A historical perspective of the neuropsychiatrie disorders associated with stroke must logically begin with a discussion of the word "stroke." Although many clinicians do not like the term "stroke," it has become so ingrained in both the public and professional literature that it will likely remain the primary word used to describe this cerebrovascular disorder.
One of the problems with the word "stroke" is that it has multiple meanings. A stroke of luck or a tennis stroke have very different meanings from the catastrophic medical disorder. Originally the term was used in medicine to describe being struck down by an illness, especially one which rendered the victim unconscious or paralytic (Millikan et al. 1987). The use of the word stroke to indicate apoplexy (plexus meaning stroke and apo meaning from) began in the 17th century. The recognition, however, of apoplexy as an important medical condition is evident from the writings of Hippocrates (460-370 bc). He noted that unaccustomed attacks of numbness and anesthesia were a sign of impending apoplexy and that when patients, who were not febrile, complained of headache, noises in the head, vertigo, slowness of speech, or numbness of the hands, there was a high likelihood that they would become epileptic or suffer from apoplexy (Millikan et al. 1987). It was not until the development of the microscope by Leeuwenhoek (1632-1723), however, that an understanding of the nature of stroke occurred. Bichat (1771-1802) was the first to describe cerebral softening and Rostan (1823) identified that brain softening found in victims of apoplexy was not due to inflammation. Hughlings-Jackson (1875) wrote that cerebral softening was always focal, "it is localized by vessels, mostly arteries." Information about the physiology of the cerebral circulation, however, began with the observations of Monro (1783). He reported that the volume of blood in the brain was constant and that blood was continually flowing in through arteries and out through veins. Hughlings-Jackson also noted that the middle cerebral artery, or some of its branches, were almost always the vessels occluded. Furthermore, Hughlings-Jackson distinguished between cerebral softening due to arterial disease and cerebral softening due to embolism.
The earliest reports of emotional disorders related to stroke were descriptions of patients by neurologists and psychiatrists. Disturbances of language function have frequently been associated with emotional disorders because aphasia is a common and easily recognized behavioral manifestation of dominant hemisphere brain damage. Furthermore, speech is intimately associated with emotions and thoughts. Pierre Paul Broca, a surgeon and anthropologist (1861) described a single case of aphasia in a patient who was able to utter only one syllable "tan." At autopsy the patient was found to have a large lesion of the left hemisphere including the posterior aspect of the inferior frontal gyrus which has been named Broca's area (Fig. 2.1). Carl Wernicke (1874) proposed that aphasia was the result of impairment in elementary psychic processes which were localized in different brain areas. Wernicke described the first patients with impairment in verbal comprehension with lesions involving the temporal occipital-parietal junction of the left hemisphere which has become known as Wernicke's area.
Broca (1878) also first described an area of cortex which he called the limbus cortex that surrounded the midbrain. This included phylogenetically older areas of cortex such as the inferior temporal lobe, hippocampal gyri, cingulate cortex, and
Figure 2.1 Schematic lateral view of the brain indicating functional brain regions. Broca's and Wernicke's areas play an important role in the production and comprehension of language. The anterior basal portion of the temporal cortex is part of the limbic circuit and the frontal association cortex plays an important role in coordinating motor and cognitive functions of the frontal lobe. The motor, sensory, and visual corticis have topographic and columnar organization for focal motor, sensory, and visual functions.
Figure 2.1 Schematic lateral view of the brain indicating functional brain regions. Broca's and Wernicke's areas play an important role in the production and comprehension of inferior frontal cortex. He noted that all mammals had this large cerebral convolution which formed a ring or limbus around the lower brain stem structures. Limbus cortex has given rise to the term "limbic system." In 1937, Papez (1937) suggested, based purely on anatomical observations (i.e., the older phylogenetic age of the limbic cortex and its circular anatomical organization), that this limbus cortex or limbic system formed the anatomical basis for emotion (this proposal will be discussed more fully in Chapter 3).
Some of the earliest writings about the cerebral basis of emotion, however, were published by Hughlings-Jackson (1915). Hughlings-Jackson, widely regarded as the father of English neurology, was appointed to the National Hospital in 1862. Jackson was the first to identify that brain lesions were associated with a duality of symptoms. That is, brain lesions produced both a loss of specific function as well as a positive symptom such as a movement disorder or a mental process not previously seen. He explained this emergence of "positive symptoms" as a result of removal of higher controls normally inhibiting these functions. This culminated in his view that there was a hierarchy in the organization of the nervous system with the pre-frontal cortex mediating the highest level of mental function.
Similar to his concept of duality of symptoms associated with brain injury, Hughlings-Jackson conceptualized language as an expression of brain function existing in two forms. Language was either intellectual (conveying content) or emotional (expressing feelings). He proposed that these components might be separated by disease. This was the first suggestion that emotional expression was distinct from spoken language and that stroke might produce disorders of emotion without producing disorders of language function.
Adolph Meyer (1904), on the other hand, conceptualized emotion, as he did psychopathology, as a response to multifaceted influences including both physiological and mental processes that he referred to as psychobiology (Lewis 1957):
In the concept of emotion one is able to see most clearly the basic psychobiological premise of the unity of "mental" and "bodily" functions. Emotion as, in fact, the middle ground serves as a striking refutation of an artificial parallelism. An emotion is a reaction which by its very nature covers the entire range of human reactivity, including in the response the non-conscious vasomotor and other organic changes as well as the conscious feelings of rage, joy, etc. In fact, it is in the emotion, permeating and coloring as it does the entire psychobiological activity that one has most definitively and convincingly the feeling of self.
Based in part on his background in neuropathology, Adolph Meyer became very interested in focal brain injury associated with trauma. He stated, "considering the meager knowledge of unmistakably reliable facts of etiology in mental disease, trau-matism would seem to furnish unusually clean-cut conditions of interference with the mechanisms of motor sensory plasticity. The first question is: has the localization of the injury, as such, anything to do with the production of specific symptoms? An examination in detail of the many cases in which laceration has occurred in different regions of the brain affords some reason to believe that purely intellectual and emotional disorders can be directly connected with the localization of the injury. Lesions of the left frontal lobe were all accompanied by some mental aberration or deficiency apart from stupor and, in 10 cases, with lesions of both frontal lobes that 8 showed specific mental disturbance." He identified delirium, dementia, and aphasia as disorders which he attributed to the direct result of brain injury. In keeping with his psy-chobiological view of most mental "reactions," however, he saw disorders such as manic-depressive illness and paranoiac conditions as arising from a combination of head injury (specifically citing left frontal lobe and cortical convexities) as well as family history of psychiatric disorder and other premorbid vulnerabilities such as a personal history of prior psychiatric disorder.
Bleuler (1951) described the long-term nature of depressions following stroke when he stated that "melancholic moods lasting for months and sometimes longer appear frequently." Another example of the psychiatric perspective is that of Post (1962) who in his classic empirical study of 100 elderly patients with depression remarked that the association of brain ischemia with a first episode of depressive disorder was so common that it suggested the causes of atherosclerotic disease and depression may be "etiologically linked."
Early 20th century neurologists, on the other hand, described disorders which were associated with specific lesion locations, such as frontal lobe or parietal lobe syndromes, or behavioral disorders which were unique to brain injury. Babinski (1914), for example, described patients with stroke who would not acknowledge the existence of an obvious motor deficit. These patients were said to have "anosog-nosia" (gnosia meaning knowledge and anos meaning without). When confronted with their physical impairment, patients with anosognosia simply denied that anything was wrong. Babinski also noted that they frequently displayed indifference to their impairments or an inappropriate level of cheerfulness. These disorders of recognition of impairment and inappropriate affect are often associated with right hemisphere lesions.
Another example of an emotional disorder which is unique to brain injury is the catastrophic reaction. Goldstein (1939) described the catastrophic reaction as the abrupt onset of emotional symptoms of frustration, depression, and embarrassment. Lasting from a few seconds to a few minutes, the catastrophic reaction is characterized by a display of emotion (shouting, swearing, pounding fists, and throwing things) followed by return to the previous calm emotional state. Mixing explanation with description, Goldstein (1939) described the catastrophic reaction as "a sudden outburst of emotion provoked by a cognitive task which is based on the inability of the organism to cope when faced with a serious defect in physical and cognitive functions." "Survival," he wrote, "becomes paramount, in a pathologically changed organism. Survival may be normal and ordered or disordered and inconsistent." He referred to this latter type of survival, embedded in physical and mental shock, as "catastrophic."
Another emotional disorder, felt to be unique to patients with brain injury, is the indifference reaction. This disorder was first described by Hecaen et al. (1951) and Denny-Brown et al. (1952) and is associated with right hemisphere lesions. Gainotti (1972) described the indifference reaction as indifference towards failures, lack of interest in family and friends, making foolish, inappropriate jokes, and minimization of physical disability. The indifference reaction was also noted to be frequently associated with severe perceptual deficits and impairment in orientation.
The final emotional disorder that is unique to brain injury is pathological laughter or crying. Although pathological laughter and crying can occur with a variety of lesions, Ironside (1956) described a particular type of disorder in which pathological laughter or crying is a prominent feature, that is pseudobulbar palsy. This disorder is associated with bilateral and often multiple lesions affecting the corticobulbar pathways at any level above the pons. These upper motor neuron lesions produce dysphagia, dysarthria, and paralysis of the voluntary facial muscles. Patients with pseudobulbar palsy may also have uncontrollable episodes of crying or sometimes laughter which usually last only a few seconds but may be totally disconnected from their mental state. Sudden noises or non-emotional conversation may trigger an episode of crying or laughter and lead to embarrassment and social withdrawal.
Beginning in the early 1960s, most reports about poststroke emotional symptoms attributed them to understandable psychological responses to the associated impairments. For example, Ullman and Gruen (1960) reported that stroke was particularly stressful to the organism, as Goldstein had suggested, because the organ governing the emotional response to injury had itself been damaged. Adams and Hurwitz (1963) reported that discouragement and frustration caused by disability could themselves impede recovery from stroke. Fisher (1961) described depression associated with cerebrovascular disease as reactive and understandable because "the brain is the most cherished organ of humanity." Thus, depression was empathically understood and, therefore, explained as a natural emotional reaction to a decrease in self-esteem produced by the combination of a life-threatening injury, the associated physical and intellectual disability, and the resulting loss of independence.
A few investigators, such as Post (1962), however, impressed by the frequency of the association between brain injury and emotional disorders, hypothesized the existence of direct causal connections between stroke and depression. The first systematic study, however, which examined emotional reactions in patients with stroke and other forms of brain damage was conducted by Gainotti (1972). Depressive catastrophic reactions were found more frequently among 80 patients with left hemisphere brain damage, particularly those with aphasia, than among 80 patients with right hemisphere brain injury. Patients with right hemisphere lesions, however, were noted to have an increased frequency of indifference reactions. The indifference reaction was also associated with neglect for the opposite half of the body and space. Gainotti agreed with Goldstein's explanation that the catastrophic reaction was a psychological response to severe physical disability. The indifference reaction, on the other hand, was not as easy to explain. Gainotti suggested that denial of illness and disorganization of the non-verbal type of synthesis may have been responsible for this emotional symptom.
Another systematic study conducted prior to the 1980s was done by Folstein et al. (1997), in which 20 patients between 1 and 2 months following stroke were compared to 10 patients with hip fracture or severe arthritis for frequency of depressive disorder as defined by having 8 or more of 13 depressive symptoms on a semi-structured mental state exam. Although the physical impairment in both groups was comparable (and matched in a subgroup), the stroke patients had a 45% frequency of depression compared to 10% in the orthopedic group. The authors concluded that, "mood disorder is a more specific complication of stroke than simply a response to motor disability."
Thus, explanations for the cause of emotional disorders produced by stroke have followed two lines of reasoning. One line suggested that brain injury may provoke specific emotional disorders, mediated through pathophysiological responses of the brain to injury. The other line of reasoning emphasized that emotional disorders were an understandable psychological response to the loss of ego integrity produced by brain injury. McHugh and Slavney (1998) have termed these differences as "perspectives of psychiatry." Each perspective is based on different, underlying assumptions and methods of reasoning. Poststroke emotional disorders are usually viewed from either the "disease perspective" in which the brain injury provokes a pathophysiological response which leads to clinical symptoms or from the "life story perspective" in which a person becomes vulnerable based on their life experience and in the midst of a stressful life event they develop an empathically understandable psychological disorder. These different perspectives have led to many of the continuing controversies and uncertainties about emotional disorders following stroke. Some clinicians, for example, using the life story perspective, wonder whether the depressive disorders associated with stroke are "real" depressions or whether they represent an entirely different category from major depressions seen in patients with unipolar or bipolar mood disorders (Gainotti et al. 1999). Similarly, empathic life story reasoning has led some health care professionals to speculate that these depressions should be encouraged or at least tolerated as a way of promoting the patient's "adjustment" and acceptance of the limitations imposed by the stroke. Baker and Baker (1976), for example, state in their discussion of Broca's aphasia that the patient's recognition of their deficit can be considered a more favorable prognostic finding in a patient who is depressed and apathetic. "We have seen patients who make no gain in aphasia therapy until some degree of depression appears, at which time benefit from the program can be noted." On the other hand, most health care workers now target emotional disorders such as depression for vigorous therapeutic intervention. Numerous studies (see Chapter 18) have demonstrated that depressed patients do not recover physically, cognitively, or in language function as well as comparable patients who are not depressed.
Although these differences in underlying assumptions about the cause of emotional disorders accompanying stroke can be viewed as obstacles to progress, they also represent fuel for research since it is only through systematic empirical research that these controversies can be resolved and a clear understanding of the nature, cause, and treatment of emotional disorders following stroke can be gained.
In summary, for more than 100 years, clinicians have recognized that emotional disorders accompany stroke. The clinical disorders produced by brain injury have fallen into two major categories. One category has included disorders in which the brain injury is viewed as a cause of emotional disorders which are also seen in patients without brain injury. These disorders are sometimes called symptomatic or secondary disorders. Examples of these disorders include depression, mania, anxiety disorders, and personality disorders. Another category of emotional disorders that occur after brain injury includes those that are unique to brain injury, including the catastrophic reaction, the indifference reaction, anosognosia or denial of illness, aprosodia (the inability to comprehend or express emotion), and the pathological display of emotion. The causes of these disorders are also viewed from two perspectives, one a direct result of pathophysiological changes produced by brain injury termed the disease perspective or alternatively as empathically understood psychological responses to impairment and/or loss in a vulnerable individual termed the life story perspective. Both of these concepts and etiological viewpoints continue to be endorsed by different groups of investigators as well as practicing clinicians.
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