Medical Student Morning Report Presentation

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Medical Student Morning Report Presentation

• Jamison Strahan, Omar Hernandez, Toby Natividad,
  Tawana Smith, Justin McInnis

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HPI

• 17 y/o LAM with new onset seizure. Sz, observed
  by brother, lasted 12 min with post-ictal period
  of 6 min. Patient was evaluated at Clear Lake
  Medical, no laboratory or radiologic tests were
  performed, no meds prescribed, patient was D/C
  home.
• At 6 am next morning, pt had 2nd seizure lasting
  10min with a 6 min post-ictal period. Following
  both seizures, patient was not aware of the
  incident, no encopresis, incontinence or biting
  of his tongue. No associated fevers, N/V,
  abdominal pain, diarrhea, no aura or HA prior to
  seizure.

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History

• PMH
• HA approximately every 10 days since childhood,
  resolved with Advil/Tylenol, never formally
  evaluated.
• Gastritis x 3 yrs.
• Asthma at 10 yrs old-resolved.
• Several episodes of inability to move his
  extremities when awakening from sleep
  (hypnopompic paralysis) during childhood.
• FHx
• Non-contributory, parents live in Guatemala.
• Two brothers, five sisters, all healthy.
• PSHx None
• Developmental Hx Completed 6th grade.
• Immunizations Unsure, last vaccination at age
  13 yrs.

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History, Contd

• Hospitalizations Fx left clavicle 6 yo, Fx right
  ankle 8 yo, no complications.
• Social Hx Moved from Guatemala 2 yrs ago.
  Lives with brother (19), and two friends in an
  apt. No tobacco, alcohol, drug use. Denies any
  sexual activity ever. No sick contacts. No
  travel outside of country since moving here. No
  food from outside of country. Works as a bus boy
  at a Mexican restaurant.
• Meds None. Takes herbal supplement Sukkol
  (Glutamic acid, Lecithin) qod x 1 month for
  memory and energy and Chamomile tea for
  gastritis.
• Allergies NKA

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OSH Labs
80N 14.8L 3.8M 0.8E

• LFTs
• SDS Digoxin 0.1, Acetaminophen lt 10,
  Salicylate lt 2.8, ETOH 0.003
• UDS Neg
• UA SG 1.020, Blood 1, pH 5, 0 LE, 0 Nit, WBC
  3-4, RBC 3-5, Bacteria 3
• CT 7 cm low density intra-axial lesion in
  posterior right temporal lobe. 4 cm low
  density extra-axial lesion in left mid-cranial
  fossa.
• EEG pending

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Physical Exam

• Ht 58 in (50th for 11.5 y/o) Wt 104 lbs (50th
  for 13.5 y/o)
• T 37.6 po BP 104/59 P 86 R 24
• Gen A O x 3, NAD, cooperative
• HEENT PERRL, EOMI, MMM
• Neck Supple, Brudzinski-Neg, no nuchal
  rigidity no LAD
• CV RRR, Normal S1/S2, No M/R/G
• Lung CTA bilaterally
• Abd BS, NTND, soft, No HSM
• GU Normal testicular exam (Tanner IV), Tanner IV
  ax hair
• Skin No rashes, petechiae or lesions
• Ext No C/C/E, LBP muscular origin
• Neuro CN II-XII grossly intact. LE DTRs 2.
  Normal heel-shin test. Mild past pointing and
  decreased concentration with finger to nose test
  both UEs. No dysdiadochokinesia. Negative
  Rhomberg. Gait slight decrease in balance
  (secondary to Phos phenytoin infusion from OSH
  per subjective report).

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Problem List?
Differential Diagnosis?
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DDX for Pediatric Brain Mass

• Neoplasm
• Primary
• Pilocytic Astrocytoma (24)
• Medulloblastoma (16)
• Ependymoma (10)
• Hemangioblastoma
• Craniopharyngioma
• Glioblastoma multiforme
• Tuberous Sclerosis
• Pinealoma
• Benign cyst
• Choroid Plexus Papilloma
• Secondary
• Lymphoma (also 1)
• Germ cell (testicular)
• Blood/Vascular
• Hemorrhage
• AVM
• Aneurysm

• Pus
• Infectious
• Abscess
• Toxoplasmosis
• Neurocysticercosis
• Tuberculosis
• CMV
• Amebic Meningoencephalitis
• Lyme Disease
• Toxocariasis
• Trichinosis
• Fungal Infx (Histoplasma/Blastomyces)
• Inflammatory
• Sarcoidosis
• Other Granulomatous Dz
• Vasculitis
• Water (hydrocephalus)
• Obstructive
• Communicating

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UTMB Labs

• UA WNL
• Urine Cx Negative.
• EEG Very abnormal, 2 independent foci of
  underlying dysfunction (R frontal and R posterior
  regions) with potential epileptogenicity
• Stool OP Endolimax nana, Entamoeba hartmanni,
  Dientamoeba fragilis, few Blastocystis homonis.

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Image MRI
T1 Weighted Image
T2 Weighted Image

• 1.1 cm rim enhancing cystic lesion in right
  temporal lobe with suspected scolex and
  surrounding edema highly suspicious for
  neurocysticercosis.

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Image CT
Calcification?

• Hypodense region - 1 cm in diameter in R
  temporal/parietal region which may have a tiny
  punctate calcification inferiorly, leading
  differential possibility is neurocysticercosis.

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DiagnosisNeurocysticercosis
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Diagnostic Criteria

• Minor
• Compatible lesion on image
• Clinical manifestations
• Positive CSF ELISA Ab/Ag
• Other organ involvement demonstrated
• Epidemiologic
• Household contact
• Immigrant from endemic area
• Frequent travel to endemic area

• Absolute
• Confirmatory biopsy
• Image of cyst w/ scolex
• Funduscopic exam
• Major
• Highly suggestive lesion on image
• Positive serum Ab
• Cyst resolution after anti-parasitic med
• Spontaneous resolution single cyst

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Diagnostic Criteria

• Definitive
• 1 absolute OR
• 1 major 2 minor 1 epidemiologic
• Probable
• 1 major 2 minor
• 1 major 1 minor 1 epidemiologic
• 3 minor 1 epidemiologic

Del Brutto, OH et al. Proposed diagnostic
criteria for neurocysticercosis. 2001 Neurology
57(2)177-183.
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Neurocysticercosis Background
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Epidemiology

• Most common parasitic infection of the central
  nervous system
• Affects 50 million people worldwide
• Endemic to Mexico, Central and South America,
  sub-Saharan Africa and Asia
• gt 1,000 cases per year in the United States,
  particularly in the Southwestern region where
  immigration is prevalent

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Transmission

• Humans develop NCC through ingestion of T. solium
  ova
• Contaminated food (i.e. fruits and vegetables
  irrigated with water containing human feces)
• T. solium carrier contaminating foods directly
  (carriers often contain eggs under fingernails)

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Pathophysiology

• Ingested ova develop into embryos in the small
  intestine and invade the bowel wall
• The embryos then disseminate hematogenously to
  the tissues and develop into cysticerci over a 3
  wk 2 mo period.
• The cysticerci that enter the central nervous
  system do not cause inflammation in surrounding
  tissues initially (asymptomatic) and can be
  parenchymal and extraparenchymal
• The asymptomatic phase lasts an average of 3-5
  years but can last as long as gt 30yrs.
• Neurologic symptoms occur when cysticeri
  die/degenerate and the human host mounts an
  associated inflammatory response

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Pathogenesis
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Morbidity and Mortality

• NCC typically is benign most lesions resolve
  spontaneously within 2-3 months
• Mortality depends on whether NCC is simple or
  complicated
• Simple NCC occurs in children with only a single
  exposure to cysts most commonly seen in the U.S.
  and other non-endemic countries (few
  complications)
• Complicated NCC occurs in children in endemic
  areas who are constantly re-exposed to ova (less
  favorable prognosis)

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Clinical Manifestation

• Seizures (particularly focal) (87)
• Headache (32)
• Nausea/Vomiting (32)
• Altered Mental Status (13)
• Cranial Nerve palsies, gait abnormalities,
  papilledema, decreased visual acuity (lt10)
• Fever is uncommon
• Physical exam is commonly normal

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Labs

• Enzyme-linked immuno-transfer blot assay (EITB)
• Specificity is 100 and sensitivity 90 for
  children with gt2 lesions
• Sensitivity only 50-70 in children with just 1
  lesion
• Lumbar Puncture (contraindicated with increased
  ICP)
• Reveals pleocytosis (often lymphocytic, but
  occasionally eosinophilic) in 50 of cases
• Glucose- decreased
• Protein- increased
• Stool sample
• 3 consecutive daily stool specimens
• Presence of ova may be sole diagnostic
  confirmation
• Stool test for T. Solium is rarely positive
• Enzyme-linked immunosorbent assay (ELISA)
• Serum or CSF sample
• Can aid in diagnosis in cases with few lesions
  and mild disease
• Sensitivity 75-80

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Radiographic Correlation
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Parasite Stages

• Vesicular
• No cellular response, prominent scolex
• Colloidal
• Cyst degenerating, mild inflammation
• Nodular
• Prominent inflammation, surrounding edema
• Calcified
• Resolving cellular response, calcified remnant

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Vesicular Phase

• MRI shows cysts having CSF-like density WITHOUT
  surrounding high-intensity signal
• CT shows round hypodensities WITHOUT enhancement

Scolex
MRI with contrast
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Colloidal Phase

• Contrast-CT or MRI shows slight pericystic
  contrast uptake due to thickened capsule
• Symptoms (Sz) may begin in this stage

MRI with contrast
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Nodular Phase

• Intense inflammation and surrounding edema cause
  typical ring-enhancement with contrast
• Symptoms most prominent at this stage

MRI with contrast
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Calcified Phase

• Only calcified remnants
• CT without contrast shows high intensity signal

CT w/o contrast
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Treatment
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Neurocysticercosis is not a single disease for
which one therapy can be recommended -Current
Consensus Guidelines for Treatment of
Neurocysticercosis. Clin Micro

Reviews. Oct 2002 pg 747-756

• Factors Influencing Treatment
• Number of parasites
• single lesion
• few lesions (lt5 cysts)
• massive infection (gt100 cysts)
• Location of Lesion (intra-parenchymal vs
  extra-parenchymal)
• Parasite Viability
• Growing, living, degenerating, calcified
• Current Treatments Antihelminthics,
  Anticonvulsants, Anti-inflammatory and Surgery

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Antihelminthic Therapy

• Albendazole
• - Inhibits microtubule synthesis in nematodes
• - standard dosing is 15mg/kg/day given for 15
  days (several studies have shown similar
  efficacy for 3d and 8d courses)
• Why?
• - Standard course kills 75-90 of cysts
• - More rapid cyst clearance from brain
• Why not?
• - Most Pt with NCC become symptomatic only when
  cyst begin to degenerate. This is secondary
  to development of edema and inflammation
  around dying cyst.
• - Anti-helminthic drugs can worsen neurological
  problems due to rapid increase in number of
  degenerating cysts (risk of pericystic
  vasculitis/stroke).
• Praziquantel
• - Interacts with both steroids and
  anticonvulsants (P450)
• - Poor CNS penetration
• - New studies show 75-100mg/kg given in 3
  divided doses 2hrs apart have similar efficacy
  as standard Albendazole therapy

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Anti-Inflammatory Therapy (Steroids)

• Should be given concomitantly with Albendazole
• Dexamethasone 12-16 mg/day or Prednisolone 30-40
  mg/day (up to 1 mg/kg/day) x 5 days then a 2 week
  taper.
• Primary management for chronic cysticercosis and
  cysticercosis encephalitis

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Anticonvulsant Therapy

• Carbamazepine and Phenytoin 1st line.
• Risk of seizure greatest during degenerative
  phase
• Calcified cysts can serve as epileptic focus
  after active infection cleared.
• Current practice Anticonvulsant therapy for 1yr.
  Medication can be stopped if Pt has been seizure
  free.

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Guidelines for Intra-parenchymal Cysts

• Growing cysts Always treat with antihelminthics
  (AH) and steroids especially when there is risk
  of ventricular involvement
• Live cysts
• Few - AH /- steroids or Neuroimaging f/u only
• Moderate(gt5) - AH steroids
• Heavy(gt100) - AH high dose steroids or chronic
  steroid management with neuroimaging follow-up
• Degenerating Cysts
• Few to Moderate - Neuroimaging f/u
• Heavy (cysticercosis encephalitis) - high dose
  steroids and osmotic diuretics to decrease ICP.
• Calcified Cysts No treatment regardless of
  number

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Questions??