Brain Tumours

Intracranial tumours are common in dogs and cats and may include meningiomas, gliomas or pituitary adenomas (see below). Meningioma is the most common intracranial neoplasm in dogs and cats. Astrocytomas and oligodendrogliomas represent one-third of histologically confirmed canine brain tumours. Choroid plexus tumors comprise approximately 10% of all primary brain tumours in dogs. The availability of advanced imaging techniques such as computed tomography (CT) and magnetic resonance imaging (MRI) has resulted in a growing number of dogs and cats diagnosed with intracranial neoplasia. The therapy arsenal for brain tumours is growing vast with the developmental advances in the veterinary field of neurology, anaesthesia, emergency and critical care, neurosurgery and radiotherapy, that allow dogs and cats to be treated with a favourable prognosis. In academia or specialised veterinary institutions the treatment options are: neurosurgery with total or subtotal resection of brain tumours; primary or adjuvant radiotherapy with linear accelerator, intralesional radiation therapy; or medical therapy with chemotherapeutic agents or hormonal agents. However, the big challenge for the veterinary surgeon remains the diagnosis of intracranial neoplasia at an early stage, when clinical signs may be aspecific. Prognosis will dramatically improve when brain tumours are caught in the early stage, improving the outcome of neurosurgery and radiation therapy.

The dog or cat with an intracranial tumour may present as: a patient with an additional mass within the bony calvarium creating a mass effect on surrounding unaffected brain tissue; a patient with an endocrine disorder due to an endocrine-active tumour (pituitary adenoma, see below); or both. The patient with an intracranial tumour is a diagnostic challenge since the mass effects can initially be absent or very subtle. Historical findings include subtle to overt altered behaviour (e.g., hiding, personality changes, lethargy, poor appetite, disorientation and aggressive behaviour); seizures; impaired vision; weakness (para-, hemi- or tetraparesis); altered consciousness (e.g., depressed, obtunded, stuporous or comatose). The severity of clinical signs depends on the tumour location, size, invasiveness and growth rate. For example, tumours close to the cerebellum will give ataxic gait whereas tumours close to the optic chiasm will impair vision. Behavioural changes (and not seizures) are the first and most common complaints in dogs and cats with brain tumours.

Abnormal clinical findings associated with brain neoplasia include weight loss despite normal appetite, hyporexia, anorexia, decreased thirst and/or bradycardia. Neurological abnormalities include seizures, circling, locomotor disturbances, visual deficits, hearing loss, altered states of consciousness and head pressing. Characteristic neurological signs of focal intracranial lesions affecting the forebrain (seizures), cerebral cortex (head pressing), thalamus (personality changes, visual deficits), hypothalamus (diabetes insipidus), brainstem (cranial nerve deficits), vestibular systems (nystagmus) and cerebellum (ataxia, intention tremor) may help neurolocalisation but precise pinpointing remains difficult.

Skull radiography is rarely a valuable diagnostic tool for intracranial neoplasia since calcifications and invasiveness into bone structures are rare. Exceptions are hyperostosis adjacent to the meningioma with invasion of the calvarium causing erosion or complete calvarial disruption, invasion of the calvarium and brain by local extension (e.g., with skull osteosarcomas, nasal adenocarcinomas and squamous cell carcinomas of the middle ear); calcification or mineralisation of the intracranial neoplasm (e.g., with meningioma). Cerebrospinal fluid (CSF) is rarely diagnostic for intracranial neoplasia. The most common CSF abnormality due to brain tumours is increased protein concentration; however, normal CSF does not preclude neoplasia.

When an intracranial mass is suspected the imaging tool of choice is MRI (Figure 1A). However, contrast-enhanced CT is also a valuable diagnostic tool, since brain tumours usually damage the blood-brain barrier resulting in enhancement of tumour tissue next to unaffected brain tissue. CT and/or MRI are also necessary because definitive therapy (surgery, chemotherapy, radiotherapy) requires knowledge of precise anatomical location and size of the brain tumour. In rare instances a brain biopsy under imaging guidance (e.g., free-hand, CT-guided, or frameless (Brainsight) stereotactic neuronavigation using MRI data) is indicated to determine the best treatment option. Patients with suspected metastatic intracranial neoplasia should have thoracic and abdominal CT to identify the primary tumour.

Figure 1. MRI scan of an Intracranial meningioma in an 8-year-old West Highland White Terrier with seizures, before (A) and 3 months after (B) rostrotentorial transparietal craniotomy.

Surgery of Brain Tumours

Craniotomy requires specific medical and anaesthetic management with respect to intracranial pressure and blood flow, antibiotics, anticonvulsants and diuretics. Arterial catheterisation is used to constantly monitor arterial blood pressure and end-tidal capnography is used for continuous monitoring of carbon dioxide. Periodic arterial blood sampling for carbon dioxide levels aids anaesthetic monitoring. Modest hyperventilation using a mechanical ventilator reduces arterial carbon dioxide, decreases cerebral blood flow and lowers intracranial pressure.

The term 'craniectomy' is used when the bone flap that is created during craniotomy is not replaced. The most common approaches to the calvarium are:

 Rostrotentorial transparietal or transtemporal craniotomy with or without osteotomy of the zygomatic arch

 Unilateral or bilateral transfrontal sinus craniotomy

 Caudotentorial craniotomy

 Suboccipital craniotomy

In the case of a meningioma the tumour usually arises from the dura itself and then the dura mater needs to be circumferentially excised together with the tumour. In gliomas the dura mater can be preserved and used for closure after tumour extraction. In the case of peripheral brain tumours, the tumour margins are carefully explored with neurosurgical probes. In the case of meningiomas there is usually a sharp border between tumour and normal brain parenchyma and the tumour may roll out of the calvarium. Debulking of gliomas is done based on abnormal colour (grey, glassy-like, dark) and consistency (necrotic, haemorrhagic, mucoid, cystic compartments) and available imaging during surgery. In limited craniotomies the bone flap is usually not replaced. When the dura mater cannot be sutured a fascia transplant (from the temporal muscle) can be sutured to the dura mater to close the calvarium. In the case of osteotomy of the zygomatic arch, the arch is restored with cerclage wire or monofilament sutures. After surgery of the neurocranium, patients should recover in a padded cage in an intensive care unit.

Surgical removal of a solitary meningioma (Figure 1B) results in excellent long-term survival, especially in cats. The results of craniotomy in 42 cats indicated a median survival of 26 months (range 3 days to 54 months) and overall survival was 71% at 6 months, 66% at 1 year, and 50% at 2 years. The higher incidence of atypical tumours may contribute to the poorer therapeutic response in dogs with meningiomas. There is a significant morbidity and mortality associated with the surgical removal of gliomas, and especially when located in the caudal fossa and brainstem. Partial removal of a brain neoplasm may relieve signs of cerebral dysfunction and, in turn, may render an animal a better candidate for other forms of therapy. Cytoreduction lessens the volume of tumour needing therapy using other treatment regimes, such as radiation therapy.

Pituitary Adenomas

Pituitary adenomas are considered benign tumours. The manifestations of pituitary adenomas in dogs and cats may be both endocrine and non-endocrine. The endocrine excess syndrome caused by corticotrophic (adrenocorticotropin (ACTH) cell) adenoma is called Cushing's disease (dog and cat) and that caused by the somatotrophic (growth hormone (GH) cell) adenoma is acromegaly (cat). In cats, ACTH and GH pituitary adenomas manifest themselves by diabetes mellitus that may delay the diagnosis. Clinically non-functioning adenomas occur in dogs and cats and comprise 9% of feline intracranial neoplasia and lead to neurological signs due to the tumour mass effect on the brain. Pituitary adenomas in dogs and cats can be approached by the oral route to the brain, i.e., trans-sphenoidal hypophysectomy (see: Pituitary Surgery in Dogs and Cats: Where Do We Stand Today? Extreme Surgery).

References

1.  Gordon LE, Thacher C, et al. Results of craniotomy for the treatment of cerebral meningioma in 42 cats. Veterinary Surgery 1994;23:94–100.

2.  Hanson JM, Teske E, et al. Prognostic factors for outcome after transsphenoidal hypophysectomy in dogs with pituitary-dependent hyperadrenocorticism. Journal of Neurosurgery 2007;107:830–840.

3.  Meij BP, Auriemma E, et al. Successful treatment of acromegaly in a diabetic cat with transsphenoidal hypophysectomy. Journal of Feline Medicine and Surgery 2010;12:406–410.

4.  Seim III HB. Surgery of the brain. In: Fossum TW, ed. Small Animal Surgery. 3rd ed. St. Louis: Mosby Elsevier, 2007:1379–1401.

5.  Sturges BK, Dickinson PJ, et al. Magnetic resonance imaging and histological classification of intracranial meningiomas in 112 dogs. Journal of Veterinary Internal Medicine 2008;22:586–595.