Janica Walden, Michael Solle, Neuroradiology
Case 1: History

1-2008:
 26 male with ventriculomegaly & symptoms
concerning for hydrocephalus with papilledema &
headaches.
Case 1: Head CT
Case 1: MRI (FLAIR)
Case 1: MRI (CISS)
Case 1: Surgery

Multiple cysts were visualized &
removed from lateral & 3rd ventricles.
Case 1: Pathology

Light Microscope:
 Sections showed fragments of degenerating
wall of a cysticercal cyst. Wall shows a small
amount of calcification.

Diagnosis: Cysticercosis
Neurocystircercosis

Cysticercosis is the most common parasitic
infection in immunocompetent patients:
 incidence is not increased in patients with AIDS,
 Cysticercosis is generally acquired by ingesting fruits
or vegetables contaminated with eggs (Taenia
solium,.
 ingesting larvae (undercooked pork) results in
intestinal teniasis.




Most common cause of acquired seizures.
Gray-white junction- hematogenous spread (?)
Intraventricular lesions (20-50%).
Subarachnoid space lesions (racemose typecluster of grapes) (less than 10%).
Neurocystircercosis

Vesicular stage:
 cyst-like lesion w/mural nodule (larva with full bladder &
scolex, generally no contrast enhancement).

Colloidal stage:
 cyst dies & produces inflammatory reaction (incomplete
ring-enhancing lesion w/edema).
 Occasionally, multiple lesions are in the colloidal stage &
produce an encephalitis-like picture.

Granular stage:
 dead organism produces classic ring-enhancing lesion.

Nodular stage:
 final stage in which lesion calcifies.
Case 2:

History:
 27 male with HIV, lumbar puncture was
done… & india ink stained positive for
cryptococcus.
Case 2: Intial study
Case 2: 1st Follow up study
-Operation

A single burr hole was made. Dura was
opened & underlying pia was cauterized.
Following this, using stereotaxy, a
biopsy needle was advanced. Once the
target was achieved, mild aspiration
yielded gross purulence. Multiple
specimens were obtained.
Case 2: 2nd Follow up study, post op

Patient non-compliant with medications.
Case 2: 3rd Follow up study

Improved compliance.
Case 2: 4th Follow up study, further
improvement
IRIS (immune reconstitution
syndrome)
HIV pts initiated on retroviral therapy.
 Restored immune system now reacting/overreacting (?) to intact pathogens and/or
residual antigens.
 Paradoxical worsening of a known condition,
or appearance of a new condition following
initiation of therapy.

IRIS
Most commonly involved include CMV,
mycobacterium, varicella zoster, herpes,
PCP, & cryptococcus .
 Clinical presentation involves recurrence
of symptoms related to a latent TB
infection, or cryptococcal meningitis.

References:
www.aidsrestherapy.com/content/4/1/9
 http://en.wikipedia.org/wiki/Immune_rec
onstitution_inflammatory_syndrome

Case 3
Case 3
Case 3
Operation & pathology:
Right frontal sinus mass pedunculated off of
the posterior table of frontal sinus, which was
noted to be dehiscent. Most consistent with
an encephalocele.
 Fragments of central-nervous-system tissue,
consistent with encephalocele/heterotopia.

Case 4: History
3 year old girl with presented with left leg
weakness & limp x 3 weeks.
 Fell 3 weeks prior & had been limping ever
since.
 2 days prior to presentation she began not
using her left hand.

Arterial spin label cerebral
blood flow map.
Case 4: Pathology

Sections show a proliferation of neoplastic
astrocytes.
 Moderate nuclear atypia & mitotic figures. No
necrosis, histologic findings consistent with
anaplastic astrocytoma.
Neoplastic cells diffusely stained for GFAP.
 Many nuclei of neoplastic cells stained
positive for p53.
 A Ki-67 immunostain reveals a labeling
index of 12% in area sampled.

Case 5

74 year old male with diabetes & hypertension
presented with weakness/extreme fatigue,
weight loss & CN V & VI palsies.
CT
Findings

Enhancing soft tissue mass at left petrous
apex & left posterolateral wall of the left
cavernous sinus.
 Measures 1.8 cm x 1.2 cm.
 Extends along cavernous sinus, erodes through
sphenoid sinus wall.
 Extends along cisternal portion of V & into
brainstem.

Narrowing of adjacent left petrous internal
carotid artery.
Pathology

Acutely inflamed necrotic debris with
fungal hyphae and giant cells present.