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Behavior and Treatment of Strokes in Later Life
Behavior and Treatment of Strokes in Later Life LEWIS J. POLLOCK, M.D. *
ALTHOUGH one may speak of the ordinary diseases of childhood, there are no ordinary diseases of later life. There are some diseases which develop slowly and progressively, and one of these is arteriosclerosis. It most frequently begins later in life, therefore one may anticipate the occurrences of strokes in larger numbers in the elderly than would be encountered in early life. This does not mean that an old brain is necessarily an arteriosclerotic one. Tilney has said, "No evidence thus far adduced is sufficient to convince us that there is such a thing as a strictly old brain. The brain in aged people may present certain marked changes, but these are in their turn incident to many pathological assaults upon the tissues sustained during life which in one individual more, in others less, are in all alike the consequence of infection, intoxications or other marked influences. All of this is a strong argument in favor of the theory that holds old age in the brain, as in other organs, to be the result of life's successive and cumulative intoxications." We do not know what the signs and symptoms of aging as separated from disease would be; we only know those which occur as age progresses. The consequences of a cerebral vascular accident depend in considerable measure upon the mental and physical status of the patient who sustains one. Upon the background of the signs and symptoms occurring in later life a stroke may result in residuals of one type, in an otherwise vigorous younger person another. At any age we are the total of all that has occurred before. It has been said that "discipline obtained in earlier life permits us to age gracefully. Through appropriate learning and practice and the effort to prolong mobility and plasticity in the earlier years, effective mental control may be achieved, knowledge accumulated, wisdom increased, thus extending mental longevity" (Miles). A cerebral vascular accident in one with such antecedents results in a far less catastrophe than in one whose personality may have been defective throughout his former life.
* Professor Emeritus, Department of Nervous and Mental Diseases, Northwestern University Medical School, Chicago. 211
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Lewis J. Pollock
When a cerebral vascular accident occurs in later life it is of some importance to differentiate the signs and symptoms of a stroke, which is not a condition sui generis, from the antecedent ones of the older person, whatever their cause, upon which the former are engrafted. Among these antecedent signs and symptoms is a diminution in acuteness of perception not entirely the result of aging alone. Thus pain and vibration senses are less acute, as is vision, hearing, taste and smell. The reaction time is lengthened; motility is slower, memory for recent events and names diminishes. The patient predisposed to stroke is likely to be more affected by the death of friends and relatives, and more aware of aging of acquaintances. He probably has difficulty in obtaining new positions or adequately fulfilling obligations of old ones. There develops a lack of insight into his own character and a sense of change in behavior in others. Indecision, caution because of protective attitude, and a readiness to defend one's position develop out of a sense of insecurity and anxiety. At times suspicion, depression, narrowed interest and a sense of hopelessness are seen. Most characteristic are the increasing lack of plasticity and the unbending rigid attitudes. The Federal Security Agency reports that chronic diseases are the leading causes of death in the older age groups. In 1900 they were also the leading killers of persons 65 years old and over. Then, as now, heart disease headed the list. Cerebral vascular lesions were the second leading cause of death in 1900 and the third in 1948. The percentage distribution of deaths from cerebrovascular accidents for persons 65 years or over has shown a slight increase over this period; from 12.2 per cent in 1900 to 12.4 per cent in 1948 (AlIen). The incidence in younger groups is less, Irish finding it to be 8 per cent in 12,500 autopsies of both young and aged persons. There has been a dramatic increase in the longevity of man in recent years. Whereas in 1900, 4 per cent of the population was over 65 years of age, in 1935, 6 per cent was over 65, and it is estimated that in 1980, 15 per cent will be over 65 years of age. It behooves us, therefore, carefully to consider by what means we "may add more life to years than more years to life" (Piersol). This is particularly applicable to the residuals of strokes, fo! ."the hemiplegic patient can and frequently does live for many years. In other words, the cardiovascular catastrophe that initiates hemiplegia is not necessarily the beginning of the end of life but merely the beginning of a long period of torment and despair" (Davidson). The treatment of the consequences of a stroke is conditioned not only by the neurologic deficit but also by the underlying conditions which precipitated it. Spontaneous massive cerebral hemorrhage, cerebral thrombosis or embolism, cardiovascular insufficiency, coronary thrombosis, mural thrombi, arachnoiditis, thromboangiitis obliterans, peri-
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arteritis nodosa and other collagenous diseases, arteriosclerosis, hypertension, miliary and other aneurysms, infectious periarteritis, emboli due to extra cardiac sources (lung and other abscesses), tumor of the brain, basilar artery insufficiency and thrombi of the internal carotid artery in the neck-all may be responsible for the precipitation of hemiplegia. Obviously, the treatment of the acute phase will differ in all. The treatment of the re si duals also will differ. Despite the similarity of the neurological deficit the underlying disease remains, and what may be indicated in one case may be contraindicated in another. Arteriosclerosis is said to be responsible for many strokes, including the "little strokes," to which more attention will be paid in succeeding paragraphs. The frequency of atheroma and arteriosclerosis as the cause varies from 18 per cent of the cases reported by Hicks and Black to 46 per cent in those reported by Wilson, Rupp, Riggs and Wilson. Although "little strokes" are generally linked to arteriosclerosis, they occur in many other conditions already mentioned. One must keep in mind particularly thrombosis of the internal carotid artery and insufficiency of the basilar artery. Since a diagnosis of the pathological process is necessary if a stroke is to be treated intelligently, it is appropriate to discuss some of these processes. BIG STROKES
At present we lack dependable information on the relative frequency of cerebral hemorrhage, thrombosis and embolism; on the relation of any of these conditions to systemic disorder, hypertension, arteriosclerosis, coronary thrombosis, mural infarct, cardiac hypertrophy or kindred ailments; on the manner in which cerebral hemorrhage is produced (whether by rupture of a blood vessel or confluence of thrombi or softening); and on the source of bleeding (whether on the arterial or venous side of the cerebral vascular system). Nowhere in the field of medicine is there greater need for the cooperation of internist and neurologist. When the presenting signs are those of cerebral involvement, the neurologi::;t should associate himself with an internist, and in the case of a cardiac catastrophe the internist might benefit from the advice of a neurologist. The differential diagnosis between intracerebral hemorrhage, thrombosis and often embolism may in the majority of instances be effected by the neurologist. Since subarachnoid hemorrhage resulting from a ruptured aneurysm of the circle of Willis, massive cerebral hemorrhage, thrombosis of the internal carotid artery in the neck and a few other conditions may be treated surgically, and since thrombi may respond to prophylactic and active medical treatment, their differentiation is most important. This may readily be seen from the fact that although anticoagulants may be useful in thrombi, they would be disastrous in hemorrhage.
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The neurological deficit resulting from a stroke, irrespective of its cause, depends upon the part of the nervous system involved. One of the severe deficits is that of motion. Paralysis may develop in one extremity, in an arm and leg of one side, or in all extremities. It is usually associated with spasticity, increased deep refiexes, pathological refiexes as a Babinski sign; often contractures, abnormal postures, sustained spasm; at times pain, rarely atrophy. In cortical lesions, since the representation of motion is widespread, the paralysis may be limited to a segment of the body. In the more peripheral lesions, as those of the internal capsule and brain stem, the paralysis may affect a whole side of the body. When limited to the motor cortex, Jacksonian or motor focal fits may be part of the clinical picture. When the internal capsule is the seat of the lesion, the paralysis may be associated with loss of sensation and homonymous hemianopsia. When the distal brain stem is involved, crossed paralysis may occur. Ipsilateral paralysis of cranial nerves, contralateral paralysis of extremities and crossed anesthesia may occur, as well as cerebellar ataxia, paralysis of muscles of deglutition and phonation. If the lesion affects the basal ganglia, parkinsonism and other hyperkinesias, such as athetosis, may result or arteriosclerotic rigidity ensue. When the frontal lobes are involved motor disturbances, grasping, groping, inattention or extinction of visual or other stimuli and psychic disorders are present. When the parietal lobe is involved, apraxia, astereognosis, other agnosias such as body identification, loss of ability to calculate, loss of apperception of time, direction, distance or location occur and when the adjacent occipital lobe is involved, possibly hemianopsia and unsystematized visual hallucinations. These are systematized and often lilliputian when the temporal lobe is affected, the hallucinations consisting of little images, animals or men, in action. In addition, hallucinations of smell and taste, as well as quadrantic anop:!'ia, may be present. When the lesions are bilateral, pseudobulbar palsy with dysarthria, dysphagia and convulsive unmotivated laughing and crying are seen. When the lesion affects the dominant hemisphere, as the left in patients of right-handed stock, various aphasias-motor, sensory (either auditory or visual), transcortical or associative-and agraphia occur. It is apparent that plans for treatment must vary in each patient and be related to the deficit present-not too simple a matter even in young patients. INTERMITTENT STROKES
Of these but three will be described: those due to thrombosis of the internal carotid artery in the neck, the syndrome of intermittent insufficiency of the basilar arterial system, and "little strokes."
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Strokes Due to ThrOlubosis of the Internal Carotid Artery in the Neck
One of the remarkable and long-lasting blind spots in medicine relates to spontaneous thrombosis of extracranial vessels such as the carotid arteries. In 1914 J. Ramsay Hunt wrote, in an article on "The Role of the Carotid Arteries in the Causation of Vascular Lesions of the Brain, with Remarks on Certain Special Features of the Symptomatology," "Hemiplegia from occlusion of the intracranial branches of the internal carotid artery is one of the most frequent clinical features met with in general practice and yet apparently one of the rarest from obstruction of the main arterial pathway in the neck." This observation was overlooked until T. G. Illyd James, 35 years later, quoted it. When one considers that these vessels are frequently ignored, both in clinical and pathologic studies, it is not unlikely that many such thrombi are overlooked. That this is true may be seen from the information given to me by Wetzel, that in 41 angiograms of patients with residual hemiplegia at the United States Veterans' Administration at Hines and at Passavant Memorial Hospital, Chicago, there were seven instances of carotid artery thrombosis in the neck~a little over 17 per cent. Before an attack leads to complete hemiplegia, many attacks of short duration may occur with hemiparesis and especially blindness on the ipsilateral side of the lesion. Alvarez cites an instance of such blindness when describing "little strokes." Intermittent Insufficiency of the Basilar Arterial System
Siekert and Millikan now feel that their formerly described syndrome of intermittent insufficiency of the basilar system seems to be the first phase of thrombosis of the basilar artery. Arteriosclerosis was present to a severe degree in 24 of the 28 patients; 19 had hypertension. "Many of the 28 patients had had previous neurologic symptoms. Transitory episodes occurred months or even years before the onset of the final illness. These periodic episodes were fleeting and apparently minor in character. They varied from momentary confusion to one lasting several hours, with diplopia, blurred vision, vertigo, slurred speech, and numbness. Ten patients had periods of hemiparesis. When this alternates from side to side, it is characteristic of insufficiency of the basilar artery. The final illness began like one of these previous episodes, but the symptoms did not abate. Instead, additional ones occurred, with a progression, often stepwise, that continued until death." The first phase may last for weeks, months or years. The final phase, which may last for days or weeks, was characterized by quadriparesis in 11, and 17 had evidence of hemiparesis. Twelve of these became quadriparetic within two days. The chief neurologic signs were paresis of extremities and the face, pseudobulbar weakness, and ocular abnormalities.
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"Little Strokes"
Those who have read the perceptive and brilliant descriptions of Alvarez on "The Little Strokes" owe him a debt of gratitude. Because of his work, many patients will be spared needless procedures, even operative treatment, for disorders apparently unconnected with the nervous system that do not exist. Moreover, the patient, his family, and his employers will profit when they are informed of the real character of his illness. Although, as we have said, not all intermittent strokes are the result of arteriosclerosis, under which heading Alvarez described them, all else that he says of them is true and illuminating. Of them he says, "One of the commonest diseases of man is a slow petering out toward the end of life, and one of the commonest ways of petering out is that in which the brain is slowly destroyed by the repeated thromboses of small sclerotic blood vessels." Alvarez recounts the statement of a patient, "I don't mind dying of a stroke, but I dread not dying with the first big one. I don't want to take ten years to peter out, a nuisance to myself and my family." Also, "Doctor," as a sweet old lady once said with great clairvoyance, "death is taking little bites of me!" He quotes OsIer who spoke of those many men and women "who take as long to die as they did to grow up," who go through "cold gradations of decay" and live a sort of death in life. He also quotes OsIer on Oliver W. Holmes; Holmes went quickly, "His friends were spared the most distressing of all human spectacles." Alvarez relates that he remembers "a man who lived for 30 years after he had been made childish by a series of three little strokes that did not affect either his speech or his muscles." However, he has seen many patients who after a stroke became remarkably well, and cites the case of Pasteur who, for 27 years after his big stroke, did much of his best work. Interestingly, his barber told a friend of Alvarez that through the years Pasteur must have had 50 little strokes. Alvarez has seen many persons go for 10 or 15 years in good health before another little stroke occurred. The symptoms and signs of the intermittent strokes which Alvarez designates as "little strokes" differ from those of either the early phase of basilar artery thrombosis or thrombosis of the internal carotid artery in th~ neck. This is easily understood, since in many of his cases the "little strokes" result from successive lesions of little arteries occupying in a random fashion scattered areas in the cerebral hemispheres. Better to project the treatment, it is necessary to know the signs and symptoms and from them deduce the areas of the brain involved. The signs and symptoms may be divided into those produced by neural deficit, those which seem remote from neurologic causes, and those which especially in later life are produced by an acceleration and periodic progression of psychologic changes which may be seen in aging l"ersons
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in lesser degree. One of the characteristics is the occurrence of a sudden unexpected episode following which and thereafter steplike, equally sudden, and frequently nocturnal attacks result in the often bizarre symptomatology. These may be of such minor significance as to escape the notice of the patient and may only be discerned by a searching inquiry. Another characteristic is the relatively short duration of some, especially signs of neural defect. Frequently, therefore, they are attributed to vascular spasm. Among the signs of neural deficit may be mentioned the temporary aphasias, weakness of arm and leg, at times only of the face, blindness of usually one, rarely both eyes which is common to thrombosis of the internal carotid artery in the neck. In thrombosis of the basilar artery and its branches there may occur temporary symptoms seen in a lasting form in a large attack. Also may be mentioned convulsions which, when focal, may be succeeded by Todd's paresis, disagreeable taste and pain in the tongue especially unilateral, parkinsonism, thalamic signs, and rigidity. Mysterious indeed are the signs and symptoms seemingly remote from cerebral causes. Among them are dizziness, not true vertigo, tinnitus, paresthesias, especially burning and itching over areas not corresponding to anatomical divisions, gastrointestinal disturbances, pain, nausea and vomiting, belching, tympanites, cardiac-like episodes of tachycardia, oppression, heart consciousne5s, sudden drops in blood pressure. However, one must be alert to concomitant little thrombi in the heart. In many cases the symptoms of sudden appearance give rise to fear of a subsequent attack under similar conditions as in church, public places, restaurants, riding in trains, walking on the streets, so that the picture has characteristics of a phobia. I am certain that very often I have made a diagnosis of a psychoneurosis with phobias and have overlooked the underlying pathology. However, from the success attending reassurance and explanation the patient was relieved of symptoms until another attack occurred, and it also was attributed to phobias. So often has the condition resulted in anxiety and depression that hypochondriasis has frequently been the diagnosis. Of the greatest importance are the mental changes since it is these which lead to the greatest misery of the patient, relatives and employers. Moreover, it is here that sensible advice may result in banishing fear and anxiety, unjust criticism, futile adjuration to "snap out of it," and in protection against business and professional failure. Among the mental changes may be mentioned a change in character wherein a previously intelligent, orderly, kindly and well-groomed person turns into a suspicious, slovenly, asocial, profane, amoral, hypochondriacal, depressed and self-centered one.
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TREATMENT AND REHABILITATION
I have described a number of varieties of intermittent thrombotic lesions of blood vessels. It is appropriate now to discuss some of the procedures that have been proposed for use during the acute episode of these as well as the "big attacks" brought about by thrombosis. SYlllpathetic Block
Svien and Karavitis found continuous stellate block disappointing, and James observed no striking improvement from cervical sympathectomy or from arterial stripping. Poppen and Baird, however, advocated continuous stellate block. Ruben and Mayer reported that 60 per cent of acute and 27 per cent of chronic strokes showed improvement after stellate block. This view was also held by Gilbert and deTakats, who report improvement in all of 10 cases with embolism, 8 of 12 with thrombosis, and 1 of 3 with cerebral hemorrhage. Quite favorable results were reported by Amyes and Perry, when the block was done within six hours of the development of neurologic symptoms. This is also true of those cases coincident with cardiac decompensation. Although Sherman and Grinker noted the good results claimed by others to occur in a little better than half their cases, they go on to say, "This treatment appears to have no sound physiologic basis, since the effect upon the caliber of the vessels is not great and it has been shown that it produces no increase of cerebral blood flow. Its effect early in the course of vascular accident is also open to question because many such lesions show early and rapid improvement spontaneously. The final opinion waits careful controlled studies." Fischer believes that the reports upon the efficacy of cervical sympathectomy are not conclusive and that further studies are necessary. Millikan and Moersch did not find the block to be significant, either in prevention of death or of residuals. Harmel, reporting upon the effects of bilateral stellate block in 13 normotensive and hypertensive patients, failed to find any effect whatsoever. Scheinberg confirmed his work. Alvarez, in regard to its use in little strokes, said, "1 cannot see what good that could do (i.e., vasodilatation) after a thrombus has become well stuck in one spot and the resulting lack of blood has led to the complete and permanent destruction of a bit of the brain." Anticoagulant Therapy
Siekert and MilIikan were favorably impressed by the use of anticoagulants in the early treatment of the syndrome of intermittent insufficiency of the basilar artery. Using Tromexan in some and Dicumarol in others, they conclude that, "While their effectiveness is still unproved, treatment for this devastating cerebrovascular syndrome may be available in the form of anticoagulants." Of course, if they will prove valuable in insufficiency of the basilar artery, they should be equally valuable in
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involvement of other arteries. Cortisone has been reported by a few as successful. Rehabilitation
From the moment a stroke, whether little or big, occurs, rehabilitation must begin. Associated with the physician is Nature, and not all of the good results-disappearance of mental changes, recovery of use of arms, ambulation and recovery from aphasia, agraphia or agnosias-can be attributed solely to treatment, whether psychiatric, speech training, physical medicine, or use of drugs designed to diminish spasticity or to treat the underlying cause. Nature, after injury, begins a reparative process. Not all of the disability following a neural injury is the result of irreversible changes in the neural tissue. Often, and to a surprising degree, only a blocking of impulses, not a permanent interruption, occurs. At times some recovery of function begins even years after injury. This I have observed in the case of sensation, which in injuries of the spinal cord and cauda equina may begin to recover as long as three or four years after. In peripheral nerves it is well known that branching of adjacent uninjured sensory fibers occurs after long delay and results in imperfect restoration in what is known as the area of overlap. It is possible that it may occur in the central nervous system. Moreover, some collateral circulation may be established since not all of the cerebral arteries are "end arteries." Whether the stroke be big or little, if its cause is vascular the reason for its OCcurrence must be discovered. It is here that the counsel of an internist is invaluable. The neurologist can differentiate the types of vascular disturbances in the brain or find other lesions as tumor or inflammation, but if the underlying cause is extra cerebral he should be guided in respect to treatment by the internist. There is some difference of opinion as to the therapeutic or diagnostic value of spinal puncture. Considerable judgment must be exercised to determine when it is indicated. It is fraught with some danger and as a diagnostic procedure it is necessary in only a few cases. Careful nursing and medical supervision is necessary to sustain nutrition, provide adequate fluid intake, promote evacuation of bowel contents, and prevent bed sores, urinary and other infections, contractures, thrombophlebitis and ankylosis of joints. In big strokes bed rest is, of course, necessary for some time; in little strokes not. The duration of the period of bed rest is not agreed upon by all. Early ambulation, now so popular after operative procedures, particularly in older patients, in my opinion is not followed by as quick or complete a recovery of the neural deficit following severe strokes, as is a period of bed rest of three to six weeks. Bed rest does not mean immobilization. By intelligent management by physiatrists and nurses the complications of atrophy of muscles, decalcification of bones, throm-
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bophlebitis and the like can be prevented. This entails the employment of bed exercises, frequent changes of posture, passive movement, massage and heat. Unless such treatment be made available, contractures and particularly painful freezing of joints (especially the shoulder) occur. If there is no contraindication because of cardiovascular or other disease, the patient may be permitted to sit up in bed and to dangle the legs out of bed. Soft splinting of parts of extremities, especially the feet, is indicated. In addition to the medicinal treatment necessary for the underlying disease, measures must be instituted for the relief of insomnia, restlessness, agitation, tension, pain in the head and stiff and painful joints. For a short time the paralysis may be a flaccid one, later to become spastic. The countless remedial drugs manufactured for the relief of spasticity are usually worthless. One may, of course, block the myoneural junction by curare-like drugs, but they are dangerous and serve but little purpose. As soon as compatible with the general condition of the patient, an attempt should be made to induce him to assist in selfcare-to feed himself, brush teeth, shave, comb hair and later to get in and out of bed, use the toilet, and so forth. The subsequent program of rehabilitation should be directed toward continued progress in self-care. This includes writing (if the paralysis is not the result of a lesion in the dominant hemisphere), the use of the telephone, and dressing and undressing as well as possible. Ambulation should be taught by the accepted procedures of physiatrists, who begin with the most simple task of rising and standing with aid of parallel bars, successively proceeding to activity as complete as may be possible. Efforts should be made to interest the patient in activities, but there is no simple prescription suitable for all. Careful study of the patient's previous interests, intellectual status, avocations and hobbies are indicated. A doctor of philosophy, for example, would find basket weaving or rug making intellectually frustrating. If unable to read, patients should have read to them selected literature and news and fiction relating to their former occupations and interests. They should have available music, radio and intelligent television programs. Collecting stamps, preparing an album, or painting may interest the patient and permit development of agility and precision. Card playing and other suitable games should be made available. When the dominant hemisphere is affected, aphasia may occur. In some cases it may disappear spontaneously after an undetermined period of time. One cannot say how much re-education may have to do with recovery, how much spontaneous restoration. I have an impression that the latter plays a large role. However, speech therapists and psychologists have devised methods of re-education and in a number of instances have been rewarded by restoration of function in varying degrees. I would interpose here that frustration from failure to regain speech is often so
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hard for the patient to bear that efforts toward recovery of speech may not be warranted. I feel it is better for older patients without much life expectancy to be happy, while slowly dying, than to learn to speak again. There are other sequelae of a stroke: parkinsonism is one. Although numerous drugs have been reported to be highly successful in reducing tremor and rigidity, I have found most of them to compare unfavorably with hyoscine, especially when combined with pilocarpine nitrate and caffeine citrate. Convulsive disorders are another sequela. Numerous anticonvulsants have been manufactured and some are efficacious. The bromides have been maligned by many who have had but little experience with them. I have found them very useful when one follows the blood bromide level to determine proper dosage. The upper level of concentration permissible without intoxication is much higher than reported. Many of my patients tolerate 300 mg. per 100 cc. of blood. In small doses given during the day they are preferable to strong hypnotics given at night. In depression, the powdered extract of opium in doses of 16 to 48 mg. (>i to ~ grain) several times a day has been found useful. So that the patient will not know what he is taking, the drug should be called by its old name thebaicum. However, it is not habit forming. In the case of intermittent or little strokes, especially those which result from thrombi of the small arteries of the cerebrum, special consideration should be given to the enlistment of family, friends, doctor and nurse to surround the patient with kindness, understanding, patience and forgiveness. When all understand that the change in character, mentality, manner and behavior is the result of an organic disease, that the patient cannot be held responsible or voluntarily again assume the characteristics of his old self, the gradual but progressive slow death may be made more bearable. 122 S. Michigan Avenue Chicago 3, Illinois
ALTHOUGH one may speak of the ordinary diseases of childhood, there are no ordinary diseases of later life. There are some diseases which develop slowly and progressively, and one of these is arteriosclerosis. It most frequently begins later in life, therefore one may anticipate the occurrences of strokes in larger numbers in the elderly than would be encountered in early life. This does not mean that an old brain is necessarily an arteriosclerotic one. Tilney has said, "No evidence thus far adduced is sufficient to convince us that there is such a thing as a strictly old brain. The brain in aged people may present certain marked changes, but these are in their turn incident to many pathological assaults upon the tissues sustained during life which in one individual more, in others less, are in all alike the consequence of infection, intoxications or other marked influences. All of this is a strong argument in favor of the theory that holds old age in the brain, as in other organs, to be the result of life's successive and cumulative intoxications." We do not know what the signs and symptoms of aging as separated from disease would be; we only know those which occur as age progresses. The consequences of a cerebral vascular accident depend in considerable measure upon the mental and physical status of the patient who sustains one. Upon the background of the signs and symptoms occurring in later life a stroke may result in residuals of one type, in an otherwise vigorous younger person another. At any age we are the total of all that has occurred before. It has been said that "discipline obtained in earlier life permits us to age gracefully. Through appropriate learning and practice and the effort to prolong mobility and plasticity in the earlier years, effective mental control may be achieved, knowledge accumulated, wisdom increased, thus extending mental longevity" (Miles). A cerebral vascular accident in one with such antecedents results in a far less catastrophe than in one whose personality may have been defective throughout his former life.
* Professor Emeritus, Department of Nervous and Mental Diseases, Northwestern University Medical School, Chicago. 211
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Lewis J. Pollock
When a cerebral vascular accident occurs in later life it is of some importance to differentiate the signs and symptoms of a stroke, which is not a condition sui generis, from the antecedent ones of the older person, whatever their cause, upon which the former are engrafted. Among these antecedent signs and symptoms is a diminution in acuteness of perception not entirely the result of aging alone. Thus pain and vibration senses are less acute, as is vision, hearing, taste and smell. The reaction time is lengthened; motility is slower, memory for recent events and names diminishes. The patient predisposed to stroke is likely to be more affected by the death of friends and relatives, and more aware of aging of acquaintances. He probably has difficulty in obtaining new positions or adequately fulfilling obligations of old ones. There develops a lack of insight into his own character and a sense of change in behavior in others. Indecision, caution because of protective attitude, and a readiness to defend one's position develop out of a sense of insecurity and anxiety. At times suspicion, depression, narrowed interest and a sense of hopelessness are seen. Most characteristic are the increasing lack of plasticity and the unbending rigid attitudes. The Federal Security Agency reports that chronic diseases are the leading causes of death in the older age groups. In 1900 they were also the leading killers of persons 65 years old and over. Then, as now, heart disease headed the list. Cerebral vascular lesions were the second leading cause of death in 1900 and the third in 1948. The percentage distribution of deaths from cerebrovascular accidents for persons 65 years or over has shown a slight increase over this period; from 12.2 per cent in 1900 to 12.4 per cent in 1948 (AlIen). The incidence in younger groups is less, Irish finding it to be 8 per cent in 12,500 autopsies of both young and aged persons. There has been a dramatic increase in the longevity of man in recent years. Whereas in 1900, 4 per cent of the population was over 65 years of age, in 1935, 6 per cent was over 65, and it is estimated that in 1980, 15 per cent will be over 65 years of age. It behooves us, therefore, carefully to consider by what means we "may add more life to years than more years to life" (Piersol). This is particularly applicable to the residuals of strokes, fo! ."the hemiplegic patient can and frequently does live for many years. In other words, the cardiovascular catastrophe that initiates hemiplegia is not necessarily the beginning of the end of life but merely the beginning of a long period of torment and despair" (Davidson). The treatment of the consequences of a stroke is conditioned not only by the neurologic deficit but also by the underlying conditions which precipitated it. Spontaneous massive cerebral hemorrhage, cerebral thrombosis or embolism, cardiovascular insufficiency, coronary thrombosis, mural thrombi, arachnoiditis, thromboangiitis obliterans, peri-
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arteritis nodosa and other collagenous diseases, arteriosclerosis, hypertension, miliary and other aneurysms, infectious periarteritis, emboli due to extra cardiac sources (lung and other abscesses), tumor of the brain, basilar artery insufficiency and thrombi of the internal carotid artery in the neck-all may be responsible for the precipitation of hemiplegia. Obviously, the treatment of the acute phase will differ in all. The treatment of the re si duals also will differ. Despite the similarity of the neurological deficit the underlying disease remains, and what may be indicated in one case may be contraindicated in another. Arteriosclerosis is said to be responsible for many strokes, including the "little strokes," to which more attention will be paid in succeeding paragraphs. The frequency of atheroma and arteriosclerosis as the cause varies from 18 per cent of the cases reported by Hicks and Black to 46 per cent in those reported by Wilson, Rupp, Riggs and Wilson. Although "little strokes" are generally linked to arteriosclerosis, they occur in many other conditions already mentioned. One must keep in mind particularly thrombosis of the internal carotid artery and insufficiency of the basilar artery. Since a diagnosis of the pathological process is necessary if a stroke is to be treated intelligently, it is appropriate to discuss some of these processes. BIG STROKES
At present we lack dependable information on the relative frequency of cerebral hemorrhage, thrombosis and embolism; on the relation of any of these conditions to systemic disorder, hypertension, arteriosclerosis, coronary thrombosis, mural infarct, cardiac hypertrophy or kindred ailments; on the manner in which cerebral hemorrhage is produced (whether by rupture of a blood vessel or confluence of thrombi or softening); and on the source of bleeding (whether on the arterial or venous side of the cerebral vascular system). Nowhere in the field of medicine is there greater need for the cooperation of internist and neurologist. When the presenting signs are those of cerebral involvement, the neurologi::;t should associate himself with an internist, and in the case of a cardiac catastrophe the internist might benefit from the advice of a neurologist. The differential diagnosis between intracerebral hemorrhage, thrombosis and often embolism may in the majority of instances be effected by the neurologist. Since subarachnoid hemorrhage resulting from a ruptured aneurysm of the circle of Willis, massive cerebral hemorrhage, thrombosis of the internal carotid artery in the neck and a few other conditions may be treated surgically, and since thrombi may respond to prophylactic and active medical treatment, their differentiation is most important. This may readily be seen from the fact that although anticoagulants may be useful in thrombi, they would be disastrous in hemorrhage.
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The neurological deficit resulting from a stroke, irrespective of its cause, depends upon the part of the nervous system involved. One of the severe deficits is that of motion. Paralysis may develop in one extremity, in an arm and leg of one side, or in all extremities. It is usually associated with spasticity, increased deep refiexes, pathological refiexes as a Babinski sign; often contractures, abnormal postures, sustained spasm; at times pain, rarely atrophy. In cortical lesions, since the representation of motion is widespread, the paralysis may be limited to a segment of the body. In the more peripheral lesions, as those of the internal capsule and brain stem, the paralysis may affect a whole side of the body. When limited to the motor cortex, Jacksonian or motor focal fits may be part of the clinical picture. When the internal capsule is the seat of the lesion, the paralysis may be associated with loss of sensation and homonymous hemianopsia. When the distal brain stem is involved, crossed paralysis may occur. Ipsilateral paralysis of cranial nerves, contralateral paralysis of extremities and crossed anesthesia may occur, as well as cerebellar ataxia, paralysis of muscles of deglutition and phonation. If the lesion affects the basal ganglia, parkinsonism and other hyperkinesias, such as athetosis, may result or arteriosclerotic rigidity ensue. When the frontal lobes are involved motor disturbances, grasping, groping, inattention or extinction of visual or other stimuli and psychic disorders are present. When the parietal lobe is involved, apraxia, astereognosis, other agnosias such as body identification, loss of ability to calculate, loss of apperception of time, direction, distance or location occur and when the adjacent occipital lobe is involved, possibly hemianopsia and unsystematized visual hallucinations. These are systematized and often lilliputian when the temporal lobe is affected, the hallucinations consisting of little images, animals or men, in action. In addition, hallucinations of smell and taste, as well as quadrantic anop:!'ia, may be present. When the lesions are bilateral, pseudobulbar palsy with dysarthria, dysphagia and convulsive unmotivated laughing and crying are seen. When the lesion affects the dominant hemisphere, as the left in patients of right-handed stock, various aphasias-motor, sensory (either auditory or visual), transcortical or associative-and agraphia occur. It is apparent that plans for treatment must vary in each patient and be related to the deficit present-not too simple a matter even in young patients. INTERMITTENT STROKES
Of these but three will be described: those due to thrombosis of the internal carotid artery in the neck, the syndrome of intermittent insufficiency of the basilar arterial system, and "little strokes."
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Strokes Due to ThrOlubosis of the Internal Carotid Artery in the Neck
One of the remarkable and long-lasting blind spots in medicine relates to spontaneous thrombosis of extracranial vessels such as the carotid arteries. In 1914 J. Ramsay Hunt wrote, in an article on "The Role of the Carotid Arteries in the Causation of Vascular Lesions of the Brain, with Remarks on Certain Special Features of the Symptomatology," "Hemiplegia from occlusion of the intracranial branches of the internal carotid artery is one of the most frequent clinical features met with in general practice and yet apparently one of the rarest from obstruction of the main arterial pathway in the neck." This observation was overlooked until T. G. Illyd James, 35 years later, quoted it. When one considers that these vessels are frequently ignored, both in clinical and pathologic studies, it is not unlikely that many such thrombi are overlooked. That this is true may be seen from the information given to me by Wetzel, that in 41 angiograms of patients with residual hemiplegia at the United States Veterans' Administration at Hines and at Passavant Memorial Hospital, Chicago, there were seven instances of carotid artery thrombosis in the neck~a little over 17 per cent. Before an attack leads to complete hemiplegia, many attacks of short duration may occur with hemiparesis and especially blindness on the ipsilateral side of the lesion. Alvarez cites an instance of such blindness when describing "little strokes." Intermittent Insufficiency of the Basilar Arterial System
Siekert and Millikan now feel that their formerly described syndrome of intermittent insufficiency of the basilar system seems to be the first phase of thrombosis of the basilar artery. Arteriosclerosis was present to a severe degree in 24 of the 28 patients; 19 had hypertension. "Many of the 28 patients had had previous neurologic symptoms. Transitory episodes occurred months or even years before the onset of the final illness. These periodic episodes were fleeting and apparently minor in character. They varied from momentary confusion to one lasting several hours, with diplopia, blurred vision, vertigo, slurred speech, and numbness. Ten patients had periods of hemiparesis. When this alternates from side to side, it is characteristic of insufficiency of the basilar artery. The final illness began like one of these previous episodes, but the symptoms did not abate. Instead, additional ones occurred, with a progression, often stepwise, that continued until death." The first phase may last for weeks, months or years. The final phase, which may last for days or weeks, was characterized by quadriparesis in 11, and 17 had evidence of hemiparesis. Twelve of these became quadriparetic within two days. The chief neurologic signs were paresis of extremities and the face, pseudobulbar weakness, and ocular abnormalities.
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"Little Strokes"
Those who have read the perceptive and brilliant descriptions of Alvarez on "The Little Strokes" owe him a debt of gratitude. Because of his work, many patients will be spared needless procedures, even operative treatment, for disorders apparently unconnected with the nervous system that do not exist. Moreover, the patient, his family, and his employers will profit when they are informed of the real character of his illness. Although, as we have said, not all intermittent strokes are the result of arteriosclerosis, under which heading Alvarez described them, all else that he says of them is true and illuminating. Of them he says, "One of the commonest diseases of man is a slow petering out toward the end of life, and one of the commonest ways of petering out is that in which the brain is slowly destroyed by the repeated thromboses of small sclerotic blood vessels." Alvarez recounts the statement of a patient, "I don't mind dying of a stroke, but I dread not dying with the first big one. I don't want to take ten years to peter out, a nuisance to myself and my family." Also, "Doctor," as a sweet old lady once said with great clairvoyance, "death is taking little bites of me!" He quotes OsIer who spoke of those many men and women "who take as long to die as they did to grow up," who go through "cold gradations of decay" and live a sort of death in life. He also quotes OsIer on Oliver W. Holmes; Holmes went quickly, "His friends were spared the most distressing of all human spectacles." Alvarez relates that he remembers "a man who lived for 30 years after he had been made childish by a series of three little strokes that did not affect either his speech or his muscles." However, he has seen many patients who after a stroke became remarkably well, and cites the case of Pasteur who, for 27 years after his big stroke, did much of his best work. Interestingly, his barber told a friend of Alvarez that through the years Pasteur must have had 50 little strokes. Alvarez has seen many persons go for 10 or 15 years in good health before another little stroke occurred. The symptoms and signs of the intermittent strokes which Alvarez designates as "little strokes" differ from those of either the early phase of basilar artery thrombosis or thrombosis of the internal carotid artery in th~ neck. This is easily understood, since in many of his cases the "little strokes" result from successive lesions of little arteries occupying in a random fashion scattered areas in the cerebral hemispheres. Better to project the treatment, it is necessary to know the signs and symptoms and from them deduce the areas of the brain involved. The signs and symptoms may be divided into those produced by neural deficit, those which seem remote from neurologic causes, and those which especially in later life are produced by an acceleration and periodic progression of psychologic changes which may be seen in aging l"ersons
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in lesser degree. One of the characteristics is the occurrence of a sudden unexpected episode following which and thereafter steplike, equally sudden, and frequently nocturnal attacks result in the often bizarre symptomatology. These may be of such minor significance as to escape the notice of the patient and may only be discerned by a searching inquiry. Another characteristic is the relatively short duration of some, especially signs of neural defect. Frequently, therefore, they are attributed to vascular spasm. Among the signs of neural deficit may be mentioned the temporary aphasias, weakness of arm and leg, at times only of the face, blindness of usually one, rarely both eyes which is common to thrombosis of the internal carotid artery in the neck. In thrombosis of the basilar artery and its branches there may occur temporary symptoms seen in a lasting form in a large attack. Also may be mentioned convulsions which, when focal, may be succeeded by Todd's paresis, disagreeable taste and pain in the tongue especially unilateral, parkinsonism, thalamic signs, and rigidity. Mysterious indeed are the signs and symptoms seemingly remote from cerebral causes. Among them are dizziness, not true vertigo, tinnitus, paresthesias, especially burning and itching over areas not corresponding to anatomical divisions, gastrointestinal disturbances, pain, nausea and vomiting, belching, tympanites, cardiac-like episodes of tachycardia, oppression, heart consciousne5s, sudden drops in blood pressure. However, one must be alert to concomitant little thrombi in the heart. In many cases the symptoms of sudden appearance give rise to fear of a subsequent attack under similar conditions as in church, public places, restaurants, riding in trains, walking on the streets, so that the picture has characteristics of a phobia. I am certain that very often I have made a diagnosis of a psychoneurosis with phobias and have overlooked the underlying pathology. However, from the success attending reassurance and explanation the patient was relieved of symptoms until another attack occurred, and it also was attributed to phobias. So often has the condition resulted in anxiety and depression that hypochondriasis has frequently been the diagnosis. Of the greatest importance are the mental changes since it is these which lead to the greatest misery of the patient, relatives and employers. Moreover, it is here that sensible advice may result in banishing fear and anxiety, unjust criticism, futile adjuration to "snap out of it," and in protection against business and professional failure. Among the mental changes may be mentioned a change in character wherein a previously intelligent, orderly, kindly and well-groomed person turns into a suspicious, slovenly, asocial, profane, amoral, hypochondriacal, depressed and self-centered one.
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TREATMENT AND REHABILITATION
I have described a number of varieties of intermittent thrombotic lesions of blood vessels. It is appropriate now to discuss some of the procedures that have been proposed for use during the acute episode of these as well as the "big attacks" brought about by thrombosis. SYlllpathetic Block
Svien and Karavitis found continuous stellate block disappointing, and James observed no striking improvement from cervical sympathectomy or from arterial stripping. Poppen and Baird, however, advocated continuous stellate block. Ruben and Mayer reported that 60 per cent of acute and 27 per cent of chronic strokes showed improvement after stellate block. This view was also held by Gilbert and deTakats, who report improvement in all of 10 cases with embolism, 8 of 12 with thrombosis, and 1 of 3 with cerebral hemorrhage. Quite favorable results were reported by Amyes and Perry, when the block was done within six hours of the development of neurologic symptoms. This is also true of those cases coincident with cardiac decompensation. Although Sherman and Grinker noted the good results claimed by others to occur in a little better than half their cases, they go on to say, "This treatment appears to have no sound physiologic basis, since the effect upon the caliber of the vessels is not great and it has been shown that it produces no increase of cerebral blood flow. Its effect early in the course of vascular accident is also open to question because many such lesions show early and rapid improvement spontaneously. The final opinion waits careful controlled studies." Fischer believes that the reports upon the efficacy of cervical sympathectomy are not conclusive and that further studies are necessary. Millikan and Moersch did not find the block to be significant, either in prevention of death or of residuals. Harmel, reporting upon the effects of bilateral stellate block in 13 normotensive and hypertensive patients, failed to find any effect whatsoever. Scheinberg confirmed his work. Alvarez, in regard to its use in little strokes, said, "1 cannot see what good that could do (i.e., vasodilatation) after a thrombus has become well stuck in one spot and the resulting lack of blood has led to the complete and permanent destruction of a bit of the brain." Anticoagulant Therapy
Siekert and MilIikan were favorably impressed by the use of anticoagulants in the early treatment of the syndrome of intermittent insufficiency of the basilar artery. Using Tromexan in some and Dicumarol in others, they conclude that, "While their effectiveness is still unproved, treatment for this devastating cerebrovascular syndrome may be available in the form of anticoagulants." Of course, if they will prove valuable in insufficiency of the basilar artery, they should be equally valuable in
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involvement of other arteries. Cortisone has been reported by a few as successful. Rehabilitation
From the moment a stroke, whether little or big, occurs, rehabilitation must begin. Associated with the physician is Nature, and not all of the good results-disappearance of mental changes, recovery of use of arms, ambulation and recovery from aphasia, agraphia or agnosias-can be attributed solely to treatment, whether psychiatric, speech training, physical medicine, or use of drugs designed to diminish spasticity or to treat the underlying cause. Nature, after injury, begins a reparative process. Not all of the disability following a neural injury is the result of irreversible changes in the neural tissue. Often, and to a surprising degree, only a blocking of impulses, not a permanent interruption, occurs. At times some recovery of function begins even years after injury. This I have observed in the case of sensation, which in injuries of the spinal cord and cauda equina may begin to recover as long as three or four years after. In peripheral nerves it is well known that branching of adjacent uninjured sensory fibers occurs after long delay and results in imperfect restoration in what is known as the area of overlap. It is possible that it may occur in the central nervous system. Moreover, some collateral circulation may be established since not all of the cerebral arteries are "end arteries." Whether the stroke be big or little, if its cause is vascular the reason for its OCcurrence must be discovered. It is here that the counsel of an internist is invaluable. The neurologist can differentiate the types of vascular disturbances in the brain or find other lesions as tumor or inflammation, but if the underlying cause is extra cerebral he should be guided in respect to treatment by the internist. There is some difference of opinion as to the therapeutic or diagnostic value of spinal puncture. Considerable judgment must be exercised to determine when it is indicated. It is fraught with some danger and as a diagnostic procedure it is necessary in only a few cases. Careful nursing and medical supervision is necessary to sustain nutrition, provide adequate fluid intake, promote evacuation of bowel contents, and prevent bed sores, urinary and other infections, contractures, thrombophlebitis and ankylosis of joints. In big strokes bed rest is, of course, necessary for some time; in little strokes not. The duration of the period of bed rest is not agreed upon by all. Early ambulation, now so popular after operative procedures, particularly in older patients, in my opinion is not followed by as quick or complete a recovery of the neural deficit following severe strokes, as is a period of bed rest of three to six weeks. Bed rest does not mean immobilization. By intelligent management by physiatrists and nurses the complications of atrophy of muscles, decalcification of bones, throm-
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bophlebitis and the like can be prevented. This entails the employment of bed exercises, frequent changes of posture, passive movement, massage and heat. Unless such treatment be made available, contractures and particularly painful freezing of joints (especially the shoulder) occur. If there is no contraindication because of cardiovascular or other disease, the patient may be permitted to sit up in bed and to dangle the legs out of bed. Soft splinting of parts of extremities, especially the feet, is indicated. In addition to the medicinal treatment necessary for the underlying disease, measures must be instituted for the relief of insomnia, restlessness, agitation, tension, pain in the head and stiff and painful joints. For a short time the paralysis may be a flaccid one, later to become spastic. The countless remedial drugs manufactured for the relief of spasticity are usually worthless. One may, of course, block the myoneural junction by curare-like drugs, but they are dangerous and serve but little purpose. As soon as compatible with the general condition of the patient, an attempt should be made to induce him to assist in selfcare-to feed himself, brush teeth, shave, comb hair and later to get in and out of bed, use the toilet, and so forth. The subsequent program of rehabilitation should be directed toward continued progress in self-care. This includes writing (if the paralysis is not the result of a lesion in the dominant hemisphere), the use of the telephone, and dressing and undressing as well as possible. Ambulation should be taught by the accepted procedures of physiatrists, who begin with the most simple task of rising and standing with aid of parallel bars, successively proceeding to activity as complete as may be possible. Efforts should be made to interest the patient in activities, but there is no simple prescription suitable for all. Careful study of the patient's previous interests, intellectual status, avocations and hobbies are indicated. A doctor of philosophy, for example, would find basket weaving or rug making intellectually frustrating. If unable to read, patients should have read to them selected literature and news and fiction relating to their former occupations and interests. They should have available music, radio and intelligent television programs. Collecting stamps, preparing an album, or painting may interest the patient and permit development of agility and precision. Card playing and other suitable games should be made available. When the dominant hemisphere is affected, aphasia may occur. In some cases it may disappear spontaneously after an undetermined period of time. One cannot say how much re-education may have to do with recovery, how much spontaneous restoration. I have an impression that the latter plays a large role. However, speech therapists and psychologists have devised methods of re-education and in a number of instances have been rewarded by restoration of function in varying degrees. I would interpose here that frustration from failure to regain speech is often so
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hard for the patient to bear that efforts toward recovery of speech may not be warranted. I feel it is better for older patients without much life expectancy to be happy, while slowly dying, than to learn to speak again. There are other sequelae of a stroke: parkinsonism is one. Although numerous drugs have been reported to be highly successful in reducing tremor and rigidity, I have found most of them to compare unfavorably with hyoscine, especially when combined with pilocarpine nitrate and caffeine citrate. Convulsive disorders are another sequela. Numerous anticonvulsants have been manufactured and some are efficacious. The bromides have been maligned by many who have had but little experience with them. I have found them very useful when one follows the blood bromide level to determine proper dosage. The upper level of concentration permissible without intoxication is much higher than reported. Many of my patients tolerate 300 mg. per 100 cc. of blood. In small doses given during the day they are preferable to strong hypnotics given at night. In depression, the powdered extract of opium in doses of 16 to 48 mg. (>i to ~ grain) several times a day has been found useful. So that the patient will not know what he is taking, the drug should be called by its old name thebaicum. However, it is not habit forming. In the case of intermittent or little strokes, especially those which result from thrombi of the small arteries of the cerebrum, special consideration should be given to the enlistment of family, friends, doctor and nurse to surround the patient with kindness, understanding, patience and forgiveness. When all understand that the change in character, mentality, manner and behavior is the result of an organic disease, that the patient cannot be held responsible or voluntarily again assume the characteristics of his old self, the gradual but progressive slow death may be made more bearable. 122 S. Michigan Avenue Chicago 3, Illinois