Neurocysticercosis

Findings

Figure 1: CT scan demonstrates a right-sided parietal lobe intraaxial cystic structure with a central “dot” representing a scolex.
Figure 2: CT scan reveals multiple cysts at the level of the brainstem and right temporal lobe. These cysts show wall enchancement on postcontrast imaging with surrounding edema. These findings, combined with the patient’s acute symptoms, are consistent with the diagnosis of cysts in the colloidal vesicular stage.
Figure 3, Figure 4, and Figure 5: T1 , FLAIR and T1 postcontrast images, respectively, show cysts with surrounding edema in the region of the brainstem that enhance with contrast.


Diagnosis: Neurocysticercosis


Neurocysticercosis is an intracranial parasitic infection caused by the pork tapeworm, Taenia solium. The parasite is endemic in parts of Mexico, Central and South America, Asia, Africa, and Eastern Europe. The parasite is acquired by ingestion of insufficiently cooked pork containing the encysted larvae or through fecal-oral route. The larva develops into adult tapeworms within the human intestinal tract. The oncospheres (active embryo) released from the ova of the adult tapeworm by gastric digestion burrow through the intestinal tract to the bloodstream.

The most common presenting symptom is seizure; however, the interval between the date of infection and symptoms varies from less than one year to 30 years. Symptoms do not present until larval death. Once the larva dies, there is an acute inflammatory response that may cause meningitis. Disease presentation varies depending on the location of the cysts. Cysts in the subarachnoid space can produce basal meningitis, hydrocephalus, and mass lesions. However, cysts in the suprasellar cistern, cerebellopontine angle, and sylvian cistern may cause cerebral arteritis with subsequent infarction of the middle cerebral or posterior cerebral distribution.

There are four stages of cyst formation that parallel the imaging findings:
1) Vesicular stage: The larvae are alive and the cyst contains clear fluid. There is minimal edema and the cyst has a thin capsule. The cyst is isointense to CSF on MR, and an eccentric scolex can be identified as a mural nodule.
2 & 3) Colloidal vesicular and granular nodular stage: The fluid within the cyst becomes turbid as the larvae dies and leaks into the surrounding tissue, causing a strong inflammatory response. Imaging studies show ring enhancement and capsular thickening. The cyst shrinks in the granular nodular stage to approximately 33% of its original size and shows nodular enhancement. Cysts are usually isodense or hyperintense to CSF on T1-weighted imaging and T2-weighted imaging or FLAIR.
4) Nodular calcified stage: During this stage, CT is more specific than MR. There will be low-density cysts with focal calcifications.

Completion of the four stages ranges from two to 10 years, with an average of five years. Serologic testing of serum or CSF for specific antibodies, or ELISA, aid in determining a diagnosis. Travel history is often essential in reaching a diagnosis.

Chiari I malformation

Findings

Figure 1 and Figure 2: Sagittal T1 and Sagittal T2 images showing tonsillar herniation, as well as the presence of syringomyelia at the level of the cervical cord.
Figure 3 and Figure 4: Axial imaging demonstrates the presence of a cervical syrinx on T1 and T2.


Diagnosis: Chiari I malformation


Chiari malformations are a spectrum of anomalies associated with a reduction of posterior cranial fossa volumes and CSF while conserving overall brain volume. Chiari I malformations refer to a greater than 5 mm herniation of the cerebellar tonsils down through the foramen magnum. The cerebellar vermis and ventricular system are typically unaffected, and the fourth ventricle is usually normal. In its pure form, the tonsils fall to the C1-C2 level, with the brain stem seen in normal position.

Hydromyelia (a dilatation of the central canal within the spinal cord) or syringomyelia (paracentral canal dilatation) is seen in 20% to 70% of Chiari I individuals. In symptomatic patients with herniation greater than 5 mm, syringomyelia has been seen in approximately 50% of the cases. Dilatation occurs, as there is backup of CSF and increased pressure within the affected canal. In addition, 20% of Chiari I patients have hydrocephalus.

Chiari I is also associated with numerous skeletal abnormalities. Unlike Chiari II malformations, Chiari I is not associated with myelomeningocele.

A genetic basis for Chiari I has been suggested by its association with achondroplasia, Hadju-Cheney syndrome (a very rare connective tissue and bone disorder affecting skull base, mandible, and fingers), and Klippel-Feil syndrome (C2-C3 fusion), along with reports of familial pattern of occurrence and concordance in monozygotic twins.

Patients typically present in the second or third decade of life with suboccipital headaches, retro-orbital pressure or pain, clumsiness, dizziness, vertigo, tinnitus, muscle weakness, and lower cranial nerve symptoms. Women are more frequently affected than men.

X-ray will show the associated skeletal anomalies, such as skull base invagination, scoliosis, kyphosis, cervical ribs, and many other skeletal anomalies. Axial images with CT may demonstrate an obliterated cisterna magna, tonsillar ectopia, and a normal fourth ventricle. CT may be useful in patients who have contraindications to MRI. MRI is the study of choice, as tonsillar position and configuration are easily identified along with other associated findings, such as syringomyelia. Most findings are best viewed in the sagittal plane.

Giant paraclinoid ICA aneurysm

Findings

Noncontrast CT: Peripheral calcifications. High density lumen (Figure 1) representing nonthombosed blood in the aneurysm lumen.
T1-weighted MRI (Figure 2), T2-weighted MRI (Figure 3): Hemorrhage of varying ages in aneurysm wall including T1 bright, T2 bright crescent-shaped hyperacute periluminal blood in wall (Figure 2 and Figure 3) representing methemoglobin. Pulsation artifact due to blood flow in patent lumen (Figure 2 and Figure 3).


Diagnosis: Giant paraclinoid ICA aneurysm


Giant cerebral aneurysms, defined as cerebral aneurysms greater than 2.5 cm in size, typically occur in the fifth to seventh decade with slight female preponderance. These aneurysms commonly present with symptoms related to subarachnoid hemorrhage – severe headache, nausea, vomiting, and loss of consciousness – or progressive neurologic dysfunction due to mass effect. Patients may also present with signs and symptoms caused by cerebral ischemia secondary to dislodged intramural thrombus.

Partially thrombosed giant aneurysms have a characteristic MRI appearance due to its dual component nature (thrombosed portion with layering clot, and patent portion with flowing blood). Typically, they appear as well-circumscribed mass lesions with mixed signal intensities and varying ages of clot in the thrombosed portion of the aneurysm. The patent portion will demonstrate evidence of flow including signal void, enhancement, and pulsation artifact.

Giant aneurysms are classified as saccular, fusiform, or serpentine giant types:
1) Saccular aneurysms are believed to arise from smaller saccular aneurysms. Proposed mechanisms include turbulent flow, which induces endothelial damage from turbulent flow that induces recurrent scarring, and mural thrombus formation. Another theory is that there are recurrent hemorrhages in the aneurysm wall, causing expansion.

2) Fusiform aneurysms develop from artherosclerotic degeneration of the arterial wall and involve longer segments of intracranial arteries.

3) Serpentine aneurysms are a type of fusiform aneurysm with irregular, tortuous lumen. Development is not well understood.

Treatment options are varied and are dependent on each individual case, including direct clipping of the neck (particularly for narrow-necked saccular aneurysms), surgical ligation, endovascular treatment, and surgical bypass