Handbook of Pediatric Neurosurgery

some patients but then became progressively
narrower.48 No patients achieved full restoration
of disk space.
● In virtually all series of SEA, the best predictor of
neurological outcome is the patient’s
preoperative neurological condition.2
● For intramedullary spinal cord abscesses,
prognosis is inversely related to the acuity of
onset of symptoms and directly related to the
use of antibiotics in conjunction with prompt
surgical drainage. Mortality among patients
treated nonoperatively is 100%, whereas
surgically treated patients improve or have a
complete recovery in approximately 78% of
cases.22 Death is most frequently due to the
presence of multiple CNS abscesses.
54.10 Surgical Pearls
● Surgical intervention for tuberculous
osteomyelitis may be either via laminectomy
with antibiotics and bracing or via anterior
vertebrectomy and reconstruction. The two
approaches do not di er in e cacy for local
disease control, but vertebrectomy is associated
with a reduced rate of complications related to
kyphosis and angulation.
● For every spine biopsy, send tissue for
appropriate cultures and pathological study.
Uncommon infections such as tuberculosis and
fungal infections will often be identified first by
microscopic evaluation.
54.11 Common Clinical
Questions
1. What are the surgical indications for a
laminectomy over a more radical surgery for
dealing with spinal infection?
2. How do you minimize the surgical site
infections following high-risk pediatric spinal
surgery?
3. What is the standard treatment for childhood
diskitis sand osteomyelitis, and surgical site
infections?
54.12 Answers to Common
Clinical Questions
1. Laminectomy remains the preferred procedure
when the primary problem for most surgical
decompression and biopsy. However, if there is
significant mobility of the spine with significant
vertebral body disease, instrumented fusion
with possible corpectomy is necessary given the
potential for delayed kyphosis and the inability
to address any significant ventral disease.
2. (a) Preoperative recommendations include a
chlorhexidine skin wash at home the night
before surgery, urine cultures, a Patient
Education sheet, and a nutritional assessment.
(b) Perioperative guidance includes clipping
over shaving if removing hair, IVcefazolin and
prophylaxis for gram-negative bacilli, limited
OR access, intraoperative wound irrigation, and
vancomycin powder applied in bone grafts and
to surgical sites.
(c) Postoperatively, impervious dressings are
preferred, and dressing changes should be
minimized to the extent possible.46
3. (a) Child diskitis: 7 to 10 days of IVantibiotics
followed by up to 6 weeks of PO antibiotics
based on imaging. Patients should be followed
for up to 12 to 18 months and reassessed if
symptoms recur or ESR/CRP fail to return to
normal.
(b) Osteomyelitis and spinal epidural abscess: 6
weeks of targeted IVantibiotic therapy with
extension to 8 to 12 weeks depending on
clinical and laboratory findings.
(c) Surgical site infections: 4 to 6 weeks of
targeted antibiotic therapy with possible
maintenance on oral antibiotic therapy
depending on clinical and laboratory findings.
References
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[47] Martin RJ, Yuan HA. Neurosurgical care of spinal epidural,
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470–477
Evaluation and Management of Pediatric Spinal Infections
459

55 Surgical Considerations in Tuberculosis, Fungal,
and Parasitic Infections of CNS in Children
Chandrashekhar Deopujari, Dattatraya Muzumdar, Sonal Jain
55.1 Introduction
Tuberculosis (TB) is a chronic granulomatous dis-
ease caused by acid-fast bacilli, in the Mycobacte-
rium tuberculosis complex. It has a propensity to
a ect multiple organs and is potentially life threat-
ening. It is still regarded as a leading cause of
death worldwide due to a single infectious agent.
The incidence of TB is on decline in developing as
well as industrialized countries, but the emergence
of multidrug-resistant form of tuberculosis is of
concern since it has worsened morbidity and mor-
tality. Children who are persistently exposed to
individuals with tuberculosis are usually at high
risk of contracting the dreaded illness. Low
immunity, malnutrition, and overcrowding are the
principal contributing factors. Central nervous sys-
tem (CNS) TB is a devastating manifestation of the
infection, accounting for about 10% of all cases of
TB especially TB meningitis.1 The occurrence of
vasculitis, arachnoiditis, direct parenchymal
injury, and raised intracranial pressure (ICP) is
responsible for the poor outcome.1,2 Delay in diag-
nosis is another significant cause for mortality in
underdeveloped countries. Involvement of the
spine, also known as Pott’s disease accounts for 1
to 2% of the world spinal deformity. It can result in
complications, such as arachnoiditis, intramedul-
lary tuberculoma, and spinal cord compression
from epidural abscess. There are no specific inter-
national guidelines for the diagnosis and treat-
ment of CNS tuberculosis and the treatment is
largely institution specific. There are no studies,
which demonstrate the superiority of an individ-
ual treatment protocol over another.
55.2 Pathogenesis
Mycobacterium TB commonly causes CNS tubercu-
losis, although in immunocompromised patients
other species may be involved. Following initial
pulmonary infection, the tuberculous bacteria may
enter the systemic circulation and subsequently
reach the CNS, which is rich in oxygen establishing
in the meninges, subpial or subependymal region
of the brain, or the spinal cord. It is known as
the Rich focus, which may rupture into the subar-
achnoid space or ventricular system leading to
meningitis. Alternatively, the meninges can be
involved due to rupture of a tuberculoma into a
vessel in the subarachnoid space, or rupture of
miliary tubercles in miliary TB. It can rarely be
involved following contiguous spread of infection
from the adjacent bone.
The classic feature of tuberculous CNS disease is
the formation of dense, gelatinous, inflammatory
exudate along the basal surface of the cerebrum. In
advanced cases, it may involve the leptomeninges
over the cerebral convexities, and extend into the
ventricular system, can cause ependymitis and
choroid plexitis.1,2
Cell-mediated immune response is usually seen.
The parenchymal tuberculous focus can develop
into tuberculoma or brain abscess if the immunity
is low.
The tuberculous a iction of the CNS manifests
in a variety of clinical syndromes.
55.3 Tuberculous Meningitis
Tuberculous meningitis (TBM) in developing coun-
tries is more common among infants and children.
The basal exudates can cause obstruction to cere-
brospinal fluid (CSF) flow, causing hydrocephalus. It
can also result in obliterative vasculitis due to occlu-
sion of blood vessels at the base of the brain.3,4
Tuberculous meningitis is characterized by basal
exudates, which cause abnormal meningeal en-
hancement, hydrocephalus, and cerebral infarction.
This triad is specific for the diagnosis of TBM.
The complications of meningitis include hypona-
tremia, hydrocephalus, vasculitis, cranial nerve
involvement, and associated multiple tuberculomas.3
55.3.1 Hyponatremia
Hyponatremia is common in TBM and is independ-
ently associated with worse outcome. In conjunc-
tion with raised ICP, it may contribute to poor
outcome through worsening cerebral edema, and
its surveillance and prevention are of paramount
importance. It manifests as either syndrome of
inappropriate antidiuretic hormone secretion
(SIADH) or cerebral salt-wasting syndrome (CSW).3
It usually results due to hypothalamic injury or
inflammation.
460

55.3.2 Hydrocephalus
Hydrocephalus is a sequelae or complication of
tubercular meningitis.1,2,3,4
The inflammatory
basal exudates cause obstruction to the CSF flow
resulting in a communicating type of hydrocepha-
lus in about 80% of the cases. Noncommunicating
or obstructive hydrocephalus can occur either
because of obstruction of fourth ventricular outlet
foramina by the basal exudates, or when there is
obstruction of the aqueduct either due to a stran-
gulation of the brainstem by exudates or by a sub-
ependymal tuberculoma. Trapped or loculated
ventricle is also seen due to entrapment of a part
of a ventricle by ependymitis. Sometimes, there is
a combination of noncommunicating (obstructive)
and communicating (defective absorption) hydro-
cephalus, which may be di cult to treat. It is
found to be a cause of failure of endoscopic third
ventriculostomy. About 50% of patients with TBM
have chest X-rays suggesting active or previous
pulmonary tuberculosis; 10% have miliary disease,
which strongly suggests CNS involvement.4,5
55.3.3 Vasculitis
The inflammatory basal predominantly involving
the circle of Willis. The adventitial and media are
a ected initially and later the lumen of the vessel.
It causes reactive subendothelial cellular prolifera-
tion leading to complete occlusion and thrombus
formation. Middle cerebral and lenticulostriate
arteries are the most common vessels involved.
55.3.4 Cranial Nerve Involvement
Cranial nerve involvem ent in TBM is variable and
is seen in 17 to 70% of patients. It prim arily
occurs due to ischem ia of the nerve or entrap-
m ent of the nerve in basal exudates causing
neuritis or perineuritis or there m ay be a tuber-
culom a on the nerve within the subarachnoid
course. The proxim al portion of the nerve at root
entry zone is usually a ected. The brainstem
nucleus of the nerve in proxim ity can be a ected.
Perm anent loss of function can ensue in late
stages due to fibrosis.1,2,3,4,5,6
55.3.5 Tuberculous Encephalitis
and Encephalopathy
Tuberculous encephalitis results from parenchy-
mal inflammation adjacent to the meninges. It
shows edema, perivascular infiltration, and a
microglial reaction, known as border zone reac-
tion. Tuberculous encephalopathy is a delayed type
IV hypersensitivity reaction caused by tuberculous
protein. It is a fulminant immunological mecha-
nism resulting in extensive damage to the white
matter and perivascular demyelination. Infants
and young children with pulmonary TB are com-
monly a ected. There is a high incidence of mor-
tality despite antituberculous medication.5,6
55.3.6 Tuberculomas
Tuberculomas are among the most common intra-
cranial mass lesions.7,8,9 They can occur at any age.
They can be solitary or multiple and can occur
anywhere in the brain parenchyma.10,11,12 In chil-
dren, they predominate in the infratentorial
compartment.10
Tuberculomas arise when
tubercles in the parenchyma of brain enlarge with-
out rupturing into the subarachnoid space. They
usually occur in the absence of TBM, but may occur
with meningitis because of the extension of CSF
infection into the adjacent parenchyma via cortical
veins or Virchow–Robin spaces. Presence of tuber-
culomas at the corticomedullary junction suggests
the hematogenous spread of infection, because
there is narrowing of the arterioles at the gray/
white matter junction. Initially, tuberculomas
show typical noncaseating granulomatous reac-
tion, which is predominantly lymphocytic and
subsequently develops a central area of caseating
necrosis. The central area of necrosis is initially
solid and later may liquefy. Miliary tuberculomas
are usually associated with meningitis and most of
these patients have a primary pulmonary focus of
infection. They are usually less than 2 to 5 mm in
size. The occurrence of intramedullary tubercu-
loma is rare.13,14,15
55.3.7 Tuberculous Brain Abscess
Tuberculous brain abscess is rare.16,17,18,19,20,21 It
can be solitary or multiple. It is an encapsulated
collection of pus with abundant viable tubercle
bacilli without classic tubercular granuloma for-
mation. The wall is thicker than pyogenic abscess.
They can mimic ontogenic–pyogenic abscess.18 It
can occur from parenchymal tuberculous granulo-
mas or via the spread of tuberculous foci in the
meninges to the brain. According to the Whitener
criteria for tuberculous abscess, it should reveal
macroscopic evidence of abscess formation within
the brain parenchyma, and, on histological confir-
mation, the abscess wall should be composed of
Surgical Considerations in Tuberculosis, Fungal, and Parasitic Infections of CNS in Children
461

vascular granulation tissue containing acute and
chronic inflammatory cells and tubercle bacilli.19,20
55.3.8 Calvarial Tuberculosis
Calvarial tuberculosis is rare, even in areas where
tuberculosis is endemic because of paucity of lym-
phatics in the calvarial bone.21,22 It occurs secon-
dary to hematogenous spread from the primary
focus such as pulmonary, cervical or hilar lymph-
adenitis, renal or systemic tuberculosis. Less com-
monly it can arise from tuberculous mastoiditis or
spinal tuberculosis. The outer table is usually the
first to be destroyed, though eventually both tables
can be a ected. It could occur as small, circum-
scribed punched out defect in the bone with gran-
ulation tissue covering both internal and external
aspect with little tendency for osteitis to spread in
the bone or periosteum surrounding the defect or
widespread destruction of the inner table with
abundant extradural granulation tissue in the form
of pachymeningitis externa.23,24 In circumscribed
and sclerotic type, there is marked thickening of
the bone because of lack of blood supply to the dis-
eased bone. Younger population is at higher risk to
develop calvarial tuberculosis and it is rare in
infancy. The most common sites of involvement
are frontal and parietal bones, both the bones have
large amount of cancellous bone.25,26,27 They com-
monly present as scalp swelling, discharging sinus,
and pain, rarely patient may present with seizure
or motor deficit. Plain X-ray of the skull can be
helpful. Areas of rarefaction are seen early in the
disease, which develop into punched out defects
with a central sequestrum later on.28 Both osteo-
lytic and osteoblastic areas may be seen. Rarely,
sclerosis may be seen and indicates secondary
infection. CT scan of the brain is helpful in
assessing the extent of bone destruction, scalp
swelling, and degree of intracranial involvement
(Fig. 55.1).27 Combination of surgical excision
and antitubercular therapy are the preferred treat-
ment. With early diagnosis and a combination of
surgical and medical management, all cases of cal-
varial tuberculosis are potentially curable. Surgery
is indicated to establish the diagnosis, to remove
thick extradural granulation tissue and necrotic
bone, and in patients with sinus discharge, intra-
cranial extensions, and large collections of caseat-
ing material causing mass e ect.21,22,23,24,25,26,27,28
55.3.9 Spinal Tuberculosis
TB spondylitis, also called as Pott’s disease, was
first described by Percival Pott in 1779. Tubercu-
lous spondylodiskitis is an important cause of
spinal infection in developing countries. Early
diagnosis and prompt treatment are essential to
avoid morbidity. It constitutes 2 to 4% of all cases
of osteomyelitis. The lumbar spine is the most
commonly a ected region, followed by the thora-
cic and cervical spine and, rarely, the sacrum. The
thoracolumbar junction is a common site involved
in tuberculous spondylitis. It results from hema-
togenous spread, both arterial and venous; direct
contamination; and direct spread from adjoining
abscess. The arteries at the anterior aspect of the
vertebra possess the richest supply, accounting for
the initial infective focus in the anterior subchon-
dral bone. The Batson paravertebral venous plexus
of valveless veins provides a potential route of ret-
rograde spread from abdominal veins. Direct con-
tamination of the spine may occur after surgery or
after spinal canal puncture, although the incidence
is low. It could manifest as solitary vertebral
body involvement, multifocal skip lesions, pure
Fig. 55.1 (a) Axial CT bone window
showing right greater wing of sphe-
noid bone erosion. (b) Axial contrast
CT showing hypodense poorly en-
hancing granulation tissue in the right
greater wing of sphenoid bone.
Infections
462

posterior element involvement. Spinal meningitis,
arachnoiditis, or myelitis may ensue. Epidural
abscess may occur.
55.3.10 Clinical Profile, Imaging,
and Diagnosis
The most common signs include fever, headache,
vomiting, and an altered sensorium. Neck rigidity
and cranial nerve palsies are commonly seen.1,6
Variable degrees of encephalitis, hydrocephalus,
and infarction are responsible for altered senso-
rium in tubercular meningitis.
Focal deficits may occur in the forms of mild to
total weakness of the limbs or varying degrees of
cranial nerve palsy. The cranial nerves are involved
via arachnoiditis, and motor weakness is usually
secondary to infarctions of the subcortical white
matter. Among the cranial nerves, the abducens
and oculomotor nerves are frequently involved.
Motor deficits are measured by the Barthel index,
which are categorized by activities of daily living.
Patients with tuberculomas usually present with
headache, seizures, focal neurological deficit, and
features of raised intracranial tension. Infratento-
rial tuberculomas may present with brainstem
syndromes, cerebellar symptoms, and multiple
cranial nerve palsies.10 Hydrocephalus has been
described as a marker of visual impairment.
Tuberculous abscesses have an acute clinical pre-
sentation and a rapid deteriorating course than
tuberculomas, with symptoms of fever, headache,
and focal neurological signs. The clinical symptoms
of spinal TB in children are often insidious and
include back pain, fever, paraparesis, sensory dis-
turbance, and bowel and bladder dysfunction.
About 3% of children with spinal TB develop severe
kyphosis greater than 60 degrees. The risk factors
for the development of severe kyphotic deformity
are the following: being younger than 10 years of
age, involvement of three or more vertebral
bodies, and thoracic spine localization. Severe
kyphosis results in spinal cord compression over
the apex of the deformity and cardiopulmonary
dysfunction from restrictive lung disease and is
cosmetically unacceptable.
On clinical suspicion of tubercular meningitis,
CSF examination is the initial modality of investi-
gation.3 The diagnosis of tubercular meningitis is
based on definite and probable criteria. Definitive
diagnosis of tuberculous meningitis depends on
the detection of the tubercle bacilli in the CSF,
either by smear examination or by bacterial
culture.5,6,7 The predominance of CSF lymphocyto-
sis is highly suggestive of tubercular meningitis,
which is reported to be greater than 50% in 80 to
83% of patients. Low levels of CSF glucose and ele-
vated levels of protein are also seen. The polyme-
rase chain reaction (PCR) constitutes a rapid
method of detecting the M. tuberculosis genome in
CSF, and allows for a rapid and specific diagnosis of
tuberculous meningitis.6
The identification of
bacilli is di cult since cultures take a long time for
processing and the bacilli may disappear rapidly
from CSF after treatment has been instituted.6
Acid-fast bacilli in the context of centrifuged CSF
may be evident in 20 to 90% of cases. However, the
small sample volume, low bacillary load, and the
presence of PCR inhibitors in samples may account
for low sensitivity. The yield of positive mycobac-
terial cultures from CSF in tubercular meningitis
varies from 19 to 70%.5,6,7,8 The diagnostic utility of
skin testing being positive for CNS tuberculosis
varies from 10 to 20% to 50%.
Molecularly based techniques include commer-
cially available nucleic acid amplification (NAA)
methods and other PCR-based methods, antibody
detection, antigen detection, or chemical assays
such as adenosine deaminase (ADA) and tubercu-
lostearic acid measurements.29 Commercial nucleic
acid amplification (NAA) assays for the diagnosis of
TBM are 56% sensitive and 98% specific and the
diagnostic yield of NAA increases when large vol-
umes of CSF are processed. The sensitivity of CSF
microscopy and culture falls rapidly after the start
of treatment, whereas mycobacterial DNA may
remain detectable within the CSF until 1 month
after the start of treatment. The measured sensi-
tivities and specificities of ADA in the CSF range
from 44 to 100% and 71 to 100%, respectively.
Standardized cuto s of ADA values for the diagno-
sis of TBM have not been established, and the val-
ues used in various studies ranged from greater
than 5 to greater than 15 IU/L. It is helpful in pre-
dicting poor neurological outcomes among pedia-
tric TBM cases.30,31A raised ADA activity in the CSF
of patients with CNS TB lacks specificity. CSF ADA
activity is not recommended as a routine diagnos-
tic test for CNS tuberculosis. Tuberculostearic acid
has good sensitivity, but requirement of expensive
equipment has limited its clinical use.31
The imaging findings are summarized in
Table 55.1.
Contrast-enhanced computed tomography (CT)
is the investigation of choice since it is easily avail-
able and can be quickly performed to establish
diagnosis. CT scan can depict the presence of
Surgical Considerations in Tuberculosis, Fungal, and Parasitic Infections of CNS in Children
463

hydrocephalus, infarcts, and basal exudates.32 The
presence of periventricular lucency in isolation
can suggest ischemia but along with a rounded
third ventricle is suggestive of interstitial edema
and raised ICP syndrome. In some series, normal
results are reported in up to 5% of cases. Hydroce-
phalus is a frequent accompaniment of tube-
rculous meningitis with an incidence varying
between 50 and 80%. CT cannot predict the level of
CSF block in TBM because both types of hydroce-
phalus can present with panventricular dilation.32
The presence of basal enhancement, hydrocepha-
lus, tuberculoma, and infarction were more
common in TBM than in children with pyogenic
meningitis. They reported that basal enhancement,
tuberculomas, or both were 100% specific and 89%
sensitive for the diagnosis of TBM. Andronikou and
colleagues suggested nine criteria for the diagnosis
of TBM on CT. Przybojewski and colleagues eval-
uated these nine criteria and showed high specific-
ity for all the criteria, and 100% specificity for four
individual criteria.32 It has been shown that sensi-
tivity has been improved when more than one
criterion was present. Presence of hyperdensity on
precontrast scans in the basal cisterns might be the
specific sign of TBM in children. The reported inci-
dence of infarcts on CT varies from 20.5 to 38%.
Magnetic resonance imaging (MRI) has been
shown to be superior to CT in evaluating patients
with suspected meningitis and its associated com-
plications.33,34,35 Noncontrast MRI shows little or
no evidence of meningitis in early stages of the
disease. Contrast-enhanced MRI shows abnormal
meningeal enhancement in the basal cisterns, and
sylvian fissures (Fig. 55.2). The cerebral convex-
ities show enhancement in severe and late-stage
TBM. Tentorial and cerebellar meningeal involve-
ment is less common. There could be minimal or
absent meningeal enhancement in immunocom-
promised patients although some reports show no
significant di erence. The newer sequences of MR
imaging along with qualitative and quantitative in-
formation of CSF flow and dynamics is helpful to
di erentiate between types of hydrocephalus and
postoperative evaluation in patients with third
ventriculostomy. However, the flow around fourth
ventricle may not be easily appreciated. MR ventri-
culography has been used to evaluate CSF flow
dynamics and in patients with hydrocephalus. MRI
depicts hemorrhagic transformation of infarcts
better. Multiple infarcts in the anterior circulation
territory favored tuberculous etiology.
Table 55.1 Imaging features
MR imaging

Tuberculous
meningitis
Tuberculoma

Cysticercosis

Fungal
granuloma
Hydatid cyst
T1 WI

Hyperintense

Hypointense

Hypointense with
hyperintense dot
within cyst
Variable, low to
intermediate to
isointense
Hypointense
T2 WI

Nonspecific

Hypointense

Hyperintense

Hypointense

Hypointense
Contrast

Basal
enhancement
Homogenous/ring
enhancement
with central
hypointensity
Present

Peripherally
enhancing
Nil
Magnetic
transfer
Hyperintense

-

-

-

-
Diffusion WI

Restriction
(infarction)
-

-

-

-
Abbreviations: MR, magnetic resonance; WI, weighted.
Fig. 55.2 Axial contrast CT showing basal meningeal
inflammation with dilated ventricles and periventricular
ooze suggestive of meningitis with hydrocephalus.
Infections
464

MR angiogram reveals small segmental narrow-
ing, uniform narrowing of large segments, irregu-
lar beaded appearance of vessels, or complete
occlusion with contrast-enhanced MRI being more
sensitive to detect smaller vessels. The infarcts
mostly involve thalamus, basal ganglia, and inter-
nal capsule regions. Di usion-weighted MR imag-
ing helps in early detection of infarction and in
delineating the extent of infarction.
Magnetic transfer (MT) MRI is considered supe-
rior to conventional MRI for showing abnormal
meninges.36 It also helps in di erentiating tuber-
culous meningitis from other causes of meningitis.
The abnormal meninges appearing hyperintense
on precontrast T1-weighted (T1W) MT images is
considered to strongly suggest tuberculous menin-
gitis. Also, the MT ratio (MTR) is significantly dif-
ferent from brain parenchyma and inflamed
meninges, because the inflammatory exudate in
TBM is composed of cellular infiltrate, degenerated
and partially caseated fibrin, tubercles, and, less
commonly, bacilli.
Radiograph/CT pneumoencephalography or con-
trast-enhanced cisternography done via lumbar
puncture may help in di erentiating communicat-
ing and noncommunicating hydrocephalus, if MRI
is not available.32,33,34,35,36
Imaging findings of tuberculoma depends on
whether it is noncaseating or caseating with solid
or liquid center. A solid noncaseating tuberculoma
is isodense or slightly hypodense to the surround-
ing brain parenchyma on CT and hypointense on
both T1 W and T2 W images on MRI. It shows
homogeneous enhancement on contrast adminis-
tration ( Fig. 55.3 and Fig. 55.4). The cellular
components of the noncaseating tuberculomas
appear brighter on MT T1 W imaging di erentiat-
ing it from metastases, lymphomas, and other
infective granulomas.32,33,34,35,36 The target sign, a
central calcification or nidus surrounded by ring
Fig. 55.3 (a) Axial contrast CTshowing ring-enhancing conglomerate lesions in the left cerebellum. (b) Axial T2 image
showing hypointense solid lesion with perifocal edema in the left frontoparietal brain. (c) Axial contrast image showing
hypointense thick irregularly ring-enhancing lesion in the left frontoparietal brain.
Fig. 55.4 (a) Axial T2 image showing
hypointense solid conglomerate le-
sions in the suprasellar and bilateral
sylvian fissures. There is severe peri-
focal edema. (b) Axial contrast image
showing the peripheral enhancing sol-
id lesions depicting crenated margins.
Surgical Considerations in Tuberculosis, Fungal, and Parasitic Infections of CNS in Children
465

enhancement on postcontrast images, is consid-
ered pathognomonic of tuberculoma. Solid caseat-
ing granulomas with T2 hypointense center can be
confused with lymphoma and fungal and cysticer-
cus granulomas. These lesions appear hypointense
on T1 W MT images surrounded with a hyperin-
tense rim. En plaque tuberculomas are hyperdense
on noncontrast CT scans, isointense to brain on
T1 W MRI, and isointense to hypointense on T2 W
images with homogeneous postcontrast enhance-
ment. Tuberculomas can mimic neurocysticercosis,
fungal granulomas, and tumors like lymphomas,
glioma, and metastases. Newer imaging techni-
ques, like di usion imaging, MR spectroscopy
(MRS), and MT imaging may help in di erentiating
these conditions.33,34,35,36
MRS is specific for the diagnosis of tuberculoma,
which show large cellular component appearing
bright on MT imaging and with a choline peak on
spectroscopy. Dynamic contrast enhancement
(DCE) MRI has been used by to correlate the rela-
tive cerebral blood volume values with the cellular
and necrotic components of tuberculomas and also
with the expression of various immunohistochem-
ical markers. Serial di usion tensor imaging (DTI)
has been used to evaluate brain tuberculomas and
may be of value in assessing the therapeutic res-
ponse of tuberculomas that are treated only with
specific antituberculous drugs. Fluorodeoxyglu-
cose positron emission tomography can be helpful
in di erentiating an atypical tuberculoma from
other neoplastic and nonneoplastic CNS lesions. It
can also be used in the follow-up of tuberculomas.
Imaging findings of tuberculous brain abscess
are usually nonspecific. They present as large,
frequently multiloculated, ring-enhancing lesions
with perilesional edema and mass e ect
(Fig. 55.5). Di usion-weighted imaging shows
restricted di usion with low apparent di usion
coe cient (ADC) values because of the presence of
inflammatory cells in the pus. MRS helps in di er-
entiating tuberculous abscess from those of pyo-
genic and fungal causes.33,34,35 MRS shows lipid,
lactate, and phosphoserine without evidence of
cytosolic amino acids, in contrast with pyogenic
abscess. MT imaging can di erentiate tuberculous
from pyogenic abscesses. The rim of tuberculous
abscesses shows lower MTR values compared with
pyogenic abscesses.36
55.3.11 Spinal Tuberculosis
MRI is currently the imaging modality of choice,
given its superior ability in the detection of soft
tissue and bone marrow changes even in patients
with normal radiographs.34,35 MRI of the entire
spine should be performed to exclude multilevel
involvement and skip lesions. Bone marrow edema
is an early sign of infection that is seen as areas of
hypointensity on T1 W images, and hyperintense
areas on T2 W, short tau inversion recovery (STIR),
and proton density fat-suppressed sequences
(Fig. 55.6). T1 W images are the most sensitive in
detecting marrow edema. A contrast-enhanced
T1 W sequence with fat suppression provides val-
uable additional information and is highly recom-
mended. Vertebral end plate erosion is seen as loss
of the normal T1-hypointense line on sagittal MR
images. Diskal enhancement patterns include
homogeneous disk enhancement, patchy noncon-
fluent areas of disk enhancement, and varying
areas of peripheral disk enhancement, most often
being T1 hypointense, T2-heterogeneously hyper-
intense, and epidural masses, which are slightly T1
hypointense and T2 hyperintense. Compression or
displacement of the spinal cord should be looked
for in the presence of epidural masses, which may
show craniocaudal migration. Spinal cord involve-
ment in the form of infarction and syringomyelia
may occur as a complication of arachnoiditis.
Tuberculous pus formation may occur between the
dura and the leptomeninges and may appear
Fig. 55.5 Axial contrast CT image showing conglom-
erate of multiple ring-enhancing lesions in the left
posterior temporal brain.
Infections
466

loculated. It appears hyperintense on T2 W and
isointense to hypointense on T1 W images. The
dural granulomas appear hypointense to isoin-
tense on T2 W and isointense on T1 W images. Rim
enhancement can be seen on postcontrast images.
Epidural TB lesions generally appear to be isoin-
tense to the spinal cord on T1 W images and have
mixed intensity on T2 W images. In postcontrast
images, uniform enhancement can be seen if the
TB inflammatory process is phlegmonous, whereas
peripheral enhancement is seen if true epidural
abscess formation or caseation has developed. Epi-
dural tuberculous abscess may occur as primary
lesions or may be seen in association with arach-
noiditis, myelitis, spondylitis, and intramedullary,
and dural tuberculomas.
55.3.12 Treatment
The primary line of treatment for tuberculous
meningitis is medical therapy with antitubercu-
lous multidrug chemotherapy.1,4,5,6,7,8,9,31
The
primary drugs include rifampicin (10 mg/kg), iso-
niazid (5 mg/kg), ethambutol (20 mg/kg) or strep-
tomycin (20 mg/kg), and pyrazinamide (25 mg/kg)
for 3 months followed with isoniazid and rifampi-
cin daily for the next 6 months and continued
with isoniazid and ethambutol for 15 months.
The therapy is prolonged and is continued for
2 years.1,4,5,6,7,8,9 In certain situations like relapse,
therapy can be continued for 1 more year. Steroids
can be added if the patient has pronounced men-
ingitis and appears sick. All patients with TBM
may receive adjunctive corticosteroids regardless
of disease severity at presentation.4,5,6,7,8,9,31 Adults
(>14 years) should be administered dexametha-
sone 0.4 mg/kg/24 h with a tapering course over 6
to 8 weeks. Children can be given prednisolone
4 mg/kg/24 h (or equivalent dose dexamethasone:
0.6 mg/kg/24 h) for 4 weeks, followed by a tapering
course over 4 weeks. It has been shown to signifi-
cantly improve survival rate. They are withheld if
the patient has also manifested with lung tubercu-
losis. Patients with multidrug-resistant tuberculo-
sis are administered second and third line of
antituberculous drugs including kanamycin or
ethionamide. The liver and renal functions are
closely monitored during the course of therapy.
Visual charting is performed to detect abnormality
with color vision.
The therapy for children with TB meningitis
includes controlled ventilation maintaining nor-
mal oxygenation and paCO2 concentrations.1,3,6
Intravascular volume should be maintained at all
times with blood and fluids, maintaining normal
hematocrit and electrolyte concentration. Fluid
restriction is not recommended. Hypotonic fluids
should be avoided to prevent hyponatremia. The
head of the bed may be elevated to reduce intra-
cranial venous pressure as long as norm al central
venous pressures are maintained by adequate vol-
ume replacement.
55.3.13 Hyponatremia
The mainstay of treatment for SIADH has been
based on fluid restriction unless patients are
severely symptomatic, in which case hypertonic
saline is used. Diuretics and urea have been used.
Demeclocycline has been used in chronic SIADH.
The treatment of CSW revolves around fluid and
Na replacement because these patients develop
hyponatremia in the setting of volume depletion.37
Fludrocortisone or hypertonic saline has yielded
good results. Correction of chronic hyponatrem ia
should be performed very slowly (<0.5 mM/h) or
Fig. 55.6 Axial T2 image of the dorsolumbar spine
showing destruction and collapse of D12–L1 vertebra
resulting in kyphosis and spinal cord compression.
Surgical Considerations in Tuberculosis, Fungal, and Parasitic Infections of CNS in Children
467

rapid correction risks the development of central
pontine myelinolysis.1,3
55.3.14 Hydrocephalus
The hydrocephalus is graded as mild if the third
ventricle or temporal horns were dilated (>2 mm),
as moderate if rounding of the frontal horns
occurred, and as severe if periventricular lucency
was present on imaging. Patients with sympto-
matic hydrocephalus or radiologically worsening
hydrocephalus benefit from CSF diversion proce-
dures. The Palur grading system (Vellore grading
system) was based on the presence or absence of
neurological deficits and level of sensorium
(Table 55.2).38 The grading system is useful to
grade the patients in retrospective studies, but it
has some degree of subjectivity in assessing senso-
rium. Therefore, the modified Vellore grading sys-
tem is used which includes the Glasgow Coma
Scale ( Table 55.3). The latter grading system is
reproducible across di erent levels of clinical
expertise and across di erent disciplines of health
care workers and is, therefore, a more reliable sys-
tem. However, both grading systems correlate well
with outcome and prognostication.
Medical management with tapering doses of
steroids and decongestants including acetazola-
mide (100 mg/kg) and frusemide (1 mg/kg) can be
tried for a few days or a week in patients in grades
I and II.38 Grades II and III patients should be moni-
tored closely during this period to detect any wor-
sening or lack of improvement and a shunt should
be promptly o ered in case of failure of medical
management. In good grade patients, prolonging
medical therapy could be harmful and may lead to
irreversible brain damage. Grade IV patients
should undergo external ventricular drainage and
shunt should be inserted if they show neurological
improvement.39,40
Ventricular tap is sometimes indicated as an
emergency measure to assess and reduce the CSF
pressure and stabilize the neurological condition.
It can also yield ventricular CSF for examination.
Serial ventricular tap every 6 to 8 hours can be
done till definitive CSF diversion procedure is con-
templated. The initial choice of surgical procedure
is ventriculoperitoneal shunt. Bhagwati et al have
observed that reduction in ICP and size of the ven-
tricles is helpful to improve periventricular perfu-
sion and enhance drug delivery to the tissues in a
more e ective manner.41 The complications of
shunt surgery include shunt infection and shunt
blockade requiring one or multiple revisions. Poor
general condition of patient and high CSF protein
and cellular content were responsible for frequent
shunt blockages. Agarwal et al reported shunt-
related complications in 11 (30%) children and
three of 37 children had to undergo multiple shunt
revisions. Palur et al reported that 26 of 114
(22.8%) patients had to undergo one or more shunt
revisions, one patient requiring more than three
revisions.38 Sil and Chatterjee reported a shunt
infection rate of 15.6% and revision rate of 43.8% in
their series of 37 children who underwent shunt
surgery for TBM with hydrocephalus.42 Multiple
revisions were done in 18.7% of patients.
Endoscopic third ventriculostomy is an option
for patients who have completed at least 4 weeks
of antituberculous therapy.43
It is technically
demanding and should be performed by a surgeon
who is skilled in endoscopic procedures.44,45,46,47,48
It is di cult to recognize anatomical landmarks
since the floor of the third ventricle is frequently
thick and the subarachnoid space is also likely to
Table 55.2 Palur’s grading for TB meningitis–induced
hydrocephalus
Description
I. 1.
Headache, vomiting, fever, and/or neck stiffness
2.

No neurological deficit
3.

Normal sensorium
II 1.
Normal sensorium
2.

Neurological deficit present
III 1. In altered sensorium but easily arousable
2.

Dense neurological deficit may or may not be
present
IV 1. Deeply comatose
2.

Decerebrate or decorticate posturing
Abbreviation: TB, tuberculosis.
Table 55.3 Modified Vellore Grading Scale for TB
meningitis–induced hydrocephalus
Grade Variables
I

GCS 15 Headache, vomiting, fever ± neck
stiffness. No neurological deficit
II

GCS 15 Neurological deficit present
III

GCS 9–14 Neurological deficit may or may not
be present
IV

GCS 3–8 Neurological deficit may or may not
be present
Abbreviations: TB, tuberculosis; GCS, Glasgow Coma
Scale.
Infections
468

be obliterated by exudates in early stages of the
disease.47,48 The basilar artery and its branches are
at enhanced risk of injury. The tubercles and gran-
ulation tissue on the thick floor of third ventricle
bleed when touched and obscure the endoscopic
field. Patients with longer duration of symptoms
and ATT were more likely to benefit from the
ETV.47
With the advent of e ective antitberculous che-
motherapy and steroids, the indication for surgery
is rare.1,6,31 The role of routine adjunctive cortico-
steroids for all patients with tuberculomas without
meningitis is controversial. They may be helpful in
those patients whose symptoms are not con-
trolled, or are worsening, on anti-tuberculosis
therapy. Intrathecal hyaluronidase has been tried
in children with communicating hydrocephalus
but does not o er any particular advantage over
shunt insertion in terms of regression of specific
neurological deficit or overall functional improve-
ment.49
Surgical excision of tuberculomas or
tuberculous abscess is performed only when there
is a rapid clinical deterioration following optimal
medical therapy.49,50,51,52 Intraventricular tubercu-
lous abscess threatening to develop acute obstruc-
tive hydrocephalus or formation of a subdural
empyema may necessitate a craniotomy. Biposy
correlation may be warranted to establish diagno-
sis in cases of coinfection with HIV contributing to
di erential diagnosis.
55.3.15 Outcome and
Prognostication
The factors contribute to this poor outcome
include cerebrovascular involvement with resul-
tant cerebral ischemia, abscess formation, hydro-
cephalus and raised ICP, direct parenchymal injury,
hyponatremia, seizures, and delayed diagnosis.
The grade at presentation is the best and most
consistent predictor of outcome following shunt
surgery in patients with TBM. The presence of
infarcts in the basal ganglia and internal capsule
are also likely to indicate a poor outcome following
shunting.1,3,6,38,41,42
The outcome of TBM with hydrocephalus is
finally dependent on the response of the disease to
antituberculous therapy.38,41,49,50,51,52 It is under-
standable that in patients with drug-resistant TB
either multidrug-resistant TB (MDR-TB) or exten-
sively drug-resistant TB (XDR-TB), the outcome is
likely to be poor. There are, however, no studies,
which have reported on the outcome following
surgery for drug-resistant TBM. Home-based treat-
ment of childhood neurotuberculosis is feasible in
selected patients under close supervision in areas
where there is high incidence of tuberculosis
coupled with HIV infection resulting in severe bed
shortages in secondary and tertiary hospitals.53
55.3.16 Pott’s Disease
The early TB spondylitis without spinal cord com-
pression or neurological deficits can be treated
conservatively with chemotherapy. However, sur-
gery is recommended for patients with spinal cord
compression or neurological compromise, signifi-
cant spinal deformity, persistent severe axial pain,
or disease progression on maximal medical
therapy.54 Steroids may be helpful in patients who
are deteriorating on antituberculous therapy.
Various surgical approaches have been reported
in the treatment of TB spondylitis in the pediatric
age group.55,56 Short- and long-term clinical out-
comes were similar when radical surgery was
compared with debridement alone, but the correc-
tion of kyphosis and deformity was better in chil-
dren undergoing radical surgery with anterior
reconstruction than in patients undergoing
debridement alone. In addition, radical surgery
seems to decrease the length of drug therapy
because clinical and radiographic outcomes were
similar for chemotherapeutic regimens prescribed
for 6, 9, or 18 months when combined with radical
surgery.54,55,56 In children, the skeletal immaturity
of young children should be recognized minimiz-
ing the number of fused segments, especially in
the thoracic spine, to avoid complications such as
iatrogenic short trunk, crankshaft deformity, and
pulmonary hypoplasia from restricted growth of
the rib cage. Moreover, younger patients exhibit a
more progressive form of TB, with increased risk of
extrapulmonary disease and progressive vertebral
body collapse placing them at a higher risk for dis-
abling complications than adults.
The surgical technique of choice for spinal TB
has been a matter of continuous debate.56 Poste-
rior-only operations in spinal TB traditionally have
had unfavorable outcomes because they were usu-
ally limited to laminectomy with or without
fusion, whereas the unaddressed spinal cord com-
pression was located anteriorly.55,56 Modern tech-
niques, such as vertebral column resection via a
posterior approach, allow circumferential decom-
pression of the spinal cord, correction of acute seg-
mental deformity, and resection of the infectious
focus.56
Surgical Considerations in Tuberculosis, Fungal, and Parasitic Infections of CNS in Children
469

55.3.17 Fungal Diseases of Central
Nervous System
Intracranial fungal infections are reported but
intracranial fungal masses requiring neurosurgical
intervention are uncommon.57,58,59,60 They are rare
in children.61 However, in the recent years it has
seen an upsurge due to HIV infections, increased
use of immunosuppressants, increased incidence
of diabetes mellitus and prolonged survival in
organ transplants, and patients undergoing cancer
adjuvant therapy.62,63,64,65,66,67,68,69 There is relative
paucity of literature on this subject and hence the
management of intracranial fungal masses is not
standardized.62,63,64 The mainstay of fungal infec-
tions, however, is still antifungal therapy. It is still
unclear whether the role of surgery involves a
biopsy, partial or radical excision and its relation
to the long-term outcome.
55.3.18 Pathogenesis
Fungi are ubiquitous organisms. They are often
nonpathogenic or result in a self-limited illness in
otherwise healthy humans. Fungi that grow as
yeast include Candida and Cryptococcus, whereas
Aspergillus and mucormycosis grow with branching
hyphae. Coccidioidomycosis is an example of a
dimorphic fungus. Fungi that grow as yeasts
spread hematogenously, entering the meningeal
m icrocirculation ow ing to their sm all size, result-
ing in seeding of the subarachnoid space and
m eningitis. Although parenchym al disease is less
com m on with yeast organism s, both Candida and
Cryptococcus m ay m anifest as prim arily paren-
chym al abnorm alities with the form ation of
granulom as or abscesses. The hyphal form s of
fungal pathogens often cause parenchym al dis-
ease, because the larger m orphology precludes
access to the m eningeal m icrocirculation. The
larger cerebral vessels m ay also becom e involved,
resulting in vasculitis with throm bosis and
mycotic aneurysm form ation.
The commonest fungus that produces intracra-
nial fungal masses (IFM) is the Aspergillus
species.57,58,59,60
Aspergillus flavus is generally
implicated as the causative organism in patients
who are immunocompetent, whereas Aspergillus
fumigatus is more frequently reported in immuno-
compromised individuals. The other fungi causing
IFMs include Cryptococcus, mucormycosis, Can-
dida, Cladosporium, and dematiaceous fungi.
Inhaled fungal spores, which travel to the lung
parenchyma, are most often removed by an
immunocompetent immune system. They can also
occur related to indwelling catheters, fungal dis-
ease in other organs, or trauma, with the infection
subsequently being eliminated by a combination
of the host’s reticuloendothelial, cellular, and
humoral defense system. Direct penetration of the
blood–brain barrier through hematogenous route,
in immunocompromised or rarely immunocompe-
tent patient may result in meningitis or cerebritis.
It may also result following setting of neurosurgi-
cal procedures or secondary to adjacent sinus dis-
ease. Fungal aneurysms are caused usually by
Aspergillus or mucormycosis.62,63,64 The angioinva-
sive nature of these organisms leads to the
digestion of the elastic lamina of the vessels by the
production of the enzyme elastase.
The commonest focus of infection for intracra-
nial fungal masses is the paranasal sinuses (PNSs)
and the mastoid sinuses, rarely lungs and heart
especially in the presence of artificial heart
valves.62,63,64,65,66,67,68,69 In some patients with IFM,
however, no obvious systemic source for the fungal
infection is discernible.62 Rarely, fungal infection
may follow direct inoculation of the brain during
intracranial or transsphenoidal surgery or follow-
ing trauma. Sharma et al reported two patients
who developed IFMs following intracranial sur-
gery.70 IFM include, HIV infection organ transplan-
tation, cancer chemotherapy, prolonged steroid
therapy, autoimmune disorders such as systemic
lupus erythematosus and tuberculosis.
Fungal infections can lead to meningitis, menin-
goencephalitis, vasculitis, abscess formation, and
granuloma formation.57,58,59,60,61,62
Most reported
studies have identified Cryptococcus, Aspergillus, and
Candida species as the most common organisms in
fungal infections of the CNS.62,63,64,65,66,67,68,69 How-
ever, granuloma formation has been reported to be
most common with Aspergillus.
55.3.19 Prevalence and Clinical
Profile
Intracranial fungal masses can be seen in any age
group, but most patients are in the third, fourth,
and fifth decades of life.57,58,59,60,61,62 They have
been reported even in neonates, infants, and
young children. Intracranial fungal masses in
immunocompetent patients have been predomi-
nantly reported from Indian subcontinent, Middle
east, Africa, and California in the United States. The
hot, dry climate coupled with a high content of
Aspergillus spores in the atmosphere may be a
Infections
470

probable cause. Nearly 50% of patients with IFMs
have no overt predisposing illness or evidence of
immunosuppression. There might be a subclinical
impairment of cell-mediated immunity. There has
been an increase in the number of invasive fungal
infections in recent times. The incidence was 5.1%
in 1992, 6.6% in 1996, and 10.4% in 2005. The
cumulative prevalence of IFMs in transplant recipi-
ents varied between 0.5 and 1%.57,58,63,64,65,66,67,68,69
It has been observed that IFMs would constitute
about 1 per 1,000 neurosurgical procedures per-
formed at major neurosurgical centers accounting
for their rarity.
The clinical presentation can be indolent and
vary from a few days to several months or even
years.64 The clinical presentation is not specific but
can be divided into the following five distinct
types depending on the nature of the disease:64
● Involvement of the cranial nerves I to VI with
orbital and nasal symptoms. These symptoms/
signs are common in patients with fungal
infections that originate in the PNS and spread to
the intracranial compartment by the contiguous
route.
● Focal neurological deficits due to involvement of
any part of the neuraxis.
● “Stroke-like” presentation with sudden onset of
hemiparesis reported in 6 to 10% of patients.
Fungal aneurysms can present with
subarachnoid hemorrhage.
● Raised ICP, seizures, and altered sensorium. The
altered sensorium can result from raised ICP,
ischemia due to the vasculitis associated with
the concomitant fungal meningitis and fungal
meningoencephalitis.
● Fever is an infrequent symptom, seen in only 10
to 31% of patients.
55.3.20 Imaging and Diagnosis
CT scans can show paranasal sinusitis, small areas
of bony destruction, and absence of separation of
periosteum from the medial orbital wall. Jinkins et
al described five cases with varying radiological
findings, including large tumor-like enhancing
granulomatous masses within the brain tissue,
nodular meningeal granuloma, paranasal sinusitis,
orbital masses with brain destruction, infections
with vasculitis, and aneurysm formation. The dif-
ferential diagnosis of a similar mass in isolation
included an abscess, tuberculoma, meningioma,
and glioma (depending on location).
The characteristic MRI appearances for various
fungal granulomas have been described and have
shown some variability among organisms.
For example, cryptococcoma appears to have low
T2-weighted signal intensity, contrasting with
the surrounding hyperintense cerebral edema
(Fig. 55.7). Aspergillomas, however, have inter-
mediate signal intensity for the granuloma, sur-
rounded by perilesional edema on T2-weighted
images (Fig. 55.8). Gupta et al who reported an
intracranial aspergilloma that simulated a menin-
gioma by demonstrating isointense T1 signal to
the brain parenchyma and isointense T2 signal to
the white matter.71
Parenchymal involvement of CNS fungal disease
may result in granuloma formation, cerebritis,
and/or abscess formation. Imaging findings of cer-
ebritis are nonspecific but typically include
increased T2/fluid-attenuated inversion recovery
(FLAIR) signal abnormality associated with a
variable amount of enhancement. The common
locations involved are the frontal lobes, anterior
cranial fossa without frontal lobe involvement, and
followed by middle cranial fossa, sellar and tempo-
ral regions.
Fungal abscesses often multiple and near the
gray–white matter junction related to the hemato-
logic distribution of fungal organisms. Fungal
Fig. 55.7 Axial contrast CT image showing the hypo-
dense center with peripherally enhancing lesion in the
right parietal brain. There is perifocal edema.
Surgical Considerations in Tuberculosis, Fungal, and Parasitic Infections of CNS in Children
471

abscesses may also involve the deep gray matter
nuclei involvement of the deep gray matter nuclei.
Bacterial abscesses are more often single and spare
the basal ganglia. The imaging appearance of an
intracranial fungal abscess is similar to a pyogenic
abscess typically demonstrating a ring-enhancing
lesion with a hypointense T2 rim, which may
show restricted di usion. Immunocompromised
patients may have a variable imaging appearance,
as shown by Enzmann and colleagues, who
studied 15 immunocompromised patients with
CNS infections and concluded that six of eight
patients a icted with Aspergillus had minimal to
no enhancement on imaging with intravenous
contrast.72 MRS demonstrated identification of
multiple signals between 3.6 and 3.6 ppm and
may confer further specificity to the diagnosis.
Fungal infections that a ect immunocompetent
hosts include Cryptococcus neoformans, Cocci-
dioides immitis, Histoplasma capsulatum, and
Blastomyces dermatitidis, whereas Aspergillus and
Candida are most often seen in immunocompro-
mised hosts.
Aspergillus is among the most commonly iso-
lated organism from fungal brain abscesses. Asper-
gillus abscesses may be surrounded by low signal
intensity on T2-weighted and gradient-echo
images. The hypointense T2 signal rim has been
attributed to small amount of hemorrhage with
hemosiderin-laden macrophages and a dense pop-
ulation of hyphae at the abscess rim. Peripherally
restricted di usion may be present. Another strik-
ing feature of Aspergillus is the tendency for the
organism to invade blood vessels. In the retrospec-
tive analysis by Nadkarni and Goel,63 3 of 10
patients were found to have autopsy-proven evi-
dence of intracranial vascular invasion with secon-
dary thrombosis. Vascular invasion is facilitated
by the release of the enzyme elastase, which
facilitates intramural vascular invasion. Secondary
complications of vascular invasion include vasculi-
tis, infarction, rarely mycotic aneurysms, and
intracranial hemorrhage. Imaging findings of
hemorrhage are common in association with
Aspergillus infection.
55.3.21 Treatment
Surgical treatment is required in the following
situations: (1) stereotactic biopsy as a means to
establish diagnosis and identification of organism;
(2) surgical excision, to remove or reduce the mass
e ect; and (3) external ventricular drain to treat
sequelae such as hydrocephalus and conversion to
ventricular shunt placement, if necessary. In addi-
tion, intracavitary administration of amphotericin
B has been advised.65,66,67,68,69 Stereotactic drain-
age of aspergillosis brain abscesses with long-term
survival has been reported by Goodman et al.73
Stereotactic procedures might yield a good out-
come in selected patients, but whenever feasible,
safe radical excision of the IFM along with normal
nervous tissue around it should be done. Medical
therapy with antifungal agents is required for pro-
longed periods following surgery in patients with
IFM.57,58,59,60,61,62,63,64,65,66,67,68,69
Surgical extirpa-
tion of the paranasal sinus disease by functional
endoscopic sinus surgery (FESS) should be per-
formed whenever it is associated with intracranial
fungal masses.64,74,75,76,77,78,79,80,81,82,83,84
Fungal
aneurysms should be treated with clipping or
endovascular treatment after su cient duration of
antifungal therapy.85 However, the ultimate out-
come may not be always gratifying.86
The treatment of cryptococcal meningitis is
essentially chemotherapy.87 A 4-week regimen is
advocated for patients who have no underlying
disease or immunosuppressive therapy and early
Fig. 55.8 (a) Coronal T2-weighted MR
image showing the hypointense left
cavernous sinus lesion characteristic of
Aspergillus. (b) Axial T1-weighted con-
trast MR image showing the hetero-
genous enhancement.
Infections
472

recognition of meningitis without concomitant
neurological sequelae. After 4 weeks of therapy,
the CSF India Ink preparation should be negative
and CSF cryptococcal antigen titers b1: 8 at 4
weeks. Patients who do not meet the above criteria
should receive at least 6 weeks of therapy and
long-term maintenance treatment should be con-
sidered for patients with the AIDS.
55.3.22 Outcome
In spite of advances in the management of fungal
CNS infections, there is a uniformly high mortality
and morbidity reported in almost all series of
patients with IFMs. The mortality rates range from
around 40% in immunocompetent patients to 92%
in transplant recipients. The newer drugs and
more aggressive surgical procedures have not sig-
nificantly improved the mortality and morbidity
rates of patients with intracranial fungal
masses.70,74,75,76,77 However, earlier diagnosis has
reduced the mortality rate. The cause of delay in
treatment could be multifold. In India, most
patients are treated with antituberculous therapy
on empirical basis. Amphotericin B is notorious for
causing renal and liver failure and has other seri-
ous side e ects. Other contributing factors were
presence of extensive paranasal sinus involvement,
postoperative meningoencephalitis, and ventricu-
litis. Sometimes, the diagnosis is revealed only at
postmortem.67 Rhinocerebral mucormycosis has a
high mortality associated with it. In immunocom-
petent patients, the survival is 75% but it decreases
to 60% in patients with diabetes mellitus and to
only 20% in those with other systemic disorders.69
The outcome is better in immunocompetent
patients than those who are immunocompro-
mised. The rhinocerebral form of the disease has a
better survival than those with the primary intra-
cranial form. The main cause of mortality and mor-
bidity is vasculitis and stroke. It can occur even
distant to the site of lesion.
55.3.23 Conclusions
A high index of suspicion should be present in cases
of immunocompromised patients with intracranial
mass lesions. Diabetic patients with intracranial and
rhinocerebral mass lesions should be treated and
evaluated early for fungal etiology. Early diagnosis,
aggressive surgical procedures, and antibiotic ther-
apy for CNS fungal infections may reduce morbidity
and mortality. The presence of intracranial fungal
granulomas in immunocompromised patients is
associated with significant morbidity and mortality.
Control of the underlying condition determines the
outcome.
55.3.24 Neurocysticercosis
Cysticercosis is caused by the larval form (cysticer-
cus) of the cestode Taenia solium or the pork tape-
worm.88 Man is an accidental intermediate host
who becomes infected by consuming eggs in the
gravid proglottids of the adult tapeworm shed in
the stools of a carrier of the worm. The larvae of T.
solium lodge selectively in certain organs of the
body such as the subcutaneous tissues, eyes,
muscles, and the brain.
Neurocysticercosis (NCC) is the commonest par-
asitic infestation of the brain and it is estimated
that nearly 50 million people worldwide su er
from this disease.89 Approximately, 50,000 individ-
uals with NCC die each year due to the disease.90
Seizures or epilepsy is the commonest manifesta-
tion of NCC a ecting nearly 80% of patients.91
55.3.25 Clinicopathogenesis
of NCC
Cysticercus cysts reach the parenchyma of the
brain through the hematogenous route. Once they
are lodged in the brain, the larvae undergo degen-
eration and pass through four stages namely (i)
vesicular, (ii) colloidal, (iii) granular–nodular, and
(iv) calcific stages.91 Degeneration of the larvae in
large numbers can lead to severe edema and raised
ICP causing headache, vomiting, altered sensorium
known as “cysticercotic encephalitis,” which is
seen in some children and adolescents. It carries
high risk of morbidity and can even be fatal.
Solitary cysticercus granuloma (SCG) is the com-
monest cause of focal seizures in Indian patients.91
The seizures are usually complex partial seizures
of short duration, rarely status epilepticus (1.7%).92
It can be associated with hippocampal sclerosis
responsible for mesial temporal lobe epilepsy. It
can cause obstructive hydrocephalus by blocking
the circulation of CSF. Papilledema has been
reported in 2.3 to 6.6% of children, less common
than in adults.92 The cysts, which reside dormant
in the subarachnoid spaces at the base of the brain
or the sylvian fissures, are termed as ‘‘racemose
cysticercus cyst.’’ They can cause infarcts of the
brainstem and the basal ganglia. Focal deficits
were seen in 4% of children,92 as compared to 16%
of adults.93
Surgical Considerations in Tuberculosis, Fungal, and Parasitic Infections of CNS in Children
473

Extraparenchymal cysts are rare in children.94
They may be found in the ventricular and subar-
achnoid spaces presenting as chronic meningitis,
basilar arachnoiditis, or obstructive hydrocepha-
lus. Ophthalmic cysticercosis may lodge in subreti-
nal space, vitreous humor, anterior chamber, or
conjunctiva. They may cause sudden blindness,
ocular palsy, or visual diminution.
NCC rarely a ects the spinal cord. Intramedullary
cysticercus granulomas are occasionally known to
cause paraparesis.95
55.3.26 Diagnosis of NCC
CTscan and MRI of the brain and spinal cord reveal
the primary diagnosis. On CT scan, lesions are sin-
gle and less than 20 mm in size—termed as single
small enhancing computed tomographic lesion
(SSECTL).96
Some children may have multiple
lesions; disseminated NCC with numerous cysts
may give the so-called “starry-sky” appearance,
which is typical of NCC ( Fig. 55.9). Vesicular cysts
are nonenhancing with no perifocal edema while
colloidal cyst have ring enhancement with scolex
appearing as bright high-density eccentric nodule.
Calcified cysts are small and generally without any
edema. In extraparenchymal NCC, CT may show
hydrocephalus, enhancement of tentorium and
basal cisterns due to arachnoiditis, and occasion-
ally infarcts.97 On MRI, visualization of the cysts is
better, isointense to w hite m atter and bright on
T2-weighted im ages, scolex being seen well
with proton-density sequences. Calcified lesions
appear hypointense on all MRI sequences and
m ay at tim es be m issed. 3DCISS is m ore sensitive
in diagnosis of intraventricular cysts. High ADC is
seen in core of cysticercus cyst than tubercular
abscess.97
Serological tests include enzyme-linked immu-
nosorbent assay (ELISA), which is 50% sensitivity
and 65% specificity in the CSF. Most of the labora-
tory tests are usually noncontributory.94
The di erential diagnosis includes tuberculoma,
microabscess, low-grade neoplasm, metastasis,
toxoplasmosis, and fungal infection.
55.3.27 Surgery for NCC
The prim ary treatm ent of NCC is m edical therapy
and prim arily consists of symptom atic treatm ent
including analgesics, anticonvulsants, and
steroids.90,94 Cysticidal drugs (praziquantel and
albendazole) are know n to destroy live larval
cysts whether in the parenchym a, ventricles, or
the subarachnoid spaces and possibly hasten the
resolution of granulom as. Albendazole is pre-
ferred over praziquantel for its lower cost and
side e ects. A dose of 15 mg/kg body weight
in two divided doses for 15 days is the m ost
com m only used regim e. The bioavailability of
albendazole increases w ith coadm inistration of
steroids and is not a ected by phenytoin and car-
bam azepine, w hich is a ected w ith praziquan-
tel.94 Patients w ith cysticercotic encephalitis m ay
have a fatal outcom e if treated with cysticidal
drugs due to the increase in edem a around the
degenerating cysts.90
The primary indication for surgery in NCC is as
follows:
● Extraparenchymal NCC: Intraventricular cysts,
hydrocephalus due to racemose cysts,
hydrocephalus due to ependymitis caused by
NCC.
● Spinal cysticercosis: Intramedullary,
extramedullary.
In addition to above, surgery may be required for a
large parenchymal colloidal or subarachnoid cyst
causing mass e ect, confirm diagnosis in atypical
cysticercus granuloma, and surgery for intractable
epilepsy.90,94,98
Fig. 55.9 Axial CT image showing multiple disk lesions
with central scolex in bilateral cerebral hemispheres
suggestive of disseminated cysticercosis.
Infections
474

55.3.28 Surgery for
Intraventricular Cysts
Patients with intraventricular cysts usually
present with persistent or interm ittent features
of raised ICP. A CT or MRI shows the cyst, w hich
has sim ilar density to CSF and occasionally a sco-
lex is seen as a hyperintense dot within the cyst
( Fig. 55.10). 3DCISS or FLAIR MR sequences
m ay confirm the diagnosis. The com m onest loca-
tion of the cyst is in the fourth ventricle followed
by the lateral and third ventricles. An inflam ed
cyst will enhance on contrast adm inistration and
be densely adherent to the surrounding epen-
dym a and choroid plexus.
Medical therapy for intraventricular cyst may
take several days or weeks to act and clinical dete-
rioration might occur during that period. Sudden
death with intra–third ventricular cysts has been
reported.99,100,101 The minimally invasive endo-
scopic excision of the cyst is the procedure of
choice since it avoids a large craniotomy and
reduces the manipulation of the brain. However,
the surgeon should have adequate experience in
endoscopic surgery, which will help minimize
complications and inadequate excision. A rigid
scope is su cient for use in the lateral and third
ventricular cysts, but a flexible scope is better for
posterior third ventricle and aqueductal cysts. The
excision of lateral and third ventricular cysts can
be combined with other procedures such as sep-
tostomy to create a communication between both
the lateral ventricles and a third ventriculostomy
to relieve hydrocephalus due to an obstruction in
the region of the aqueduct.102 Endoscopic surgery
for fourth ventricle cyst is more demanding, which
can be approached through the precoronal burr
hole using rigid scope. The cyst can be excised
through the aqueduct. It is paramount that the
entire scope assembly with the cyst should be
delivered through the burr hole. A flexible endo-
scope is needed for cysts presenting at the fora-
men of Magendie. Dense adhesions in this region
might preclude safe excision of the cyst and the
procedure may need to be abandoned. In such a si-
tuation, a shunt would be needed to treat the
hydrocephalus and medical therapy with albenda-
zole and praziquantel is required.103 Inadvertent
rupture of intraventricular cyst during excision
has rarely lead to an untoward incident. It does not
cause dissemination of the disease or anaphylactic
reaction. Madrazo et al devised a pipette to per-
form an atraumatic removal of the cysts.104 In
patients who have multiple cysts, oral albendazole
(15 mg/kg body weight in two daily divided doses)
for 2 weeks is administered. A course of steroids
(prednisolone or dexamethasone) can be given for
the first 5 to 7 days of albendazole therapy. The
hydrocephalus usually resolves in about 70% of
patients. A shunt is necessary in cases where there
is ependymitis following degeneration of cysts
within the ventricles or subarachnoid spaces.
Repeated shunt revisions may be required since
the CSF may have high protein or cell content and
even due to obstruction of the shunt by small cysts
or inflammatory exudates. Shunts have also been
known to be the cause of migration of fourth ven-
tricular cysts into the third or lateral ventricles due
to a siphon e ect.90,94,102,103 A standard shunt sys-
tem is suitable for use in patients with hydroce-
phalus due to NCC. Long-term steroid therapy with
daily oral prednisone at a dose of 50 mg three
times a week for up to 2 years has been shown to
reduce the rate of shunt dysfunction from 60 to
13%.90,102,103 However, prophylaxis for tuberculosis
with isoniazid is recommended as prolonged ste-
roid therapy, can predispose a patient to tubercu-
lous infection.104
Fig. 55.10 (a) Sagittal T1-weighted
MR image showing a cyst in the fourth
ventricle, hypointense center with a
smooth peripheral margin. (b) Axial
T1-weighted MR image showing the
fourth ventricular cyst with a scolex in
the center.
Surgical Considerations in Tuberculosis, Fungal, and Parasitic Infections of CNS in Children
475

55.3.29 Surgery for Parenchymal
and Racemose Cysts
They present with signs of acute to subacute raised
ICP and focal neurological deficits. They are usually
in the colloidal stage of evolution. Di usion-
weighted sequences may be needed to distinguish
these lesions from epidermoid cysts.
Surgery might be required on an emergent basis
to reverse the deficits and reduce the raised ICP.90,
94,98 Craniotomy and excision of cyst leads to good
outcome. Cysts are usually delivered easily. How-
ever, if the cyst wall is densely adherent to the
neurovascular structures in the vicinity, they can
be subtotally excised. The cysts might present
in suprasellar cisterns, cerebellopontine cisterns
causing pressure e ect on the adjacent critical
structures.
A typical solitary cysticercus granuloma pre-
senting with seizures does not require surgery. In
7% of patients, the granuloma can enlarge and
can have atypical radiology and mimic tubercu-
loma or an abscess.90 In such situation, stereotactic
excision or biopsy may be needed especially in
eloquent areas of brain. If there is a high index of
suspicion, then serum should be tested for cysti-
cercus antibodies and if found positive, then either
symptomatic therapy or treatment with albenda-
zole will avoid a surgical exploration.
NCC can cause intractable epilepsy due to an
epileptogenic scar around a cortical cysticercus
lesion such as a granulom a or m esial temporal
sclerosis (MTS) associated w ith NCC.94,105 It can
cause MTS by various m echanism s such as kin-
dling, seizures, and due to inflam m ation spread-
ing from an adjacent degenerating cysticercus
cyst. These patients should undergo presurgical
evaluation for epilepsy surgery and dealt with
accordingly.
55.3.30 Spinal Cysticercosis
Intramedullary and extramedullary cysticercal
cysts in the spinal cord are rare (Fig. 55.11). They
need to be excised in case of spinal cord compres-
sion or if the diagnosis is uncertain. If there is no
spinal cord compression and there is evidence of
cysticercal infection from a positive enzyme-
linked immunotransfer blot (EITB) for cysticercal
antibodies in the serum, medical therapy can be
administered using steroid therapy alone for a
maximum of 2 weeks or albendazole with steroid
therapy for 2 weeks.90,94,95
55.3.31 Complications and
Prevention
The major complications for endoscopic surgery
include intraventricular hemorrhage, forniceal
damage, CSF leak, seizures, and meningitis.99,102,
103,104 These complications occur in fewer than 5%
of patients. Patients with intraventricular cysts,
large parenchymal cysts, large racemose cysts
causing mass e ect, and for biopsy or excision of
atypical SCG have an excellent outcome. About
75% of patients with NCC who underwent surgery
had improved at a follow-up of 3 years. Shunt sur-
gery for hydrocephalus caused by cysticercotic
meningitis is complicated by frequent shunt revi-
sions for blockages or infection in as many as 68%
of patients and carries a mortality of 50% on
long-term follow-up.90,94,98,100 Mortality is high in
patients with basal racemose cysticercosis.
The possible strategies to control cysticercosis
include health education emphasizing the need for
hygienic practices such as hand washing after def-
ecation and before eating, mass chemotherapy for
taeniasis and vaccination of pigs.89,90,94
55.3.32 Conclusions
NCC is primarily treated with medical therapy.
Surgery is required in patients with NCC include
Fig. 55.11 Coronal T1 contrast MR image showing the
thoracic intramedullary large hypointense cyst with a
scolex in the center.
Infections
476

large parenchymal cysts, spinal cord cysts, atypical
SCG, and surgery for intractable epilepsy. Endo-
scopic surgery is the procedure of choice for exci-
sion of intraventricular cysticercal cysts as it is
minimally invasive. Shunt surgery is needed for
hydrocephalus associated with cysticercotic men-
ingitis. Hydrocephalus has a poor outcome with
the need for multiple shunt revisions and a high
morbidity and mortality.
55.3.33 Hydatid Disease
Cerebral involvement by hydatid disease occurs in
1 to 4% of patients infected with the parasite.106,107
The majority are males, belonging to younger age
group. They usually reach considerable size before
the patient becomes symptomatic. The common
signs and symptoms are usually attributable to
raised ICP. In children, they present with increas-
ing head size. This is probably because of the slow
growth and expansion of these cysts within the
cranial cavity. Posterior fossa cysts obstruct the
CSF pathways, causing hydrocephalus. Other
symptoms such as hemiparesis, seizures, visual
field defects, and gait disturbances may vary with
the cyst location.108,109 Intracranial hydatid cyst
may also be classified as primary or secondary.
The primary cysts are formed as a result of direct
infestation of the larvae in the brain without
demonstrable involvement of other organs. In
primary multiple cysts, each cyst has a separate
pericyst with brood capsule scolices and these
originate from multiple larvae a ecting brain after
crossing the gastrointestinal tract, liver, lungs, and
right side of heart without a ecting them. The pri-
mary cysts are fertile as they contain scolices and
brood capsules, hence rupture of primary cyst can
result in recurrence. The secondary multiple cysts
results from spontaneous, traumatic, or surgical
rupture of the primary intracranial hydatid cyst
and they lack brood capsule and scolices. The sec-
ondary intracranial hydatid cysts are therefore
infertile and the resultant risk of recurrence after
their rupture is negligible. Primary multiple cysts
are uncommon and isolated case reports of pri-
mary multiple hydatid cysts have appeared in the
literature.109
CT/MRI reveals a well-defined, smooth, thin-
walled, spherical homogenous cystic lesions. The
intensity of the cystic contents is similar to that of
CSF. On unenhanced CT scans, the cyst wall is iso-
dense or hyperdense to brain tissue ( Fig. 55.12).
The cyst wall has low intensity on both T1- and
T2-weighted images (Fig. 55.13). Usually, no en-
hancement of the walls is noted in simple cysts.
Based on the presence or absence of pericystic
edema and contrast enhancement, hydatid
cysts are classified into simple (noncomplicated)
cysts with no edema or contrast enhancement,
Fig. 55.12 Axial CT image showing a large right
frontoparietal cyst with smooth margins.
Fig. 55.13 Sagittal T2-weighted MR image showing
hyperintense cyst with smooth margins in the posterior
parietal brain causing mass effect. There is no perifocal
edema.
Surgical Considerations in Tuberculosis, Fungal, and Parasitic Infections of CNS in Children
477

and infected or complicated cysts with edema and
contrast enhancement.107,108,109 The growing cyst
produces a compressed layer of host tissue sur-
rounding it, called the pericyst. The compressed
cerebral parenchyma (the pericyst) shows
increased vascularity and reactive gliosis.
The di erential diagnosis of cerebral cystic
hydatidosis includes abscess, cystic tumor, arach-
noid cyst, glioependymal cyst, and porencephalic
cyst.106,107,108,109 Brain abscess and cystic tumor
usually have significant rim enhancement, sur-
rounding edema, and mural nodules. Other cystic
lesions are not spherical in shape and are not sur-
rounded entirely by brain parenchyma.
Multiple cerebral hydatid cysts are rather
rare and result from spontaneous, traumatic, or
surgical rupture of a solitary primary cyst or as a
consequence of a cyst rupture elsewhere and
embolization of hydatids to the brain.109,110 Only
three cases of multiple primary hydatid cysts of
the brain have been described.109,110
Rupture of hydatid cysts can occur in three
ways: contained, communicating, and direct.107,108,
109,110,111 Contained rupture occurs when only the
endocyst ruptures and the cyst contents are con-
fined within host-derived pericyst.
Complicated hydatid cysts may further be classi-
fied according to the status of the germinal mem-
branes. Intact complicated hydatid cysts have
well-preserved germinal membranes while rup-
tured-complicated hydatid cysts have intact peri-
cysts with ruptured, free-floating membranes.
Intact complicated cysts need to be excised along
with the pericyst, especially when multiple in
number, owing to the absence of any plane of dis-
section. Ruptured-complicated but contained
hydatid cysts are analogous to brain abscesses
with floating hyaline membranes, acting as foreign
bodies within purulent material. Surgery remains
the treatment of choice, with intact cyst removal
without spillage of fluid being the main prognostic
factor.112,113,114,115,116,117 Care should be exercised
to prevent cyst migration while managing intra-
ventricular small cysts. Irrigation with scolicidal
agents like 1% cetrimide and 10% formalin is
not recommended as prophylaxis.111,112 Antihel-
minthics such as albendazole (oral 10 mg/kg for 3
months) should be administered, including during
the perioperative period.
55.3.34 Conclusion
Intracranial hydatid cysts can occur as primary
solitary cysts, in both the supra- and infratentorial
compartments. Both these locations may also have
multiple primary hydatid cysts. Cyst wall enhance-
ment is a rare finding, but can be present at times.
Gravity can be put to use in removing these cysts,
supplementing the Dowling technique. Infected
hydatid cysts that have ruptured in contained
manner behave just like a brain abscess containing
a foreign body and can be tackled in the same
fashion.
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Surgical Considerations in Tuberculosis, Fungal, and Parasitic Infections of CNS in Children
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(Trang không có chữ)

XI
Section XI
Operating Room Basics
56 Neuronavigation in Pediatric
Neurosurgery

484

56 Neuronavigation in Pediatric Neurosurgery
Ulrich-Wilhelm N. Thomale
56.1 Introduction
Among other recent advances in Pediatric neuro-
surgery, neuronavigation is one of the relevant
ones. This technique has made surgical procedures
shorter with smaller approaches, more e ective
and thus safer. Although for neuronavigation, only
a very few prospective randomized trials were
performed to proof its e cacy, this technique
became routine use in all neurosurgical fields over
the past decades. In the development of its broad
application, boundaries of surgical indications
have partially been crossed by navigation techni-
ques since the precise planning and execution of
surgery especially of deep seated became better
accessible. In the following chapter, we would like
to define di erent techniques of neuronavigation
and go through the wide range of indications as
used in pediatric neurosurgery.
56.2 Terminology
56.2.1 Definition
Navigation is the process of determining, estab-
lishing, and maintaining a course or trajectory to a
target location.1
Neuronavigation is technically a neurosurgical
computer-assisted guiding system in which an
anatomical image dataset is registered in its spatial
orientation to the related patients’ anatomy using
virtual coordinates defined in an invisible refer-
ence system.
56.2.2 Related Terminology
Computer-a ssisted sur ger y is a broader definition
for surgical planning and performance systems, in
which computer data processing is used to assist
specific steps before or within the surgical proce-
dure. Neuronavigation is one possible computer-
assisted technique.
In frameless stereotaxy, unlike frame-based
stereotaxy, where the mechanical frame is used as
coordinate system fixed toward the patients’ head
and visualized in an image dataset, the frame is
replaced by a virtual coordinate system defined by
an optical (camera) or magnetic (electromagnetic
source) reference system.
Image guidance defines any surgical procedure
guided by imaging or image data, which may also
include intraoperative imaging techniques (ultra-
sound, computed tomography [CT], magnetic reso-
nance imaging [MRI]) besides navigation.
56.3 Technique
56.3.1 Systems
Optical Navigation
A camera is used to register any spatial orientation
of two to three markers defining the geometry of a
reference frame,2,3,4,5,6 which is rigidly attached to
the fixed patient positioning system (e.g., pin
clamp) and instruments in order to localize their
spatial relation to the patients’ anatomy in correla-
tion to the image dataset (mean system accuracy:
0.22 mm).7 In infants with open fontanelles in
which rigid pin fixation is not possible, indirect
fixation of the patient to the table as well as refer-
ence frame attachment to the table can overcome
this problem (Fig. 56.1a). As an alternative, the
reference frame may directly be attached to the
bone structures overcoming the need for head fix-
ation or pinless fixation systems are used.8,9,10
Children with closed fontanelle until the age of, for
example, 10 years should be fixated with a four-
pin pediatric clamp system (Fig. 56.1b). Free line
of sight from the camera toward the surgical site
including the reference frame and all navigated
instruments are warranted during surgery
(Fig. 56.2).
Active Reference Marker System
Markers are giving active infrared signals toward
the camera system to detect their spatial localiza-
tion. Electric supply is needed with batteries or
cables integrated or attached to the reference
frame or instruments.
Passive Reference System
Infrared signals are emitted by the camera
reflected by passive markers attached to the refer-
ence frame or instruments to detect their spatial
position. No cable or batteries are needed.
484

Fig. 56.1 Age- and system-dependent
positioning. (a) Infant positioning for
optical navigation system on a vacuum
mattress secured with tape toward the
table. Reference frame is attached to
the table. (b) Child positioning for
optical navigation (closed fontanelle
with age up to 10 years) four-pin
fixation clamp with the reference
frame attached to the clamp. (c)
Positioning for electromagnetic navi-
gation without head fixation attaching
the reference localizer to the forehead
(electromagnetic source: box on left).
Fig. 56.2 Schematic arrangement of
the OR components during micro-
scopic navigation using an optical
system. An, anesthetist; As, assistance;
M, microscope; N, nurse; Nav, optical
navigation system; P, patient;
Rf, reference frame; S, surgeon.
Neuronavigation in Pediatric Neurosurgery
485

56.3.2 Electromagnetic
Navigation
An electromagnetic source is building a magnetic
field in which active magnetic sensors either rig-
idly attached to the patient may localize the regis-
tered anatomy (reference localizer) or integrated
within navigated instruments which can be spa-
tially detected and visualized in the image dataset
in relation to the patient’s anatomy (mean system
precision: 0.99–2.24 mm).7,11 The system is easier
to handle during surgery since no rigid fixation of
the head is needed (advantageous for infants,
Fig. 56.1c).12,13,14,15 Line of sight is not an issue
during surgery, however, any magnetic material
within the positioning table or surgical instru-
ments brought into the electromagnetic field may
negatively influence the system-related accuracy.
56.3.3 Workflow
● Image data acquisition.
● Virtual planning: definition of regions of
interests, targets and trajectories, definition of
landmarks and registration points.
● Registration of the image data in correlation to
the related patient’s anatomy.
● Tracking and navigation of the surgical
procedure.
Imaging
Volum e dataset of CT (thin-sliced sections, m ay
be reconstructed from spiral CT scan), MRI con-
trast enhanced, (MP-Rage, 3D-FFE, T1 sequence
w ith high anatom ical resolution), m ay be fused
to thin sliced T2 sequences which can be recon-
structed along virtual planes and along any
defined trajectories.
Registration
Marker Registration
May be performed with visible markers attached
to the patients’ anatomy and defined within
the image dataset (skin—fiducials, bone—screw
markers) or by anatomical landmarks which are
clearly identified on the patient’s anatomy and
within the images (e.g., nasion, epicanthus, lateral
orbital rim, tragus, etc.). Fiducial skin marker
(n ≥6) registration reveals a mean precision of 1 to
1.9 mm.16,17
Screw marker registration was
described to be more precise than skin fiducials
(1.35 vs. 1.85 mm),18 however, with the necessity
of further intervention for its placement.
Surface Registration
Surface registration is achieved with multiple point
acquisition along the most characteristic anatomical
structures (facial mask) and widest possible regions
which is then correlated to the 3D surface recon-
struction of the volume dataset. This is nowadays
routinely used and may be acquired with a laser
scanner (mean precision: 1.8–3 mm)16,17
or an
active touch-sensitive pointer, which is advanta-
geous for including haired skin regions in the regis-
tration in parietal and occipital approaches.
Tracking and Navigation
Patient position and attachment of any reference
localizer (optical or electromagnetical) must be
carefully planned to establish good registration
quality and to avoid interference during surgery and
navigation. Intraoperative tracking and navigation
includes pointer-based techniques to identify the
preplanned entry point on the patient’s anatomy
and trajectory toward the respective target. Regis-
tered surgical instruments may be included in the
navigation process such as catheter stylets,13,19,20
forceps,21,22,23 or endoscopes8,24,25,26,27 tracked with
their geometric information and tip position.
Microscope integration into navigation includes
tracking of the focus level and viewing direction
visualized in the image dataset of the navigation.28,29
Augmented reality may be integrated by contour
guidance displaying any targets or regions of inter-
est in the microscopic field of view. This has the
advantage that navigation can be performed parallel
to microsurgical intervention without interruption
by pointer integration.
56.3.4 Multimodal Image
Integration in Navigation
Functional imaging, metabolic imaging, and angiog-
raphy might be integrated in the visualization of the
image dataset and fused to high-resolution image
data guiding surgical-related information. Avoiding
morbidity close to eloquent areas might better be
avoided by visualizing them in the image data.30,31,32
Integrating di usion tensor imaging (DTI) tractogra-
phy into the navigation has high value for surgical
planning but must be interpreted carefully during
surgery due to the brain shift and changes by tumor
compression.33 Angiography integration may help
Operating Room Basics
486

to localize feeder entry into a nidus of arteriove-
nous malformations (AVMs) or intraoperative
visualization of aneurysm-related anatomy.34,35,36
Metabolic imaging is relevant for targeted biopsies
for metabolic active tumor parts and to correlate
image information with histological evaluation
(Fig. 56.3).37,38,39,40
56.3.5 Intraoperative Imaging and
Navigation
Intraoperative imaging together with navigation
may be conducted together with preoperative
imaging data and later updating the surgical modi-
fied anatomy. It may also be used for combining
registration by using the intraoperative image
dataset of the patient. That might be achieved
when the image source is directly linked to the
navigation system.
Ultrasound Navigation
Ultrasound navigation is an easy and cost-e ec-
tive tool for gaining an im age update w ith rea-
sonable time e ort. Navigation system s are
available with direct integration of the ultra-
sound probe as navigated tool. Ultrasound
im age interpretation m ay require experience by
the user w hich is more likely established in
pediatric neurosurgery.41,42,43,44,45
Intraoperative MRI may be of relevance in pedia-
tric brain tumor surgery in extensive mass lesions or
low-grade tumor entities. The need for high invest-
ments and the time-consuming e orts does restrict
its use in big medical centers and for selected cases.
Updating the surgical-related spatial changes (brain
shift) over time and identifying tumor remnants is
possible with high image quality. Low-field MRI
machines are more often integrated in the operating
room (OR), while high-field 3Tesla machines are
often used in a dual OR concepts for parallel diag-
nostic use during long surgeries.46,47,48,49,50,51
Intraoperative CT is less relevant for pediatric
neurosurgery in order to avoid radiation expo-
sure.52,53,54,55 Spinal instrumentation, however, is a
relevant indication in which 3D C-arm imaging
combined with navigation may e ectively be used
for proper pedicle screw placement.56
56.4 Indications
56.4.1 Ventricular Catheter
Placement
Guided placement of ventricular catheters has
shown to be beneficial for more accurate placement
Fig. 56.3 Multimodal image integra-
tion in a postcentral paracallosal lesion
with nodular FET–PET hotspot and
visualization of the pyramidal tract
anterior to the lesion, selecting a
postcentral approach.
Neuronavigation in Pediatric Neurosurgery
487

and longer survival of the functioning catheters.13,57
Neuronavigation was introduced as an e ective
guiding tool. Indications were described for slit ven-
tricle syndrome, narrow and displaced ventricles in
shunt surgery, reservoirs for intrathecal chemother-
apy, and external ventricular drains for traumatic
brain injury. Frameless stereotactic systems,19,58,59
electromagnetic navigation,13,20,57,60,61 ultrasound-
guided navigation,41 and navigated endoscopic sys-
tems62 are used. These introduce high technical and
time-consuming e orts for a relative short surgical
intervention, which are justified especially for
applying accuracy in lifelong implants.
Recently, a simple navigation system based on
guiding tool assisted by smartphone technology
was introduced in order to reduce the time e ort
and to apply accuracy of ventricular placement in
a high number of patients, which has significantly
reduced incorrect catheter placement within a
prospective randomized trial.63,64
56.4.2 Endoscopy
Combining neuronavigation together with endos-
copy is reasonable and useful since endoscopy
often uses small openings and the freedom of
action is limited by this entry. Thus, the point of
entry as well as the trajectories must be well
defined in preoperative planning as well as intra-
operative application by navigation. Brain shift
during intraventricular surgery may be a relevant
problem in navigated endoscopy necessitating
constant verification of the endoscope’s view and
position depicted in the navigation system. This
problem may be reduced by establishing continu-
ous irrigation with balanced in and outflow to void
collapse of the paraventricular structures. Navi-
gated endoscopy is used for several indications.
Ventricular Endoscopy
For endoscopic third ventriculostomy (ETV), navi-
gation has been discussed to be useful.26,65 In
enlarged ventricles, navigation may not be neces-
sary and the entry point can accurately be meas-
ured in the sagittal image with a trajectory from
the floor of the third ventricle through the fora-
men of Monro toward the skull surface in relation
to the nasion and 2 cm lateral to the midline.66 In
narrow ventricles, navigation is reasonable to
enter the lateral ventricle safely.67,68,69
Ventricular cysts are heterogeneous and fenes-
tration toward regular cerebrospinal fluid (CSF)
spaces is most often the surgical aim. The entry
point must be individually defined in each patient
and the trajectory should enable free working
space at the target of fenestration. Indications for
arachnoid cysts of di erent locations,70,71,72,73,74
for septum pellucidum cysts,75,76 intraventricular
cysts,25 and Dandy–Walker–like malformations77,78
are described.
Multiloculated hydrocephalus (MLHC) is a com-
plex situation after ventriculitis during neonatal
period. Anatomical distortion causing lack of ana-
tomical landmarks and multiple compartments
are presented often with active volume changes.
Navigation is necessary to apply an individual and
e ective plan for surgical therapy in order to sim-
plify the most often necessary shunt system with
minimal amount of catheter placements.24,79,80
Repeated navigated endoscopy procedures are
often necessary in early active state of MLHC.
Isolated ventricles alone are the simpler form of
MLHC and must be treated with fenestration fora-
men of Monro plasty,81 septostomy, or stent place-
ment especially in isolated forth ventricle82,83 by
navigated endoscopic guidance.
Ventricular tumors have also an individual
appearance and are often initially diagnosed or
treated by navigated endoscopy. Endoscopic resec-
tion is possible if they are small or well accessi-
ble.84,85,86 Cystic tumor compartments might need
fenestration or stent placement.87,88
Endoscopic biopsy is also relevant in pineal re-
gion tumors especially challenging when com-
bined with ETV.89 Single burr hole entry points
may well be planned with navigated techniques.90
Skull Base Surgery
Endoscopy was introduced for accessing skull base
lesions transnasally or transorally.91,92,93 In smaller
children, this techniques might be limited or be
less standardized since pneumatization develops
at later stage.94,95 Navigation is especially helpful
in approaching either very small lesions or exten-
sive destructing lesions when the regular anatomy
is destroyed either by endoscopic means ore
microsurgical technique.93,96,97,98,99,100,101
Addi-
tionally, X-ray exposure can be reduced while pen-
etrating the skull base. Not only tumor surgery,
but also CSF leaks due to trauma or malformations
may well be treated.102,103 The clivus and cranio-
cervical junction may also be approached by navi-
gated endoscopic-assisted techniques.104,105,106
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488

Endoscopic Assistance for
Intraparenchymal Lesions
Deep-seated intraparenchymal lesions may be
approached with navigated endoscopic assistance
directly or with the help of port devices.86,107
Pineal region tumors were described to be
approached transtentorially by navigated endo-
scopic assistance.108 Similarly, hippocampal depth
electrodes have been placed.109
56.4.3 Navigated Microsurgery
Since early times of neuronavigation, caver noma s
were the classical indication for navigated micro-
surgical resection.36,110,111,112,113,114 This was asso-
ciated with a more comfortable and safer surgery
in children.115
Most of the supratentorial located tumors in
pediatric cohort are deep seated tumors in which
neuronavigation is helpful. Hemispheric, intraven-
tricular, thalamic, and hypothalamic tumors are
approached by the help of neuronavigation on a
routine basis in most countries.116,117,118,119,120 By
the means of neuronavigation, deep seated tumors
can be precisely targeted and by using augmented
reality contour overlays in the miscroscope, the ex-
tension of the tumor can better be estimated at
di erent microscopic magnifications to aim
for more extensive resection.120 Especially, for
intraventricular tumors, navigated placement of
tubular retraction devices are developed.121,122 In
surgical resection of tumors close to eloquent
areas, the combination of neuronavigation and
brain mapping123 or transcranial magnetic stimu-
lation is used.124 For infratentorial lesions, intrinsic
cerebellar hemispheric tumors and often brain-
stem tumors are operated by guidance of neurona-
vigation.125,126,127 This also holds true for extensive
skull base128 or orbitocranial tumors.129,130
Intraoperative imaging might further enhance
the grade surgical resection by intraoperative
imaging using ultrasound42,44,131 or MRI46,132,133,134
in extensive tumor lesions or deep-seated low-
grade lesions with similar appearance characteris-
tics like brain tissue.
56.4.4 Frameless Stereotaxy
For navigation, di erent frameless stereotactic sys-
tems are available which have the major advantage
that preoperative imaging can be used saving
significant time of anesthesia, and that no
stereotactic frame needs to be attached to the child-
ren’s head which represents di culties in all
younger children. However, the accuracy of frame-
less stereotactic systems are described to be
lower.135 Using these systems, lesions should exceed
diameters of 10 to15 cm depending on their depth
location.21,135,136 Diagnostic yield and complication
rates were described to be similar in frame-based
compared to frameless techniques.137,138 Indications
are generally biopsies,22,136,139,140 catheter place-
ment, for example, for cyst aspiration or stent
placements,4,141,142 or the placement of depth elec-
trodes for seizure monitoring as stereo EEG.15
56.4.5 Epilepsy Surgery
Neuronavigation is widely used in epilepsy sur-
gery for di erent reasons.143,144,145 Resection of epi-
leptogenic hamartomas85,146 is regularly navigated
procedures similar to other heterotopic147 or focal
epileptogenic lesions.148,149 The placement of intra-
operative electrodes for seizure mapping being either
grid electrodes or depth electrodes can accurately be
placed by navigation.15,150,151,152 The correlation of
monitoring results by defining epileptogenic regions
as targets can intraoperatively well identified by
navigation.28,153,154,155
Complex epilepsy surgeries
such as insular surgery156,157 hemispherotomies158
and callosotomies159 can additionally be guided by
neuronavigation.
56.4.6 Spine
Spinal instrumentation in scoliosis surgery160,161
or craniocervical junction reconstruction105,162
was described to be guided by neuronavigational
techniques alone and/or together with intraopera-
tive imaging.56,163 In addition, spinal tumors or
neurenteric cysts were approached with navigated
techniques.54,164,165
56.5 Common Clinical
Questions
1. How do you practically gain maximal accuracy
by fiducial marker or surface registration?
2. Is it obligatory to have an optical parallel to an
electromagnetic navigation system?
3. What are the possible solutions for navigating
suboccipital approaches in prone positioning?
4. What are the limitations of stenting the sylvian
aqueduct in an isolated fourth ventricle?
Neuronavigation in Pediatric Neurosurgery
489

56.6 Answers to Common
Clinical Questions
1. For skin fiducial marker registration, the
following essentials are necessary to
acknowledge during registration. First, at least
six fiducials must be placed. Second, the
fiducials must be placed so that they can be
reached by the pointer in the respective
position. Third, the area of fiducial placement
should be as wide as possible including tight
skin areas over the forehead, temporal region,
and the mastoid. For surface matching, active
sensitive touch pointers might have the
disadvantage to take longer for multiple surface
point acquisition, but the great advantage over
the laser pointer is that hairy skin and the
entire face mask can be included in the
registration. To combine landmark registration
together with surface registration gives highest
accuracy and best practicability.
2. Electromagnetic navigation system is an easy
and fast usage system but includes most often
the disadvantage that multimodal image
datasets and individual instruments cannot as
easily be included in the navigation procedure.
That makes it a decent navigation system for
simple tasks such as ventricular catheter
placement. Those can also be established by
optic navigation systems with only low amount
of additional e orts. Optical navigation system
should cover the entire range of indications
needed in navigated neurosurgery.
3. For optical navigation systems, registration in
prone positioning might be painful. However, it
is well possible when the camera is positioned
on the side of the patient focusing on the area
in front of the face below the table. Surface
registration can then be performed by touch
pointer registration including landmarks,
multiple points on the facial mask, and the wide
range of hairy skin in parietal and occipital
regions. After registration, the camera might be
moved back at the foot of the table for free line
of sight during surgery.
4. Stenting the sylvan aqueduct is generally
indicated only in isolated fourth ventricle and in
cases with short aqueductal stenosis. To avoid
any injury to the midbrain while approaching
the stent, the direction of the sylvian aqueduct
defines the trajectory toward the skull surface
which determines the entry point at relative
close proximity to the midline (1.5–2 cm).
Under endoscopic vision and with great care to
the deviating structures around the foramen of
Monro, the catheter is then approached through
the aqueduct into the fourth ventricle. In cases
where the roof of the fourth ventricle is already
deviated supratentorially, the catheter might be
advanced through a double layer membrane at
this location under navigated endoscopic
guidance.
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57 Appendices

497

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m
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d
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h
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b
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s
498
Appendices

A
p
p
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d
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x
A
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2
(
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t
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.
6
499
Appendices