Sagittal T2, Transverse T2 and T1 FLAIR, pre and post contrast transverse FSPGR, post contrast sagittal.
T2 FLAIR, T2*, DWI, ADC are currently not available.

Multifocal, asymmetric, rim-enhancing T1-W, T2-W and T1- and T2-FLAIR hypointense linear meandering tracks are present throughout the infra- and supratentorial brain parenchyma to include the left and right cerebellar hemispheres, dorsal mesencephalon, left myelencephalon and to a lesser degree/diencephalon, to include right thalamic brain parenchyma. Mild T2W and T2 FLAIR perilesional hyperintensity is seen along some of the linear tracks. Mild T2 FLAIR hyperintensity is noted adjacent to the ventral aspect of the right lateral ventricle and periventricular white matter. Multifocal T2* signal voids are seen along the described tracks to include a 4 mm x 2 mm, cigar-shaped void within the left cerebellar hemisphere and multiple punctate and meandering voids within the right mesencephalon.

A poorly defined, ovoid, 5 mm x 2 mm, focus of contrast enhancement is seen within the right epaxial musculature adjacent to the cranial aspect of C2. Hypointense, heterogeneity and asymmetric contrast enhancement of multiple small vessels along the surface of the cerebrum and within a small vertical branch of the right caudal cerebellar artery along the right surface of the cerebellum adjacent to the vermis, is noted. Multifocal (2-3, less than 1 mm – 2mm, linear areas of hyperintensity are noted on the diffusion weighted images within the left cerebellar hemisphere and right diencephalon. These corresponded to signal voids on ADC mapping.

Incidental finding: A small, less than 1mm, round to ovoid, contrast enhancing structure is seen within the left-dorsal aspect of the nasopharynx consistent with mucosal inflammation/irregularity or small polyp.

Differential diagnosis

Differential diagnosis included myelitis due to parasitic infection with migration throughout the neuropil. Consideration was given to Cuterebral sp. myiasis and aberrant nematode migrans such as Dirofilaria sp.,or less likely Gurlitia sp. (due to limited travel history) given the parasitic tracts seen throughout the brain parenchyma on MRI. Concurrent viral, bacterial or fungal encephalidites were considered less likely.

The clinical diagnosis was cerebral larval migrans. The patient was euthanized two weeks after imaging as the owner reported the patients’ condition progressed and worsened at home. Cerebrospinal fluid (CSF) obtained from the cerebellomedullary cistern following MRI demonstrated an eosinophillic and neutrophilic pleocytosis supportive of verminous myelopathy.(1)

Necropsy, performed 19 days following imaging on the day of euthanasia, demonstrated moderate hemorrhage surrounding the spinal cord at the dorsal atlanto-occipital junction. The brain had several areas of degeneration and hemorrhage within multiple parasitic migration tracts. The meninges were mildly dehydrated and blood filled. The right cerebral hemisphere was larger than the left and there was a minimal amount of cerebral edema. Cuterebral myiasis is caused by larval development and migration of bot flies of the Cuterebra and Trypoderma genera.

Central parasitic migrans of this species is often overlooked as a cause of central nervous system signs in felines.(1)  The cat is an atypical host of cuterebra, generally acquiring infections when outdoors hunting for rodents or lagomorphs.(1)  Cuterebra cases are seasonal in the northern United States and occur more commonly in the midsummer to early fall months.(1,2)  In warmer climates flies are multivoltine, so infections occur year round.(2)  Clinical signs can vary depending on the migration of the parasite in the host. Cuterebral myiasis commonly occurs in the skin and subcutis.(1)  Aberrant migrations within the trachea, pharynx and upper respiratory tract are reported, and migration can be extensive.(1)  Intracranial forms of cuterebral myiasis are frequently preceded by upper respiratory signs. Larvae enter the calvarium via the cribiform plate by way of the nasal passages, middle ear by way of the external ear canal or the cranial nerve foramina.(1) Reported clinical signs of central nervous system (brain) migration include, status epileptics, head tilt, unilateral or bilateral central blindness, head pressing, dementia and pacing.(1,2)  Often, clinical signs in acute cases rapidly progress and are generally fatal. Intracranial larvae may be found within the brain parenchyma or within the spinal cord at necropsy.(2,4)  Diagnosis depends heavily on history, clinical signs and MR imaging. CT findings are less specific as associated brain lesions demonstrate a mottled CT appearance consistent with encephalitis.(1)  Reported T1-W and T2-W MR findings are similar to the described lesions of the patient of the current report.(1,4,5)  However, we report herein the first description of the T2*, T1- and T2 FLAIR, and DWI/ADC mapping MR characteristics. Previously, the described T2-W hyperintensity surrounding the hypointense tracks was attributed to edema. T1- and T2-FLAIR hyperintensity negate the presence of pure edema and support the presence of large molecules or protein-bound fluid. The T2* signal voids seen in this case support the presence of acute blood degradation by-products (most likely intracellular deoxyhemoglobin) given the isointensity of the regions on T1-W images and hypointensity on T2-W images.

CSF analysis results may fail to disclose abnormalities may be supportive of a mild inflammatory process (with increased total protein, red blood cells and leukocytes, with a predominance of macrophages) or may reveal an eosinophilic pleocytosis with elevated protein fraction.(1,5,6)  Definitive diagnosis is often achieved at necropsy. Histopathologically, lesions are consistent with suppurative inflammation and multifocal meningoencephalitis with malacia, hemorrhage and parasitic tracks being seen throughout the brain or spinal cord parenchyma. (4)  Edema and mass effect are usually minimal.(4)  Lesions may also include hemorrhage, necrosis, astrogliosis and focal granulomatous encephalitis.(3)

The author’s would like to acknowledge Drs. Michaela Beasley and Gabriel Garcia for their involvement in the case.

References

1. James, Fiona. Poma, Roberto. Neurological manifestations of feline cuterebriasis. The Canadian Veterinary Journal. 2010 Feb;51(2):213-215.

2. The American Association of Veterinary Parasitologists. Cuterebra species. June 25, 2014. Retrieved 10/24/15 from: http://www.aavp.org/wiki/arthropods/insects/cuteribridae/cuterebraspecies/

3. Williams KJ, Summers BA, de Lahunta A. Cerebrospinal cuterebriasis in cats and its association with feline ischemic encephalopathy. Veterinary Pathology 1998 Sept;35(5):330-343.

4. Thomas WB. Nonneoplastic disorders of the brain. Clinical Techniques in Small Animal Practice. S 1999 Aug;14(3):125-147.

5. Tieber LM, Axlund TW, Simpson ST, Hathcock JT. 2006. Survival of a suspected case of central nervous system cuterebrosis in a dog: clinical and magnetic resonance imaging findings. Journal of the American Animal Hospital Association. 2006 May-June;42(3):238-242.

6. Glass EN, Cornetta AM, deLahunta A, Center SA, Kent M. Clinical and clinicopathologic features in 11 cats with Cuterebra Laraemyiasis of the central nervous system. Journal of Veterinary Internal Medicine. 1998 Sep-Oct;12(5):365-368.