Meningioma in a 9-year-old chocolate Lab: Neurology perspective

Dr. Courtney SampsonCanine meningiomas tend to be slow growing, so a chronic and progressive course of neurologic signs is common.1,2 Most canine meningiomas are located over the cerebral convexities and below the brain stem.3 Neurologic signs depend on location and size of the mass. Seizures are the most common presenting clinical sign with forebrain meningiomas.4,5 Therefore, intracranial neoplasia should not be excluded based on a normal neurologic examination in older patients with new-onset seizures or behavior change.1 Other neurologic deficits associated with a unilateral forebrain mass may include behavior or mentation changes, central blindness, and contralateral menace, facial sensation, nasal response, and proprioceptive deficits. Clinical signs associated with brainstem meningiomas are associated with lesion location and may include cranial nerve deficits, hemiparesis or tetraparesis, and mild to profound mentation change. If primary therapy is not implemented, survival time is usually short.1

Palliative treatment for brain tumors is aimed at decreasing the severity of clinical signs. Depending on neurologic signs, corticosteroids, anticonvulsants or both may be implemented. Glucocorticoids are often used and are administered at anti-inflammatory doses with the aim of decreasing secondary effects of the tumor, which may include increased intracranial pressure, obstructive hydrocephalus, and vasogenic edema.6 In patients with seizure activity, anticonvulsant medication is indicated. The choice of antiepileptic drug should be based on the patient's neurologic status, owner limitations, and the presence of comorbidities. Phenobarbital and potassium bromide are commonly used, both of which may cause profound sedation; therefore, less-sedating anticonvulsant medications such as levetiracetam may be preferred. Patients with structural brain disease, as in meningiomas, are more likely to have difficult to control or refractory seizures.5 In addition, at-home treatment in the event of emergency events such as status epilepticus, cluster seizures, or multiple seizures without return to consciousness between events should be considered (i.e. rectal diazepam). Information regarding survival times of dogs with meningiomas treated with palliative care alone is limited, with median survival times reported from 2.5 months1 to 3.9 months.7

Cerebrospinal fluid analysis is commonly used in the routine intracranial neurologic work-up, but it is generally considered of limited value in primary brain tumors.8 In the case of a mass lesion, as with a suspected meningioma, the presence of increased intracranial pressure is considered a relative contraindication for cerebrospinal fluid collection because of the increased risk of herniation (typically cerebellar vermis herniation through the foramen magnum) and subsequent death.9 To my knowledge, meningioma has not been definitively diagnosed based on cerebrospinal fluid analysis alone. The main indication for performing a cerebrospinal tap is to attempt to rule out other causes of mass lesions that may have similar imaging characteristics such as other solitary meningeal-based masses (e.g. lymphoma or histiocytic sarcoma) or fungal granulomas.

In contrast to feline meningiomas, canine meningiomas are rarely well-encapsulated and have a tendency to infiltrate into surrounding tissue, making complete surgical resection difficult.5,9 With this in mind, the advantages of surgery include a definitive diagnosis, resolution of mass effect, and a longer median survival time as compared with treatment with palliative therapy alone.4,10 The ideal surgical candidate is neurologically stable, has a solitary and noninvasive-appearing mass on advanced imaging, and has a superficially located mass.5,8 For canine meningiomas, the median survival time with conventional surgery alone is seven months.4 The combination of surgery and radiation therapy has been shown to significantly increase median survival time in canine patients with intracranial meningiomas.4

References

1. Foster ES, Carrillo JM, Patnaik AK. Clinical signs of tumors affecting the rostral cerebrum in 43 dogs. J Vet Intern Med 1988;2:71-74.

2. Heidner GL, Kornegay JN, Page RL, et al. Analysis of survival in a retrospective study of 86 dogs with brain tumors. J Vet Intern Med 1991;5219-226.

3. Adamo PF, Forrest LJ, Dubielzig R. Canine and feline meningiomas: diagnosis, treatment, and prognosis. Compend Contin Educ Pract Vet 2004;26:951-965.

4. Axlund TW, McGlasson ML, Smith AN. Surgery alone or in combination with radiation therapy for treatment of intracranial meningiomas in dogs: 31 cases (1989-2002). J Am Vet Med Assoc 2002;221:1597-1600.

5. Bagley RS, Gavin PR. Seizures as a complication of brain tumors in dogs. Clin Tech Sm Anim Pract 1998;13:179-184.

6. Platt SR, Abramson CJ, Garosi LS. Administering corticosteroids in neurologic diseases. Compend Contin Educ Pract Vet 2005;27:210-221.

7. Platt S, Garosi L, Adams V, et al. Canine intracranial meningiomas outcome following corticosteroids, hypofractionated radiotherapy or multimodality therapy, 60 cases, in Proceedings. Euro Soc Vet Neurol Symp, 2003.

8. Lorenz MD, Coates JR, Kent M. Stupor or coma. In: Handbook of Veterinary Neurology. 5th ed. St. Louis: Elsevier, 2011.

9. Dewey CW. Encephalopathies: disorders of the brain. In: A practical guide to canine and feline neurology. 2nd ed. Ames, Iowa: Wiley-Blackwell, 2008.

10. Sessums K, Mariani C. Intracranial meningioma in dogs and cats: a comparative review. Compend Contin Educ Pract Vet 2009;31:330-339.