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CASE REPORTCerebral vascular hamartoma in a geriatric cat

Paula Martin-Vaquero DVM1*, Sarah A Moore DVM, Dipl ACVIM (Neurology)

1,Kendra E Wolk DVM

2, Michael J Oglesbee DVM, PhD, Dipl ACVP2

1Department of Veterinary ClinicalSciences, College of VeterinaryMedicine, Ohio State University,Columbus, OH, USA2Department of VeterinaryBiosciences, College of VeterinaryMedicine, Ohio State University,Columbus, OH, USA

An 11-year-old castrated male domestic medium hair cat was presented withneurological signs consistent with a right thalamocortical lesion. Computedtomography (CT) images revealed a heterogeneously, hyperattenuating, poorlycontrast enhancing intra-axial mass within the right lateral ventricle. Thehistological diagnosis at post-mortem examination was vascular hamartomawith hemorrhage and necrosis. This is the first report of a vascular hamartomaaffecting the thalamocortex in a geriatric cat. Also, this is the first time that CTimages of a feline cerebral vascular hamartoma have been reported.

Date accepted: 1 December 2010 � 2010 ISFM and AAFP. Published by Elsevier Ltd. All rights reserved.

An 11-year-old castrated male domestic me-dium hair cat was presented to the OhioState University Veterinary Medical Center

for evaluation of a 1-week history of lethargy, changesin sleep habits, and disorientation, and a 2-day historyof vision loss. The cat was current on vaccines andwas negative for feline leukemia and feline immuno-deficiency viruses.

On presentation, the cat showed dull mentation.Physical examination was unremarkable. Neurologi-cal examination revealed inappropriate mentationconsisting of disorientation, absent menace in theleft eye and decreased menace in the right eye, withbilateral normal pupillary light reflexes (PLRs). Theremainder of the cranial nerve examination was unre-markable. Postural reactions (lateral tactile placingand hopping) were mildly delayed in the right tho-racic and pelvic limbs. Spinal reflexes and cutaneoustrunci reflex were normal. Spinal palpation revealedmild discomfort at the level of the thoracolumbarjunction and diffusely throughout the lumbar spine.Based on the history and the neurological findings,a right thalamocortical lesion with possible extensionacross midline, or significantly increased intracranialpressure was suspected. Involvement of the opticchiasm was also considered as a possible explanationfor the bilateral visual deficits. Differential diagnosesincluded neoplasia (meningioma, glioma, ependy-moma, lymphoma) and inflammatory diseases, eitherinfectious (toxoplasmosis, cryptococcosis, feline

infectious peritonitis (FIP), non-FIP viruses, bacterial)or non-infectious (immune-mediated). Ophthalmolog-ical examination revealed a normal fundus and con-firmed the menace deficits and normal PLRsconsistent with central blindness.

A complete blood count showed mild neutrophilia(11�109/l, reference interval 3e9.2� 109/l) and mildmonocytosis (0.7� 109/l, reference interval0e0.5� 109/l) consistent with a mild inflammatory leu-kogram. A biochemical profile revealed mildly in-creased blood urea nitrogen (34 mg/dl, referenceinterval 13e30 mg/dl) and hypercalcemia (11.3 mg/dl,reference interval 8.4e10.1 mg/dl). Ionized calciumwas normal. A non-invasive Doppler blood pressurewas normal. Thoracic radiographs were unremarkable.

The cat was anesthetized for computed tomogra-phy (CT) (GE Lightspeed Ultra) of the brain and cere-brospinal fluid (CSF) collection. Anesthesia consistedof premedication with intravenous midazolam(0.2 mg/kg) and hydromorphone (0.05 mg/kg), in-duction with intravenous propofol (3 mg/kg) andmaintenance with inhalatory isofluorane using me-chanical ventilation. The CT study consisted of1.3 mm contiguous transverse acquisitions, pre- andpost-contrast administration (iohexol, Omnipaque240 mg/ml, dose: 2 ml/kg IV). A multilobulated,irregularly marginated, heterogeneously hyperattenu-ating mass was evident located within the right lateralventricle, extending into the left lateral ventricle(Fig 1A, B). Both lateral ventricles (right more thanleft) and the left olfactory bulb recess appeareddilated (Fig 1C). There was a marked midline shift*Corresponding author. E-mail: martin-vaquero.1@osu.edu

Journal of Feline Medicine and Surgery (2011) 13, 286e290doi:10.1016/j.jfms.2010.12.006

1098-612X/11/040286+05 $36.00/0 � 2010 ISFM and AAFP. Published by Elsevier Ltd. All rights reserved.

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with left-sided deviation of the falx cerebri (Fig 1C).The mass showed poor contrast enhancement after in-travenous contrast administration (Fig 1D, E). CSF col-lection was not attempted due to concerns aboutincreased intracranial pressure and risk for herniation.Differential diagnoses for the mass included neoplasiaand less likely granuloma (such as fungal granuloma).An intra-axial origin of the mass was considered morelikely, with choroid plexus tumor and ependymomastrongly considered due to the ventricular involvement

of themass; however, a glial cell neoplasmwith erosioninto the ventricle could not be excluded.Ameningiomaarising from arachnoid cells in the choroid plexus,though rare,was also considered. The cat recoveredun-eventfully from anesthesia. Surgical excision, radiationtherapy and palliative medical treatment options werediscussed with the owners, and palliative corticoste-roid therapy was elected. The cat was dischargedwith oral prednisolone (0.5 mg/kg PO q 12 h) and fa-motidine (0.5 mg/kg PO q 12 h). The cat improved

Fig 1. (A) Transverse pre-contrast image at the level of the thalamus showing a multilobulated, irregularly marginated, het-erogeneously hyperattenuating mass located in the mid aspect of the falx cerebri, extending into the cerebral hemispheres(right more than left) and lateral ventricles. Dilation of the ventral aspect of the lateral ventricles is also noted. (B) Transversepre-contrast image at the level of the midbrain, showing a more caudal section of the mass. (C) Dorsal reconstruction afteriohexol administration. Marked displacement of the falx cerebri and dilation of both lateral ventricles and the left olfactorybulb recess (white arrow) are noted. (D) Transverse post-contrast image, obtained at the same level as image (A). Note thepoor contrast enhancement of the mass. (E) Transverse post-contrast image, obtained at the same level as image (B). Note thepoor contrast enhancement of the mass.

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temporarily with corticosteroid therapy. Approxi-mately 8 weeks after diagnosis, the patient’s neurolog-ical signs worsened and he became anorectic, at whichtime the owners elected humane euthanasia. A com-pletepost-mortemexaminationwasperformed.Atnec-ropsy, there was a 6� 6� 4 mm, discrete, dark red,cavitated lesion which filled the rostral portion of theright lateral ventricle and extended across midlineinto the left lateral ventricle. Both lateral ventricleswere mildly dilated. No other gross abnormalitieswere noted. Microscopically, the lesion consisted ofa well-demarcated expansile mass composed of varia-bly sized blood filled spaces within the choroid plexusof the right lateral ventriclewhich extended into the leftlateral ventricle and adjacent cerebral parenchyma (Fig2A). These spaces were lined by flattened spindle cellsthat were morphologically similar but of two distinct

immunophenotypes (Fig 2B). The predominant popu-lation was immunohistochemically positive for FactorVIIIa (Von Willebrand factor), interpreted as endo-thelial cells (Fig 2C). The second population waspositive for smooth muscle actin (SMA), interpretedas pericytes (Fig 2D). The lining cells were eithersupported by a collagenous stroma (Masson’s Tri-chrome positive), or by closely spaced interveningastrocytes (fibrous astrocytosis, Glial fibrillary acidprotein (GFAP) positive) (Fig 2E). Multifocally, thetissue surrounding the blood filled spaces containedmany clusters of hemosiderin laden gitter cells anddeeply basophilic fragments of mineral, indicatingchronic hemorrhage and necrosis. A diagnosis of fo-cal vascular hamartoma with chronic hemorrhageand mild secondary obstructive hydrocephalus wasmade.

Fig 2. (A) The lesion is located within the choroid plexus, extending into the lateral ventricle (asterisk) and the adjacentcerebral parenchyma (hematoxylin and eosin, bar¼ 1 mm). (B) At higher magnification, it is clear that the lesion consistsof variably sized blood filled spaces lined by spindle cells, separated by eosinophilic matrix (hematoxylin and eosin).(C) These spindle cells are identified as endothelial cells via Von Willebrand factor immunohistochemistry. (D) The presenceof pericytes within the walls of the vascular spaces is variable as demonstrated via SMA immunohistochemistry. (E) Astro-cytic fibers are labeled dark brown via GFAP immunohistochemistry, highlighting the presence of intervening neural tissueexhibiting fibrous astrocytosis (BeE, bar¼ 100 mm).

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Cerebral vascular malformations are generally cate-gorized as hamartomas, which are non-neoplastic, de-velopmental anomalies of the vasculature.1e3 They arefurther classified into four categories: arteriovenousmalformations, venous malformations, cavernousmalformations, and capillary telangiectasias.1,3,4 Vari-ous vascular malformations of the central nervoussystem (CNS) have been described in domestic ani-mals,5e13 with the majority of these cases diagnosedearly in life.8,9,12,13 However, a delayed onset of signshas been reported in a few canine patients.7,10,11 In thiscase, the cat was 11 years old at the onset of signs. Thisis in contrast with the two previously published casesof CNS vascular hamartomas in cats, wherea 16-month-old and a 15-month-old cat developedneurological signs due to a cerebellar and a cervicalspinal cord vascular hamartoma, respectively. In hu-mans, clinical signs due to cerebral vascular malfor-mations have a peak incidence in the third decade oflife.14,15 In humans, late onset of signs has beenexplained by continued hemodynamic stress and con-sequent attenuation of the abnormal vessels whicheventually leads to hemorrhage.15,16 In addition, thereis strong evidence that some CNS vascular malforma-tions in people may be acquired, as a result of trauma,radiation, or other injury to the CNS.1

Basedon the locationof themass in this case, themaindifferential diagnoses were choroid plexus tumor, gli-oma (oligodendroglioma, astrocytoma), ependymoma,or a meningioma arising from the choroid plexus. Cho-roid plexus tumors can be hyperdense to isodense onpre-contrast CT images, but tend to enhance strongly af-ter iohexol administration,17 which was not a feature ofthis mass. Gliomas have variable density on CT andcan range from none to strong or ring enhancement.17

Ependymomas tend to also enhance strongly.Meningio-mas arising from the choroid plexus are rare, but havebeen reported in the cat.17 They, too, most often stronglyenhance after iohexol administration.17

The hyperdense appearance of intracranial masseson CT images may be attributed to hypercellularity,calcification, or hemorrhage in certain stages.18 CT ap-pearance of hemorrhage has been described exten-sively.19 The unique imaging characteristics of thismass were likely due to extensive hemorrhage andmineral deposition noted at necropsy.

The hamartoma reported here was structurally sim-ilar to the capillary telangiectasias described in people.This is based on two features: the composition of thevessel walls within the hamartoma and the presenceof intervening normal brain parenchyma between thehamartoma vessels.1,3,10,20 Capillary telangiectasiasare generally small, measuring less than 1 cm in diam-eter.1 Microscopically, they appear as a cluster of small,dilated, capillary-type vessels. The diameter of the ves-sels may be larger than expected for a normal capillary,but morphologically the vessel walls resemble those ofcapillaries, devoid of smooth muscle or elastic fi-bers.1,3,20 A key feature of capillary telangiectasias isthat the component vessels are separated from each

other by normal neural parenchyma, as noted in thecase reported here.1,3,20 Presence of factor VIII-specificstaining confirmed the endothelial nature of the ves-sel-lining cells. Also, some of these lining cells were ac-tin-positive. This feature has been previously reportedin canine CNS vascular hamartomas.10,11 These cellslikely represented pericytes, which are modifiedsmooth muscle cells that surround capillaries and ve-nules.10 Thepresence of pericytes aswell as interveningneural parenchyma within the mass suggest a malfor-mative pathogenesis rather than neoplastic, differenti-ating the diagnosis of vascular hamartoma from themorphologically similar diagnosis of cavernoushemangioma.3,10,12,20

In this case, the development of clinical signs is at-tributed to the presence of the hemorrhage observedwithin and surrounding the lesion as well as compres-sion of the surrounding cerebral parenchyma, and sec-ondary obstructive hydrocephalus.13

To the authors’ knowledge, this is the first report ofa cerebral vascular hamartoma in a cat and the firsttime that CT images of an intracranial hamartoma ina feline patient are reported. Also, it is the first timethat a cerebrovascular malformation is reported ina geriatric cat. Although this diagnosis is expected tobe rare, it is important to include vascular malforma-tions as possible differential diagnoses for intracranialmasses in cats, especially when the CT imaging fea-tures are consistent with a hemorrhagic mass.

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