What's your question? Send your pediatric/geriatric related questions to: Pediatric/Geriatric Protocol, DVM Newsmagazine , 7500 Old Oak Blvd., Cleveland, OH 44130. Your questions will be answered by Dr. Hoskins in upcoming columns.
Q How does one diagnose and manage forebrain disease in older cats?
A Dr. Joe N. Kornegay at the 2003 American College of Veterinary Internal Medicine Forum in Charlotte, N.C., gave a lecture on cerebral dysfunction in cats. Some relevant points in this lecture are provided below.
Brain neoplasia One of the most-common causes of progressive forebrain dysfunction in cats is intracranial neoplasia with meningiomas occurring far more frequently than any other tumor. Most tumors are located over the cerebral convexities. Others arise from the tela choroidea and are in the third ventricle. Caudal fossa involvement is unusual. Meningiomas involve multiple intracranial sites relatively commonly. Intracranial tumors other than meningiomas occur rarely in cats. Brain neoplasia has both primary and secondary effects. The primary effects are compression and infiltration of adjacent brain tissue by the tumor. Secondary effects include vasogenic brain edema, obstructive hydrocephalus and brain herniation. The brain usually herniates caudally through the tentorial notch, foramen magnum or both.
Most cats with meningiomas are 10 years or older, and males appear to be affected disproportionately. Clinical signs occurring secondary to intracranial neoplasia vary with the tumor's location. Signs of forebrain disease in effected cats usually occur insidiously and gradually progress. However, cats with either caudal transtentorial or foramen magnum brain herniation often deteriorate rapidly due to compression of the brain stem by the herniated tissue. Positional nystagmus is particularly common in cats with meningiomas that are caused by caudal transtentorial herniation. Cats with brain herniation also have severe upper motor neuron and long tract sensory deficits in all four limbs. Mydriasis due to oculomotor nerve compression (caudal transtentorial herniation) and apnea resulting from medulla oblongata compression (foramen magnum herniation) are other common signs seen in effected cats.
Intracranial neoplasms are diagnosed primarily based on characteristic changes seen with either survey or specialized radiographic techniques. There might be survey radiographic evidence of mineralization within the tumor or either lysis of hyperostosis in the overlying skull.
A modified occipital view, in which the radiographic beam is directed at the foramen magnum, is useful in identifying these radiographic changes. However, computed tomography (CT) or magnetic resonance imaging (MRI), if available, allow for more definitive identification of meningiomas and other intracranial neoplasms. While changes seen with CT are not specific for any particular lesion, certain generalizations can be made. Most meningiomas are superficial (extra-axial), have a broad point of attachment to the meninges, and uniformly enhance with an iodine contrast medium.
Gliomas usually can be distinguished from meningiomas because most of them originate within the brain (intra-axial). While some gliomas enhance uniformly with contrast medium, those in which there is necrosis or poor vascular perfusion at the center of the tumor can have only a peripheral rim of enhancement. A similar ring-pattern of enhancement often also occurs with metastatic tumors. Secondary effects of brain tumors, including vasogenic brain edema and obstructive hydrocephalus, also can be recognized with CT.
MRI provides even greater anatomic detail. Cerebrospinal fluid evaluation usually is unrewarding and actually can be contraindicated in some cats with intracranial neoplasia because of the potential increased risk of brain herniation subsequent to CSF removal.
However, focal inflammatory lesions can cause CT changes similar to those seen with intracranial neoplasia, so CSF evaluation should be done in cats with suspected encephalitis. The definitive diagnosis of intracranial neoplasia can be made only with biopsy.
Successful surgical resection of meningiomas located over the cerebral convexities has been reported. Clinical signs in these cats often improved within several days of surgery, if there was minimal operative brain trauma. Cats with seizures, however, might require continued anticonvulsants. Tumors other than meningiomas might not be amenable to surgery. Some noninvasive gliomas can be resected. In some cats with inoperable tumors, there could be temporary improvement associated with reduction of peritumoral edema subsequent to glucocorticoid therapy. The dosage required for clinical improvement varies. Cats with acutely progressive clinical signs and possible ongoing brain herniation should be given a higher dose (intravenous methylprednisolone at 30 mg/kg) than those with relatively static neurologic involvement (oral prednisone at 0.5 mg/kg every 48 hours and gradually increase until there is improvement). Although clinical signs in some effected cats remit for several months after glucocorticoid therapy, deterioration inevitably occurs. Some tumors also can be, at least partially, responsive to external beam radiation or chemotherapy.
Cerebral ischemic necrosis Cerebral infarction is uncommon in animals due to the relative rarity of atherosclerosis in most species. However, a syndrome of cerebral infarction occurs in cats. There is generally unilateral involvement with the cerebral cortex affected most commonly. The brain stem is affected in some cats, and multiple areas are involved in others. While the changes clearly occur because of ischemia, the nature of the responsible vascular lesion has not been defined in most cats. Cerebrocortical involvement generally occurs in the distribution area of the middle cerebral artery. While an association between this syndrome and cardiomyopathy would seem logical, changes of cardiomyopathy have not been described in effected cats. Multiple causative factors might be involved.
Adult cats of both sexes and several different breeds can be affected. Clinical signs of focal forebrain involvement, and in a small number of cats signs of brain-stem involvement, are seen. These signs do not progress unless there is brain herniation or further infarction or hemorrhage occurs. Most signs resolve completely during a period of several weeks. However, behavioral changes and seizures can persist.
Cerebral ischemic necrosis should be suspected in any cat with acute, nonprogressive forebrain disease. There might be evidence of infarction on CT or MRI, if available. On CSF evaluation, there usually is a mild increase in protein, without inflammation. Increased uptake of radionuclide might be noted in a scintigraphy study.
Methylprednisolone (30 mg/kg intravenously) should be given in severely affected cats to reduce brain edema. While anticoagulants might be helpful in some cases, there is no supportive data. Anticonvulsants are indicated in cats with seizures.
Seizures Seizures can occur in cats with forebrain disease in combination with other signs previously discussed, or they can occur alone. Seizures occur considerably less frequently in cats than in dogs. Most cats with recurrent seizures have structural brain disease. Phenobarbital at 5 mg/kg divided into twice-daily dosing is preferred for long-term seizure control.