Download Neurosurgery case 1

Neurosurgery case 1
6 months PTA
progressive on and off headache
6 months PTA
Progressive on and off headache
1 month PTA
Difficulty of walking : “dragging her left leg”
Sought consult, Dx: Stroke
Medications: metoprolol 50 mg BID
Simvastatin 10mg OD
Citicholine 500mg OD
Referred to a psychiatrist for therapy
6 months PTA
Progressive on and off headache
1 month PTA
Difficulty of walking : “dragging her left leg”
Sought consult, Dx: Stroke
Medications: metoprolol 50 mg BID
Simvastatin 10mg OD
Citicholine 500mg OD
Referred to a psychiatrist for therapy
2 weeks PTA
Progressive headache
Nausea and vomiting
Blurring of vision
6 months PTA
Progressive on and off headache
1 month PTA
Difficulty of walking : “dragging her left leg”
Sought consult, Dx: Stroke
Medications: metoprolol 50 mg BID
Simvastatin 10mg OD
Citicholine 500mg OD
Referred to a psychiatrist for therapy
2 weeks PTA
Progressive headache
Nausea and vomiting
Blurring of vision
1 day PTA
Focal seizures (L) foot, progressively
involved her leg, thigh and the whole
left half of the body lasting about 5
minutes

Past medical history:
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Dx to have migraine
Physical exam:
 PR
90/min
 BP 170/86
 RR 18/min
 T 37.0C
Physical Exam
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Awake and oriented to 3 spheres
Pupils 6mm bilateral sluggishly reactive to light
Fundoscopy – bilateral haziness of the temporal aspects of
the optic disc with areas of retinal hemorrhages
6th Nerve palsy left
Shallow L nasolabial fold
Tongue midline in protrusion
Able to do FNT, APST
L hemiparesis; grade 3/5 LE weaker than UE; Right: grade
5/5 UE grade 4/5 LE
DTR’s +++ on the left, ++on the right
Babinski on the left with ankle clonus
Know the incidence and location
of the major types of primary and
secondary brain tumors.
General clinical manifestations of
brain tumors
General clinical manifestations
of brain tumors

Intracranial tumors
Cause mass effect , dysfunction or
destruction of adjacent neural
structures, swelling, abnormal electrical
activity, or a combination of these
 Present in two major ways: focal
compression or irritation of the brain and
generalized increase in ICP
 Supratentorial vs. infratentorial

Supratentorial tumors
Focal neurologic deficit (contralateral
limb weakness or visual field deficit)
 Headache
 Seizure
 Tumor growth in a brain region
results in loss of neurologic function
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Infratentorial tumors
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Increased ICP
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Direct mass effect from tumor bulk or
hemorrhage into a tumor or from
hydrocephalus
Headache
Nausea and vomiting
Reduction in LOC
Papilledema
Infratentorial tumors
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Cerebellar hemisphere or brainstem
dysfunction
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Ataxia, nystagmus, cranial nerve palsies
Rarely cause seizures
Signs and Symptoms of
Increased ICP and its
Management
Intracranial Tumors and ICP
Two common presentations of
intracranial tumors:
1. Generalized increase in ICP
2. Focal compression and irritation of
the brain
Causes of increased ICP
1.
Direct mass effect
a.
b.
2.
from tumor bulk
Hemorrhage into a tumor
Indirectly
a.
Hydrocephalus
i.
ii.
Communicating
Non-communicating
Most common symptoms
1.
Headaches
a.
b.
2.
Nausea and vomiting
a.
3.
usually worse in the morning,
Sleep (recumbent and rise in PCO2)
pressure exerted on the area postrema
Reduction in level of consciousness
Symptoms

Mild or unnoticed
until the tumor has become very large if
the tumor growth rate is slow or
 the tumor is located near the periphery
of the brain.
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Early symptoms
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very small, with strategic location (ex.
Foramen of Monroe)
Most common signs
1.
2.
3.
4.
Papilledema
Bilateral or unilateral 6th nerve palsy
Abnormalities of the ipsilateral 3rd
nerve
Vital sign changes (Cushing’s Triad)
a.
b.
c.
Elevation of SBP – late
Bradycardia – late
Abnormal respiratory pattern
Management (Medical)
head elevation at 30-45 degrees &
keep midline
 hyperventilation: PaCO2 30-40 mmHg
 PaO2 > 70mm Hg
 systemic arterial pressure maintained
bet 100-160 mmHg for cerebral
autoregulation to be normal: CPP =/>
90mmHg
 normothermia: fever increases CBF
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Management (Medical)
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sedation & nm blockade for agitated px
anticonvulsants: seizures can inc CBF
fluid resuscitation : plain isotonic saline
cerebral decompressants
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mannitol 20% by bolus IV
hypertonic saline solution (7.2%)
diuretics: furosemide 40- 60 mg per IVT
corticosteroids: dexamethasone
barbiturate coma: to lower metabolic rate and
dec icp
Management (Surgical)
craniotomy/craniectomy for
evacuation of hematoma or mass
lession
 decompressive crainectomy
 ventriculostomy (EVD) for the release
of CSF & placement of icp monitoring

Extra axial and intra axial in brain
tumor presentation
Primary Brain tumor
 Intra-axial
brain tumor
 Extra-axial brain tumor
Intra-axial Brain Tumor

Most are derived from glia and are
called glioma
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Low metastatic potential
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Prognosis is poor; ability to infiltrate
widely
Intra-axial Brain Tumor

Spread preferentially along white
matter tracts and may cross corpus
callosum into the contralateral
hemisphere
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Resistant to both radiation and
chemotherapy
Astrocytoma
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Most common type of glioma
50% of all primary brain tumors
Four groups
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Grade 1: well-circumscribed tumor with
essentially no ability to transform into higher
grades
Grade 2: low grade; increased cellularity,
infiltrative and lack distinct boundaries
Grade 3: anaplastic; increased cellularity and
either endothelial proliferation or mitotic figures
Grade 4: glioblastoma multiforme
Oligodendroglioma
Frequently found in frontal, temporal,
or parietal lobes
 On CT scan: calcification and
hemorrhage
 On MRI: similar to those of
astrocytoma
 Tx: chemotherapy, similar to
astrocytomas
 Median survival rate: 7 to 10 years
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Ependymoma
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Frequently diagnosed in younger patients
Typically present as a mass in the 4th
ventricle and cause hydrocephalus
Symptoms: headache, nausea and
vomiting, papilledema, gait ataxia, vertigo
and diplopia
Tx: surgical resection and postoperative
radiation therapy
May spread through CSF pathway; tx is
craniospinal axis radiation
Median survival rate: 7 to 10 years
Medulloblastoma
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20 – 25% of all pediatric brain tumor
Most common primary brain tumor in children
Derived from undifferentiated precursor to
both neurons and astrocytes
Most often found in the cerebellar vermis
Symptoms: hydrocephalus and cerebellar
signs
In adults: lateral cerebellar hemisphere and
present with dysmetria
Primitive neuroectodermal tumors – outside
the posterior fossa
Medulloblastoma
Tx: maximal surgical resection
followed by radiation therapy
 Median survival time: 7 to 10 years,
with complete surgical resection and
lack of CSF spread
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Hemangioblastoma
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Most common posterior faussa tumor in
adult, after metastases
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Benign tumor composed of capillaries,
dilated vessels and foamy stromal cells
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Can occur as part of von Hippel-Lindau
(VHL) disease
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Present with cerebellar findings: headache,
ataxia, vertigo and dysmetria
Hemangioblastoma
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Most commonly found in cerebellum, also
occur in the brainstem and spinal cord
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Radiographically present as a solid
enhancing mass or as a systic tumor with
and enhancing mural nodule
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Tx: Complete surgical removal of the solid
component or nodule
Primary CNS Lymphoma
Rare intracranial tumor
 Common in elderly patients and
immunocompromised patients (AIDS)
 Highly sensitive to radiation
 Prognosis is poor
 Median survival time is 4 years in
person without AIDS and 3-6 months
in person with AIDS
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Germ cells and Pineal Region
Tumors
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Germ cells tumors
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Germinoma
Embryonal carcinoma
Choriocarcinoma
Endodermal sinus tumor
Found in pineal or hypothalamic region of
children and young adults
Often release tumor markers in the CSF
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Endodermal sinus tumor - -Fetoprotein
Choriocarcinoma --human chorionic
gonadotropin
Germinoma – placental alkaline phosphatase
Germ cells and Pineal Region
Tumors
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Germinoma
Radiosensitive tumor
 curable
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Other germ cell tumors
Carry poor prognosis
 Require both radiation and
chemotherapy
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Germ cells and Pineal Region
Tumors
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Pineal gland tumors
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originate in the posterior aspect of the 3rd
ventricle
may cause hydrocephalus from the occlusion of
aqueduct of Sylvius
Parinaud’s syndrome
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Paralysis of upward gaze
Pupils that constrict on accommodation but fail to
react to light
Nystagmus retractorius
Extra-axial Brain Tumors
Meningioma
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Second most common primary brain tumor:
20% of the total
Arising from arachnoidal cap cells
Benign tumors that originate from the dura
and displays the brain as they grow
Do not invade the brain unless they are
malignant
Can invade and erode the skull or can
cause a hyperostotic reaction
Meningioma
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Most common locations
Parasagittal regions
 Cerebral convexities
 Subfrontal region
 Cerebellopontine angle
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Found in adults, more common in
woman
Meningioma
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Diagnosis: CT or MRI is the principal
means of diagnosis
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Tx: surgery, requires completer
removal of the tumor, dural origin
and involved skull
Schwannoma
Benign tumors
 Arise from schwann cells
 Most common type:
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Vestibular schwannoma or acoustic
neuroma
 Originates
from the vestibulocochlear
 Presents with unilateral hearing loss,
tinnitus, dizziness, facial numbness
Schwannoma
Appear isointense to brain on T1 MRI
 MRI scan shows an enhancing mass
in the cerebellopontine angle that
enters the internal auditory canal
 Tx: complete surgical resection
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Pituitary Adenoma
Arise from the cells in the anterior
pituitary gland
 Functional or non-functional
 Functional tumors
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Cause an endocrinopathy from excessive
hormone production
 Prolactinoma – most common functional
tumor
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 Causes
women
amenorrhea and galactorrhea in
Pituitary Adenoma
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Non-functional Pituitary Adenomas
Presents with mass effect on adjacent
structures notably the optic chiasm
 Patients experiences a loss of peripheral
vision and describes a bitemporal field
cut on formal visual field testing
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Pituitary Adenoma
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Pituitary Microadenoma
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Appear as a non-enhancing area even the
pituitary gland that are seen best on coronal
images
Pituitary Macroadenoma
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Erode and enlarge the sella turcica in addition
to elevating the optic chiasm
MRI shows a variable degree of enhancement
and cannot usually distinguish between tumor
and normal pituitary
Pituitary Adenoma
Sublabial or intranasal incision
 Transsphenoidal craniotomy
 Conventional intracranial surgery is
chosen when the tumor is primarily
suprasellar tumor
 Radiosurgery
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Good option for patients with small
residual tumor
DIAGNOSTIC TOOLS
ROUTINE LABORATORY
STUDIES
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CBC and Blood tests
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detect markers that may indicate pineal or
pituitary tumors
Analysis of electrolytes
Glucose
BUN/Creatinine
Calcium and Magnesium
Liver function
Coagulation profile
LAB STUDIES
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Lumbar Puncture (Spinal Tap)
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needle is placed in the lower back to obtain a small
sample of cerebrospinal fluid (CSF)
look for cancer cells, blood, or tumor markers
done only after CT or MRI scan
particularly important in people with suspected brain
lymphomas
Neurological, vision, and hearing tests
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help determine the suspected tumor's effects on the
brain's functioning
Eye examination can detect changes to the optic nerve
LAB STUDIES
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Electroencephalography (EEG)
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Cerebral arteriogram (cerebral angiogram)
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noninvasive test in which electrodes are attached to a person's
scalp to measure electrical activity of the brain
an x-ray, or series of x-rays, of the head that shows the arteries
in the brain
X-rays are taken after a contrast medium (a type of dye) is
injected into the main arteries of the head
Evoked potentials
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involve the use of electrodes to measure the electrical activity of
nerves
can often detect acoustic Schwannoma
used as a guide during surgical removal of tumors that are
growing around important nerves
BIOPSY
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Removing some of the tumor tissue for examination
For Definitive diagnosis
Determines the exact type of tumor
Stereotactic biopsy
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use of a computer-assisted CT or MRI scan
drills a small hole in the skull, inserts a needle guided by
stereotaxis and withdraws a sample of tumor tissue
Skull is placed in a rigid frame
Usually takes about 10 minutes
Final diagnosis: 3 to 4 days later
Imaging
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Plain Skull X ray
Computed Tomography (CT) Scan
Magnetic Resonance Imaging (MRI)
Magnetic Resonance Angiography (MRA)
MR Spectroscopy (MRS)
Cerebral Angiography
Cranial Ultrasound, Transcranial Doppler
(Carotid Doppler Studies)
Positron Emission Tomography (PET) Scan
Electroencephalography (EEG)
Plain Skull X-rays
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We can assess for
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Fractures
Bone erosions
Bone hyperostosis
Abnormal calcifications
Midline Shift
Increased ICP
Configuration
Computed Tomography (CT)
Scan

Different densities on CT images are
related to the X-ray attenuation
properties of the tissues quantified in
Hounsfield units (Villarelli)
 Hounsfield
units range from +1000 (bone)
to -1000 (air), with water being defined as
zero

Denser tissues (bone, tumors)
appear white on CT and less dense
tissues (air or water) appear black
 Addition
of contrast makes tissues that
enhance appear more dense or white (esp.
Magnetic Resonance
Imaging (MRI)
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High tissue resolution, brain and spinal
cord are viewed with clarity and detail
superior than in any other test
The structures on MRI images depend
on the differences in proton content and
their spin properties
Superior to CT except in imaging
acute hemorrhage or bony detail
valuable in diagnosing MS, posterior
fossa lesions, temporal lobe lesions,
tumors
MR Angiography (MRA)
MR Spectroscopy (MRS)
•
•
MRA utilizes MRI and contrast material to
specifically look at cerebrovasculature; It is
particularly useful in identifying aneurysms
and occlusions of larger cerebral blood
vessels
MRS is useful in distinguishing brain
tissue whether it is neoplastic,
encephalomyelastic or of infectious in
origin
Cerebral Angiography
Use to evaluate cerebral aneurysms
and arteriovenous malformations
(AVMs), but also ventricular anatomy,
shift, and mass effect on the
cerebral vasculature from mass
lesion or edema
 “Gold Standard” for demonstrating
aneurysms,
AVMs,
tumor
vascularity,
occlusive
vascular
diseases, & abnormal vascular shunts

Positron Emission Tomography
(PET) Scan
Involves injecting a proton emitter
(FDG)
fluorodeoxyglucose,
then
computer-mapping
the
relative
metabolism of various areas of the
brain
 Useful in identifying seizure foci and
differentiating radiation necrosis
from tumor recurrence

Cranial Ultrasound, Transcranial
Doppler (Carotid Doppler Studies)
Utilizing ultrasound technology to evaluate
the carotid artery
 Utilizes high-energy pulsed wave Doppler
to image blood flow through the carotid
arteries for the evacuation of stenosis and
emboli

Electroencephalography
(EEG)
Very useful in documenting seizure
activities
 Also being used as a screening
procedure for intracranial pathology

•
Utilized in the diagnosis of coma, dementia,
and brain death
Broad treatment strategies for
brain tumors
BRAIN TUMORS:
TREATMENT STRATEGIES

Surgery: Craniotomy
GA  scalp incision; removal of small
part of skull bone  as much of the
tumor as is safely possible is removed
 bone is replaced  incision is closed
with staples or stitches
 Risk and Complications: bleeding,
infection, brain swelling, seizures, and
impairment of brain functions

Neuro-Oncology Center: University of Virginia Health Center. Brain Tumor Basics. http://www.healthsystem.virginia.edu/internet/neuro-onc/braintumor.cfm.
BRAIN TUMORS:
TREATMENT STRATEGIES

Stereotactic Radiosurgery
location-specific delivery of concentrated
radiation
 Most widely used radiosurgery devices:

 Gamma
Knife – given using a small linear
accelerator mounted on a robotic arm; used
to treat tumors and lesions of the brain and
spine; no head frame is used
 Linear Accelerator (LINAC) Based Treatment
– uses one large, powerful radiation beam;
used to treat larger brain tumors
de la Rocha. Stereotactic Radiosurgery. http://healthlibrary.epnet.com/GetContent.aspx?token=8482e079-8512-47c2-960c-a403c77a5e4c&chunkiid=112167.
Townsend, et al. Sabiston Textbook of Surgery. 17 th ed. pp 2165-2166.
Radiation Therapy
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Cell differentiation, proliferation and maturation
are potentially affected by ionizing radiation
Most sensitive target: DNA
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Single- or double-strand breaks
Cross-links
Gene transcription
Cell membrane is also radiosensitive

Lipid peroxidation
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Alters membrane fluidity and permeabilty
Affect ion fluxes and membrane-mediated transport processes
Radiation Therapy
Induction of apoptosis
 Induce delays in cell division

G2-phase arrest (most common)
 G1-phase arrest and S-phase delay
 Through tumor suppressor genes and
oncogenes encoding cell-cycle
regulatory proteins (eg. p53 and cdks)

Radiation Therapy

Radiation damage
1.
Early stages
–
–
–
2.
3.
Rapidly renewing stem cell population
Early manifestation of damage
Complete healing
Intermediate stages
Late stages
–
–
–
Lack of a separate stem cell population
Late manifestation of damage
Irreversible damage
Chemotherapy
Goal: kill rapidly dividing cells with
drugs and leave other cells unharmed
 Mechanisms:

DNA damage
 Inhibit DNA replication and transcription
 Apoptosis

 Death
receptor pathway
 Receptor-independent pathway
Drug
2
APOPTOSIS
1
Caspase cascade
Proapoptotic
molecules
Cytochrome c
Mitochodrion
APOPTOTIC PATHWAYS
Radiation and Chemotherapy
Chemotherapeutic drugs increases
the effectiveness of radiation
 Tumors sensitive:

Lymphoma
 Germinoma

The clinical manifestations of abcess and
focal infections due to local spread,
hematogenous d/s associated with immune
deficiency and how they differ from the
mimics
BRAIN ABCESS
Majority is always secondary to
purulent focus elsewhere in the body
(only 10% introduced from the
outside)
 40% related to d/s in the paranasal
sinuses, middle ear and mastoid cells
 Purulent pulmonary infection

Pathogens
• Streptococci (most common), often
anaerobic or microaerophillic
 Staphylococci (penetrating injury)
 Gram negatives, anaerobes
 Toxoplasmosis and Nocardia in
immunocompromised hosts
Risk factors
AIDS
 Immunocompromised
• IV drug abuse

Pathogenesis
Direct extension
 Metastatic (hematogenous spread)

Direct extension
Bone of the middle ear
or nasal sinuses becomes the
seat of osteomyelitis
Spread along the veins
Abcess at a considerable
distance from primary site of
focus
Metastatic (hematogenous spread)
1/3 of all brain abcess
 Majority
-ABE and septic focus
on the lungs or pleura
 Others
- congenital heart defect,
pulmonary AV
malformation
 Middle cerebral artery
 multiple

Clinical Manifestation
Headache
 Drowsiness and confusion
 Focal or generalized siezures
 Focal neurologic deficits

 Temporal
lobe
 Frontal lobe
 Parietal lobe
 Occipital lobe
 Cerebellar abcess

Fever
Temporal Lobe Abcess
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Headache is of the
same side as the
abcess
Dominant- anomic
aphasia
Upper homonymous
quadrantinopia
Weajness of the lower
face
Frontal lobe abscess

Contralateral
hemiparesis w/
motor seizures and
motor d/o of
speech
Parietal lobe abscess
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Clinical manifestations
are subtle, requiring
special techniques for
their elicitation
Agnosia
Apraxia
Cortical sensory
syndromes
Asomatognosia
Ideomotor and ideational
apraxia
Visual d/o
Occipital lobe abscess

Homonymous
hemianopia
Cerebellar abscess
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Headache in the
postauricular or
suboccipital region
Coarse nystagmus
Weakness of
conjugate gaze
Cerebellar ataxia
Ataxia of gait
Laboratory
WBC may be normal or mildly
elevated
 Culture of abscess contents
 Blood studies - mild
polymorphonuclear leukocytosis,
elevated sedimentation rate

Diagnostic Procedure
History, physical exam
- focal neurological signs and symptoms
- mass effect, increased ICP and sequelae
• Search for primary source of infection (chest xray, skull film for fracture, sinus films, etc.)
 +/– signs of systemic infection (mild fever,
leukocytosis)
 Lumbar puncture often contraindicated

Imaging Studies

CT imaging of the brain (with and without
contrast) is the most readily available
study for establishing diagnosis of brain
abscess
- Early in the course: abscess appears as a lowdensity, irregular zone
- As the disease progresses: distinctive "ring
enhancement“
Differential Diagnosis
Brain tumors
 Stroke
 Resolving intracranial hemorrhage
 Subdural empyema
 Extradural abscess
 Encephalitis

Other Causes of Pus
subdural empyema (from sinusitis,
mastoiditis - rare, 20% mortality)
 meningitis, encephalitis, AIDS,
toxoplasmosis (see Neurology Chapter)
 osteomyelitis of skull (Pott’s puffy tumour),
usually seen with sinusitis
 granuloma (TB, sarcoid)

Surgical Measures
mandatory when neurologic deficits are severe
or progressive
• used when the abscess is in the posterior fossa
 Abscess drainage - (via needle) under
stereotactic CT guidance through a burr hole
under local anesthesia, is most rapid and
effective method. May be repeated if needed.
 Craniotomy - if abscess is large or multilocular

Available online at
http://www.catalog.nucleusinc.c
Treatment
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Antibiotics according to organism if known
Pen G and metronidazole, or chloramphenicol if
unknown
Add oxacillin or nafcillin if trauma or IV drug
user ; use vancomycin in penicillin-sensitive
patients
If gram(-)organism suspected (otic, GI, GU
organ) add third-generation cephalosporin
Abscess associated with HIV infection assumed
to be due to Toxoplasma gondii - daily doses of
sulfadiazine and pyrimethamine.
Treatment


Anticonvulsants - phenytoin until abscess
resolved or perhaps longer. Obtain
anticonvulsant levels.
Following surgical procedure - corticosteroids to
reduce edema. Dexamethasone. Taper rapidly.
Use usually limited to 1 week. Continue
antibiotics for 6-8 weeks.
The common primary foci of
infection that leads to the
development of CNS infections
CNS Infections

Acute bacterial meningitis
Infection of subarachnoid spaces and
meninges
 Bacteria may spread to the subarachnoid
space from an infection of a contiguous
structure such as the paranasal sinuses
or through the bloodstream.

Causative Organisms

Newborns

Gram negative enteric organisms
 Escherichia

Children


coli and Klebsiella
H. influenzae, Pneumococcus, and
Meningococcus
Adults

Pneumoccus and Meningococcus
Brain Abscess
Infective organisms could be bacteria,
virus, fungi or parasites
 Mode of infection could be through
direct spread from adjacent
structures, hematogenous seeding, or
direct inoculation as would occur after
surgery or trauma.
 May be solitary or multiple

Brain Abscess

Multiple abscesses


Usually occur with systemic infections
that spread hematogenously
Solitary lesions

More likely to occur after direct spread
from an infected parameningeal
structure such as the middle ear or
paranasal sinus
Causative Organisms

Normal host

Anaerobic Streptococcus,
Staphylococcus, Enterobacteriaceae, H.
influenzawe or anaerobes
 May
spread from dental, pulmonary,
cutaneous, cardiac etc.

Immunocompromised host

Nocardia asteroides, L. monocytogenes,
Candida spp., C. neoformans, Mucos
spp., and Aspergillus
Spinal Abscesses
Spinal epidural abscess is a rare
condition.
 Infection usually occurs via
hematogenous spread or from direct
extension of discitis or osteomyelitis
 Predisposing factors


DM, immunocompromised state, renal
disorders, intravenous drug abuse, and
recent spinal surgery
The general principles in
treatment of brain abscess and
focal infection
Management
anatomic location
 size
 age of the patient
 Neuroimaging studies (CT, MRI)
 combination of antimicrobial agents,
surgical intervention, and eradication
of primary infected foci

TREATMENT

MEDICAL
Antimicrobial
 Corticosteroids
 Anticonvulsants


SURGICAL
Aspiration
 Excision

MEDICAL: Antimicrobial
therapy
penetrate the abscess cavity
 activity against the suspected
pathogens
 Penetration – limited by BBB
 Penetration regulation: lipid solubility
and ionization at physiological pH,
protein binding, and the molecular
weight of the drug
 6- to 8-week course

MEDICAL:
Corticosteroids and Anticonvulsants
CORTICOSTEROIDS
Recommended only for:
 edema that poses a
threat of herniation
 produces neurologic
deficits because of its
location
ANTICONVULSANTS
 Seizures are frequent
complications of brain
abscess
 seizure prophylaxis or
anti-epileptic
SURGERY: Aspiration and Excision
Strategies for the management of bacterial brain abscess
Cheng-Hsien Lu , Wen-Neng Chang, Chen-Chung Lui
25 January 2006, Journal of Clinical Neuroscience 13 (2006) 979–985
SURGERY: ASPIRATION
carried out at any stage of evolution
of the abscess.
 via a burr hole and completely
decompressed, with an immediate
reduction of mass and intracranial
pressure.
