Transcript CLINICO-PATHOLOGIC and RADIOLOGIC CORRELATION

CLINICO-PATHOLOGIC and
RADIOLOGIC CORRELATION
USTH 2009 Interns Group 5
General Data
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JA
24 year old male
Roman Catholic
Right handed
Single
4th year college student
Balic-Balic Sampaloc, Manila
Date of Admission: September 12, 2008
Chief Complaint
 twitching
the face
of the right side of
HISTORY OF PRESENT
ILLNESS
Sept 8
12MN
Sept 8
1 AM
• generalized, throbbing, grade 5/10 headache
• Upward rolling of eyeballs and rigidity of all extremities
with loss of consciousness
• right sided facial numbness
• twitching of the right lower quadrant of the face
becoming generalized ~ 15-30 seconds
• Consult USTH-TR
• Difficulty swallowing
• twitching of the right side of his face~ 5 minutes
• no headache, loss of consciousness nor stiffening of the
extremities
• Admitted to USTH pay
• MRI done
Sept. 9
• Labs done
Sept. 10
HISTORY OF PRESENT
ILLNESS
Sept 10
• Discharged stable : final diagnosis?
• THM: Albendazole, Carbazepine, Dexamethasone, Thiamine
Sept 12
4PM
• Twitching of the right side of the face lasting for 2-3 minutes
occurring at intervals of 30 minutes.
• Slurring of speech
• (-) loss of consciousness, headache, vomiting, nor blurring of
vision
HISTORY OF PRESENT
ILLNESS
Sept 12
7 PM
• Twitching of his right half of the face occurred at more
frequent intervals.
• Worsening of slurring of speech
ADMISSION
REVIEW OF SYSTEMS
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No fever
No blurring of vision
No deafness, aural discharge, dizziness,
tinnitus, ear pain
No epistaxis, nasal discharge, obstruction
No chest pains, easy fatigability, syncope,
palpitations
No dysuria, hematuria
No abdominal pain, change in bowel movement
Past Medical History
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No previous history of seizures?
No known allergies
No previous operations
No history of trauma
Not known hypertensive
Not known diabetic
Family History
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(+) Stroke - paternal grandmother
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(+) DM – Uncle
(+) Hypertension – Uncle
(+) Neurocysticercosis - cousin
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Personal and Social History
Usually eats raw fish and meat
(kilawin)
 Non-smoker
 Occasional alcoholic beverage drinker
(2-3 bottles/beer every week)
 Denies illicit drug use
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PE on admission
Conscious, coherent, ambulatory, not in
cardiorespiratory distress
 BP 130/90
PR 82 RR 20 T 36.5
 Pink palpebral conjunctiva, anicteric
sclera
 Moist buccal mucosa, no nasal nor
aural discharge
 Supple neck, no palpable cervical
lymph nodes
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PE on admission
No neck vein distention, no carotid
bruit
 Symmetrical chest expansion, clear
breath sounds, no retractions
 Adynamic precordium, AB 5th LICS
MCL, no murmurs
 Flabby abdomen, soft, no mass, no
tenderness
 Pulses full and equal, no cyanosis, no
edema
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Neurologic examination
on admission
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Conscious, coherent, dysarthic,
oriented to time, place, and person;
can follow commands; no acalculia,
apraxia, agraphesthesia,
astereognosis, right-left
disorientation, sensory extinction;
intact remote, recent and immediate
memory; MMSE: 30
Neurologic examination
on admission
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No anosmia
Pupils 2-3mm ERTL, isocoric OU, no visual
field cuts; VA: 20/50 OU; Funduscopy: clear
disc margins, no papilledema, no hemorrhage
EOM full and equal, no nystagmus
Can clench teeth, V1,V2, V3 intact
Can close eyes tightly, can raise eyebrows
equally, can frown, can puff both cheeks, can
smile, shallow R nasolabial fold
Neurologic examination
on admission
 Intact
gross hearing, no
lateralization on Weber’s; AC> BC
on Rinne’s AU
 (+) gag reflex, uvula at midline
 Can shrug both shoulders
equally against resistance, can
turn head against resistance
 Tongue deviated to the right
Neurologic examination
on admission
Cerebellar: can do APST and FTNT
with ease, bilateral
 With normal gait
 No sensory deficit as to light touch,
pain, vibration and position sense
 Reflexes: 2+ on all 4’s
 No pathologic reflexes
 No nuchal rigidity, no kernig’s sign, no
brudzinski’s sign
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Laboratories from
previous admission
CBC
CBC
Hgb
Hct
MCV
MCH
MCHC
Platelet
WBC
Neutrophil
NV
120-170
0.36-0.54
87 + 5
29 + 2
34 + 2
150-450
4.5-10
0.50-0.70
9/10/08
129
0.37
73.10
25.6
35
433
11.9
0.71
Blood chemistry
BUN
Creatinine
Sodium
Potassium
iCa
SGPT
SGOT
NV
9-23
0.5 1.2
137-147
3.8 -5
1.18-1.30
0-40
0-40
9/10/08
10.3
0.98
136
3.6
1.30
35.8
49.2
urinalysis
Urinalysis
Color
Transparency
pH
Specific gravity
Albumin
Sugar
RBC
9/10/08
Lt yellow
Turbid
6.0
1.010
(-)
(-)
0-1/hpf
Fecalysis
Fecalysis
Color
Consistency
Muscle cells
Vegetable cells
Vegetable fiber
Starch granules
Parasite /ova
9/10/08
Brown
Formed
Few
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None found
Cranial MRI(Sept. 9, 2008)
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solitary ring- enhancing cystic lesion
at the L posterior frontal cortical and
subcortical whit matterwith
surrounding vasogenic edema and
focal central calcific focus within the
lesion. Considerations include cystic
granuloma parasitic infection,
peripherally located to primary cystic
neoplasm or cystic metastases
 9/9/08
– Chest X ray normal
chest
 9/9/08
rhythm
– ECG: normal sinus
Salient Features
SUBJECTIVE:
Sudden onset of severe headache
 Numbness of the right side of the face
 Upward rolling of the eye & rigidity of all
extremities associated with loss of
consciousness
 Twitching of the right side of the face
 Difficulty speaking
 Difficulty of swallowing
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Salient Features
OBJECTIVE:
 Dysarthic
 Shallow left nasolabial fold
 Tongue deviated to the right
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Groups of symptoms pertaining to a particular
system (huh?!)
Nervous system
Differential Diagnosis
Is there a neurologic problem?
• Increased intracranial pressure
– A. (+) headache but no vomiting
– B. no papilledema
– C. no lateral rectus palsy
– D. no deterioration of level of conciousness
• Meningeal irritation
– A. (+) headache but no vomiting
– B. no nuchal rigidity
– C. no brudzinski
– D. no kernig
Is there a neurologic problem?
• Focal neurologic deficits
• A. -slurring of speech
– -twitching of R side of face
-no memory impairment
-no emotional and behavioral changes
B. -facial asymmetry
-shallow right nasolabial fold
-tongue deviated to the R
C.-no weakness of extremities
D.-no incoordination
E. -no reflex asymmetry or pathological reflex
F. -no sensory impairment
Where is the lesion?
Levelization, Lateralization, Localization
Levelization
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dysarthic
shallow left nasolabial fold
tongue deviated to the right
 upper motor neuron
Levelization
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Upper Motor Neuron
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cerebrum
cerebellum
brainstem
spinal cord
Levelization
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autonomic dysfunction
sensory level to pain
 spinal cord
Levelization
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can do APST & FTNT
can do heel to shin test
 cerebellum
Levelization
shallow left nasolabial fold
 Tongue deviated to the right
 cranial nerve deficit
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 brainstem
Levelization
Right side of the face numbness
 upward rolling of the eyes and rigidity of all
extremities associated with loss of
consciousness
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 cerebrum
Lateralization
 numbness of the right side of the face
twitching of the right side of the face
 shallow left nasolabial fold
 Tongue deviated to the right
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 left
Localization
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frontal lobe of cerebrum
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Levelize: cerebrum
Lateralize: left
Localization: frontal lobe
Differential Diagnosis
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Cystic Granuloma
Neurocysticercosis
Metastasis
Primary Neoplasm
Tuberculoma
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TB CNS infections are secondary to
hematogenous spread
Best diagnostic clue: meningitis + parenchymal
lesions
Typically parenchymal, supratentorial (parietal
lobe)
Gray-white matter junction
Solitary or multiple
Tuberculoma
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CT Findings
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NECT: hypodense to hyperdense round or lobulated
nodule/mass with moderate to marked edema
Calcium may be present
CECT: solid or ring enhancing
“target” sign
Tuberculoma
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MR Findings
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T1WI – hypointense to isointense to the brain
T2WI – hypointense rim + surrounding edema
T1 C+
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Non-caseating - nodular, homogenous enhancement
Caseating – peripheral rim enhancement
Cysticercosis
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Most common CNS parasitic infection
Etiology: Taenia Solium
Usually seen in young and middle-aged
adults
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Cysticercosis
Morphology
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Rounded or ovoid cyst, solitary in 20%-50%
Multiple, usually small number of cysts
Location: corticomedullary junction
Best dianostic clue: cyst with “dot” inside
4 patterns of neurocysticercosis:
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Parenchymal
Intraventricular
Subarachnoid
Mixed
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Cysticercosis
4 Stages:
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Vesicular Stage
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cysticercus consists of a thin capsule that surrounds a
viable larvae and its fluid containg bladder
round CSF-like cyst with a mural nodule
Colloidal Vesicular Stage
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Larvae dies and begins to degenerate
Cystic fluid becomes turbid, cyst shrinks and capsule
thickens
Release metabolic products that disrupt BBB
Cysticercosis
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Granular Nodular Stage
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Cyst retracts, capsule thickens and scolex calcifies
Edema is present
Nodular Calcified Stage
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lesion is contracted to a fraction of its initial size and
completely miniralizes
Cysticercosis
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CT Findings
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NECT
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Vesicular stage – smooth, thin-walled cyst, isodense to
CSF, no edema
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Hyperdense “dot” within cyst
Colloidal vesicular stage – hyperdense cyst fluid with
surrounding edema
Granular nodular stage – mild edema
Nodular calcified stage – small, Ca++ nodule
Cysticercosis
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CT Findings
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CECT
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Vesicular stage – no wall enhancement
Colloidal vesicular stage – thicker ring-enhancing fibrous
capsule
Granular Nodular stage – involuting enhancing nodule
Nodular Calcified stage – shrunken, calcified nodule
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Cysticercosis
MR Findings
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Vesicular stage
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T1WI, FLAIR – cystic lesion isointense to CSF; may be discrete,
eccentric scolex
T2WI – cystic lesion isointense to CSF; no surrounding edema
T1 C+ - no/mild enhancement
Colloidal vesicular stage
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T1WI – mildly hyperintense to CSF
T2WI, FLAIR – mild to marked surrounding edema
T1 C+ - thick cyst wall enhancement with marginal nodule
Cysticercosis
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MR Findings
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Granular nodular stage
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Nodular calcified stage
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T1WI, T2WI – thickened, retracted cyst wall; edema
decreases
T1 C+ - thickened, retracted cyst wall; nodular or ring
enhancement
T1WI, T2WI – shrunken, Ca++ lesion
T1 C+ - small calcified lesion; rare minimal enhancement
T2 FFE (GRE) – demonstrate calcified scolex
Metastasis
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Most common CNS manifestation of extracranial
primary neoplasm
Highest incidence: 4th to 7th decade of life
80% to 85% - supratentorial
Metastasis
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Most common primary tumors to metastasize to
the brain
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Lung
Breast
Melanoma
GI/GU tumors
Renal Cell carcinoma
Metastasis
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multiple or solitary
Best diagnostic clue: Corticomedullary junction
– most common site
Notoriously surrounded by massive vasogenic
edema
Best imaging tool: MRI+C > CECT
Metastasis
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NECT: iso- or hypodense at gray-white matter
interphase
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Peritumoral edema is variable
CECT: intense, punctate, nodular or ring
enhancement
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Metastasis
MR Findings
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T1WI – iso/hypointense
T2WI – usually hyperintense
T2FLAIR – variable (edema)
T2FFE (GRE) – blooms if
hemorrhage is present
DWI – no restriction
T1 C+ – enhances (uniform,
punctate, solid or ring enhancing)
Primary Brain Tumors
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Gliomas comprise nearly half of all intracranial
tumors
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Almost half are glioblastoma multiforme
Incidence:
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Glioblastoma – 55%
Astrocytoma – 20.5%
Ependymoma – 6%
Medulloblastoma – 6%
Peak incidence – 7th decade of life
Location – supratentorial in adults
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DIAGNOSIS:
NEUROCYSTICERCOSIS
Course in the ward
Course in the ward
referrals
 Neurosurgery
 Infectious
Disease Medicine
 Cardiovascular Medicine
1st Hospital Day
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Following laboratories were done:
CBC with platelet
Creatinine, Na, K, iCa, SGPT
CBC
CBC
Hgb
Hct
MCV
MCH
MCHC
Platelet
WBC
Neutrophil
Lymphocytes
NV
120-170
0.36-0.54
87 + 5
29 + 2
34 + 2
150-450
4.5-10
0.50-0.70
0.20-0.40
9/12/08
135
0.40
83.80
28.30
33.70
500
12.30
0.87
0.13
Blood chemistry
Creatinine
Sodium
Potassium
iCa
SGPT
NV
0.5 1.2
137-147
3.8 -5
1.18-1.30
0-40
9/12/08
0.88
136
4.4
1.28
56.8
Medications:
Albendazole 400 mg/tab 1 tab BID
 Carbamazepine 200 mg/tab 1 tab
BID
 Dexamethasone 4 mg/tab 1 tab OD
 Thiamine 300 mg/tab 1 tab OD
 Diazepam 5 mg/IV prn for seizure > 5
mins
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2nd Hospital Day
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There was slurring of speech and facial
asymmetry.
Medications:
Diazepam 50mg/IV every 8 hours ( seizure
>5mins)
Patient was observed for seizure recurrence.
3rd Hospital day
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Started on Iselpin tablet, 1 tablet 3x a day
HCTZ 12.5mg/tab 1 tablet once daily
Dexamethasone 4mg/tab ordered as 1 tablet
every other day for 7 days then discontinue.
Referred to Neurosurgery for possible
sterotactic biopsy.
5th Hospital Day
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Seizure precaution continued.
Diazepam 50mg/IV
Carbamazepine 200mg/tab given every 8 hours
6th Hospital day
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Referred to infectious diseases
Advised to continue with albendazole
400mg/tab 1 tablet twice a day.
Neurosurgery : advised with open biopsy either
sterotactic guided craniotomy for open biopsy
or frameless stereotaxy
7th Hospital day
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No seizure recurrence, afebrile
Thiamine discontinued
8th Hospital day
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Patient was febrile given PAracetamol
500mg/tab
9th Hospital day
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No seizure recurrence
OR schedule awaited
12th Hospital day
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Patient scheduled to undergo sterotactic –
guided craniotomy
13th hospital day
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Started on Amlodipine 5mg/tab 1 tab OD
(hypertension)
Infectious disease : suggested sending brain
tissue specimen for gram stain, culture and
sensitivity, AFB stain, MTB culture , KOH
smear and fungal culture.
Anesthesia : preop medications includeL
Omeprazole 20mg/tab, Amlodipine 5mg/tab
, Dexamethasone 4mg/tab and
Carbamazepine 20mg/tab.
14th Hospital day
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Patient underwent stereotactic guided left
frontal craniotomy for gross total excision of
intra-axial mass.
Intra operatively the surgeons noted that the
mass is simly a tumor and the ancillaries
requested by ID-MED were no longer necessary.
Instead the tumor was sent to the laboratory for
histopathologic evaluation.
Gross
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A yellow brown ovoid soft to fluctuant mass
measuring 2x1.3x1.0 cm.
Multiple cystic spaces measuring from 0.1 - 1.0
cm. in diameter containing clear fluid.
ACT08-3026
Microscopic
Cefazolin 1g/IV
 Phenytoin 100mg/IV
Post-op
Medications
 Dexamethasone 5mg/IV
 Paracetamol 300mg/IV
 Voltaren 50mg to every 1 liter IVF for 3 doses
 Omeprazole 20mg/IV then shifted to 20mg/tab
once the patient tolerates clear liquids.
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Cefazolin was shifted to Co-amoxyclav
625mg/tab BID for 5 days
th
15 Hospital day
 Dexamethasone was shifted to 4mg/tab OD
 Phenytoin discontinued
 Carbamazepine 20mg/tab
 Albendazole 40mg/tab were resumed pending
histopath results.
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OMeprazole was discontinued
thCOD done
16 Metoprolol
Hospital50mg/tab
day
1 tab BID was started
 Amlodipine 5mg/tab
 Referred to CV med for evalution and
management of young onset hypertension
 Iselpin was decreased to 1 tab OD
 Paracetamol was discontinued.
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CV-med suggested the ff ancillaries
thSerum TSH
17 Hospital day
 2d echo with doppler
 Lipid profile
 And UTZ – KUB with renal indices
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Underwent serum TSH and lipid profile tests –
thunable due to financial constraints
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19
Hospital day
DISCUSSION
Etiology
TAENIA SOLIUM (pork tapeworm)
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*the parasite producing taeniasis solium or pork
tapeworm infection
-Associated with eating raw or insufficient cooked pork
Etiology
Taeniasis solium - refers to infection of humans
with adult pork tapeworm
Human cysticercosis - refers to infection of
humans with larval stage of parasites
In human cysticercosis:
Man becomes the intermediate host.
Life Cycle
Human Being Harbor Cysticercus Cellulosae:
Hetero Infection – eggs liberated from
disintegrating gravid proglottides passed by one
individual get into the mouth of another and
are swallowed
Human Being Harbor Cysticercus Cellulosae:

External
autoinfection
–
eggs
maybe
transferred from anus to mouth or unclean
fingertips of an individual who has an intestinal
infection with Taeniasis solium
Human Being Harbor Cysticercus
Cellulosae:
Internal autoinfections – gravid
proglottids in an individual harboring
the adult Taenia solium may become
detached from the main strobila or
regurgitated into the stomach and
then return to duodenal canal where
they disintegrate and liberate ripened
eggs
CLINICAL
PRESENTATION
Stages of Neurocysticercosis
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Vesicular stage
Colloid stage
Granular-nodular stage
Calcific stage
Clinical Presentation
When it affects the brain parenchyma
-New onset partial seizure with or without secondary
generalization (focal or multufocal, possibly intractable)
When present in subarachnoid or ventricular space
-Increased ICP
Pseudotumor (diffuse parenchymal involvement)
Obstructive hydrocephalus (intraventricular cysts,
racemmeningealcysts)
- Intracranial space occupation (parenchymal cysts)
Meningoencephalitis
Basal arachnoiditis
Psychiatric disorders, including dementia
Spinal cysticercosis
-can mimic presentation of intraspinal tumor
DIAGNOSTICS
Diagnosis of neurocysticercosis stems from
suspicions that arises from the clinical
manifestations of the disease
Most useful diagnostic test and the primary
diagnostic criteria is neuroimaging
1. Contrast CT
2. MRI
 Useful in the evolution of cysticercus in th
eparenchyma of brain.
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4 Phases
1.
2.
3.
4.
Vesicular
Colloidal
Nodular-granular
Calcified phase
Vesicular
Colloidal
Nodulargranular
Calcified
CT
circumscribed, rounded,
hypodense areas, ave.
size 10 mm, range 4-20
mm, no enhancement
annular enhancement
surrounded by
irregular perilesional
edema
diffuse hypodense
area with irregular
borders
(non-contrast)
a small, hyperdense,
rounded, nodular
image surrounded
by edema (ff
contrast)
rounded,
homogeneous
hyperdense area
showing no
enhancement with
contrast medium
MRI
CSF-like intensity signal
on all sequences, with
no surrounding high
signal on T2-weighted
images.
higher signal than the
adjacent brain with
thick-ring
enhancement (T1)
a low-ring signal
surrounded by high
signal lesion (T2)
change in the
signal from the
cyst fluid (T2)
Both
high intensity, 2-4 mm
mural nodule, depicting
the scolex in the
interior of some
parenchymal vesicular
cysts.

When only one cyst is seen in the transitional
phase, it corresponds to the so-called "single
enhancing lesion on CT" (SECTL), signifying a
special syndrome.
Immunologic Assay
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Enzyme ImmunoBlot
The current serological assay of choice for the
diagnosis of neurocysticercosis
 CDC's immunoblot is based on detection of
antibody to one or more of 7 lentil-lectin purified
structural glycoprotein antigens from the larval
cysts of T. solium in an immunoblot format.
 It is 100% specific.
 No serum samples from patients with other
microbial infections react with any of the T. soliumspecific antigens.
 Cumulative clinical experience has confirmed that
in patients with multiple (more than two) lesions,
the test has more than 95% sensitivity.
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ELISA
- Lack of specificity has been a major problem
because of cross-reacting components in crude
antigens derived from cysticerci
- these components react with antibodies specific
for other helminthic infections, especially
echinococcosis and filariasis.
- lower sensitivity than crude antigens and do not
necessarily achieve higher specificity
Assays employing crude antigens for the detection of
antibody are not reliable for the identification of
this disease
Diagnostic Criteria
Absolute criteria
 Histologic demonstration of parasite
 Direct visualization of parasite by fundoscopic examination.
 Evidence of cystic lesions showing scolex on CT/MRI.
Major Criteria
 Lesions suggestive of neurocysticercosis on neuroimaging
studies
 Positive immunological tests
 Plain X-ray films showing calcifications in thigh and calf
muscles
Minor criteria
 Subcutaneous nodules
 Soft tissue or intracranial calcification on plain x-ray
 Clinical manifestations suggestive of neurocysticercosis
 Disappearance of intracranial lesions after a trial with
anticysticercal drug
Epidemiologic
 Living or coming from endemic area
 Frequent travel to endemic areas
 Household contact with Taenia solium infection
Definitive: 1 absolute
2 major
1 major + 2 minor + 1 epidemiologic
Probable: 1 major + 2 minor
1 major + 1 minor + 1 epidemiologic
3 minor + 1 epidemiologic
Possible: 1 major
2 minor
1 minor + 1 epidemiologic
Revised
Absolute criteria
 Histologic demonstration of parasite
 Direct visualization of parasite by fundoscopic examination
 Evidence of cystic lesions showing scolex on CT/MRI.
Major Criteria
 Lesions suggestive of neurocysticercosis on CT or MRI
 Positive serum EITB (Enzyme Immunoblot Assay)
 Resolution of cyst after therapy.
 Spontaneous resolution of single enhancing lesions.
Minor Criteria
 Lesions compatible with neurocysticercosis on CT/MRI
 Suggestive clinical features
 Positive CSF ELISA
 Cysticercosis outside CNS
Definitive diagnosis of extra-neural
cysticercosis will require one of the following:
a) histopathological demonstration of parasite
from excisional biopsy of a subcutaneous
nodule. Demonstration of larval parts (hooks,
suckers etc.) by fine needle aspiration cytology
may provide a satisfactory alternative to open
biopsy
b) plain X-ray films showing multiple "cigarshaped calcifications in the arm, thigh and calf
muscles
c) direct visualization of a cysticercosis larva in
the anterior chamber of the eye with
ultrasonography.

Epidemiologic
 Living or coming from endemic area
 Frequent travel to endemic areas
 Household contact with Taenia solium infection
Definitive: 1 absolute
2 major + 1 minor + 1
epidemiologic
Probable: 1 major + 2 minor
1 major + 1 minor + 1
epidemiologic
3 minor + 1
epidemiologic
Treatment

Treatment must be tailored to the specific needs of the
patient and may include medical drugs such as
antihelminthic drugs and corticosteroids or surgery

The introduction of praziquantel in 197927 was
enthusiastically received,28 but soon afterward, some
authors claimed that there was no need to kill a parasite
that existed in good symbiosis with the brain

an open, controlled trial published in 1995 showed no
significant differences among patients treated with
albendazole, praziquantel, or corticosteroids alone in the
evolution of seizures or even in the radiologic evolution
of cysts.13

“Albendazole is preferable over praziquantel due to its
lower cost..”

Davis, LE. “Neurocysticercosis” Emerging Neurological Infections edited by Power, C
and Johnson RT. Taylor & Francis Group, 2005. 261-287

“Albendazole is more effective than praziquantel in terms
of clinically important outcomes in patients with
neurocysticercosis”

Dimitrios K. Matthaiou, Georgios Panos, Eleni S. Adamidi,Matthew E. Falagas
“Albendazole versus Praziquantel in the Treatment of Neurocysticercosis: A
Meta-analysis of Comparative Trials” PLoS Negl Trop Dis. 2008 March; 2(3):
e194

Treatment depends on the stage of cyst development:

Immature cyst stage (stage 1)



Vesicular or viable cysts (stage 2)
Colloid cyst stage (stage 3)?


high-dose steroids
Surgery + albendazole
Dead calcified cysts stage (stage 4)

“the benefits of albendazole therapy in decreasing the
numbers of seizures outweigh the arguments..the use of
antiparasitic treatment as part of routine practice in the
management of parenchymal brain cysticercosis is
recommended”.
- A Trial of Antiparasitic Treatment to Reduce the Rate of Seizures Due to Cerebral Cysticercosis
Héctor H. Garcia, M.D., Ph.D.,et
.