

Suppuration develops between the skull and galea.

Purulent material may spread to involve the skull (osteo-
myelitis) and extend into the subdural space.

Treatment is early aspiration for drainage and antibiotics

appropriate for the bacteria causing the infection.

Osteomyelitis of the skull is associated with subgaleal

infection. It can result from skeletal traction, trauma, or
infection at the site of a craniotomy or cranioplasty. It may
result from direct extension of infection of any of the paran-
asal sinuses or mastoid air cells, or it may be the result of
hematogenous spread.'

Symptoms include pain and swelling over the site and

drainage of purulent material if an open wound is present, as
well as low-grade fever, and edema of surrounding tissue.
Diagnosis is made by x-ray and CT of the skull.

Treatment is drainage of purulent material and excision of

infected bone, followed by appropriate antibiotic ther-
apy.2,5,) 1,12,13 Repair of the cranial defect, if needed, should
be deferred until several months after the infection has
resolved.

Osteomyelitis of the skull base and petrous bone, known

as Gradenigo's syndrome, is difficult to treat because of
extensive involvement of the bone. Extensive multidisciplin-
ary surgery may be required.

Epidural abscess may develop following trauma to the

skull, osteomyelitis of the skull, or mastoiditis; most com-
monly it follows craniotomy. The dura presents a barrier

protecting the brain parenchyma; however, if venous drain-

age is compromised and becomes infected, there may be
spread of the infection into the subdural space and brain
parenchyma as well—or into the CSP, producing acute men-

508 CHAPTER 26

ingitis, cerebritis, and abscess. Diagnosis is confirmed with
CT.

Treatment is drainage of the abscess and antibiotic ther-

a p y .

Subdural empyema can be lethal if not treated early. In-

fection produces early venous thrombosis and proceeds to ful-

minating meningitis and brain abscess. It spreads most com-
monly from the paranasal sinuses, producing thrombosis of the
cortical veins and venous sinuses and extensive cerebral edema.

Symptoms include headache, lethargy, cranial nerve pal-

sies (most commonly the third cranial nerve), and papille-
dema. Hemiparesis, convulsions, and coma complete the
syndrome. Infants may develop subdural effusions secondary
to influenzal meningitis, with signs of increased intracranial

pressure (enlarged fontanel and spreading of suture lines).

Subdural taps confirm the diagnosis.

Appropriate antibiotic therapy (usually ampicillin) is in-

stituted. If the effusion does not subside, craniotomy and
removal of the membranes or subdural-peritoneal shunting
may be necessary. Chloramphenicol may be used in patients

beyond the neonatal age.

14

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15

Brain abscess is a purulent infection of the brain paren-

chyma. Abscesses develop following direct extension of
bacteria from the mastoid or paranasal sinuses, or they may
develop from hematogenous spread from the lungs, heart, or

kidneys. Children with congenital heart disease are prime
candidates for brain abscesses. Patients with HIV infection

(AIDS) are also candidates.

6

'

9

Cerebritis forms secondary to the invading organisms,

with cerebral edema and loss of structure of the white matter
of the brain secondary to focal vasculitis and thrombosis.
The brain tissue liquefies, and the glial cells and phagocytes
attempt to contain the infection by developing a capsular
wall around the diseased tissue.

If the brain is successful in containing the infection, a firm

capsule filled with degenerated brain and purulent material
develops. The abscess is surrounded by edema, which adds
to the size of the lesion, producing increased intracranial
pressure and shifting of the cranial contents. Hemiation of

the uncus of the medial temporal lobe into the tentorial
notch is a frequent consequence.

Brain abscesses may be single or multiple. If multiple in a

patient who is not immunocompromised, the cause is most
likely from hematogenous spread (congenital heart disease
or endocarditis). Patients infected with HIV are prone to
multiple abscesses. Frontal lobe abscesses are usually exten-
sions of paranasal sinus infections, and a search for middle
ear or mastoid infections is indicated in patients with a
temporal lobe abscess.' Brain abscess may be secondary to

.dental infections. (See Figs. 26-1 and 26-2A and B.)

The symptoms of brain abscess are determined by its

location and size. Headache, fever, nausea, and vomiting
occur early, followed by papilledema, lethargy, convulsions,
and hemiparesis. Abscesses occurring in the posterior fossa

produce cerebellar signs of ataxia and dysmetria, nystagmus,

and papilledema early in the illness, with rapid deterioration
of the patient's clinical status.

Figure 26-1 Computerized tomography scan, axial view
(enhanced). Brain abscess, multiloccular right parietal lobe
secondary to Pseudomonas petrous bone infection. The
abscess is surrounded by cerebral edemas.

The diagnosis is made by neurological examination,

x-rays of the skull, CT, and MRI. Spinal puncture is con-
traindicated in a patient suspected of having a brain abscess
because of the danger of precipitating an acute hemiation of
the medial surface of the temporal lobe into the tentorial
notch, thus compromising the brain stem, or because of the
danger of a hemiation of the cerebellar tonsils into the

foramen magnum, thus compromising the medulla.

Chest x-rays and blood cultures suggest possible sources

of the cause of the abscess. Cerebral angiography will reveal
a large avascular mass. However, CT and MRI suggest the
diagnosis by showing the mass lesion, often incapsulated,
and the extent of cerebral edema. (See Fig. 26-3.) There may

be multiple lesions.

Treatment of brain abscess is directed to drainage of the

abscess to reduce increased intracranial pressure and to

determine the etiological organisms, which will indicate the
type of antibiotic therapy to be used. In recent years, aspira-
tion of the abscess by stereotactic means to reduce the size
of the lesion has been popular. Most abscesses will respond
to this therapy, followed by long-term antibiotic therapy.

Large abscesses located in the frontal or temporal lobes of

the brain, may be excised with removal of the abscess
capsule and its contents. This procedure must also be fol-
lowed by antibiotic therapy. The adjacent infected tissues

INFECTIOUS PROCESSES AFFECTING THE NERVOUS SYSTEM 509

(A) (B)

Figure 26-2 A. Magnetic resonance image coronal view. Brain
abscess, right temporal lobe. The abscess extends from the petrous
bone into the right temporal lobe. B. Magnetic resonance image,

axial view. Brain abscess, right temporal lobe, secondary to
Pseudomonas infection of petrous bone. Note extensive edema
secondary to the abscess.

and bone involved in mastoidids or sinusitis must also be
treated surgically to prevent reoccurrence of the abscess. It is
important lo treat a brain abscess as soon as it is recognized

because the lesion will otherwise enlarge and rupture into
the ventricular system, producing an overwhelming infection

and death.

VIRAL INFECTIONS

Viral encephalitis develops as an extension of mumps or
herpes simplex infection. The viral infection produces dif-
fuse edema and meningeal inflammation. There is swelling
and disintegration of the cortical neurons, peri vascular in-
flammation, and focal hemorrhages of the cortex and white
matter.

Early, or prodromal, symptoms of viral encephalitis in-

clude fever, malaise, nausea and vomiting, as well as symp-
toms of upper respiratory disease.

There is a sudden onset and rapid progression of encepha-

litis with convulsions, drowsiness, and focal weakness.
Diagnostic studies should include EEG, which will show
focal slow waves in the area of the lesion but also some
diffuse slow waves over the brain. CT will reveal a large

mass, most often of the temporal lobe, but it can extend into
the frontal lobe, with decreased attenuation and occasional
hemorrhage within the lesion. (See Fig. 26-4A and B.) MR!
will reveal evidence of edema and mass effect and, possibly,
hemorrhage.

Treatment includes biopsy and microscopic examination

of the lesion. Specimens of the issue are cultured to isolate
the offending virus. In some patients, the virus may be
cultured from the spinal fluid. It is also possible to demon-
strate a specific antigen for herpes virus with immunofluo-
rescence studies. After diagnosis of heipes simplex viral
encephalitis, the specific treatment is cytosine arabinoside
and adenosine arabinoside- which are usually started imme-

diately after biopsy of ihe lesion.*-*

6

PARASITIC AND FUNGUS INFECTIONS

Parasitic and fungal infections of the brain are being seen

more frequently in the United States because of the great
amount of international travel. The presence of AIDS and
patients undergoing immunosuppressive therapy add to the
number of patients found with fungal infections.

6

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3

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17

510

CHAPTER 26

Figure 26-3 Computerized tomography (enhanced) of cerebrai
hemisphere. Brain abscess, right parietal area, secondary to
Streptococcus viridans septicemia.

Fungal and parasitic infections should be considered in

any patient with CNS symptoms.

Amebiasis (Emamoeba histolytica) is present in a small

portion of the general population of the United States, but it
is a common infection in Central America. The E. histolytica
trophozoite is ingested, it passes to the bloodstream, and
seeds to the liver and on to the brain as an embolus via the
bloodstream. The parasite produces confluent hemorrhagic
areas and infarction in the brain. Multiloculated cysts most
often occur in the frontal lobes and basal ganglia.

Symptoms include headache, seizures, and facial spasms,

and cranial nerve palsies are frequently found. Anatomic
diagnosis is made by CT examination. The lesions may be
small, with little evidence of surrounding inflammatory re-
sponse. Serum complement fixation associated with immu-
nofluorescence antibody is diagnostic.

Treatment is directed to drainage of abscesses and drug

therapy with emetine HC1, chloroquine, tetracycline, and
metronidazole. Corticosteroids are contraindicated in these
patients.

Toxoplasmosis gondii is found worldwide. It is usually

asymptomatic but most often causes symptoms in patients
who are immunosuppressed with AIDs or its therapy.

6

Symptoms and signs of diffuse encephalitis develop as the

disease becomes active. Antibody titers are increased on
complement fixation examination. The CSF reveals that
protein content is elevated, and there is an increase in
mononuclear cells. The CSF glucose is usually normal.

Roentgenograms and CT reveal multiple areas of irregular

(A)

(B)

Figure 26-4 A. Computerized tomography scan (enhanced) of
herpes encephalitis showing a large area of edema and intracerebral
hemorrhage of the right temporal lobe. B. Magnetic resonance
image, T2-weighted sequence, of the brain showing herpes
encephalitis with extensive edema and intracerebral hemorrhage ia»-
the right temporal lobe.

INFECTIOUS PROCESSES AFFECTING THE NERVOUS SYSTEM

511

nodular calcification, most often surrounding the ventricular

system.

The usual treatment of toxoplasmosis includes sulfadia-

zine and pyremethamine.

2

Corticosteroids should not be

given.

Cysticercosis (Taenia solium), or pork tapeworm, enters

the patient who eats raw or poorly cooked pork products.
The disease is prevalent in much of the world. It is rare in
most of the United States and Canada but is seen in southern
United States and California.

Cysticercosis may involve any part of the CNS. Small

cystic lesions produce multiple symptoms, depending on the
location. The basilar cisterns are frequently involved.

Diagnosis is made by identification of the parasite in the

tissue and by complement fixation tests on the CSF. No
medications will eradicate the disease. Treatment is directed
toward excision of lesions of the brain and spinal cord and
shunting any associated hydrocephalus.

Hydatid cysts are lesions occurring in the human as inter-

mediate host of the dog tapeworm. They should be distin-
guished from Cysticercosis both in cause and treatment.
Treatment is removal by large craniotomy, being careful not
to rupture the cyst. This is best accomplished by careful
corticotomy down to the cyst, which is expelled by cerebral
pulsation and irrigation. The lesions are common in southern
United States and California.

Trichinosis (Trichinella spiralis) also occurs with the in-

gestion of raw or poorly cooked pork. The nervous system is
affected in a small number of patients infested with this
parasite. CNS symptoms are those of meningoencephalitis
with cranial nerve dysfunction and progression to major
neurological deficits. Diagnosis is made by the bentonite-
flocculation immunofluorescent antibody and latex agglutin-
ation tests.

Treatment is with corticosteroids and thiabendaxole. Prog-

nosis is good with the therapy.

17

Mucormycosis is a clinical syndrome, which usually

begins in the paranasal sinuses and extends into the orbit,
causing headache, pain in one eye and the face, with perior-
bital edema, commonly ophthalmoplegia, and proptosis.
Blindness may result from occlusion of the retinal artery.

This syndrome is caused by various genera of fungi,

usually Mucor, Rhiwpus, or Absidia. The organisms are
nonpathogenic except in patients with diabetic ketoacidosis.
In clinical settings the organisms are likely to cause occlu-
sion of blood vessels, resulting in infarction. Bones at the
base of the skull are usually invaded.

Involvement of the eye may be followed by symptoms of

encephalitis, with headache and lethargy from subsequent
abscess formation.

Aggressive surgical treatment in the form of block exci-

sion of infarcted areas is followed by intense medical ther-
apy with amphotericin B and 5-fluorocytosine. Mortality

rates are high.

Aspergillosis (Aspergillus fumigatus) is a commonly en-

countered mycotic infection of the CNS. The organism is
opportunistic and frequently occurs in patients with low host

Figure 26-5 Magnetic resonance image of skull, sagittal view.
Large aspergillosis granuloma involving the sphenoid sinus, clivus,
and encasing the right carotid artery. Note the irregular enlargement
of the carotid artery within the granuloma.

resistance. Patients with leukemia, AIDS, or neoplastic dis-
eases or those on steroids or immunosuppressive therapy are
particularly susceptible.

6

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18

Exclusive involvement of the brain is rare, but the kidneys

and brain are often involved in this systemic disease. The

respiratory tree is the common source of infection, and the
brain receives the infection, most often, via the bloodstream.
This mycotic pathogen can enter the CNS through the para-
nasal sinuses by contiguous spread or by iatrogenic spread
through contaminated needles or neurosurgical procedures

Aspergillus may produce symptoms consistent with men-

ingitis, encephalitis, or granuloma. The infection may extend
from the paranasal sinuses or mastoid bone into the intra-
cranial cavity. Abscesses occur as an extension of meningeal
infections. (See Fig. 26-5.)

Granulomas are more common in patients with chronic

infection. CNS symptoms are related to the location of the
infection. The granuloma produces a sclerosing vasculitis
after invasion of the artery of the lesion. Transient ischemic
attacks occur secondary to septic emboli and may progress
to infarction. The invasion of the wall of the carotid artery
may produce mycotic aneurysms. (See Fig. 26-6A and B.)

Treatment includes decompression of the intracranial cav-

ity—with removal of the lesions if possible—and drug ther-
apy with amphotericin B and 5-fluorouracil and itracono-
zaie.

3

Tuberculosis of the intracranial cavity is rare in the United

States, but tuberculosis of the parenchyma, particularly the
posterior fossa, is common in third world countries. Tuber-
culosis also causes subdural or epidural granulomas. Isolated
brain abscesses without edema are the common CT findings.
Streptomycin, elhambutol, isonicotinic acid hydrazide, and

512 CHAPTER 2fe

(A) (B)

Figure 26-6 A. Right carotid angiogram, frontal view. Large
multilobular mycotic aneurysm of the infraclinoid portion of the
right carotid artery, secondary to aspergillosis invading the artery.

B. Lateral view of the multilobular aneurysm of the right
carotid artery.

rifampin are used in combination to treat tuberculosis of the
central nervous system.

4

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13

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20

Sarcoidosis produces multiple granulomatous lesions and

is of unknown etiology- This reiiculosis is more common in
blacks and forms noncaseating granulomatous lymphoid tis-
sue. The granulomatous lesions are found throughout the
CNS and may involve the peripheral nerves. Involvement of
the base of the brain and the cranial nerves is frequent.

Patients develop meningitis, seizures, hydrocephalus, and

dysfunction of the pituitary gland. Alterations in mental
function are common. The diagnosis can be made by chest
x-ray because the lungs are commonly involved. The only
treatment is corticosteroids and control of hydrocephalus if it

BACTERIAL INFECTIONS
OF THE SPINE

Epidural abscesses of the spine are usually the result of

blood-bome bacteria or occur postoperatively following la-
minectomy. The abscess can be related to previous spinal
puncture or an infected congenital dermal sinus.

Symptoms of spinal epidural abscess are severe back pain,

fever, and progressive compression of the spinal cord, re-
sulting in progressive paresis from compression of the neural
elements. The sedimentation rate is usually quite elevated.
Granulation tissue is commonly found in association with
epidural abscesses and may require excision during the
course of decompression.

The diagnosis is confirmed with x-ray of the spine, which

will show early osteomyelitis of the vertebra and presence of
a localized extradural collection of material shown on CT or
MRI.

Treatment is immediate decompression of the spinal cord

by laminectomy and removal of the abscess, followed by
appropriate antibiotic therapy.

2

Spinal puncture should be

avoided, as infection may be transferred from the extradural
space to the subarachnoid space and result in meningitis.

Subdural abscesses of the spinal canal are rare, and they

are usually extensions of extradural infection. Diagnosis is

made by MRI or CT scan.

Osteomyelitis of the vertebra develops from hematogen-

ous spread of infection to the vertebrae, but it may occur by
direct extension from a disk space infection or from an
intraabdominal or thoracic infection.

Deep back pain, aggravated by movement and often re-

lieved by recumbency, fever, and increased sedimentation
rate, point toward infection in a vertebral body.

TNTWTIOIIS PROCESSES AFFRCTTNO THE NERVOUS SYSTEM

513

X-rays of the spine may be normal early in the course of

the disease, but later films will show collapse of the body.
Infections of the vertebrae usually involve the intervertebral
disk space while malignant lesions do not. Diagnosis can be
made readily by CT scan, and a bone scan with gallium will

help in many cases.

Treatment of osteomyelitis of the spine is directed toward

control of the infection, comfort for the patient, and mea-
sures to prevent further collapse and deformity of the verte-
bral canal. If no deformity exists in the vertebral body,
diagnosis may be secured by CT-directed needle biopsy of
the affected vertebrae. Complications may result from mis-
directed needles, with perforation of a major blood vessel,
the spinal canal, the subarachnoid space, or the spinal cord.
Needle biopsy of the vertebrae should therefore be ap-
proached with caution.

Open biopsy may be necessary to obtain adequate tissue

for culture and correction of vertebral deformity. Correction
with corpectomy may be indicated. If instrumentation is
required, the implanted instruments should be isolated from
the site of infection.

Appropriate antibiotics are administered, depending on

the type of bacteria isolated.

2

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19

Disk space infection is usually a complication of previous

surgery or needle puncture of intervertebral disks.

The infection develops 6 to 8 weeks post-surgery, and it

produces severe pain in the area of the previous surgery,
aggravated by palpation and pressure and partially relieved
by recumbency. Fever and muscle spasm are evident in
patients with disk space infection, and their sedimentation
rates are elevated.

X-rays of the spine and CT scan are normal early in the

course of this condition. Interpretation of gallium scans is
difficult as the scan may be positive because of the recent
surgery. Later in the course, destructive changes will appear
along the edges of the intervertebral disk space, and a CT
scan will demonstrate these changes early. Narrowing of the
inter vertebral space occurs.

Treatment involves bed rest and mild medication for pain

and muscle spasms. Needle biopsy of the involved inter-

space identifies the causative bacteria—most often staphylo-
coccus—and antibiotic therapy will then be started.

2

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5

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11

Cul-

tures are often sterile, in which case a direct surgical biopsy
may be required. Some surgeons prefer to give an elective
trial of antibiotics selected for treatment of staphylococcal

organisms.

Patients who do not respond to conservative therapy may

need to undergo open surgery to remove the infected mate-
rial from the interspace. Interspace infections must be ob-

served closely, since extradural abscesses develop with spi-
nal cord compression. When the infection is controlled, the
interspace will eventually narrow, and spontaneous fusion

will occur.

Tuberculous infection of the spine with spinal cord com-

pression is a common disease in third world countries.

Tuberculosis is found most frequently in the lower thora-

cic and upper lumbar vertebrae. Usually, multiple vertebral
bodies are involved, but posterior elements rarely show
evidence of infection.

The disease starts early in life (first decade); symptoms,

however, are most obvious in young adults between 30 and
40 years of age.

Decalcificalion of the vertebral body occurs, followed by

vertebral collapse. Paravertebral abscess usually develops.
CT is most accurate in diagnosis. Medical treatment includes
streptomycin, para-aminosalicylate, and isoniazid.

13

Surgical

correction by debridement and corpectomy is appropriate if
there is collapse of the vertebral body or compression of the
spinal cord.

FUNGAL INFECTIONS OF THE SPINE

Epidural granulomas may cause compression of the spinal
cord with paraparesis or transverse myelitis following vascu-
lar occlusion secondary to arterial invasion by a granuloma.
Treatment is decompression of the spinal cord, if necessary,
and drug therapy with amphotericin B and 5-fluorouracil,
and itraconazole.

3

REFERENCES

1. Nager GT: Mastoid and paranasal infections and their relation

to the central nervous system. Clinical Neurosurgery 14:288-
313,1967.

2. Wilkowske CJ, Hermans PE: General principles of antimicro-

bial therapy. Mayo din Proc 62:789-798, 1987.

3. Terrell CL, Hermans PE: Antifungal agents used for deep

seated mycotic infections. Mayo Clin Proc 62:116-1128,

1987.

4. Van Scoy RE, Wilkowske CJ: Antituberculous agents. Mayo

Clin Proc 62:1129-1136, 1987.

5. Wright AJ, Wilkowske CJ: The penicillins. Mayo Clin Proc

62:806-820, 1987.

6. Florida Medical Association: Clinical Manual on HIV and

AIDS. Jacksonville, Florida Medical Association in Conjunc-
tion with the Florida Dept. of Health and Rehabilitation Ser-
vices, 1989, pp 53-59.

7. Schiff SJ: A surgeon's risk of AIDS. J Neurosurg 73:651-660,

1990.

8. Hermans PE, Cockerill PR III: Antiviral agents. Mayo Clin

Proc 62:1108-1115, 1987.

9. Cockerill FR III, Edson RS; Trimethoprim and sulfamethoxa-

role. Mayo Clin Proc 62:921-929, 1987.

10. Tindall GT, Ranagan JF, Nashold BS: Brain abscess and

osteomyelitis following skull traction. Arch Surg 79:638-641,

1959.

11. Edson RS, Terrell CL: The aminoglycosides: Streptomycin,

kanamycin, gentamicin, tobramycin, amikacin, netilmicin, and
sisomicin. Mayo Clin Proc 62:916-920, 1987.

12. Hermans PE, Wilhelm MP: Vancomycin. Mayo Clin Proc

62:901-905, 1987.

13. Wilson WR, Cockerill FR III: Tetracyclines, chloramphenicol,

erythromycin, and clindamycin. Mayo din Proc 62:906-915,

1987.

14. Rhodes KH, Johnson CM: Antibiotic therapy for severe infec-

tions in infants and children. Mayo Clin Proc 62:1018-1024,

1987.

15. Thompson RL: Cephalosporin, carbapenem, and monobactam

antitiotics. Mayo Clin Proc 62:821-834, 1987.

16. Whitely RJ, Soong SJ, Dolin R, Galasso GJ, Ch'ien LT.

Alford CA, and the Collaborative Study Group: Adenine ara-
binoside therapy of biopsy-proved herpes simplex encephalitis:
National Institutes of Allergy and Infectious Diseases Collabo-
rative Antiviral Study. N Engi J Med 297:289-294, 1987.

17. Martz RD, Hoff T: Parasitic and fungal diseases of the central

nervous system, in Youmans JR (ed): Neurologic Surgery, 3d
ed. Philadelphia, Saunders, 1990, chap 134, pp 3742-3751.

18. Piotrowski WP, Pilz P, Chuang I-H: Subarachnoid hemorrhage

caused by a fungal aneurysm of the vertebral artery as a
complication of intracranial aneurysm clipping: Case report. J
Neurosurg 73:962-964, 1990.

19. Walker RC, Wright AJ: The Quinolones. Mayo Clin Proc

62:1007-1012,1987.

20. Carey ME: Infections of the spine and spinal cord, in Youmans

JR (ed): Neurologic Surgery, 3d ed. Philadelphia, Saunders,

1990, chap 136, pp 3759-3781.

STUDY QUESTIONS

I. A 28-year-old diabetic male complains of nasal conges-
tion and frontal headaches for about 6 weeks before he
becomes drowsy and has a series of generalized seizures.
On examination, he is drowsy and has a left hemiparesis
and bilateral papilledema. His scalp is "boggy." There is
fluctuation beneath it and pitting edema. Palpation pro-
duces severe pain. His temperature was 39°C. Skull x-rays
show clouded frontal sinuses, and the frontal bone on the
right is "moth-eaten." CT scan shows a large mass in the

right frontal area.

1. What is the most likely cause of the mass? 2. What

surgical therapy should be administered? When? 3. How
should the diabetes be controlled? 4. When shoulfl a cranio-
plasty be performed? 5. Assuming smears and cultures indi-
cate Mucor as the etiologic agent, should the surgical ther-
apy

be altered in any way?.

II. A 37-year-old female who has experienced weight loss
and night sweats for about a month, has a sudden onset of
severe headache, nausea, vomiting, and drowsiness with a
left hemiparesis. CT shows evidence of subarachnoid hem-
orrhage in the right parietal area. An arteriogram shows an
aneurysm on a distal branch of the ascending frontoparietal
branch of the right middle cerebral artery. The patient has a
temperature of 38°C. A Westergren sedimentation rate is

115, and there is a variable systolic murmur.

1. What is the most likely cause of the aneurysm? 2. What

diagnostic procedures should be accomplished? 3. What
treatment should be instituted for the aneurysm? For infec-
tion? 4. How long should medical treatment be continued?
5. What antibiotics might be administered before organisms

, are identified?

III. A 34-year-old heterosexual male who is addicted to

heroin is admitted with chief complaints of headache and
drowsiness. The family is aware that the patient has been
deteriorating intellectually for 4 months. He has a right
hemiparesis. CT reveals multiple round "cystic" areas
throughout the brain, and there are two larger ones over the
vertex on the left at the frontoparietal junction.

1. What diagnoses should be considered? 2. What is the

most likely diagnosis? 3. What tests should be performed?
4. What therapy should be administered? 5. What diagnostic
or therapeutic procedures might a neurosurgeon have to
offer?

IV. A 39-year-old black male is hospitalized because of
progressive weakness in his lower extremities for 2 weeks.
He has been losing weight and has had night sweats for 3
months. He has a productive cough. The patient noted gen-
eralized weakness a month earlier but has developed lower
thoracic back pain and a bandlike pain around the lower
chest and abdomen. He has been unable to walk because of
weakness for the past 2 days. Chest x-ray shows bilateral
diffuse infiltrates, more in the upper fields, and there is
cavitation in the right apex. X-rays of the thoracic spine
show collapse of the lower half of T8 and the upper half of
T9. The disk space is eroded.

1. What diagnoses should be entertained? 2. What diag-

nostic studies should be performed? 3. Assuming acid-fast
organisms are obtained from the sputum, how should the
lesion of the thoracic spine be approached? 4. What antibiot-
ics should be instituted? When? 5. What is the prognosis for
the neurological deficits?

V. A 31-year-old female undergoes a diskectomy at the
L4-L5 interspace for pain in the right buttock, radiating into
the right foot. The pain is relieved except for localized back

INFECTIOUS PROCESSES AFFECTING THE NERVOUS SYSTEM

515

pain when she awakens from anesthesia, but 2 weeks later, 1. What is the most likely diagnosis? 2. What is the most
the patient begins to have increasing back pain and excru- likely offending organism? 3. What tests (procedure?) might
ciating pain in the right lower extremity in the same distri- be considered? 4. What therapy might be instituted?
bution as the pain the patient had postoperatively; but 2 days 5. Assuming the patient had a disk space infection, which
later, the patient's temperature is 102°. However, this pain is resolves on therapy, what might one expect to see on radio-
much more severe and exacerbated by any movement, graphs taken a year later?