Vascular hamartoma in the central nervous system of a foal

Borel, Nicole; Grest, Paula; Junge, H.; Eser, M. Wehrli

doi:10.1177/1040638714548681

Cited by 23 publications

(25 citation statements)

References 12 publications

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“…In contrast to congenital facial paralysis, which to our knowledge has not been reported in horses, acquired complete facial nerve paralysis in horses has been described with temporohyoid osteoarthropathy (Palus et al 2012;Koch and Witte 2014), otitis media or interna (Rand et al 2012), fractures of the temporal bone (Pownder et al 2010), encephalitis (Barton et al 2015), equine polyneuritis syndrome (Hahn 2006), diseases of the guttural pouch (Pollock 2007), developmental anomalies (Borel et al 2014) and neoplasia of the brain stem (Manso-Diaz et al 2015).…”

Section: Discussionmentioning

confidence: 88%

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Congenital unilateral facial nerve paralysis in a Warmblood filly

Schön

Eser

Kircher

et al. 2017

Equine Veterinary Education

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Summary A 17‐month‐old Warmblood filly was referred to our clinic for evaluation of congenital facial nerve (FN) paralysis. Clinical examination revealed a right‐sided facial paralysis with mild masticatory muscle atrophy, mild dysphagia and exposure keratitis. Apart from the FN deficits, neurological examination of the remaining cranial nerves showed no abnormalities. Magnetic resonance imaging (MRI) examination using a 3.0 Tesla scanner showed that in comparison to the left FN, the intracranial section of the right FN between the pons and internal acoustic canal was thinner, whereas it appeared indistinct and thickened within the internal acoustic canal and facial canal. Signs of meningitis or encephalitis were not present on MRI. Cerebrospinal fluid analysis showed mild pleocytosis. The owner of the filly requested euthanasia due to the guarded prognosis. At necropsy, the intracranial section of the right FN was macroscopically thinner than the left side and within the facial canal, a 5 mm tissue stump could be identified with an absent extracranial part of the right FN. Histological examination of the brain stem showed different architecture of the left and right motor nuclei of the FN: in the left nucleus, motor neurons of a normal size and well stainable Nissl bodies were present, whereas in the right nucleus, neurons with Nissl bodies were decreased in number and size. Further, a cytoplasmic rich cell population with a nucleus size compatible with normal neurons was present. These cells were suspected to be atrophic neurons. The tissue stump within the facial canal was histologically identified as connective tissue. Unilateral malformation of the FN has not previously been described in the horse. This filly showed a right‐sided, intracranial hypoplasia accompanied by an extracranial aplasia of the FN causing complete, congenital facial nerve paralysis, which corresponded to a difference in the architecture of the affected motor nucleus of the FN.

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Section: Discussionmentioning

confidence: 88%

“…), equine polyneuritis syndrome (Hahn ), diseases of the guttural pouch (Pollock ), developmental anomalies (Borel et al . ) and neoplasia of the brain stem (Manso‐Diaz et al . ).…”

Section: Discussionmentioning

confidence: 99%

Congenital unilateral facial nerve paralysis in a Warmblood filly

Schön

Eser

Kircher

et al. 2017

Equine Veterinary Education

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“…Although there are two reports of foals developing facial nerve dysfunction shortly after birth, Sch€ on et al (2019) in this issue is the first to document unilateral facial nerve paralysis in a foal as a developmental congenital anomaly in the veterinary literature. The postnatal nerve paralysis in the other two foals was associated with equine protozoal myeloencephalitis (Gray et al 2001) and vascular hamartoma (Borel et al 2014).…”

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confidence: 93%

Congenital facial nerve dysfunction

Russell

Aboellail

Nout‐Lomas

2017

Equine Veterinary Education

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“…VH may be differentiated of hemangioma in nervous system due to the presence of normal neuronal tissue between the vessels, which is the main feature to the diagnosis of VH [4] and is absent or rare in cases of hemangiomas [17]. Immunohistochemical assay allow the identification of lining cells of vascular structures and also normal neural and glial components between the vessels in VH [20].…”

Section: Introductionmentioning

confidence: 99%

Cerebral Vascular Hamartoma In a Campeiro Bulldog

Barros¹,

Gulgemin²,

Barreto³

et al. 2020

Acta Scientiae. Vet.

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Background: Vascular hamartomas (VH) are rare or simply underdiagnosed injuries in veterinary medicine and represent a non-neoplastic developmental anomaly disorganization and proliferation of endothelial tissue. VH occur in any region of the body, however in the brain present clinical relevance related with the potential for spontaneous bleeding, adjacent tissue compression and convulsive activity. The aim of these report is to describe clinical, pathological and immunohistochemical features of a case of cerebrovascular hamartoma and highlight the diagnosis of these rare brain disorder in dogs.Case: A 10-year-old male dog, a Campeiro Bulldog breed presented convulsions episodes and died before an elective surgical procedure for eyelid nodule removal. Three red nodules were observed in the brain, one between the parietal lobe and the left occipital lobe (in the medium suprasylviam sulcus), the other in the caudal region of the corpus callosum and the third one in the cerebellar cortex. Central nervous system, eyelids and most organs and tissues samples were collected, fixed in 10% formaldehyde and processed for histopathological analysis. Histologically, in the eyelid was detected a sebaceous adenoma. The nervous system samples revealed well-differentiated different sizes vascular structures with thin-walled and blood-filled, promoting compression of the brain. Normal neuropile was detected between the vascular structures substantiating cerebral vascular hamartoma diagnosis in the dog. Immunohistochemical assay was conducted with CD31 (monoclonal mouse antibody anti-CD31, Clone JC70A, Dako Corp.) and Von Willebrand factor (monoclonal mouse antibody anti-Von Willebrand factor, Clone F8/86, Dako Corp.) using the biotin–peroxidase–streptavidin method (PolyDetector Plus DAB–HRP, Bio SB) on CNS sections to confirm the vascular origin of the lining cells in the mass. Discussion: Hamartomas are rarely reported in domestic animals and mostly are of vascular origin. VH in nervous tissues can trigger clinical signs related to hemorrhage, brain space occupation, compression and obstructive secondary hydrocephalus. In general, cerebral VH have a slow progression and usually affected animals are asymptomatic. On the other hand, cerebral vascular hamartomas may also cause clinical signs in very young animals about 15 to 16 months old. In humans, clinical presentation of VH may be related with acquired lesions such as trauma, ionizing radiation, and other central nervous system injuries. In the present case, the dog presented convulsion episode only at 10 years old during pre-chirurgical procedures. The morphological features of the vascular hamartoma we observed in the Campeiro bulldog is classified as capillary teleangiectasia composed by well differentiated capillaries lined with well differentiated endothelial cells interspaced by normal neuronal tissue. Histopathological and immunohistochemical assay are extremely important to differentiate hamartoma from other tumors, since they may be macroscopically similar. The immunolabeling of endotelial cells by anti-CD31 and anti-Von Willebrand factor antibodies in the cerebral VH, highlight the vascular origin of the masses detected. However, it is also important to perform systematic gross examination of the brain in detail to detect even the smallest injuries in asymptomatic animals avoiding underdiagnoses of cerebral VH.

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Vascular hamartoma in the central nervous system of a foal

Cited by 23 publications

References 12 publications

Congenital unilateral facial nerve paralysis in a Warmblood filly

Congenital unilateral facial nerve paralysis in a Warmblood filly

Congenital facial nerve dysfunction

Cerebral Vascular Hamartoma In a Campeiro Bulldog

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