Brain tumours cause dysfunction either by primary destruction of brain tissue or by compression of adjacent anatomical structures. Increased intracranial pressure is often seen; this is due primarily to oedema and less commonly to haemorrhage or infarction.

As a rule, primary brain tumours grow slowly and therefore have a chronic clinical progression; in many cases this is seen by the client as normal slowing down due to age. Clinical signs are usually only seen when the brain can no longer compensate for the presence of the tumour, and in these cases the onset of neurological signs can be acute and severe. The most common clinical sign seen in patients with intracranial neoplasia is seizures. Therefore, in any older patient presenting with seizures, a primary differential should be a brain tumour. As these tumours are usually advanced at the time of diagnosis, immediate diagnostic evaluation is essential.

Primary brain tumours are usually solitary, but multiple tumours have been reported. The lack of a well-developed lymphatic system within the brain means that major patterns of spread involve local invasion and cerebrospinal fluid (CSF) seeding (LeCouteur & Withrow 2007). Multiple tumours of different histological types may occur rarely. Extracranial metastasis of primary brain meningiomas has been reported, but is considered rare (Schulman et al 1992).

Secondary tumours of the brain are seen due to metasta-tic spread, e.g. mammary carcinomas, haemangiosarcomas (HSA), prostatic and pulmonary carcinomas (LeCouteur & Withrow 2007). Of these malignancies HSA is seen most frequently and usually when there is evidence of metastasis to brain other extracranial sites are also involved (Snyder et al 2008). CNS lymphoma can occur solely within the CNS or as a secondary tumour late in the course of multicentric lymphoma or simultaneously with the initial presentation of multicentric lymphoma.

Other secondary tumours affect the brain by means of direct local extension, e.g. nasal, frontal sinus, skull, cranial nerve sheath tumours (e.g. oculomotor, vestibulocochlear and trigeminal nerves) or pituitary tumours (see Chapter 26). Skull tumours that affect the brain by local extension include osteosarcoma, chondrosarcoma and multilobular osteochondrosarcoma (LeCouteur & Withrow 2007).

Gliomas and meningiomas are the most commonly recognized intracranial neoplasms of dogs, occurring with similar frequencies (Snyder et al 2006).

Glial cell neoplasms are classified based on the predominant cell type (e.g. astrocytoma, oligodendrocytoma). They are often found in the parenchyma of the brain, and can be very invasive.

Meningiomas arise from the arachnoid layer of the meninges; they are peripherally located and most commonly broad based and extra-axial (arise outside of and push into the brain parenchyma) (Bagley 2005a). Canine meningioma is benign, but locally infiltrates along the Virchow–Robin space and invariably lacks demarcation from normal brain tissue. In cats, meningiomas are almost always well defined and have a clear demarcation (LeCouteur & Withrow 2007). The growth rate of meningiomas in cats is slow compared to dogs.

Tumours of the ependyma and choroid plexus include choroid plexus papillomas, which occur relatively infrequently.

CNS lymphoma can be either primary or secondary. Histiocytic lymphoma or neoplastic reticulosis occurs as single or multiple mass lesions characterized histologically by a perivascular proliferation of ‘reticulohistiocytic cells’ with different patterns of reticulin production, admixed with varying populations of inflammatory cells (LeCouteur & Withrow 2007).

Embryonal tumours of the CNS/primitive neuroectodermal tumours are all derived from a germinal neuroepithelial cell that has the potential to differentiate along a number of neuroectodermal cell lines (neuronal, ependymal, glial). All have an anaplastic nature and are biologically malignant (LeCouteur & Withrow 2007).

Neuronal and mixed neuronal–glial neoplasms (gangliocytoma, ganglioglioma) occur in young animals.

Primary CNS lesions reported rarely include pineal tumours, germ cell tumours (germinoma, teratoma), primary CNS melanoma, chordoma, hamartoma, epidermoid and dermoid cysts and granular cell tumour (LeCouteur & Withrow 2007).

The most common presenting clinical sign for a patient with a primary brain tumour is seizures (Bagley et al 1999, Snyder et al 2006). Changes in mentation, pacing, circling, head pressing, etc. are also common presenting signs. Other clinical signs can be seen depending on the location of the tumour within the CNS and associated secondary effects of the tumour (oedema, compression of normal brain tissue and increasing intracranial pressure). For example, neoplasms of the cerebellomedullary angle affect the vestibular system, causing vestibular signs, often with brain stem signs (paresis or loss of conscious proprioception), changes in mental status, and deficits in the fifth or seventh cranial nerve. Vertical nystagmus in any head position is most consistent with central vestibular disease. In addition, the nystagmus may change with changing head position (LeCouteur 2003).

Primary brain tumours are typically slow growing. Gradual changes in the individual may have been noticed by the client but attributed to advancing age. This means that the patient has been able to cope for a period of weeks to months before the onset of clinical signs that can be rapidly progressive due to the large size of the majority of tumours at the time of diagnosis. In any patient where a brain tumour is suspected, early diagnostic evaluation is encouraged as early diagnosis will undoubtedly contribute to longer survival times for patients and increase the treatment options available for them. It is essential, therefore, that for any middle-aged to older patient, advanced imaging is recommended. It is to be remembered that the prevalence of epilepsy as a cause of seizures declines rapidly after 5 years of age (Bagley 2005b).

Tumours that grow rapidly or obstruct a major blood vessel may show more acute signs due to haemorrhage or infarction. Metastatic lesions in the brain often lead to acute, rapidly progressive neurological signs. Localized clinical signs are seen most frequently and result from compression, invasion or irritation of a region of the brain, whereas generalized non-localizing signs result from secondary effects, e.g. increasing intracranial pressure (ICP).

A full neurological examination is required, but in many patients this may be unremarkable. In one study (Snyder et al 2006), 20% of primary intracranial tumours identified were in the olfactory area, an area of the brain that is often associated with a normal neurological examination in spite of the presence of a space-occupying lesion. An ophthalmic examination may be helpful in some patients with increased ICP because papilloedema (optic nerve oedema) may be present. If papilloedema is present, the risk of herniation is increased if CSF collection is planned. It should be remembered that papilloedema could also be seen with inflammatory disease of the CNS.

As with any older patient a minimum database should be established. Haematology, serum biochemistry and urinalysis may assist diagnosis of a primary extracranial malignancy (e.g. pancreatic insulinoma). Thoracic radiographs and abdominal ultrasound are recommended to ensure there is no evidence of extracranial neoplasia or other underlying problems (Snyder et al 2006). Rarely do primary intracranial tumours metastasize, but in patients with multifocal clinical signs, metastatic disease from another tumour should be ruled out.

Imaging, either MRI or CT, is required for definitive diagnosis (Figure 24.1). MRI is superior to CT in the evaluation of intracranial neoplasia. In the majority of cases intracranial neoplasms are not amenable to biopsy and the diagnosis is usually presumptive based on the imaging characteristics of the tumour and location within the CNS. CSF analysis is a secondary non-specific test but changes in CSF have been associated with intracranial tumours, the most common change being inflammatory. A neutrophilic pleocytosis has been associated with meningiomas (Bailey & Higgins 1986) but was not found to be a typical finding in another study (Dickinson et al 2006). The greatest elevations in CSF total protein were associated with choroid plexus tumours (Bailey & Higgins 1986). In patients with lymphoma, neoplastic cells may be identified. The value of CSF analysis is to rule out inflammatory and infectious causes of cerebral dysfunction rather than diagnose a brain tumour. Nevertheless, CSF analysis may support the diagnosis of a tumour; however, if a tumour is suspected, sampling should be taken after the MRI/CT scan as increased intracranial pressure may lead to brain herniation.

Differential diagnoses include vascular disorders (vascular accidents), trauma, immunological (e.g. granulomatous meningoencephalitis, GME), infection (e.g. protozoal), toxicity, degeneration, congenital or idiopathic (epilepsy).

Extramedullary tumours are often slow growing, gradually resulting in spinal cord compression (weeks or months), but can show an acute onset of signs and are often painful. Intramedullary lesions tend to grow quickly, causing necrosis, ischaemia or haemorrhage, and corresponding rapid neurological dysfunction, without apparent pain.

Intradural–extramedullary tumours frequently have prolonged, intermittent signs. They are usually not painful until advanced and signs are often lateralized for PNST. Isolated plasmacytomas have also been identified.

Brachial or lumbar intumescence tumours may show lameness, root signature, muscle wasting and lower motor neuron (LMN) signs to the affected limb (see below).

This comprises physical examination (including a neurological examination to localize the affected segment of the spinal cord), haematology, biochemistry, thoracic radiographs for primary or metastatic neoplasia, radiographs of vertebral column (best under general anaesthesia), CSF tap, myelography or advanced imaging (CT/MRI), and very occasionally a biopsy of the lesion.

The immediate goal is to relieve the deleterious effects of sustained spinal cord compression. Hemilaminectomy is the treatment of choice and, depending on the histological diagnosis, radiotherapy and/or chemotherapy may be indicated.