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Clinical Aspects of Cerebral Localization
CLINICAL ASPECTS OF CEREBRAL LOCALIZATION EDWIN
A.
WEINSTEIN,
M.D. *
IN our attempts to explain the function of the brain in terms of its structure, various motor, sensory and psychological phenomena have been localized in discrete areas. The evidence for this allocation has been gained from observations in disease in man, and experimental stimulations and ablations in animals. However, improved experimental technics, the development of procedures for reporting the electrical activity of nervous tissue, and the opportunity for study of ablations and stimulations in man have revised many of our concepts. Neurophysiologists no longer speak of a "center" for a particular function. Actually, no single part of the brain or individual pathway operates exclusively in the execution of any particular function. The brain acts as a whole" and in any motor or sensory phenomenon many portions of it are activated. When a finger is moved, in addition to the voluntary movement observed, there is also increased sweating and action of proprioceptors. When the same finger is pricked by a pin, impulses travel not only up the lateral spinothalamic tract to the thalamus and the cortex of the parietal lobe, but they also go to the so-called motor cortex, the hypothalamus, the cerebellum, and to other parts of the brain. Hughlings Jackson conceived of each portion of the brain as being both sensory and motor in function, and this belief is being substantiated by experimental evidence. It has been shown, for instance, that the precentral "motor" cortex receives a large afferent projection from the thalamus, as does, of course, the postcentral gyrus. Penfield has stimulated the precentral area in awake patients and produced sensory responses, and removal of the precentral cortex in man leaves a considerable sensory defiCit. A single part of the brain also has the property of both exciting and inhibiting neural activity. Thus stimulation of a given point on the "motor" cortex may either initiate a movement or stop one otherwise produced, depending upon the conditions of stimulation. In health, then, we cannot speak accurately of anyone part of the brain carrying out any isolated function. However, in clinical neurology it is possible in many instances to correlate syndromes with lesions in specific areas in the brain. In disease or injury a pattern of dysfunction appears, the recognition of which enables us to make a diagnosis of a focal pathological process. This method of localization From the Neurological Service of Dr. L S. Wechsler, Mount Sinai Hospital, New York. '" Associate Attending Neurologist, The Mount Sinai Hospital, New York City.
721
722
EDWIN A. WEINSTEIN
involves certain considerations. The pattern of dysfunction which is produced is not only dependent upon the area of the brain affected but also to a great extent on the rate of development of the causative pathological process. Thus in a slowly developing lesion there may be no neurological deficit for a long period of time because the brain has been able to compensate. The size of the lesion is also very important. When, in man, the area in the precentral cortex from which arm movements can be qbtained on stimulation is removed, the resulting paralysis is brief and leaves little residual defect. However, when both the "arm area" and "leg area" are removed, then the resulting paralysis in both the arm and the leg is much more severe and enduring. Thus, in a sense, the whole is greater than the sum of the parts. It is not infrequently found that lesions in certain areas will give no clinical symptoms. In the monkey, for instance, isolated destruction of the red nucleus or the caudate nucleus gives no observable motor deficit. This does not mean that these structures do not have important motor functions. It does mean that when these parts are destroyed, the brain is able to compensate to a great degree by utilization of other pathways. It is also important to remember that disease processes actually impair the function of more parts than can be seen on anatomical section. Thus, when one vessel is thrombosed, we may assume that other areas of the brain also have faulty nutrition. Also, by means of the surrounding edema and interference with blood supply, a tumor affects far more territory than it actually directly destroys. The presence of bilaterality of lesions is extremely important. A large amount of tissue destroyed in a cerebral hemisphere does not cause the severe changes that result when even a small amount of tissue is destroyed in both cerebral hemispheres. This is especially true with organic mental symptoms. The signs of motor dysfunction may, for convenience, be divided into disturbances of voluntary movement and release phenomena. The latter includes changes in tone, in reflexes, and the production of involuntary movements. All of these may appear in a hemiplegia. 1'he usual patteru of dysfunction in hemiplegia is one which involves mainly the distal musculature of the extremities, dealing with fine skilled movements. The upper extremity is involved more than the lower; there is increased tone, and exaggerated deep reflexes. This is the almost habitual pattern which appears in lesions from the cortex down to the brain stem. A noteworthy exception is the type of paralysis occurring in lesions involving the medial surface and most superior aspect of the hemisphere, such as occurs in parasagittal meningiomas or in occlusion of the anterior cerebral artery. Here the weakness appears predominantly in the lower limb and a foot drop may be produced. In experimental animals, particularly monkeys and chimpanzees, specific syndromes have been described after the removal of the precentral motor area, a small adjacent anteriorly situated region known
CLINICAL ASPECTS OF CEREBRAL LOCALIZATION
723
as 4-5 or the strip area, and the so-called premotor area, situated more anteriorly. Removal of precentral area 4 is said to produce only paralysis without increase in tone. Removal of the strip gives minimal paralysis lmt marked increase in tone and reflexes, while forced grasping may be produced when premotor area 6 is ablated. In man, however, such individual patterns are rarely if ever seen, perhaps because disease is not so neatly circumscribed. A hemiplegia resulting from an upper motor neuron lesion has increased tone and reflexes unless there is an accompanying sensory deficit. In a limb in which the proprioceptor pathways are interrupted, flaccidity may be present. In convulsive states produced by focal pathology the physiological differentiation of the various motor areas is useful. Jacksonian seizures produced by more anteriorly placed lesions are more likely to be of the adversive variety in which the head and eyes are turned to the opposite side, the trunk is rotated in that direction, and there are sustained movements of the contralateral limbs. More posteriorly, in the precentral area, the convulsive aura is more sharply focal, commonly involving clonic movements of the opposite thumb and index finger. In frontal lobe and thalamic lesions, signs more commonly associated with disease of the cerebellum may be seen. These include ataxia, dysdiadokokinesis, intention tremor and staggering gait. This is not surprising when it is considered that the frontal area not only sends a large contingent of fibers to the cerebellum but receives projections via the dentato-rubro-thalamic system. Another sign common to both cerebellar and cerebral lesions is the loss of ability to perform discrete movements of an individual finger without moving the others. However, in cerebellar disease the findings when unilateral are usually ipsilateral, while in frontal lobe disease they are contralateral. For the production of most of the involuntary movements seen in organic neurologic disease, multiple or diffuse lesions are necessary. The intention tremor of cerebellar disease can be produced by an isolated destruction of the ipsilateral superior cerebellar peduncle, but for the production of choreiform or athetoid movements, multiple lesions involving both the cortex and deeper structures are required. Thus the pathological lesions seen in parkinsonism, dystonia, the chore as and Wilson's disease are widespread. A possible exception is hemiballismus, a type of chorea causing wild, violent involuntary movements of large amplitude, occurring mainly in the upper extremity. This has been attributed to destruction of the opposite subthalamic body. A review of the cases in the literature, however, indicates that they occur mainly in older people with vascular disease and with evidence of previous lesions. Cases have also been reported in which the subthalamic body was intact. Neurophthalmological examination may yield information of value in localization. A discrete cortical lesion rarely yields abnormalities in oculomotor function, which is not surprising in view of the fact that
724
EDWIN A. WEINSTEIN
conjugate ocular movements may be obtained by stimulating many cortical areas. A large lesion producing a contralateral hemiparesis may also produce impairment of horizontal gaze to the opposite side. The pathways for horizontal eye movements travel in a' diffuse fashion from the cortex down to the vestibular nuclei whence they ascend in the medial longitudinal fasciculus to the third and sixth nerve nuclei. The descending pathway to the vestibular nuclei covers a wide area in the reticular formation of the brain stem and it requires a fairly large lesion in the pons to produce a paralysis of conjugate lateral gaze. However, a small lesion in the medial longitudinal fasciculus produces a characteristic syndrome. This structure is a paired one, straddling the midline, so that a lesion will usually affect both tracts. With bilateral involvement a paralysis is produced mainly in the adductor of each eye. Thus, when the patient looks to the left, the right eye comes only as far as the midline, while the left goes partially to the outer canthus, and there may be nystagmus of the left eye, a type of monocular nystagmus. The adductor paralysis seen in lesions of the medial longitudinal fasciculus is to be distinguished from the paralysis of adduction seen when the innervation of internal rectus muscle is impaired by involvement of the oculomotor nucleus or roots. There is a pattern of functional representation in the oculomotor nucleus which in a dorsoventral direction is as follows: (1) pupillary constriction, (2) downward rotation, (3) internal rotation, (4) upward rotation and (5) elevation of the lid. In intramedullary lesions, such as the hemorrhages that occur in the course of diabetes mellitus, partial involvement of third nerve functions is not uncommon. Thus, if the lesion involves the lower part of the oculomotor complex, there may be paralysis of lid elevation, upward movement and internal rotation, with sparing of other functions. In lesions affecting the oculomotor trunk, such dissociation is much less common. Disturbances of vertical conjugate eye movements are seen in lesions of the brain stem. A classical sign of a tumor in the region of the quadrigeminal plate, such as a pinealoma, is paralysis of upward gaze. With lesser degrees of paralysis, vertical nystagmus is seen and is usually an indication of brain stem compression. The presence of a Horner syndrome is of focal importance. It does not occur in unilateral lesions of the midbrain or pons because there the descending pathways for pupillary dilation destined for the cervical sympathetic are diffuse and bilateral. It is only in the medulla and cervical cord that they are sufficiently lateralized for a single lesion to produce an interruption of function. In the field of sensation, also, certain characteristic patterns of dysfunction are produced. In pathologic processes predominantly invading the cortex the sensory abnormalities) as elicited by ordinary testing, will involve mainly those modalities having to do with the relation in
CLINICAL ASPECTS OF CEREBRAL LOCALIZATION
72~
space of the limbs and the appreciation of the form of objects. Thus, in cortical lesions producing sensory loss, there is impairment in the appreciation of passive motion, of stereognosis, of two point discrimina. tion, and of the ability to localize accurately the point where a stimulus is applied. At the cortical level, the perception of touch, superficial and deep pain, temperature and vibration, as tested by ordinary clinical methods, show little or no impairment. In lesions affecting the neuraxis more caudally, there is relatively more involvement of the latter or primary modalities. In spinal cord lesions, for instance, vibratory sense may be markedly diminished or absent while position sense may be little affected. However, to this general formulation there are many exceptions. Astereognosis, disturbed position sense and loss of two point discrimination with sparing of other modalities has been observed in lesions in the foramen magnum involving the medulla and cervical cord. In these cases, unlike the finding in cortical lesions, spot localiza· tion is likely to be spared. Vascular occlusions in the brain stem, such as thrombosis of the posterior inferior cerebellar artery, may give a striking loss of pain and temperature sensation. Brain stem tumors, on the other hand, are notoriously likely to give no sensory signs referable to interruption of the spinothalamic tracts. While the phenomenon of spontaneous pain and unpleasant paresthesias is seen in vascular lesions of the thalamic region, it is rare in tumors of this area. It is not a rare occurrence for a tumor to destroy the thalamus or the spinothalamic tract without the appearance of sensory loss clinically. In fact, in certain tumors limited to the thalamus, mental symptoms may far outshadow sensory findings. These facts probably indicate that in disease other pathways may take over function in a new organization. It is also important to remember that the elicitation of sensory defects depends to a great degree on the method of examination which is used. Thus, in certain lesions, when each side of the body is stimulated individually, no deficit can be found. However, with simultaneous bilateral stimulation, the patient may not feel the stimulus on one side. The phenomenon is known as extinction. This method should be used before it is stated that a patient has no sensory or visual field abnormality. A great deal of attention has been paid to evaluation of abnormal mental phenomena in clinical localization. There are actually no mental ·symptoms that are specific for disease of any portion of the brain. We cannot state that, for instance, euphoria or loss of memory are signs of involvement of the frontal lobe. These disturbances do not occur as individual manifestations but as a part of a more general disturbance of personality. One cannot subdivide personality into emotion and intellect. We have mentioned the importance of bilaterality of involvement in the production of mental symptoms. The
726
EDWIN A. WEINSTEIN
rapidity of growth of the causative lesion is also a most significant determining factor. In a slowly progressing process, the early mental symptoms are likely to be irritability, anxiety, forgetfulness, diminution of interest, or difficulty in concentrating. In a quickly growing lesion in the same location, the initial picture may be of delirium, disorientation, confusion or stupor. Mental symptoms may also occur in focal intracranial disease, both above and below the tentorium. In the tumors studied at The Mount Sinai Hospital in the past twenty years, mental symptoms occurred about twice as frequently in supratentorial as in infratentorial growths. In tumors, intracranial hypertension was frequently associated with the presence of mental symptoms. This is not due to the increased pressure per se, but tumors producing elevated pressure are likely to be rapidly growing or close to a ventricle, an apparently favorable milieu for the development of mental changes. For instance, thalamic tumors extending alon~ the wall of the third ventricle have a very high incidence of mental symptoms. Euphoria and increased psychomotor activity may be seen not only in lesions of the frontal lobes but also in disease elsewhere in the hemisphere and often in lesions about the third ventricle. Diminished activity and somnolence may appear in lesions in the same areas. In fact, in the same patient one state may replace another. A manic type of behavior with memory loss, hallucinations and confabulation is not rare in lesions about the third ventricle. It may also be produced in tumors elsewhere, particularly those causing subarachnoidhemorrhage. This Korsakoff type of psychotic picture is hardly a focal sign as it occurs in toxic conditions, meningoencephalitis, spontaneous subarachnoid hemorrhage and other diffuse processes. Hallucinations, unassociated with other symptoms, do not help in localization. When a formed visual hallucination occurs in association with a defect in the visual field, then it points to a defect in the temporal lobe opposite the field defect. When complex hallucinations with peculiar smells or tastes are experienced, there is again strong evidence for a temporal lobe localization. In general, mental symptoms must be evaluated along with other neurological manifestations. The more diffuse and bilateral the pathological condition is, and the more rapidly it develops, the more likely one is to see disturbances in behavior.
A.
WEINSTEIN,
M.D. *
IN our attempts to explain the function of the brain in terms of its structure, various motor, sensory and psychological phenomena have been localized in discrete areas. The evidence for this allocation has been gained from observations in disease in man, and experimental stimulations and ablations in animals. However, improved experimental technics, the development of procedures for reporting the electrical activity of nervous tissue, and the opportunity for study of ablations and stimulations in man have revised many of our concepts. Neurophysiologists no longer speak of a "center" for a particular function. Actually, no single part of the brain or individual pathway operates exclusively in the execution of any particular function. The brain acts as a whole" and in any motor or sensory phenomenon many portions of it are activated. When a finger is moved, in addition to the voluntary movement observed, there is also increased sweating and action of proprioceptors. When the same finger is pricked by a pin, impulses travel not only up the lateral spinothalamic tract to the thalamus and the cortex of the parietal lobe, but they also go to the so-called motor cortex, the hypothalamus, the cerebellum, and to other parts of the brain. Hughlings Jackson conceived of each portion of the brain as being both sensory and motor in function, and this belief is being substantiated by experimental evidence. It has been shown, for instance, that the precentral "motor" cortex receives a large afferent projection from the thalamus, as does, of course, the postcentral gyrus. Penfield has stimulated the precentral area in awake patients and produced sensory responses, and removal of the precentral cortex in man leaves a considerable sensory defiCit. A single part of the brain also has the property of both exciting and inhibiting neural activity. Thus stimulation of a given point on the "motor" cortex may either initiate a movement or stop one otherwise produced, depending upon the conditions of stimulation. In health, then, we cannot speak accurately of anyone part of the brain carrying out any isolated function. However, in clinical neurology it is possible in many instances to correlate syndromes with lesions in specific areas in the brain. In disease or injury a pattern of dysfunction appears, the recognition of which enables us to make a diagnosis of a focal pathological process. This method of localization From the Neurological Service of Dr. L S. Wechsler, Mount Sinai Hospital, New York. '" Associate Attending Neurologist, The Mount Sinai Hospital, New York City.
721
722
EDWIN A. WEINSTEIN
involves certain considerations. The pattern of dysfunction which is produced is not only dependent upon the area of the brain affected but also to a great extent on the rate of development of the causative pathological process. Thus in a slowly developing lesion there may be no neurological deficit for a long period of time because the brain has been able to compensate. The size of the lesion is also very important. When, in man, the area in the precentral cortex from which arm movements can be qbtained on stimulation is removed, the resulting paralysis is brief and leaves little residual defect. However, when both the "arm area" and "leg area" are removed, then the resulting paralysis in both the arm and the leg is much more severe and enduring. Thus, in a sense, the whole is greater than the sum of the parts. It is not infrequently found that lesions in certain areas will give no clinical symptoms. In the monkey, for instance, isolated destruction of the red nucleus or the caudate nucleus gives no observable motor deficit. This does not mean that these structures do not have important motor functions. It does mean that when these parts are destroyed, the brain is able to compensate to a great degree by utilization of other pathways. It is also important to remember that disease processes actually impair the function of more parts than can be seen on anatomical section. Thus, when one vessel is thrombosed, we may assume that other areas of the brain also have faulty nutrition. Also, by means of the surrounding edema and interference with blood supply, a tumor affects far more territory than it actually directly destroys. The presence of bilaterality of lesions is extremely important. A large amount of tissue destroyed in a cerebral hemisphere does not cause the severe changes that result when even a small amount of tissue is destroyed in both cerebral hemispheres. This is especially true with organic mental symptoms. The signs of motor dysfunction may, for convenience, be divided into disturbances of voluntary movement and release phenomena. The latter includes changes in tone, in reflexes, and the production of involuntary movements. All of these may appear in a hemiplegia. 1'he usual patteru of dysfunction in hemiplegia is one which involves mainly the distal musculature of the extremities, dealing with fine skilled movements. The upper extremity is involved more than the lower; there is increased tone, and exaggerated deep reflexes. This is the almost habitual pattern which appears in lesions from the cortex down to the brain stem. A noteworthy exception is the type of paralysis occurring in lesions involving the medial surface and most superior aspect of the hemisphere, such as occurs in parasagittal meningiomas or in occlusion of the anterior cerebral artery. Here the weakness appears predominantly in the lower limb and a foot drop may be produced. In experimental animals, particularly monkeys and chimpanzees, specific syndromes have been described after the removal of the precentral motor area, a small adjacent anteriorly situated region known
CLINICAL ASPECTS OF CEREBRAL LOCALIZATION
723
as 4-5 or the strip area, and the so-called premotor area, situated more anteriorly. Removal of precentral area 4 is said to produce only paralysis without increase in tone. Removal of the strip gives minimal paralysis lmt marked increase in tone and reflexes, while forced grasping may be produced when premotor area 6 is ablated. In man, however, such individual patterns are rarely if ever seen, perhaps because disease is not so neatly circumscribed. A hemiplegia resulting from an upper motor neuron lesion has increased tone and reflexes unless there is an accompanying sensory deficit. In a limb in which the proprioceptor pathways are interrupted, flaccidity may be present. In convulsive states produced by focal pathology the physiological differentiation of the various motor areas is useful. Jacksonian seizures produced by more anteriorly placed lesions are more likely to be of the adversive variety in which the head and eyes are turned to the opposite side, the trunk is rotated in that direction, and there are sustained movements of the contralateral limbs. More posteriorly, in the precentral area, the convulsive aura is more sharply focal, commonly involving clonic movements of the opposite thumb and index finger. In frontal lobe and thalamic lesions, signs more commonly associated with disease of the cerebellum may be seen. These include ataxia, dysdiadokokinesis, intention tremor and staggering gait. This is not surprising when it is considered that the frontal area not only sends a large contingent of fibers to the cerebellum but receives projections via the dentato-rubro-thalamic system. Another sign common to both cerebellar and cerebral lesions is the loss of ability to perform discrete movements of an individual finger without moving the others. However, in cerebellar disease the findings when unilateral are usually ipsilateral, while in frontal lobe disease they are contralateral. For the production of most of the involuntary movements seen in organic neurologic disease, multiple or diffuse lesions are necessary. The intention tremor of cerebellar disease can be produced by an isolated destruction of the ipsilateral superior cerebellar peduncle, but for the production of choreiform or athetoid movements, multiple lesions involving both the cortex and deeper structures are required. Thus the pathological lesions seen in parkinsonism, dystonia, the chore as and Wilson's disease are widespread. A possible exception is hemiballismus, a type of chorea causing wild, violent involuntary movements of large amplitude, occurring mainly in the upper extremity. This has been attributed to destruction of the opposite subthalamic body. A review of the cases in the literature, however, indicates that they occur mainly in older people with vascular disease and with evidence of previous lesions. Cases have also been reported in which the subthalamic body was intact. Neurophthalmological examination may yield information of value in localization. A discrete cortical lesion rarely yields abnormalities in oculomotor function, which is not surprising in view of the fact that
724
EDWIN A. WEINSTEIN
conjugate ocular movements may be obtained by stimulating many cortical areas. A large lesion producing a contralateral hemiparesis may also produce impairment of horizontal gaze to the opposite side. The pathways for horizontal eye movements travel in a' diffuse fashion from the cortex down to the vestibular nuclei whence they ascend in the medial longitudinal fasciculus to the third and sixth nerve nuclei. The descending pathway to the vestibular nuclei covers a wide area in the reticular formation of the brain stem and it requires a fairly large lesion in the pons to produce a paralysis of conjugate lateral gaze. However, a small lesion in the medial longitudinal fasciculus produces a characteristic syndrome. This structure is a paired one, straddling the midline, so that a lesion will usually affect both tracts. With bilateral involvement a paralysis is produced mainly in the adductor of each eye. Thus, when the patient looks to the left, the right eye comes only as far as the midline, while the left goes partially to the outer canthus, and there may be nystagmus of the left eye, a type of monocular nystagmus. The adductor paralysis seen in lesions of the medial longitudinal fasciculus is to be distinguished from the paralysis of adduction seen when the innervation of internal rectus muscle is impaired by involvement of the oculomotor nucleus or roots. There is a pattern of functional representation in the oculomotor nucleus which in a dorsoventral direction is as follows: (1) pupillary constriction, (2) downward rotation, (3) internal rotation, (4) upward rotation and (5) elevation of the lid. In intramedullary lesions, such as the hemorrhages that occur in the course of diabetes mellitus, partial involvement of third nerve functions is not uncommon. Thus, if the lesion involves the lower part of the oculomotor complex, there may be paralysis of lid elevation, upward movement and internal rotation, with sparing of other functions. In lesions affecting the oculomotor trunk, such dissociation is much less common. Disturbances of vertical conjugate eye movements are seen in lesions of the brain stem. A classical sign of a tumor in the region of the quadrigeminal plate, such as a pinealoma, is paralysis of upward gaze. With lesser degrees of paralysis, vertical nystagmus is seen and is usually an indication of brain stem compression. The presence of a Horner syndrome is of focal importance. It does not occur in unilateral lesions of the midbrain or pons because there the descending pathways for pupillary dilation destined for the cervical sympathetic are diffuse and bilateral. It is only in the medulla and cervical cord that they are sufficiently lateralized for a single lesion to produce an interruption of function. In the field of sensation, also, certain characteristic patterns of dysfunction are produced. In pathologic processes predominantly invading the cortex the sensory abnormalities) as elicited by ordinary testing, will involve mainly those modalities having to do with the relation in
CLINICAL ASPECTS OF CEREBRAL LOCALIZATION
72~
space of the limbs and the appreciation of the form of objects. Thus, in cortical lesions producing sensory loss, there is impairment in the appreciation of passive motion, of stereognosis, of two point discrimina. tion, and of the ability to localize accurately the point where a stimulus is applied. At the cortical level, the perception of touch, superficial and deep pain, temperature and vibration, as tested by ordinary clinical methods, show little or no impairment. In lesions affecting the neuraxis more caudally, there is relatively more involvement of the latter or primary modalities. In spinal cord lesions, for instance, vibratory sense may be markedly diminished or absent while position sense may be little affected. However, to this general formulation there are many exceptions. Astereognosis, disturbed position sense and loss of two point discrimination with sparing of other modalities has been observed in lesions in the foramen magnum involving the medulla and cervical cord. In these cases, unlike the finding in cortical lesions, spot localiza· tion is likely to be spared. Vascular occlusions in the brain stem, such as thrombosis of the posterior inferior cerebellar artery, may give a striking loss of pain and temperature sensation. Brain stem tumors, on the other hand, are notoriously likely to give no sensory signs referable to interruption of the spinothalamic tracts. While the phenomenon of spontaneous pain and unpleasant paresthesias is seen in vascular lesions of the thalamic region, it is rare in tumors of this area. It is not a rare occurrence for a tumor to destroy the thalamus or the spinothalamic tract without the appearance of sensory loss clinically. In fact, in certain tumors limited to the thalamus, mental symptoms may far outshadow sensory findings. These facts probably indicate that in disease other pathways may take over function in a new organization. It is also important to remember that the elicitation of sensory defects depends to a great degree on the method of examination which is used. Thus, in certain lesions, when each side of the body is stimulated individually, no deficit can be found. However, with simultaneous bilateral stimulation, the patient may not feel the stimulus on one side. The phenomenon is known as extinction. This method should be used before it is stated that a patient has no sensory or visual field abnormality. A great deal of attention has been paid to evaluation of abnormal mental phenomena in clinical localization. There are actually no mental ·symptoms that are specific for disease of any portion of the brain. We cannot state that, for instance, euphoria or loss of memory are signs of involvement of the frontal lobe. These disturbances do not occur as individual manifestations but as a part of a more general disturbance of personality. One cannot subdivide personality into emotion and intellect. We have mentioned the importance of bilaterality of involvement in the production of mental symptoms. The
726
EDWIN A. WEINSTEIN
rapidity of growth of the causative lesion is also a most significant determining factor. In a slowly progressing process, the early mental symptoms are likely to be irritability, anxiety, forgetfulness, diminution of interest, or difficulty in concentrating. In a quickly growing lesion in the same location, the initial picture may be of delirium, disorientation, confusion or stupor. Mental symptoms may also occur in focal intracranial disease, both above and below the tentorium. In the tumors studied at The Mount Sinai Hospital in the past twenty years, mental symptoms occurred about twice as frequently in supratentorial as in infratentorial growths. In tumors, intracranial hypertension was frequently associated with the presence of mental symptoms. This is not due to the increased pressure per se, but tumors producing elevated pressure are likely to be rapidly growing or close to a ventricle, an apparently favorable milieu for the development of mental changes. For instance, thalamic tumors extending alon~ the wall of the third ventricle have a very high incidence of mental symptoms. Euphoria and increased psychomotor activity may be seen not only in lesions of the frontal lobes but also in disease elsewhere in the hemisphere and often in lesions about the third ventricle. Diminished activity and somnolence may appear in lesions in the same areas. In fact, in the same patient one state may replace another. A manic type of behavior with memory loss, hallucinations and confabulation is not rare in lesions about the third ventricle. It may also be produced in tumors elsewhere, particularly those causing subarachnoidhemorrhage. This Korsakoff type of psychotic picture is hardly a focal sign as it occurs in toxic conditions, meningoencephalitis, spontaneous subarachnoid hemorrhage and other diffuse processes. Hallucinations, unassociated with other symptoms, do not help in localization. When a formed visual hallucination occurs in association with a defect in the visual field, then it points to a defect in the temporal lobe opposite the field defect. When complex hallucinations with peculiar smells or tastes are experienced, there is again strong evidence for a temporal lobe localization. In general, mental symptoms must be evaluated along with other neurological manifestations. The more diffuse and bilateral the pathological condition is, and the more rapidly it develops, the more likely one is to see disturbances in behavior.