Symposium on Clinical Veterinary Oncology
Diagnosis of Intracranial Neoplasms William J. Kay, D.V.M.* This section will discuss the clinical signs and diagnostic procedures by which the veterinarian can determine whether or not an animal has a neoplastic disease of the central nervous system. It is extremely important that each sign be approached carefully in an attempt to localize and classify the lesion and prognosticate as to whether the course of the disease will be unfavorable to the animal and its owner. Neurologic cases should be approached with the objective that the animal has a "treatable disease." However, intracranial tumors are generally "untreatable conditions," except for temporary palliative measures. Chemotherapy, immunotherapy, radiation therapy, and surgery have not been completely successful in the treatment of these cases except in very selective instances. Since therapy for these neoplasms is not promising, the clinician should be highly suspicious of the presence of such a neoplasm before making a definitive diagnosis. If the history and neurologic examination lead the veterinarian to conclude that a focal lesion in the nervous system is responsible for the presenting signs, then a neoplasm would be high on the list of differential diagnoses, and a guarded prognosis would be routine.
HISTORICAL ASSESSMENT Importance
The lack of truly definitive tests to localize and etiologically classify most intracranial lesions heightens the importance of a complete history. The purpose of the history is to narrow the scope of the neurologic investigation to a specific part of the nervous system, and each question in a good history-taking session should be designed to accomplish that goal. Since neoplastic disorders of the nervous system usually progress slowly, the veterinarian should pose those questions which would en*Chief of Staff and Staff Neurologist, The Animal Medical Center, New York, New York; Diplomate, American College of Veterinary Internal Medicine
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able him to determine the time period involved in the onset of clinical signs. If a gradual onset can be ascertained, it becomes more likely that a space-occupying lesion is responsible for the signs. Specific Questions
1. Is the animal affiicted with a disorder of the central nervous system? If so, is it a lesion or process within the brain, spinal cord, or peripheral nerves? 2. If a disorder of the brain, is it cerebral, cerebellar, or of the brain stem? (To answer this question, one should be acquainted with the signs associated with focal or localized lesions in each of the sections of the brain.) Once the section of the brain involved has been determined, the veterinarian should ascertain the rate of onset of signs. Neoplasia of the nervous system often, but not always, accounts for the longest histories with the most sequential signs. Multiple seizures, for example, are not considered sequential signs but constitute a single repetitive sign of neural excitation. More typically, the signs usually appear one by one as more nervous tissue becomes involved. A detailed discussion of the life style of the animal should follow. This should include details of how the animal is housed, how it behaves in its true environment, how the animal exercises and whether it is supervised, and what its regular eating and drinking habits are. 3. What are the animal's normal activities? Have these changed even slightly over the period in question? 4. What type of personality and behavior patterns does the pet have? 5. How does the animal respond to noise? What are its drinking habits? Does it exhibit any signs of autonomic dysfunction (e.g., urinating and defecating in the house)? What are its sleeping patterns? Does the animal respond to some humans and not to others? While the previous questions might be time-consuming, they are critical to the clinician's understanding of whether any responses noted during the examination should be deemed suspicious. Intracranial mass lesions affect the brain by causing either decreased function of a particular area of the brain or a release of these areas from their influence over other parts of the brain. Increased function exists only in states of pain, such as those caused by tumors of cranial nerves or the thalamic-receiving centers, and epilepsy.
THE NEUROLOGIC EXAMINATION The neurologic examination should be done with the objective of localizing the focal lesion(s) that could be responsible for the clinical
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signs. The examination should be taken in the broadest sense- that is, what is observed is a reflection of the nervous system's ability (or inability) to function. The animal should be in the most relaxed position possible in its condition. If ambulatory, the animal should be observed running, walking, jumping, sitting, standing, and performing on command. The problem of fright in a strange environment understandably makes these observations somewhat unreliable, and conclusions should therefore be made only in light of the complete examination. In many cases, the nervous system can be better assessed prior to actually handling the animal. A vicious or extremely nervous pet is difficult to handle, and the clinician should gather as much data as possible before actual manipulation. The animal should be examined rostral-to-caudal and evaluated first as to cerebral function and then for cerebellar and brain stem function. Abnormal responses should be noted and considered with respect to abnormalities in motor and visual systems previously recorded in the history, and abnormalities in clinical pathologic data. The combination of a progressive course with additional sequential signs (especially hemiparesis, contralateral visual loss, and a hemisensory defect with or without changes in mentation) support the presence of a contralateral mass lesion. Circling, wandering, and headpressing combined with focal deficits will also support the supposition of a mass.
CoMMON CLINICAL SIGNS OF INTRACRANIAL NEoPLASMS
Unilateral Intracranial Cerebral Neoplasms Epileptiform seizures Decreased mentation Behavioral changes Circling Hemiparesis (contralateral) Head pressing Hemianopsia/visual loss (contralateral) Hemisensory changes (decreased or increased awareness of noxious stimuli)
The size, location, extent of invasion, inflammation, edema, and herniation will influence the severity of these clinical signs. They may be slowly sequential in onset or, in some cases, may appear simultaneously in clusters. As in other organ systems, the growth of intracranial tumors will determine the extent of clinical signs. A rapidly progressive lesion will usually cause readily apparent clinical signs. The nervous system can compensate more easily in cases of slow-growing lesions, and signs would not be as noticeable.
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Bilateral Intracranial Cerebral Neoplasms Occasionally there will be bilateral neoplasia affecting the cerebrum, but usually the bilateral effect is the result of: (a) unilateral lesion with herniation and edema, (b) midline neoplasm, either ventral or dorsal, (c) a tumor which begins unilaterally and subsequently grows across the midline to the other side (such as some subfrontal neoplasms, or asymmetrical pituitary or third ventricle masses). Epileptiform seizures Tetraparesis or quadriparesis (symmetrical or asymmetrical) Dementia or decreased mentation Behavioral changes Decerebrate posture Circling Head pressing Loss of autonomic control Sensory changes (usually hemihypesthesia) Visual loss (symmetrical or asymmetrical) H yperacti vi ty
Midline Cerebral Neoplasms Tumors affecting the midline structures occur frequently in domestic animals. These mass lesions often do not have focal or lateralizing signs, and this may make their diagnosis difficult. Endocrinopathy (polydipsia, polyuria, polyphagia) Visual loss Hemiparesis or tetraparesis Decrease in responsiveness and/or mentation Behavioral and personality changes Circling Head pressing Loss of autonomic control Desire for affection Hyperactivity
Tumors arising from the midline, including chromophobe adenomas, gliomas, meningiomas, and tumors of the choroid plexus, affect the optic chiasm and optic nerves and result in severe visual loss. Since there are many vital neuroanatomical structures in this area, a subtle change in the size of the lesion can. result in an array of clinical signs.
DIAGNOSTIC TESTING
Diseases of a non-neurologic origin can be ruled out by using a strong data base. Objective tests that can lead to a more definitive diagnosis of an intracranial mass include: Cerebrospinal fluid collection and examination Skull radiography
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Electroencephalography Cerebral angiography Isotope brain scan
Collection and Examination of Cerebrospinal Fluid Examination of cerebrospinal fluid is the most consistently reliable diagnostic tool currently available for determination of the existence of a brain tumor. Included in this testing is the measurement of cerebrospinal fluid pressure, and analysis of color, cellularity, protein, pH, and glucose level. There are no levels of cerebrospinal fluid pressure which are pathognomonic for an intracranial mass lesion; conversely, cerebrospinal fluid pressure can be normal in cases of very large mass lesions. Protein. Elevated levels of cerebrospinal fluid protein, particularly when present with acellularity, are indicative of a mass lesion with or without a focal neurologic deficit. There is little information on truly significant levels of protein associated with mass lesions. Increased and varied cellularity is occasionally seen with a necrotic mass lesion and, with other focal signs, can be suggestive of an inflammatory process. Exfoliative Cytology. The determination of malignant cells by exfoliative cytology is the most objective diagnostic test, but it is rarely used. Enzymes and Isoenzymes. Elevated levels of creatinine phosphokinase in cerebrospinal fluid are indicative of neurologic diseases, including tumors. Radiology Skull radiography is a routine diagnostic procedure, but is generally unrewarding unless the lesion involves bone or sinus. Tumors of the skull and sinuses will often expand to invade and compress neural tissue, causing signs similar to intrinsic mass lesions. Electroencephalography The use of the electroencephalography has recently become more widespread in localizing intracranial neoplasms. It is useful only in determining an area of electrical inactivity and not in definitively classifying this area as one involving a mass lesion. In cases where there is an increase in intracranial pressure, a more diffuse pattern of electrical abnormality can exist. Cerebral Angiography The use of angiography to localize intracranial neoplasms has been limited. In the future, cerebral angiography may be useful in the localization of intracranial mass lesions. Radioisotope Brain Scan The technology for interpretation has been limited but warrants futher investigation. The cost of the instrumentation is prohibitive, but
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the advantages of this procedure far outweigh this one drawback. It is a noninvasive and safe procedure, and is objective, once certain criteria are established.
SECONDARY EFFECTS OF INTRACRANIAL NEOPLASIA Many of the clinical signs associated with intracerebral and extracerebral lesions are caused by the phenomena of brain edema and brain herniation. The clinician should carefully observe for signs of midbrain, pons, and cerebellar dysfunction, even in those animals whose signs are seemingly only cerebral.
BRAIN EDEMA
Brain edema occurs primarily in cerebral white matter and is the result of an alteration in blood-brain and blood-cerebrospinal fluid barriers. It is routinely present in frontal lobe mass lesions, but even small brain tumors can have significant edema. The onset of edema can occur so rapidly that the clinical signs of a diffuse neurologic process are sometimes seen. As in other organ systems, the rapidity with which a pathologic process occurs can result in more profound clinical signs than are present in a more slowly progressive disease.
BRAIN HERNIATION
The brain is a soft malleable organ located in a bony immovable vault. Thus, when a lesion(s) occupies space in the brain, the affected portion must necessarily move to another position within the vault. This mechanism of brain herniation occurs as a sequela to brain edema and results in one portion or side of the brain squeezing or compressing another portion or other side. The degree of herniation is usually directly proportional to the amount of edema and the size of the lesion. Cingulate Gyrus Herniation
In cingulate gyrus herniation, the side of the cerebrum under the influence of a mass lesion expands and then compresses the other side of the cerebrum under the hard falx cerebri which separates the two cerebral hemispheres. The falx is the meningeal tissue which extends in a dorsoventral manner. The cingulate gyrus on the side of the lesion expands and slides under the falx cerebri to push and compress the other side of the brain. This condition is quite common in lateralizing brain tumors, and
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the clinical signs often indicate a bilateral lesion; the compression of the uninvolved hemisphere causes clinical signs similar to those with the lesion. The amount of compression is quite important: the extent of dysfunction is directly proportional to the amount of compression, edema, and rapidity of onset.
Transtentorial Herniation In this process, the lesion expands, and the posterior portions of the cerebrum will move under the bony tentorium cerebelli to begin to compress the cerebellum and brain stem. What was originally a cerebral lesion now clinically involves also the cerebellum and brain stem. The maximum effect of transtentorial herniation results in either unilateral or bilateral midbrain compression. Coma, dilated pupils, and decerebrate posture rapidly ensue.
Herniation through the Foramen Magnum In cases of severe or large mass lesions with edema, the brain is actually squeezed through the foramen magnum. Lesions which originate in either the cerebrum, cerebellum, or brain stem can result in neural tissue being forced through the only large openings within the skull, the foramen magnum. The variety of signs that exists when the medulla and cerebellum are forced through the foramen magnum are determined by the rapidity of onset and the location of the lesion. Usually an animal with intracranial contents which have swelled to this extent is so neurologically debilitated that death is imminent. The cascading clinical signs of edema and herniation make it mandatory that therapy is rapidly instituted. If the herniation is not controlled, death follows in several hours because of brain stem compression. The signs of herniation, however, are not limited to brain tumors, and the clinician should not assume that all clinical signs of herniation are due to "untreatable lesions" and irreversible diseases.
TREATMENT OF INTRACRANIAL NEOPLASIA The current therapy for intracranial neoplasms has been, for the most part, palliative and noninvasive.
Medical Treatment The objectives of the medical treatment of intracranial neoplasms are the control of brain edema and herniation and the alleviation of seizures. The long-term management of intracranial lesions is, of course, dependent on their location, rapidity of growth, and tumor type. The use of steroids and anticonvulsants can often alleviate symptoms for extended periods of time.
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Surgical Treatment The neurosurgical management of brain tumors has been limited to the removal of meningiomas and bony lesions which compress the brain. Chemotherapy and immunotherapy are rarely used because of the difficulty in obtaining a tissue diagnosis. The difficulty in determining treatable lesions should not deter the clinician and neurosurgeon from attempting to localize surgically treatable lesions. The removal of some extracranial lesions has been quite successful, resulting in improved neural function.
LESIONS RESEMBLING INTRACRANIAL NEOPLASMS Certain inflammatory conditions, including bacterial viral and fungal diseases, mimic the clinical signs of intracranial lesions. Reticulosis, which falls somewhere between neoplasia and inflammation, is a commonly seen condition which exhibits many of the clinical and pathologic characteristics of brain tumors. Other fungal diseases, including cryptococcosis, can present with a mass lesion effect, and only discriminating diagnostic tests can rule out intracranial neoplasia.
SUGGESTED READING J. Greene, H.]., Blauch, B., Leipold, H. W., et al.: Neoplasia in the central nervous system of three canines. J .A.A.H.A., 9:369-373, 1973. 2. Kay, W. ].: Neuroophthalmology. In Home Study Course in Ophthalmology. Section 9. South Bend, Indiana, American Animal Hospital Association, 1974. 3. Kay, W. ].: Epilepsy. In Kirk, R. W. (ed.): Current Veterinary Therapy V. Philadelphia, W. B. Saunders Co., 1974. 4. Kay, w~ ]., Israel, E., and Prata, R. G.: Cerebrospinal fluid. VET. CuN. NoRTH AM., 4:419-435, 1974. 5. Palmer, A. C.: Tumours of the central nervous system. Proc. Roy. Soc. Med., 69:4951, 1976. 6. Miller, M. E., Christensen, G. C., and Evans, H. E.: Anatomy of the Dog. Philadelphia, W. B. Saunders Co., 1964. 7. Zaki, F. A., and Hurvitz, A. I.: Spontaneous neoplasms of the central nervous system in the cat.]. Small Anim. Pract., in press. The Animal Medical Center 510 East 62nd Street New York, New York 10021
Diagnosis of Intracranial Neoplasms William J. Kay, D.V.M.* This section will discuss the clinical signs and diagnostic procedures by which the veterinarian can determine whether or not an animal has a neoplastic disease of the central nervous system. It is extremely important that each sign be approached carefully in an attempt to localize and classify the lesion and prognosticate as to whether the course of the disease will be unfavorable to the animal and its owner. Neurologic cases should be approached with the objective that the animal has a "treatable disease." However, intracranial tumors are generally "untreatable conditions," except for temporary palliative measures. Chemotherapy, immunotherapy, radiation therapy, and surgery have not been completely successful in the treatment of these cases except in very selective instances. Since therapy for these neoplasms is not promising, the clinician should be highly suspicious of the presence of such a neoplasm before making a definitive diagnosis. If the history and neurologic examination lead the veterinarian to conclude that a focal lesion in the nervous system is responsible for the presenting signs, then a neoplasm would be high on the list of differential diagnoses, and a guarded prognosis would be routine.
HISTORICAL ASSESSMENT Importance
The lack of truly definitive tests to localize and etiologically classify most intracranial lesions heightens the importance of a complete history. The purpose of the history is to narrow the scope of the neurologic investigation to a specific part of the nervous system, and each question in a good history-taking session should be designed to accomplish that goal. Since neoplastic disorders of the nervous system usually progress slowly, the veterinarian should pose those questions which would en*Chief of Staff and Staff Neurologist, The Animal Medical Center, New York, New York; Diplomate, American College of Veterinary Internal Medicine
Veterinary Clinics of North America- Vol. 7, No. 1, February 1977
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WILLIAM
J.
KAY
able him to determine the time period involved in the onset of clinical signs. If a gradual onset can be ascertained, it becomes more likely that a space-occupying lesion is responsible for the signs. Specific Questions
1. Is the animal affiicted with a disorder of the central nervous system? If so, is it a lesion or process within the brain, spinal cord, or peripheral nerves? 2. If a disorder of the brain, is it cerebral, cerebellar, or of the brain stem? (To answer this question, one should be acquainted with the signs associated with focal or localized lesions in each of the sections of the brain.) Once the section of the brain involved has been determined, the veterinarian should ascertain the rate of onset of signs. Neoplasia of the nervous system often, but not always, accounts for the longest histories with the most sequential signs. Multiple seizures, for example, are not considered sequential signs but constitute a single repetitive sign of neural excitation. More typically, the signs usually appear one by one as more nervous tissue becomes involved. A detailed discussion of the life style of the animal should follow. This should include details of how the animal is housed, how it behaves in its true environment, how the animal exercises and whether it is supervised, and what its regular eating and drinking habits are. 3. What are the animal's normal activities? Have these changed even slightly over the period in question? 4. What type of personality and behavior patterns does the pet have? 5. How does the animal respond to noise? What are its drinking habits? Does it exhibit any signs of autonomic dysfunction (e.g., urinating and defecating in the house)? What are its sleeping patterns? Does the animal respond to some humans and not to others? While the previous questions might be time-consuming, they are critical to the clinician's understanding of whether any responses noted during the examination should be deemed suspicious. Intracranial mass lesions affect the brain by causing either decreased function of a particular area of the brain or a release of these areas from their influence over other parts of the brain. Increased function exists only in states of pain, such as those caused by tumors of cranial nerves or the thalamic-receiving centers, and epilepsy.
THE NEUROLOGIC EXAMINATION The neurologic examination should be done with the objective of localizing the focal lesion(s) that could be responsible for the clinical
INTRACRANIAL NEOPLASMS
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signs. The examination should be taken in the broadest sense- that is, what is observed is a reflection of the nervous system's ability (or inability) to function. The animal should be in the most relaxed position possible in its condition. If ambulatory, the animal should be observed running, walking, jumping, sitting, standing, and performing on command. The problem of fright in a strange environment understandably makes these observations somewhat unreliable, and conclusions should therefore be made only in light of the complete examination. In many cases, the nervous system can be better assessed prior to actually handling the animal. A vicious or extremely nervous pet is difficult to handle, and the clinician should gather as much data as possible before actual manipulation. The animal should be examined rostral-to-caudal and evaluated first as to cerebral function and then for cerebellar and brain stem function. Abnormal responses should be noted and considered with respect to abnormalities in motor and visual systems previously recorded in the history, and abnormalities in clinical pathologic data. The combination of a progressive course with additional sequential signs (especially hemiparesis, contralateral visual loss, and a hemisensory defect with or without changes in mentation) support the presence of a contralateral mass lesion. Circling, wandering, and headpressing combined with focal deficits will also support the supposition of a mass.
CoMMON CLINICAL SIGNS OF INTRACRANIAL NEoPLASMS
Unilateral Intracranial Cerebral Neoplasms Epileptiform seizures Decreased mentation Behavioral changes Circling Hemiparesis (contralateral) Head pressing Hemianopsia/visual loss (contralateral) Hemisensory changes (decreased or increased awareness of noxious stimuli)
The size, location, extent of invasion, inflammation, edema, and herniation will influence the severity of these clinical signs. They may be slowly sequential in onset or, in some cases, may appear simultaneously in clusters. As in other organ systems, the growth of intracranial tumors will determine the extent of clinical signs. A rapidly progressive lesion will usually cause readily apparent clinical signs. The nervous system can compensate more easily in cases of slow-growing lesions, and signs would not be as noticeable.
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Bilateral Intracranial Cerebral Neoplasms Occasionally there will be bilateral neoplasia affecting the cerebrum, but usually the bilateral effect is the result of: (a) unilateral lesion with herniation and edema, (b) midline neoplasm, either ventral or dorsal, (c) a tumor which begins unilaterally and subsequently grows across the midline to the other side (such as some subfrontal neoplasms, or asymmetrical pituitary or third ventricle masses). Epileptiform seizures Tetraparesis or quadriparesis (symmetrical or asymmetrical) Dementia or decreased mentation Behavioral changes Decerebrate posture Circling Head pressing Loss of autonomic control Sensory changes (usually hemihypesthesia) Visual loss (symmetrical or asymmetrical) H yperacti vi ty
Midline Cerebral Neoplasms Tumors affecting the midline structures occur frequently in domestic animals. These mass lesions often do not have focal or lateralizing signs, and this may make their diagnosis difficult. Endocrinopathy (polydipsia, polyuria, polyphagia) Visual loss Hemiparesis or tetraparesis Decrease in responsiveness and/or mentation Behavioral and personality changes Circling Head pressing Loss of autonomic control Desire for affection Hyperactivity
Tumors arising from the midline, including chromophobe adenomas, gliomas, meningiomas, and tumors of the choroid plexus, affect the optic chiasm and optic nerves and result in severe visual loss. Since there are many vital neuroanatomical structures in this area, a subtle change in the size of the lesion can. result in an array of clinical signs.
DIAGNOSTIC TESTING
Diseases of a non-neurologic origin can be ruled out by using a strong data base. Objective tests that can lead to a more definitive diagnosis of an intracranial mass include: Cerebrospinal fluid collection and examination Skull radiography
INTRACRANIAL NEOPLASMS
149
Electroencephalography Cerebral angiography Isotope brain scan
Collection and Examination of Cerebrospinal Fluid Examination of cerebrospinal fluid is the most consistently reliable diagnostic tool currently available for determination of the existence of a brain tumor. Included in this testing is the measurement of cerebrospinal fluid pressure, and analysis of color, cellularity, protein, pH, and glucose level. There are no levels of cerebrospinal fluid pressure which are pathognomonic for an intracranial mass lesion; conversely, cerebrospinal fluid pressure can be normal in cases of very large mass lesions. Protein. Elevated levels of cerebrospinal fluid protein, particularly when present with acellularity, are indicative of a mass lesion with or without a focal neurologic deficit. There is little information on truly significant levels of protein associated with mass lesions. Increased and varied cellularity is occasionally seen with a necrotic mass lesion and, with other focal signs, can be suggestive of an inflammatory process. Exfoliative Cytology. The determination of malignant cells by exfoliative cytology is the most objective diagnostic test, but it is rarely used. Enzymes and Isoenzymes. Elevated levels of creatinine phosphokinase in cerebrospinal fluid are indicative of neurologic diseases, including tumors. Radiology Skull radiography is a routine diagnostic procedure, but is generally unrewarding unless the lesion involves bone or sinus. Tumors of the skull and sinuses will often expand to invade and compress neural tissue, causing signs similar to intrinsic mass lesions. Electroencephalography The use of the electroencephalography has recently become more widespread in localizing intracranial neoplasms. It is useful only in determining an area of electrical inactivity and not in definitively classifying this area as one involving a mass lesion. In cases where there is an increase in intracranial pressure, a more diffuse pattern of electrical abnormality can exist. Cerebral Angiography The use of angiography to localize intracranial neoplasms has been limited. In the future, cerebral angiography may be useful in the localization of intracranial mass lesions. Radioisotope Brain Scan The technology for interpretation has been limited but warrants futher investigation. The cost of the instrumentation is prohibitive, but
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the advantages of this procedure far outweigh this one drawback. It is a noninvasive and safe procedure, and is objective, once certain criteria are established.
SECONDARY EFFECTS OF INTRACRANIAL NEOPLASIA Many of the clinical signs associated with intracerebral and extracerebral lesions are caused by the phenomena of brain edema and brain herniation. The clinician should carefully observe for signs of midbrain, pons, and cerebellar dysfunction, even in those animals whose signs are seemingly only cerebral.
BRAIN EDEMA
Brain edema occurs primarily in cerebral white matter and is the result of an alteration in blood-brain and blood-cerebrospinal fluid barriers. It is routinely present in frontal lobe mass lesions, but even small brain tumors can have significant edema. The onset of edema can occur so rapidly that the clinical signs of a diffuse neurologic process are sometimes seen. As in other organ systems, the rapidity with which a pathologic process occurs can result in more profound clinical signs than are present in a more slowly progressive disease.
BRAIN HERNIATION
The brain is a soft malleable organ located in a bony immovable vault. Thus, when a lesion(s) occupies space in the brain, the affected portion must necessarily move to another position within the vault. This mechanism of brain herniation occurs as a sequela to brain edema and results in one portion or side of the brain squeezing or compressing another portion or other side. The degree of herniation is usually directly proportional to the amount of edema and the size of the lesion. Cingulate Gyrus Herniation
In cingulate gyrus herniation, the side of the cerebrum under the influence of a mass lesion expands and then compresses the other side of the cerebrum under the hard falx cerebri which separates the two cerebral hemispheres. The falx is the meningeal tissue which extends in a dorsoventral manner. The cingulate gyrus on the side of the lesion expands and slides under the falx cerebri to push and compress the other side of the brain. This condition is quite common in lateralizing brain tumors, and
INTRACRANIAL NEOPLASMS
151
the clinical signs often indicate a bilateral lesion; the compression of the uninvolved hemisphere causes clinical signs similar to those with the lesion. The amount of compression is quite important: the extent of dysfunction is directly proportional to the amount of compression, edema, and rapidity of onset.
Transtentorial Herniation In this process, the lesion expands, and the posterior portions of the cerebrum will move under the bony tentorium cerebelli to begin to compress the cerebellum and brain stem. What was originally a cerebral lesion now clinically involves also the cerebellum and brain stem. The maximum effect of transtentorial herniation results in either unilateral or bilateral midbrain compression. Coma, dilated pupils, and decerebrate posture rapidly ensue.
Herniation through the Foramen Magnum In cases of severe or large mass lesions with edema, the brain is actually squeezed through the foramen magnum. Lesions which originate in either the cerebrum, cerebellum, or brain stem can result in neural tissue being forced through the only large openings within the skull, the foramen magnum. The variety of signs that exists when the medulla and cerebellum are forced through the foramen magnum are determined by the rapidity of onset and the location of the lesion. Usually an animal with intracranial contents which have swelled to this extent is so neurologically debilitated that death is imminent. The cascading clinical signs of edema and herniation make it mandatory that therapy is rapidly instituted. If the herniation is not controlled, death follows in several hours because of brain stem compression. The signs of herniation, however, are not limited to brain tumors, and the clinician should not assume that all clinical signs of herniation are due to "untreatable lesions" and irreversible diseases.
TREATMENT OF INTRACRANIAL NEOPLASIA The current therapy for intracranial neoplasms has been, for the most part, palliative and noninvasive.
Medical Treatment The objectives of the medical treatment of intracranial neoplasms are the control of brain edema and herniation and the alleviation of seizures. The long-term management of intracranial lesions is, of course, dependent on their location, rapidity of growth, and tumor type. The use of steroids and anticonvulsants can often alleviate symptoms for extended periods of time.
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Surgical Treatment The neurosurgical management of brain tumors has been limited to the removal of meningiomas and bony lesions which compress the brain. Chemotherapy and immunotherapy are rarely used because of the difficulty in obtaining a tissue diagnosis. The difficulty in determining treatable lesions should not deter the clinician and neurosurgeon from attempting to localize surgically treatable lesions. The removal of some extracranial lesions has been quite successful, resulting in improved neural function.
LESIONS RESEMBLING INTRACRANIAL NEOPLASMS Certain inflammatory conditions, including bacterial viral and fungal diseases, mimic the clinical signs of intracranial lesions. Reticulosis, which falls somewhere between neoplasia and inflammation, is a commonly seen condition which exhibits many of the clinical and pathologic characteristics of brain tumors. Other fungal diseases, including cryptococcosis, can present with a mass lesion effect, and only discriminating diagnostic tests can rule out intracranial neoplasia.
SUGGESTED READING J. Greene, H.]., Blauch, B., Leipold, H. W., et al.: Neoplasia in the central nervous system of three canines. J .A.A.H.A., 9:369-373, 1973. 2. Kay, W. ].: Neuroophthalmology. In Home Study Course in Ophthalmology. Section 9. South Bend, Indiana, American Animal Hospital Association, 1974. 3. Kay, W. ].: Epilepsy. In Kirk, R. W. (ed.): Current Veterinary Therapy V. Philadelphia, W. B. Saunders Co., 1974. 4. Kay, w~ ]., Israel, E., and Prata, R. G.: Cerebrospinal fluid. VET. CuN. NoRTH AM., 4:419-435, 1974. 5. Palmer, A. C.: Tumours of the central nervous system. Proc. Roy. Soc. Med., 69:4951, 1976. 6. Miller, M. E., Christensen, G. C., and Evans, H. E.: Anatomy of the Dog. Philadelphia, W. B. Saunders Co., 1964. 7. Zaki, F. A., and Hurvitz, A. I.: Spontaneous neoplasms of the central nervous system in the cat.]. Small Anim. Pract., in press. The Animal Medical Center 510 East 62nd Street New York, New York 10021
