In the eighteenth century, hysteria was called English malady, and although the various paralytic symptoms and unusual seizures were attributed to a disorder of the emotions, the biologic mechanism that mediated these symptoms remained a mystery. A prominent explanation relied on the newly discovered laws of gravity; it was postulated that the mind caused paralysis an arm by an “action at a distance,” just as gravity made the apple fall (Vieth, 1965). While medicine has made great advances since the eighteenth century and our understanding of the central nervous system has increased enormously, we still have trouble delineating the exact mechanisms that cause patients to express their emotional discomfort through somatic symptoms. We still do not have laboratory measures that will tell us whether an isolated neurological symptom is caused by a neurological illness or by a specific emotional state. Consequently, much of what is included in this chapter the clinical lore that has been gathered since the time of Charcot about how to differentiate neurological disorders from psychiatric disorders.
P.230
Commonality of Neurological and Psychiatric Symptoms
A solitary neurological symptom can have many different etiologies. Headache can be caused by anxiety, brain tumor, or head trauma and it is the task of the physician to determine the correct etiology so that appropriate treatment can be instituted. Although there is some help from imaging and other laboratory measures, the correct etiology (or the inability to stipulate an etiology) is most often determined by the clinical examination and history. As both neurological psychiatric disorders are related to dysfunctions of the central nervous system, it is not surprising that the major differential diagnosis is between a neurological or a psychiatric disorder.
Many general medicine patients suffer from symptoms that are frequently associated with disorders of the central nervous system. Kroenke and Mangelsdorf (1989) reviewed the records of 1000 patients followed in an internal medicine clinic. They found that 567 patients had at least one or more of the following possible neurological symptoms: fatigue, dizziness, headache, back pain, insomnia, numbness, impotence, as well such general symptoms chest pain, abdominal pain, dyspnea, edema, weight loss, cough, and constipation. A biologic etiology to the symptoms could be found in only 16 percent of patients; 10 percent of the symptoms were classified as psychological (the authors speculated that many of the unexplained symptoms were probably related to undiagnosed psychiatric disorders). Several studies of neurology inpatient admissions show that 30%-40% of the patients were given a psychiatric diagnosis of somatization disorder, whereas no specific diagnosis could be made for approximately 30 percent (Creed et al., 1990; Ewald et al., 1994). Carson et al. (2000a) found that 47 percent of 300 referrals to a neurology outpatient clinic met the criteria for a DSM-IV anxiety or depressive disorder. Raja (1995) found that 13.5 percent of acute psychiatric inpatients and 68.1 chronic psychiatric inpatients also had a neurological disorder. This enormous overlap of psychiatric and neurological disorders unexplained symptoms is precisely what makes the clinical practice of psychiatry and neurology so intriguing.
Such symptoms as dizziness, headache, syncope, and motor problems, are common to all patients, and particularly psychiatric neurological patients (Kroenke et al., 1992, 1993; Kapoor et al., 1995; Crimlisk et al., 2000). In the past when no cause for such symptoms could be found, they were labeled hysterical. With the advent of DSM-III term hysteria was banished from psychiatric nomenclature. In large part this was caused by the fact that hysteria had taken on so many different and sometime pejorative meanings, e.g., a paralysis; a personality disorder, or simply gross disorganized emotional discharge. Somatic symptoms of psychological origin are now grouped under the heading Somatoform Disorders, which in DSM-IV encompasses somatization
P.231
conversion, pain, and hypochondriasis disorders; all of these disorders manifest the presence of physical symptoms that suggest a general medical condition but are not fully explained by that condition. The somatoform disorders are descriptive categories and may represent one end of a continuum that ends with somatization disorder and begins with somatic symptoms related to anxiety depressive disorders (Katon et al., 1991).
Panic Disorder/Hyperventilation as A Cause of Common Neurological Symptoms
The symptoms of a panic attack, e.g., palpitations, sweating, trembling, shortness of breath, feeling of choking, chest pain, nausea and abdominal distress, dizziness, feelings of unreality, fear losing control or dying, paresthesias, and chills or hot flashes (DSM-IV, 1994) are very real and frightening to the patient. They are the symptoms that patients most frequently consult their physicians about. The question for the physician is do the symptoms represent a panic attack or do they represent some other medical disorder. Although panic attacks may occur spontaneously, most are precipitated by feelings of anxiety. There is a significant comorbidity between panic attacks and hyperventilation (Cowley and Roy-Byrne, 1989; Spinhoven et al., 1993). Hyperventilation usually causes any or all of the following symptoms: faintness, visual disturbances, inability to concentrate, nausea, vertigo, headache, a feeling of fullness in the head, chest, and/or epigastrium, breathlessness, palpitations, feelings of being hot or cold, sweating, paresthesias, and occasionally vomiting. The overlap of symptoms with a panic attack is evident.
Hyperventilation causes symptoms by lowering of PCO2. Two deep breaths produced by yawning or sighing are enough to alter PCO2 significantly and produce symptoms. The lowered PCO2 reduces cerebral blood flow, since there is a direct relation between PCO2 and the caliber of the cerebral blood vessels. In 240 seconds of over breathing, cerebral blood flow can be reduced by 40 percent (Plum and Posner, 1972) Thus, hyperventilation leads to cerebral hypoxia, and this is the cause of the EEG slowing so often seen with over breathing (Gotoh et al., 1965). Prolonged hyperventilation can produce respiratory alkalosis, which in turn can induce tetany. Hyperventilation also precipitate panic attacks (Katon et al., 1991).
Hyperventilation is a routine part of electroencephalographic testing and may induce an epileptiform abnormality. Of course, it can also induce actual seizures. Hyperventilation in response to anxiety may, fact, be a major mechanism by which emotional tension induces seizures in susceptible individuals (Mattson et al., 1970). The cerebral hypoxia caused by hyperventilation, when compounded by a mild degree of orthostatic hypotension and/or the Valsalva maneuver, may
P.232
reduce cerebral blood flow to the degree that the patient faints or has a tonic convulsion. (Many young boys have learned to induce syncope by over breathing and then performing the Valsalva maneuver for the amusement of their friends.)
Hyperventilation can also cause nonspecific ST-and T-wave changes in the electrocardiogram (EKG) (Christensen, 1946), and many hyperventilation syndrome patients showing such EKG changes have been admitted to coronary care units. Hyperventilation is often associated with air swallowing and this, in turn, can lead to epigastric distress and gastrointestinal symptoms.
Hyperventilation is a very common response to anxiety. One might almost call it a universal human reaction to anxiety, since is part of the autonomic response to threatening situations. The somatic symptoms it causes may often cause the unwary physician to pursue an extensive workup that only serves convince the patient that something is physically wrong with him thus reinforcing the medical symptoms and ignoring source of the anxiety (Katon, 1991).
Somatization Disorder
Somatization disorder as defined in DSM-IV encompasses what has been previously referred to as hysteria or Briquet's syndrome. DSM-IV defines somatization disorder as a polysymptomatic disorder that begins before the age of 30 and is characterized by at least four pain symptoms, two gastrointestinal symptoms, one sexual symptom, and one pseudoneurological symptom. This is a descriptive category and one can see why when a patient complains of many somatic symptoms he or she is likely to be assigned the category of somatization rather than medical disorder (Katon et al., 2001). Historically, the DSM-IV criteria were developed from the work of Perley and Guze (1962). In their view the term hysteria had been used indiscriminately for any psychosomatic symptom so they developed an elaborate and restrictive system for diagnosing hysteria (Briquet's syndrome). They assigned the diagnosis if patients had (1) a dramatic or complicated medical history before age 35; (2) a minimum of 15 symptoms distributed in at least 9 of 10 organ systems and (3) no medical diagnosis that adequately explained their symptoms. For 6 to 8 years, Perley and Guze studied 39 patients who met these criteria. Ninety percent of the sample did not develop any other illness that might explain their symptoms, however, the patients tended to develop additional psychosomatic complaints over the years. Using criteria first designed by Perley and Guze and incorporated in DSM-IV a patient so labeled usually has an almost lifelong history of unexplained somatic symptoms.
P.233
Unexplained Symptoms
If a patient presents with long history of many different unexplained somatic symptoms it should make one think immediately of a possible somatization disorder or other psychiatric illness A large number of unexplained medical symptoms often indicates that the patient has an anxiety or depressive disorder (Katon et al., 1991d; 2001). In a recent study, Carson et al. (2000b) found a high incidence of unexplained symptoms and psychiatric disorders in neurology practice. They studied 300 new referrals to a neurology clinic at general hospital who had unexplained symptoms. A third of these cases remained unexplained. Seventy percent of the patients in unexplained group had anxiety and depressive disorders, whereas only 32 percent of the explained group had a psychiatric diagnosis. Interestingly this high number of unexplained symptoms is not much different than is found in other medical specialty clinics. Kroenke and Mangelsdorf (1989) reported that only 16 percent of unexplained physical complaints were explained by organic disease. Hamilton et al. (1996) found that the symptoms of 53 percent the patients referred to a GI clinic and 32 of patients referred to a cardiac clinic could not be medically explained. They also noted that the patients with unexplained symptoms complained of significantly more symptoms, more bodily pain, and had impaired social functioning.
The most pressing clinical concern is whether the unexplained symptoms represent the early symptoms of a neurological disorder or instead are manifestations of a psychiatric disorder presenting with neurological symptoms. In classic study Slater and Glithro (1965) attempted to answer this question. They evaluated 85 patients 10 years after they had received a diagnosis of hysteria (most would now be called conversion reactions). Of the 85 patients with a chart diagnosis of hysteria, they found on follow-up that 22 had later been given a diagnosis of an organic disease that could have explained their initial symptoms. At the time they were diagnosed as hysterical, 19 of the patients had medical illnesses that could have explained their symptoms. Eight had died of their medical conditions. Well over half the total population of “hysterics” had medical problems that were mistaken as psychogenic or that had precipitated emotional reactions. Four patients had committed suicide. In 1998 Crimlisk and colleagues published a paper entitled “Slater Revisited” reporting how they replicated, with modern research techniques, Slater and Glithro's study of 1965. Their paper highlights the changes in research methods that have taken place since 1965. They used clearly defined diagnostic criteria, standardized interviews, and rating scales to examine 73 consecutively admitted patients a neurological clinic, who had unexplained motor symptoms. The patients were followed up 5–7 years after the initial visit. During follow-up period only three subjects developed a neurological disorder that fully or partly explained their initial symptoms.
P.234
Seventy-five percent of the patients met criteria for a psychiatric diagnosis (45% had personality disorders) and in 75 percent of those given a psychiatric diagnosis; this diagnosis coincided with the onset of the motor symptoms. Only one patient developed a new psychiatric diagnosis that could have explained his symptoms. Interestingly, 42 percent had a history of neurological disorder. This study indicates that conversion disorder is not a benign condition in the sense that at follow-up only 33 percent of the patients were employed full time and the symptoms in 52 percent had remained the same or got worse.
Conversion Disorders
Conversion disorders can be a symptom of somatization disorder or a separate diagnostic category. Conversion disorders are defined in DSM-IV as unexplained symptoms or deficits affecting voluntary motor sensory functions that suggest a medical or neurological condition. The differentiation of conversion symptoms from neurological disease is a frequent problem in neurological, medical, and psychiatric practice. Some physicians believe that somatization disorder, as defined above, can be differentiated from isolated conversion symptoms. In our experience, conversion symptoms rarely occur in isolation. When doctors label unexplained findings “conversion reaction” in patients lacking a history of hypochondriasis, the diagnosis is almost invariably wrong. We have found that two criteria are extremely important in making a positive diagnosis of conversion reaction. Unless both are present, the diagnosis should be held in doubt. These criteria are (1)that no medical diagnosis explains the patient's symptoms and (2) that there is, even in children, a past history of psychosomatic illness (conversion reaction, hypochondriasis, or psychophysiological reaction).
The two classic hallmarks of conversion, la belle indifference and secondary gain, have been, in our experience, more often misleading than helpful establishing the diagnosis. Apparent indifference is often a sign of stoicism, and stoical hospitalized patients are often seriously ill. Indifference to illness is also a common sign of brain damage. This is the basis the therapeutic effect frontal lobotomy. Many patients with progressive brain disease are mercifully indifferent to their desperate condition. Conversely, individuals may be excited and anxious when they develop conversion symptoms, though it is true that some do manifest la belle indifference.
The secondary gain, which refers to the reward for the patient who develops a conversion disorder, is often difficult to identify. Sometimes it is no more than staying in the hospital and avoiding contact with the family, sometimes it may be a subtler or even a fantasized gain. On the other hand, patients who have been injured in automobile or industrial accidents often have lawsuits or compensation claims pending, which are justified but could be mistaken as secondary
P.235
gain by their physicians. No one has ever put forward criteria which one can distinguish a legitimate from secondary gain. The gain may be quite clear after the diagnosis is established, but as a diagnostic aid, it is almost useless.
It has been our experience that most medical doctors consider a patient conversion disorder or somatizer either when the physician cannot imagine an organic lesion that could explain his symptoms or when a patient with well-known history of psychosomatic illnesses presents himself for examination. Mistakes are made because the physician's diagnostic acumen is naturally a function of his previous experience and knowledge. No one can know everything, peculiar facets of difficult cases organic disease that even the most experienced clinician has not encountered before can appear. Also, the tendency toward psychosomatic illness does not confer immortality, and even hysterics can become sick and die.
Certain neurological diseases seem to predispose conversion symptoms. Patients whose judgment is impaired by mental retardation, intoxications or other encephalopathies, encephalitis, brain tumor, or multiple sclerosis may elaborate symptoms and signs or exaggerate real symptoms. This may draw attention away from the real disease, sometimes with tragic results.
It may be worthwhile to consider some of the classic conversion symptoms that mimic neurological conditions. In doing so, we wish to demonstrate that symptoms that cannot be easily ascribed to an organic lesion constitute an inadequate basis for the diagnosis of conversion disorder or somatization. The diagnosis requires such symptoms in addition to a past history of psychosomatic illnesses. Both are necessary; neither is sufficient.
Specific Classical Conversion Symptoms
Inability to swallow or feeling a lump in the throat is typical of globus hystericus. Normal results on direct examination of the nasal and oral pharynx on barium swallow studies are sufficient to rule out most lesions that could cause similar symptoms. On the other hand, both myasthenia gravis and polymyositis may begin with intermittent weakness of the swallowing mechanism. At the time of examination, patient may be able to swallow normally and appear to be well. Similarly, pseudobulbar palsy, which interferes with swallowing, may wax and wane in severity. When unassociated with other signs of neurological disease, such symptoms have been mistakenly considered hysterical.
Hemisensory loss conversions usually involve half the entire body from head to foot and from the extremities to the midline. A pinprick felt normally on one side of the linea alba will not be felt on the other side. Sensory splitting at the
P.236
exact midline and a shift of perception toward the side normal sensation are considered by many to be hard-and-fast signs of conversion; organic hemisensory deficits typically appear 1 or 2 cm toward the anesthetic side of the midline. This is because segmental sensory nerve fibers extend 1 or 2 cm across the midline from the “good” side into the anesthetic side. It is also said that diagnosis of conversion can be confirmed by testing vibratory sensation. A tuning fork placed on the skull or the sternum to one side of midline should be felt by neurological patients no matter which side the hemisensory loss is on because the oscillations of the tuning fork are transmitted throughout the entire bone. If the patient claims not to feel vibrations on one side, he may have a conversion reaction.
Unfortunately, these sensory signs of conversion are rather unreliable because some patients with neurological diseases report what they think their examiner wishes them to report, claiming that a change in sensation occurs at the midline when in fact this may not be so. In addition, it is conceivable that minorities of patients have a physiologically variant pattern sensory function in which the anesthesia caused by a brain lesion does, in fact, change at the midline or to the “wrong” side of midline. Patients who report absent vibratory sensation on the anesthesia side of their skull or sternum may in fact feel the vibrations less on that side but report to the examiner they feel nothing be consistent. Whatever the reason, it is an empirical fact that patients with lesions that are undeniably organic—strokes, tumors, demyelinating diseases— have reported sensory changes with characteristics that are considered typical of hysteria.
Hemiplegic conversions may be diagnosed in the following way: placing his hands underneath the patient's paralyzed heel while the patient is supine, examiner asks the patient to raise his normal leg. The examiner can thereby determine whether or not the patient is able to move his paralyzed leg because the normal response while raising one leg is to push down with the other. If the patient pushes down with his paralyzed leg, the factitious nature of his paralysis should be clear. By reversing the process and asking patient to raise paralyzed leg, the examiner can determine whether or not the patient is actually trying to lift it. If the patient does not push down with the good leg, examiner can conclude that he is not trying to raise the paralyzed leg. This test is only useful in complete hemiplegia, however, and will not help in distinguishing conversion hemiparesis (which is more common than conversion hemiplegia) from true hemiparesis. The presence of unilateral changes in deep tendon reflexes, spasticity, and Babinski's reflex provides objective evidence indicating neurological disease. The absence of these alterations, however, cannot establish the diagnosis of conversion.
Paralysis of the extraocular muscles, those face and the tongue, does not occur in conversion syndromes. Paresis of the cervical muscles, with difficulty elevating the head from a pillow or with drooping of the onto the
P.237
chest, is extremely rare. Paralysis of the trunk muscles also rare. Thus, conversion paralysis or paresis usually involves one or more of the extremities. Conversion weakness of the leg is more frequently encountered than weakness of the arm.
If the patient is ambulatory, manner in which he moves, dresses, undresses, and mounts an examining table should be noted; for conversion paralysis is, mainly one of paralysis of movement as opposed to individual muscles. The patient with a conversion disorder may complain that all movements at one joint are affected, but the object of the examination is to note the distribution of the paralysis as well muscles affected and to determine if the patient can still use the affected muscles to perform movements that he does not realize entail their use. On examination, patients with conversion weakness may manifest simultaneous and equal contraction of agonistic antagonistic muscles, hence “paralysis.”
Hemiparesis conversion is characteristically associated with give-way weakness. This means discontinuous resistance during direct muscle testing. Give-way weakness is absolutely diagnostic of factitious weakness, but occasionally a patient will exaggerate mild, real weakness in order to convince the examiner that he is, in fact, weak. In such cases, the patient may feel that examiner is going to miss the diagnosis and so he helps out. Reflex abnormalities, when present, can rule out conversion but the absence of such abnormalities will not establish the diagnosis.
Astasia-abasia, or gait conversion, can sometimes be extremely difficult to differentiate from movement disorders. Physicians routinely place emphasis on the following indications that a disordered gait is hysterical. The patient walks well, never falls, and does not injure himself when unaware that be is being observed. The conversions involving gait are usually recognized by their bizarre character and dissimilarity from any disorder of gait produced by organic disease. In hemiplegia, the affected leg may ostentatiously be dragged along ground and not circumducted as in organic hemiplegia. When severe, astasiaabasia will be manifested by the patient's attempting to fall as opposed organic patient who does his best to support himself. Some patients, walk with great difficulty, cling to walls and furniture to the examiners, but manifest normal power and coordination while lying in bed. This kind of inconsistency suggests conversion.
Because almost all movement disorders are worsened by anxiety, it is not wise to accept without reservation reports by nurses and other staff the effect that the patient is able to walk nearly normally when unaware that he is being observed. If the patient is made nervous by an examiner or a large group of physicians on rounds, his organic movement disorder may worsen. Sometimes patients with gait conversion problems do, in fact, fall and may accidentally hurt themselves, so a history of falls with occasional scrapes and bruises does not necessarily rule out conversion.
P.238
Inconsistency of gait disturbance is common in apraxias caused by frontal or subcortical cerebral disease. Peculiarities of affect in such patients and an absence of Babinski's sign may lead to an incorrect diagnosis conversion. Formal mental status and examination (seeChapter 7) are helpful in identifying these patients.
Gait disorders, whether neurological or psychosomatic, often cause a certain amount of confusion among clinicians. It is not at all uncommon to find a minority of competent neurologists who will consider a patient to have either neurological or a conversion disorder even in the face of an opposite majority view. Fortunately, there are relatively safe and fairly objective tests for conversion in such cases: amytal infusion and hypnosis. Amytal is infused intravenously at a rate of 50 mg per minute until nystagmus develops. This usually requires 250 to 500 mg. As soon as nystagmus develops, the infusion is stopped and the patient is asked to perform motor task that he previously found difficult. If there is a substantial improvement in his movement disorder, the diagnosis of conversion is supported. If the gait deteriorates, the diagnosis neurological disorder is supported. This test often extremely helpful but it can be misinterpreted. When anxiety is responsible for marked worsening of an organic movement disorder, amytal or hypnosis might improve the gait by relieving anxiety. When neither deterioration nor improvement is clear-cut, no inference about the etiology of the gait disturbance can be made.
It is probably fair to say that conversion dystonia and/or chorea virtually never occur together. It is possible to be misled by certain inconsistencies. Some inconsistencies are diagnostic. For example, in torticollis the examiner may not be able to straighten the patient's head even by exerting maximal effort, and yet the patient can often straighten his own head by merely touching forehead with an index finger on the side toward which his head is tilted. This inconsistency is unexplained but is characteristic of dystonia neurologic origin.
Conversion rigidity increases in proportion to the effort made by examiner to move the rigid extremity. This feature may also be present in the frontal lobe disorders that lead to gegenhalten or counterpull. Gegenhalten is a semivoluntary resistance the patient increasingly offers to passive movement of his limbs. When the examiner attempts to extend the patient's elbow, for example, patient will resist, and his resistance will increase as the elbow is extended further. Forced grasping may be seen in response to tactile stimulation of the patient's palm by the examiner's fingers. In frontal lobe disorders, when the examiner attempts to extend the patient's fingers while disengaging his own from patient's grip, he may encounter counterpull.
Visual conversion symptoms include monocular diplopia, triplopia, tunnel vision, and blindness. Though monocular diplopia is, in most cases, caused by hysteria, ocular pathology such as dislocated lenses, cataracts, and parietal lobe lesions can give rise to it (Kestenbaum, 1961). A patient under our care who
P.239
was recovering from well-documented disseminated leukoencephalitis reported triplopia, which is theoretically a physiological impossibility.
A test for the psychological etiology of tunnel vision depends upon the fact that the normal visual field expands in a cone of vision as the distance from target to the patient is increased. If patient's field is identical at 2 meters from his eye to what it is at 1 meter from eye, the inconsistency suggests conversion. Patients who are blind on the basis of neurological disease usually have no pupillary response to light. In disease of the parietal or occipital lobes, however, cortical blindness may be present and pupillary reflexes will remain normal. If a patient with blindness and normal pupillary responses is presented with a slowly rotating, vertically striped drum and develops involuntary tracking movements (optokinetic nystagmus), his blindness can be considered factitious.
There are two tests that can be useful in detecting unilateral conversion blindness. The patient is asked to read a line of alternating black and red letters while a red glass is held over the good eye. In conversion blindness patient will be able to see the red letters with the bad eye and will read all the in the line. Also, a distorting prism can be placed over the good eye and the patient will still be able to perform tasks requiring intact vision. Convergence spasms and blepharospasm (the result of spasm the orbicularis oculi) can be manifestations of hysterical disturbances ocular movements. Defects in the lateral and vertical planes of gaze caused by hysteria may induce a kind coarse nystagmus. However, blepharospasm can also be a sign of Meigs' syndrome, which is an involuntary, dystonic syndrome.
Conversion deafness can be easily demonstrated as the patient awakened from sleep by sound. A conversion reduction of hearing (as opposed to deafness) is difficult to distinguish from neurologic disease of the ears. Variability of responses to audiological tests can reflect a neurological syndrome as well as conversion.
Conversion amnesias, fugue states, and pseudodementia can also confound the diagnostician. In earlier chapters, particularly the one on epilepsy, we noted that transient fluctuations in consciousness can be associated with epileptic conditions and we suggested some guidelines for diagnosis. Conversion states may partially mimic epilepsy and can be confused with it. It is a rare psychiatrist or neurologist who has not been confronted with a patient says he does not know who he is, or who he was at a particular time, or where he came from. Such conversions states are most often seen in times of stress, for instance, among soldiers during war or in individuals indicted for crimes. Characteristics that help to distinguish those with psychogenic amnesia or dissociative states from neurological patients include the following: (1) the patient is able to carry out complex functions during the time of amnesia. (2) Memory loss and shift of identity to another person or personality are usually sudden. (3) The patient's behavior is fairly well integrated in that he usually has enough money to get
P.240
where he is going and takes time to eat and drink. (4) Loss of memory usually affects a specific section of life or ability, that is, arithmetic recognition certain relatives. (5) The transition to a normal state is abrupt. (6) There no history or physical evidence of neurological disease.
Berrington et al. (1956) studied 37 cases of fugue state and noted that depression was a frequent concomitant. Interestingly, they noted that a high proportion of the patients had a history head injury and they speculated that this may have precipitated the fugue state. They also observed that the patients were usually completely unaware of their identity and past life and acted as if they were in a dream. During the episodes, they could travel and seemed able to answer complex questions adequately. They had either partial or complete amnesia for the episodes.
Even if all of the characteristics of amnesia indicate hysteria, unless the past history indicates a psychosomatic tendency, the diagnosis should be held in doubt. Other conditions can cause dissociative states. For example, the clearly neurological syndrome of “transient global amnesia,” described by Fisher and Adams (1964) and by Shuttleworth and Morris (1966) is marked by periods of confusion and disorientation to time and place that usually last a few hours. Patients in these two studies had no recollection of events and described them-selves as feeling strange during the episodes of amnesia. In contrast to the abovementioned syndromes of conversion amnesia and fugue state, which usually affect individuals in the third or fourth decade, these patients were all middleaged or elderly and had a history of hypertension atherosclerosis. Although they did not lose their identity, they could not retain new information during these episodes. It was hypothesized that the episodes resulted from transient ischemia, specifically ischemia of the mamillary-hippocampal complex.
Complaints of pain are rarely completely fabricated. Patients who are considered to have conversion pain syndromes complain of severe pain, but they exhibit none of the physical reactions that are expected to be associated with pain of neurologic origin and thus present an appearance that belies their allegations of intense suffering. The diagnosis of conversion pain may also be applied to patients who are unusually distressed and agitated by their pain. Some of the most common syndromes ascribed to conversion are headaches, low back pain, abdominal pain, and atypical facial pain.
Many physicians regard low back pain as a common syndrome that can result from conversion and are likely to consider the diagnosis if there is no muscle spasm, if the neurological examination is normal, and if the standard imaging studies are completely normal. Complete investigation might also include pelvic and rectal examinations, prostatic specific antigen and alkaline phosphatase determinations. An incomplete and negative evaluation can erroneously seem to support the diagnosis of conversion.
P.241
Undiagnosable abdominal pain is very often the result of aerophagia. The statements of many physicians who attend pain clinics to the effect that two-thirds to three-quarters of their patients have solely psychosomatic pain (i.e., conversion pain) are incorrect in our opinion. Though patients often exaggerate real pain, it is the responsibility of the physician to determine its underlying physical cause.
A variety of diagnostic myths that have been perpetuated with regard to pain: (1) Continuing pain in patients who have undergone multiplesurgical procedures for pain without improvement means the is either psychogenic or an undesirable side effect of surgery. Often, all this may imply is that the original cause of the pain has not been diagnosed or treated. (2) A high intake of analgesics, or patient requests for analgesics more often than every 4 hours, indicate that the patient's problem is not pain but addiction. In fact, some analgesics have a duration of action that is shorter than 4 hours (Goodman and Gilman, 1990). (3) A lawsuit combined with an undiagnosable pain problem is a sure sign of psychogenic origin. If the lawsuit is settled, pain will disappear. The data supporting this common assumption are lacking. Lawsuits often justified and patients who settle them do not necessarily improve. (4) Negative findings on repeated tests and bizarre complaints with no physical findings indicate that pain is psychogenic. Some of the most bizarre head pains we have seen were easily diagnosed as temporomandibular joint (TMJ) syndromes. True, repeated CT scans, EEGS, and standard neurological examinations revealed no abnormalities in these cases, but few physicians routinely palpate the head and face in headache patients. This is essential for the diagnosis of TMJ syndrome. Pain syndromes in other parts of the body may also be diagnosed when the correct test is done.
What we have tried to demonstrate with these examples is that the diagnosis of conversion can be made in error, even when the symptoms are classic. It is exceedingly rare for conversion disorder to be the first manifestation of a psychosomatic tendency. Conversion disorders are nearly always preceded, even in children, by other symptoms deemed psychosomatic, many of which have not resulted in a visit to the physician. Stomachaches and headaches with frequent school absences, sleep disturbances, and/or school phobia, precede conversion hysteria by many months or years in childhood. Unless there is a history of previous psychosomatic disorders, the diagnosis of conversion reaction should remain open to question. On the other hand, psychosomatic illness is so common that its presence should not blind the physician to the possibility of organic disease. Of patients referred for neurological examination, 25 to 40 percent have psychosomatic complaints (Creed et al., 1990; Ewald et al., 1994; Carson et al., 2000a).
P.242
Headache
The cause of headache is one of the most critical determinations a physician has to make. Headache can be a symptom of anxiety or depression, it can be the first symptom of a brain tumor. It is not our purpose to provide a comprehensive discussion of the disorder. For this the reader is referred to two excellent books, Diamond and Dalessio (1999) Dalessio's Silbersteins 7th edition of Wolf's Headache(2001). We will merely put forward the criteria from patient's history that are helpful in distinguishing headaches of psychogenic origin from those of neurological origin.
In general, if the headache is worst headache ever experienced by the patient, if it is a new headache, or if it is associated with neurological signs, the physician must assume that an acute or life-threatening situation may be present, and a full investigation should be promptly initiated. A CT scan should the first test. If normal, lumbar puncture should follow. When this rule is followed, the diagnoses of subarachnoid hemorrhage, meningitis, encephalitis, or brain tumor will not often be missed. For teaching purposes, we advise medical students to fully investigate any headache that is “the worst, the first, or cursed (by neurologic abnormalities).” Conversely, any headache that has been present for more than a year, almost irrespective of its character, is rarely caused by a serious or progressive disorder. In general, one should not think of headaches as related to emotional factors if the headache is of sudden onset, caused by reclining or by coughing, awakens the patient from sleep, is unilateral, even if the headache persists for days, weeks, or months.
Headaches that are dull, generalized, and constant for many days in a row usually have no neurological cause. Patients with such headaches often describe, a pressure feeling, which is what they mean by headache. These patients almost always have an impressive past history of psychosomatic illness and are depressed. The unremitting character of the headaches and the patient's complaints of their severity usually contrast with the fact that patient is nonetheless able to work. Analgesics, tranquilizers, and sedatives are usually ineffective, but antidepressants often help.
Tension headaches are presumably caused by muscle tension. When the muscles in the posterior neck and temples are under the stress of continuous contraction, they begin to ache just as muscles anywhere in the body do when they have been overworked. The pain reflection is then generalized over the head. Such headaches are dull and steady, though occasionally, a sustained muscle contraction headache is followed by a typical vascular (throbbing) headache, and the two types of headache will coexist in an attack. Tension headaches can usually be attributed to emotional tension, but sometimes cervical pathology, such as osteoarthritis or cervical disc disease, will cause headache by inducing cervical muscle contraction. Tension headaches characteristically occur in the
P.243
morning on awakening or in the late afternoon. These headaches are worse during the work week and tend to be relieved on weekends vacations. Aspirin and sedatives generally relieve them. Tension headaches are often mistakenly attributed to essential hypertension or chronic sinusitis. With few exceptions, by the time a patient comes to a doctor for treatment of tension headaches, they will have occurred for months or years. Surprisingly, this holds true children too. Some patients who initially deny the long-standing nature of their headaches, when pressed will admit that they have had similar headaches in the past, though perhaps not so severe or so frequent. This point is important in distinguishing ordinary tension headaches from those caused by brain tumors.
Headaches are caused by brain tumors in two ways, increased intracranial pressure and by traction of the mass on pain-sensitive structures within the skull. No single headache is characteristic of a brain tumor. Headaches caused by increased intracranial pressure are, if anything, remarkable for being nonspecific. They are mild, dull, aching, and very often bifrontal or bioccipital. They may be present in the morning on awakening, last a few hours, and get better as day goes on. They may not occur every day. Thus, they be similar to tension headaches. Headaches produced by increased intracranial pressure, however, are characteristically of recent onset, usually starting within a few weeks before the patient presents himself to the physician. We have found this to be the single most important feature in distinguishing tension headaches from those caused by increased intracranial pressure. When brain tumors cause headaches by traction on pain-sensitive structures, headaches are often lateralized or localized to one spot. Intraventricular tumors can cause headaches that may be exacerbated or relieved by changes in position. Thus, when a patient complains of a headache that is brought on by putting his head in one position and relieved by changing the position, a mechanical factor must be considered and the possibility of a tumor investigated thoroughly. It is an ominous sign if sitting up relieves headache.
Prostrating headaches that are relieved by sleep, whether they throbbing and severe, lasting several hours, and associated with nausea, and/or vomiting, are usually migraines. This is so whether or not they are unilateral preceded by typical ischemic symptoms such as flashing lights, scintillating scotomata, or sensory or motor symptoms. Migraine headaches begin with throbbing but when the pain reaches its zenith, the throbbing may stop. Usually at this time is unbearable, prostrating, and associated with vomiting photophobia. Curiously, at this point in the headache, many patients can fall asleep and if so, they awaken improved. The incidence of migraine is the same in men and women but, presumably because of hormonal factors, headaches are usually more severe and more frequent in women. Patients with such prostrating headaches usually have a positive family history of migraine, which suggests hereditary basis. There is a familial comorbidity with anxiety and affective disorders
P.244
(Merikangas et al., 1993). Migraine headaches occur primarily in the young, often begin in the first decade, and seldom develop for the first time after the age of 30 years. They may tend to occur more frequently on weekends and vacations and are not satisfactorily relieved by ordinary nonnarcotic, orally administered analgesics. Recent studies have found a strong association between migraine, with or without aura, and affective panic disorders. Panic disorder was also comorbid with other types of severe headache; in most cases the headache syndrome preceded the onset of panic disorder but not in all cases (Breslau et al., 2001). There also is a significant comorbidity with epilepsy and stroke (Breslau and Rasmussen, 2001). Propranolol, other beta-blockers, have become useful therapeutic agents in reducing the frequency and severity of attacks. Antidepressants, particularly the tricyclics and the SSRIs, are also widely used with good effect but one wonders if tension headaches associated with depression have been labeled migraine in many patients who have experienced relief from antidepressants (Merikangas, 1991). Ergot-containing preparations are usually effective in stopping such headaches if they are taken the early stages of the attack, especially during the prodromal period. Sumatriptin and other serotonin agonists have become the first line of therapy for severe attacks.
The syndrome of TMJ is often misdiagnosed as atypical migraine, atypical facial pain, or a functional disorder. The steady, nonthrobbing nature of the pain at onset distinguishes it from migraine. The occasional very brief headache, lasting minutes, and the lack of throbbing at the onset are other helpful features in distinguishing the TMJ syndrome from migraine. The tenderness of affected muscles distinguishes it from atypical facial pain, and the unilateral nature of the pain should distinguish it from functional or ordinary tension headache.
Temporomandibular joint pain is characterized by a usually unilateral, deepseated pain in the side of face, which is brought on or exacerbated by movements of the lower jaw. The pain is related to spasm muscles that operate the jaw, mainly temporalis and pterygoid, but rarely, masseter. It is not usually associated with actual pathology of the temporomandibular joint so that the name is somewhat misleading. Radiographs of the joint are abnormal in only a minority of cases. The syndrome is most common in young women. The characteristics of the pain are typical muscle pain: it is steady (nonthrobbing) and severe. After several hours, throbbing can develop. The pain is exacerbated by quick stretches of the muscle, as in mouth opening, and by more prolonged use of the painful muscle, as in chewing. It may follow visits to the dentist when prolonged opening of the mouth and stretching muscles mastication are necessary. Bruxism, yawning, shouting, singing, fellatio, and direct trauma to the jaw are other contributing factors.
Given that TMJ pain is usually experienced around or behind the eye and along the temple, palpation of the temporalis muscle and attempted lateral movement of the jaw against pressure usually produces pain. When the body pterygoid muscle is palpated from inside the mouth, there great tenderness,
P.245
and the muscle itself often feels tense and hypertrophied to the examiner. Direct pressure over the temporomandibular joint may also cause pain. Many patients with this syndrome are depressed, do not sleep well, and awaken feeling tired. They often grind their teeth during sleep and yawn a great deal in the morning after awakening. Thus, bruxism and yawning seem to be the major contributing factors in many cases.
The syndrome is easier to diagnose than treat. Conservative therapy consists of heat applied to the affected area, a diet of soft foods, limitation mouth opening, and mild analgesics muscle relaxants. Certain exercises surgical interventions have been helpful, and antidepressants are appropriate in some cases in which depression has caused sleeplessness, bruxism, lassitude, and frequent yawning and these manifestations of depression have caused pain, but no one specific treatment has emerged (Gaudet and Brown, 2000).
Another form of headache that is common but perhaps little known to psychiatrists often follows minor or major head trauma. This occurs in the posttraumatic stress syndrome, which also involves giddiness, irritability, sensitivity to noise, and minor memory concentration difficulties. Lishman (1968) noted that the symptoms were unrelated to either extent or the location of brain damage. Jacobsen (1969), however, reported that the symptoms were more likely to occur if the patient had been rendered unconscious at time of impact. He observed that the headaches usually stopped within 2 months of the iniury and that most patients were free of all symptoms within 4 years. This syndrome is not usually associated with radiographic or electroencephalographic changes and many have questioned its organic basis. The distinctiveness of the syndrome argues against this psychosomatic view of its etiology, in our opinion, as does the fact that it may occur in individuals with no history of psychosomatic disease or pending lawsuits. Recently McAllister et al. (1999) showed that patients 1 month after traumatic brain injury had FMRI evidence of significant differences in the right parietal and dorsolateral cortical regions when asked to do a working memory task, as compared to controls, thus lending some physiological basis to the symptoms of poor concentration following traumatic closed head injury. Arciniegas et al. (2000) has also shown impaired auditory gating manifested by nonsuppression of P50 evoked waveforms in patients with persistent symptoms following traumatic brain injury. He postulates that this defect may represent a persistent cholinergic dysfunction and has found that low-dose donepezil provides some symptomatic improvement (Arceniegas, 2002).
Conclusion
Conversion disorders and somatization have long perplexed physicians. The serious study of these syndromes was inaugurated by the neurologist, Jean Martin Charcot (1825–1893). His studies provided the springboard for modern psychiatry
P.246
through the work of one of his most illustrious pupils, Sigmund Freud. Conversion and somatization have been designated variously as a neurological syndrome, a psychiatric syndrome, and a disease of society (Vieth, 1965). To a degree these disorders crystallized the dilemma we have had in writing this book: We have had to constantly check ourselves from referring to psychiatric illnesses as functional, thereby implying a separateness from neurological illnesses that do not exist. It should be apparent that one or more neurological syndromes could produce almost every abnormal emotional state. It is selfevident that all behavioral symptoms, whatever their etiology, are mediated by the central nervous system, a common pathway for many different pathological processes. Though most conversion syndromes exist in the absence of neurological disease, one wonders why one patient and not another develops conversion in response to apparently similar life stresses. There is no clear answer this problem. Genetic aspects have been incompletely explored, and we have not been able to identify causative environmental influences. Though our knowledge of these conditions has increased considerably over the years (we no longer believe that the varied symptoms are related to a wandering uterus, and we have been able to formulate criteria for their diagnoses), our skills are still exercised fundamentally at a descriptive level. This is still true of many neurological and psychiatric conditions. Though we look to basic medical research for the full understanding of these diseases, it behooves us meanwhile to polish our clinical skills and learn what we can from observation and description.
References
Arciniegas, D., A. Olincy, J. Topkoff, et al. Impaired auditory gating and P50 nonsuppression following traumatic brain injury. J Neuropsychiatry 12:77, 2000.
Arciniegas, D., J. Topkoff, C. Anderson, et al. Low-dose donepezil normalizes P50 physiology in traumatic brain injury patients. J Neuropsychiatry 14:115, 2002.
Berrington, W. P., D. W. Liddell, G. A. Foulds. A re-evaluation of the Fugue J Ment Sci 102:280, 1956.
Breslau, N., L. Schultz, W. Stewart, et al. Headache types and panic disorder. Neurology 56:350, 2001.
Breslau, N., B. Rasmussen. The impact of migraine. Neurology 56 (Suppl 1):S4, 2001.
Carson, A., B. Ringbauer, L. MacKenzie, et al. Neurological disease, emotional disorder, and disability. J Neurol Neurosurg Psychiatry68:202, 2000.
Carson, A., B. Ringbauer, J. Stone, et al. Do medically unexplained symptoms matter? A cohort study of 300 new referrals to a Neurology outpatient clinic. J Neurol Neurosurg Psychiatry 68:207, 2000.
Christensen, B. Studies on hyperventilation. II. Electrocardiographic changes in normal man during voluntary hyperventilation. J Clin Invest 24:880, 1946.
Cowley, D., P. Roy-Byrne. Panic disorder and hyperventilation syndrome. In: Anxiety New Findings For the Clinician, P. Roy-Byrne, ed. American Psychiatric Press, Washington DC, 1989, p. 19.
P.247
Creed, F., D. Firth, M. Timol, et al. Somatization and illness behavior in a neurology ward. J Psychosom Res 34:427, 1990.
Crimlisk, H., Bhatia, H. Cope, et al. Slater revisited: 6-year follow-up study of patients with medically unexplained symptoms, BMJ316:582, 1998.
Crimlisk, H., Bhatia, H. Cope, et al. Patterns of referral in patients with unexplained motor symptoms. J Psychosom Res 49:217, 2000.
Dalessio, D., J. Silberstein. Wolfe's Headache and Other Head Pain, 7th Ed. Oxford University Press, New York, 2001.
Diamond, S., D. Dalessio. The Practcing Physicians Approach to Headache, 6th Ed. Saunders, Philadelphia, 1999.
Ewald, H., T. Rogne, K. Ewald, et al. Somatization in patients newly admitted to a neurological department. Acta Psychiatr Scand 89:174, 1994.
Fisher, C. M., R. D. Adams. Transient global amnesia. Acta Neurol Scand 40 (Suppl. 9):7, 1964.
Gaudet, E., D. Brown. Tempromandibular disorder treatment and outcomes. Cranio 18:9, 2000.
Goodman, L. S., A. Gilmans. The Pharmacological Basis of Therapeutics, 8th Ed. A. G. Gilman, T. W. Rall, A. Nies, P. Taylor, eds. Pergamon, New York, 1990.
Gotoh, F., J. S. Meyer, Y. Takagi. Cerebral effects of hyperventilation in man. Arch Neurol 1 2:410, 1965.
Hamilton, J. et al. Anxiety, depression and the management of medically unexplained symptoms in medical clinics, J R Coll Physicians Lond 30:18, 1996.
Jacobson, S. A. Mechanisms of the sequellae minor craniocervical trauma. In: The Late Effects of Head Injury, A. E. Walker, W. F. Caveness, M. Critchley, eds, CC Thomas, Springfield IL., 1969, p. 35.
Kapoor, W., M. Fortunato, B. Hanusa, et al. Psychiatric illnesses in patients with syncope. Am J Med 99:502, 1995.
Katon, W. Panic Disorder in the Medical Setting. American Psychiatric Press, Washington DC, 1991.
Katon, W., E. Lin, M. Von Korff, et al. Somatization. Am J Psychiatry 148:34, 1991.
Katon, W., M. Sullivan, E. Walker. Medical symptoms without identified pathology. Ann Int Med 134:917, 2001.
Kestenbaum, A. Clinical Methods of Neuro-ophthalmologic Examination, 2nd Ed. Crune and Stratton, New York, 1961.
Kroenke, K, D. Mangelsdorf. Common symptoms in ambulatory care. Am J Med 86:262, 1989.
Kroenke, K., C. Lucas, M. Rosenberg, et al. Causes of persistent dizziness. Ann Int Med 117:898, 1992.
Kroenke, K., R. Price. Symptoms in the community. Arch Intern Med 153: 2474, 1993.
Lishman, W. A. Brain damage in relation to psychiatric disability after head injury. Br J Psychiatry 114:373, 1968.
Mattson, R. H., G. R. Heninger, B. B. Gallagher, et al. Psychophysiological precipitants of seizures in epileptics. Neurology 20:406, 1970.
Merikangas, J. Headache syndromes in Medical Psychiatric Practice, Vol 1. A. Stoudemire, B. Fogel, eds. American Psychiatric Press, Washington DC, 1991, p. 393.
Merikangas, K. J. Merikangas, J. Angst. Headache syndrome and psychiatric disorders. J Psychiatry Res 27:197, 1993.
McAllister, T. W, A. Saykin, L. Flashman, et. al. Brain activation during working memory one month after traumatic brain injury.Neurology 53:1300, 1999.
P.248
Mattson, R. H., G. R. Heninger, B. B. Gallagher, C. H. Glaser. Psycbophysiological precipitants of seizures in epileptics. Neurology20:406, 1970.
Perley, M. J., S. B. Guze. Hysteria-the stability and usefulness of clinical criteria. A quantitative study based on a follow-up of six to eight years in 39 patients. N Engl J Med 266:421, 1962.
Plum, R, J. B. Posner. Diagnosis of Stupor and Coma, 2nd Ed. Contemporary Neurology Series. F. A. Davis, Philadelphia, 1972.
Raja, M. Neurological diagnosis in psychiatric patients. Ital J Neurol Sci 16:153, 1995.
Shuttleworth, E. C., C. E. Morris. The transient global amnesia syndrome. Arch Neurol 15:515, 1966.
Slater, E., E. Glithero. A follow-up of patients diagnosed as suffering from “hysteria.” J Psychosom Res 9:9, 1965.
Spinhoven, P., E. Onstein, P. Stark, et al. Hyperventilation and panic attacks in general hospital patients. Gen Hosp Psychiatry 15:148, 1993.
Veith, I. Hysteria. University of Chicago Press, Chicago, 1965.