Functional Paralysis and Sensory Disturbance

Jon Stone

Michael Sharpe

ABSTRACT

Paralysis or sensory loss unexplained by disease and often described as functional or psychogenic is a common clinical presentation, especially in neurologic practice.

Despite their frequency, functional paralysis and sensory loss have received remarkably little research attention. In this chapter, we summarize the available epidemiologic and clinical research literature that specifically relates to functional paralysis and sensory symptoms. We also discuss hypotheses that try to answer the question of why patients develop paralysis rather than another symptom such as fatigue or pain. Lastly, we suggest how conceptualizing these symptoms as arising from reversible dysfunction of the nervous system, rather than as purely psychogenic, is both consistent with recent research findings and a way of achieving greater transparency of communication with the patient.

TERMINOLOGY

Doctors use a wide variety of terms to describe symptoms unexplained by disease. All have theoretic and practical shortcomings, however (1,2). Table 13.1 lists some of the commonly used words, together with their respective advantages and pitfalls.

In Edinburgh we have studied the perceptions of different diagnostic terms for paralysis by general neurology outpatients. We asked them to imagine that they had a weak leg, that their tests were normal, and that the doctor was giving them one of ten diagnoses (see Table 13.2) (4). The diagnoses “all in the mind,” “hysterical,” and “psychosomatic” were interpreted as meaning “mad,” “imagining symptoms,” or “making up symptoms” by more than half of the subjects. The diagnosis of functional weakness was, however, no more offensive than that of stroke.

The diagnosis of functional nervous disorder was in common use as a description of “hysterical” symptoms from the late 19th century to the middle of the 20th century. Using it avoids having to make a meaningless distinction between symptoms that are arising from the mind rather than from the brain; it implies that the problem is one of nervous system functioning rather than structural damage. However, the term “functional” continues to have a pejorative meaning for some doctors. Whilst this is perhaps more of a problem for doctors than patients, it may also be argued that the term will inevitably acquire stigma with the general public if widely used. The term may also be criticized as being simply too broad in meaning, as other conditions such as epilepsy and migraine can also be described as functional. Despite these reservations, we will use the term “functional” because we consider it to be the best currently available, theoretically and practically.

HOW COMMON IS FUNCTIONAL PARALYSIS AND SENSORY LOSS?

Studies in Nonneurologic Populations

There have been few population-based studies of functional weakness. These have estimated the prevalence at 2% (5,6). One of these, a study of functional symptoms in over 2,000 people found this rate was maintained even in people aged less than 45 years (Rief, personal communication, 2000). By way of contrast, another study of 600 people did not find anyone with functional paralysis (7). A prospective consecutive study of neurologic inpatients with functional paralysis in Sweden found a minimum population incidence of functional paralysis of 5 per 100,000 (8). This incidence is similar to that of other neurologic disorders, for example, amyotrophic lateral sclerosis (2 per 100,000) and multiple sclerosis (3 per 100,000) (9).

TABLE 13.1 WORDS USED TO DESCRIBE PARALYSIS UNEXPLAINED BY DISEASE

Diagnosis
Psychogenic	Suggests a purely psychological etiology, when increasingly most workers in the field of somatic symptoms accept that a biopsychosocial model fits the data best.
Psychosomatic	In its true intended sense, it means an interaction between mind and body, but has become shorthand for “psychogenic” (3). Likely to offend (4).
Nonorganic	A “nondiagnosis” that indicates what the problem isn’t rather than what it is.
Hysterical	Suggests uterine etiology. Likely to offend (4). It has the advantage that it cannot mean malingering.
Conversion disorder	Little clinical evidence to support the psychodynamic conversion hypothesis for most cases. Conversion symptoms typically have a high rate of comorbid distress.
Dissociative motor disorder	Although dissociation can be an important mechanism in some cases, there is no evidence that all patients develop paralysis or sensory loss because of dissociation.
Medically unexplained	More theoretically neutral but untrue since we do have some understanding of these symptoms and can recognize them clinically. Does not distinguish symptoms that present with a hallmark of inconsistency from symptoms which are consistent but with poorly understood pathology (e.g., cervical dystonia or unexplained spastic paraplegia). Also impractical when talking to patients (4).
Functional	Avoids psychological vs. physical debate in keeping with biopsychosocial model. Describes abnormal functioning of nervous system. Not offensive to patients. Can also mean malingering. Too broad a term for some.

TABLE 13.2 PERCEPTION OF DIAGNOSTIC LABELS FOR WEAKNESS “IF YOU HAD LEG WEAKNESS, YOUR TESTS WERE NORMAL, AND A DOCTOR SAID YOU HAD X, WOULD HE BE SUGGESTING THAT YOU WERE Y (OR HAD Y)”^a

Y Connotations (% response, n = 86)
X Diagnoses	Putting It On (Yes)	Mad (Yes)	Imagining Symptoms (Yes)	Can Control Symptoms (Yes)	Medical Condition (No)	Good Reason to be Off Sick from Work (No)	Offense Score (%)^b	The Number Needed to Offend (95% CI)^c
Symptoms all in the mind	83	31	87	83	66	70	93	2 (2-2)
Hysterical weakness	45	24	45	48	33	42	50	2 (2-3)
Medically unexplained weakness	24	12	31	33	37	41	42	3 (2-4)
Psychosomatic weakness	24	12	40	28	21	28	35	3 (3-4)
Depression-associated weakness	21	7	20	28	15	28	31	4 (3-5)
Stress-related weakness	9	3	14	30	14	23	19	6 (4-9)
Chronic fatigue	9	1	10	23	19	14	14	8 (5-13)
Functional weakness	7	2	8	17	8	20	12	9 (5-16)
Stroke	2	5	5	7	6	12	12	9 (5-16)
Multiple sclerosis	0	1	3	2	3	8	2	43 (13-∞)
CI, confidence intervals.
^aPercent responses among 86 new neurology outpatients, offense score, and number needed to offend (i.e., the number of patients to whom you would have to give this diagnostic label before one patient is offended). ^bThe proportion of subjects who responded “Yes” to one or more of: “putting it on,” “mad,” or “imagining symptoms.” ^cCalculated according to the offense score.
Adapted and reprinted from Stone J, Wojcik W, Durrance D, et al. What should we say to patients with symptoms unexplained by disease? The “number needed to offend.” BMJ. 2002;325:1449-1450, with permission.

In older studies from the St. Louis group, the lifetime reported prevalence of an episode of unexplained paralysis in psychiatric patients, postpartum women, and medically ill patients was much higher at 7%, 9%, and 12%, respectively (10, 11, 12).

Carrying out high-quality epidemiology on a symptom such as weakness is not easy, and there are significant limitations to all of the studies listed above. First, functional weakness can be a difficult clinical diagnosis, and basing figures on patient self-report or retrospective note review is likely to lead to errors in over- and underreporting, respectively. Second, doctors and patients are likely to have varying views on what “medically unexplained weakness” encompasses. For example, is sleep paralysis—a type of paralysis that many people have experienced at one time or other in their lives—unexplained by disease? Or is the temporary weakness felt in a limb that has been injured normal or abnormal? Consequently, a much more detailed survey than any carried out so far will be needed to obtain robust estimates of the nature, incidence, and prevalence of various forms of functional weakness in the general population.

Outpatients

There have been no studies that have specifically examined the prevalence of functional paralysis and sensory loss in neurologic outpatients. A number of studies in European practice have established that around one third of all outpatients seen by neurologists have symptoms that are only somewhat or not at all explained by disease (13,14). Unfortunately, it remains unclear how many of these patients have paralysis or sensory loss. The best estimate is from a case series reported by a neurologist in London who diagnosed conversion hysteria in 3.8% of 7,836 consecutive patients (15).

Inpatients

The reported frequency of functional paralysis in neurologic inpatients varies from 1% to 2% (8,16) and after back surgery, as high as 3% (17). Further information comes from studies of the prevalence of “hysteria” or conversion disorder in neurologic inpatients which varies between 1% to 18% (18, 19, 20, 21). Between a third to a half of patients with conversion disorder have paralysis as their main symptom (22), which would suggest the true frequency may be even higher.

In conclusion, the limited epidemiologic evidence available suggests that the symptoms of functional paralysis and sensory disturbance are relatively common in neurologic practice and may also have a surprisingly high prevalence and incidence in the general population.

ETIOLOGY OF FUNCTIONAL PARALYSIS AND SENSORY LOSS:

General Factors

There is a large literature on the possible causes of conversion disorder/hysteria. It approaches the problem from a variety of perspectives: psychoanalytic, psychogenic, cultural, and biologic. However, the fundamental problem with these general approaches is that they make the assumption that all patients presenting with symptoms imitating neurologic disease have the same disorder (23,24). Until the validity of grouping together patients with different pseudoneurologic symptoms can be established, it seems more sensible to study patients defined by sharing specific symptoms.

There has been only one controlled study that has addressed the etiology of functional paralysis and none in patients with functional sensory symptoms. There have, however, been several studies of wider groups of patients that have contained high proportions of patients with paralysis or sensory loss (25, 26, 27, 28, 29, 30, 31, 32).

Binzer et al. carried out a prospective case control study of 30 patients with functional paralysis and 30 patients with neurologic paralysis (8,33,34). They found a higher rate of so-called axis 1 psychiatric disorders (such as depression) as well as axis 2 disorders (personality disorders) in the functional paralysis group. They also found that functional paralysis patients tended to have received less education and to have experienced more negatively perceived life events prior to symptom onset. Contrary to many other studies of conversion disorder (26), they did not find a higher rate of childhood abuse in the cases, although the cases did report their upbringing to be more negative (34). A study of illness beliefs in the same cases and controls was remarkable for showing that patients with motor conversion symptoms were more likely to be convinced that they had a disease and to reject psychological explanations than were patients who actually had a neurologic disease.

Other studies have examined patients with conversion disorder, a high proportion of whom have paralysis. They have confirmed the importance of childhood factors, psychiatric comorbidity, personality variables, and the importance of organic disease as risk factors for functional symptoms.

The problem remains that all of these studies, although relatively specific to patients with functional paralysis, are still examining questions relating to the generality of why people might develop symptoms unexplained by disease. Childhood factors, psychiatric morbidity, disease, and personality factors are relevant to the development of many
kinds of functional somatic symptoms, and for that matter, depression and anxiety (35). What researchers have found much harder to tackle is the specific question, “Why do people develop paralysis and not some other symptom?”

Why Do People Develop Paralysis?

The Psychodynamic Perspective

For the last century, the dominant view of the etiology of functional paralysis has been psychodynamic. Figure 13.1 shows a classic case of a soldier who has lost the ability to perform his duties because of paralysis of the right hand. He complained, “I cannot salute and I cannot handle a gun with this hand; it has to be treated.” Figure 13.1A shows the patient at presentation and Figure 13.1B after psychotherapeutic treatment.

According to the psychodynamic model, the loss of function implicit in paralysis is said to arise as a result of mental conflict in a vulnerable individual—the mental conflict being partially or even completely resolved by the expression of physical symptoms—so-called primary gain. In addition to communicating distress that cannot be verbalized and “escaping” the conflict, the individual receives the status and advantage of being regarded as an invalid—so-called secondary gain. Some have regarded conversion hysteria purely as a form of communication. In the case of paralysis, the symptom may be regarded as communicating a conflict over action, for example, a pianist who cannot move his or her fingers. In the case shown in Figure 13.1, the potential symbolism of the loss of the saluting hand is obvious.

While the hypothesis that conversion results from a transformation of distress into physical symptoms is clinically plausible for some patients, it remains merely a hypothesis. The evidence is that most patients have obvious “unconverted,” emotional distress as demonstrated by a number of studies which have found greater prevalence of emotional disorder in patients with functional symptoms compared to controls with an equivalently disabling symptom caused by disease (8). Further evidence against the conversion hypothesis is the poor sensitivity and specificity of la belle indifférence as a clinical sign (see below). When emotional distress is apparently hidden, it is often the case that the patient is not unaware of their emotional symptoms; rather, they simply do not want to tell a doctor about them for fear of being labeled as mentally ill. Wessely (36) has made a cogent plea for revision of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria to a more practical and theoretic symptom-based classification which would entail removing the name “Conversion Disorder.” In our view, this would be a great step forward, although it would be wrong to abandon all of the things we have learned from psychodynamic theory in doing so.

Figure 13.1 A soldier with functional paralysis before (A) and after (B) treatment. (Reprinted from Abse W. Hysteria and Related Mental Disorders. Bristol: Wright, 1966.)

The Psychogenic Perspective and Dissociation

Ross Reynolds (37), Charcot (38), and others observed more than a century ago that ideas and suggestion could play a central role in the formation of particular symptoms. Janet extended this notion further with the idées fixes and dissociation (39). Here is a famous example:

A man traveling by train had done an imprudent thing: While the train was running, he had got down on the step in order to pass from one door to the other, when he became aware that the train was about to enter a tunnel. It occurred to him that his left side, which projected, was going to be knocked slantwise and crushed against the arch of the tunnel. This thought caused him to swoon away but happily for him, he did not fall on the track, but was taken back inside the carriage, and his left side was not even grazed. In spite of this, he had a left hemiplegia (39).

Janet referred to the principle process in hysteria as a “retraction of the field of personal consciousness and a
tendency to the dissociation and emancipation of the system of ideas and functions that constitute personality.” In the example above, the idea of paralysis, brought on by terror of an imminent injury, has become dissociated from the patient’s consciousness and is acting independently. He was keen to point out, however, that it is not necessarily the idea itself that is the cause of the symptom, but the action of that idea on a biologically and psychologically vulnerable individual. His conception of the idées fixes was also more sophisticated than “I’m paralyzed” or “I’m numb.” He thought in many cases the idées fixes could be something less immediately related to the symptom, for example, the fixed idea of a mother’s death or the departure of a spouse.

Surprisingly, there has been little systematic work since the efforts of Janet (39) that has examined the phenomenon of dissociation in patients with functional paralysis, even though dissociation assumes the role of a principal etiologic factor in the International Classification of Diseases (ICD-10) classification. Two studies by Roelofs et al. found relationships between somatic and cognitive aspects of dissociation, hypnotisability, and child abuse in a cohort most of whom had functional motor symptoms (26,40). More work is needed in this area, specifically controlled data, and studies looking at dissociation as a transient trigger of symptoms rather than a general trait.

The Social Perspective

A social perspective on the generation and shaping of functional paralysis can also be advanced (41). It has been suggested that patients respond to social pressures and expectations by choosing, consciously or subconsciously, to present with certain symptoms. The symptoms of paralysis may be chosen because it is a more culturally accepted presentation of ill health than is depression. This idea is supported by studies finding greater disease conviction among patients with functional paralysis compared to neurologic controls (33). A strong belief in, or less often fear of a disease, is a recurring theme in this patient group. However, in our experience, the conviction that, whatever it is, it is “not a psychological problem” is even more prevalent and may reflect socially determined stigma about psychological problems. The social dimension of hysterical paralysis is explored further in Shorter’s book From Paralysis to Fatigue (42), although his hypothesis that paralysis is “now a rare symptom and seen mostly in ‘backward’ working-class and rural patients” (43) requires revision in light of more recent studies.

The Biologic Perspective

For decades, researchers have been sporadically searching for biologic correlates of functional paralysis or sensory loss. Only with the advent of functional neuroimaging is this avenue proving fruitful, although studies thus far remain preliminary.

Transcranial Magnetic Stimulation

Eleven studies and case reports (17,44, 45, 46, 47, 48, 49, 50, 51, 52, 53) with a total of 73 patients have used transcranial magnetic stimulation (TMS) to test motor function in patients with functional paralysis. Almost without exception they have reported normal findings. This suggests that TMS may be a useful adjunct in distinguishing neurologic from functional weakness. Two papers have described therapeutic benefit from diagnostic (50) and repetitive TMS (54), although one suspects the mechanism here is primarily persuasion that recovery is possible rather than anything specific to TMS itself.

Evoked Responses and the P300 Response

An early study of functional hemianesthesia suggested that patients may have impaired standard evoked sensory responses in their affected limbs (55), but this was refuted by several even earlier (56) and later studies (57, 58, 59, 60, 61, 62) including a recent study using magnetoencephalography (63). Most recently transiently absent scalp somatosensory evoked responses have been seen in two patients with conversion disorder that subsequently recovered (64).

Of greater interest are the nature of the P300 and other late components of the evoked response in patients with functional sensory loss. One study found that it was diminished in one case of unilateral functional sensory loss but not in a subject feigning sensory loss (65), and another found reduction in P300 components in patients with hypnotically induced sensory loss (66).

Cognitive Neuropsychology

Two older studies (both with around ten patients each) found that patients with conversion symptoms had reduced habituation compared to ten controls with anxiety, suggesting an impairment in attention (67,68). These studies found different degrees of physiologic arousal detectable in patients with conversion symptoms compared to controls. Another study suggested that arousal was high even when la belle indifférence was present (69). A series of studies in this area by Roelofs et al. have suggested deficits in higher level central initiation of movement with relative preservation of lower level motor execution (as measured, e.g., by reaction times) in patients with functional paralysis (70,71). Detailed studies of attention in this patient group have been consistent with a high-level voluntary attentional deficit (72). Spence has argued that functional paralysis is a disorder of action, drawing analogies with other disorders, including depression and schizophrenia (73).

Functional Imaging

Charcot spent many years later in his career applying the clinicoanatomic method to hysteria. He believed that there must be a dynamic lesion in the brain to explain the symptoms he was observing. The small body of work on the
functional neuroimaging of hysteria that is now able to look for such a dynamic lesion is presented elsewhere in this symposium. The studies published in relation to the symptom of paralysis and sensory loss are summarized in Table 13.3 below.

The data so far published is conflicting. This is perhaps not surprising and was acquired from different experimental paradigms. It is discussed further in Chapter 26.

TABLE 13.3 STUDIES OF FUNCTIONAL BRAIN IMAGING IN FUNCTIONAL, FEIGNED AND HYPNOTIC PARALYSIS AND SENSORY LOSS

First Author/year		Subjects	Paradigm	Activations and Deactivations Seen
Conversion Disorder
Tiihonen, 1995 (74)	1	Weak + sensory (L)	SPECT during electrical stimulation of left median nerve, before and after symptoms	Increased perfusion of right frontal lobe and hypoperfusion in right parietal lobe during symptomatic state compared to recovery
Marshall, 1997 (75)	1	Paralysis (L)	PET, attempted movement of leg against resistance	Activation of right anterior cingulate and orbitofrontal cortex
Yazici, 1998 (76)	5	Gait (L + R)	SPECT	Predominantly left-sided temporal (4/5) and parietal (2/5) hypoactivation
Spence, 2000 (77)	3	Paralysis (L + R)	PET, a hand joystick task of affected limb	Hysterical paralysis associated with deactivations in left dorsolateral prefrontal cortex during movements but not at rest; feigners showed deactivation in right anterior frontal cortex regardless of laterality of weakness
Vuilleumier, 2001 (78)	8	Weak + sensory (L + R)	SPECT, buzzers applied to all four limbs. Four patients had before and after scans	Reduced cerebral blood flow in the contralateral thalamus and basal ganglia; less severe hypoactivation predicted recovery
Mailis-Gagnon, 2003 (79)	4	Pain + sensory (L + R)	fMRI, sensory stimulation	When stimulus not perceived—anterior cingulate activation; deactivation in somatosensory, prefrontal, inferior frontal and parietal cortex; failure to activate thalamus and posterior cingulate
Werring, 2004 (80)	5	Visual loss controls	fMRI, 8 Hz visual stimulation	Reduced activation of visual cortices, with increased activation of left inferior frontal cortex, left insula-claustrum, bilateral striatum and thalami, left limbic structures, left posterior cingulate cortex
	7
Hypnotically (Hyp) induced paralysis
Halligan, 2000 (81)	1	Hyp paralyzed (L)	PET, attempted movement of paralyzed leg	Right anterior cingulate and right medial orbitofrontal cortex activation similar to that seen in the single patient described by Marshall et al.
Ward, 2003 (82)	12	Hyp paralyzed (L)	PET, attempted movement of paralyzed leg	Hypnotic paralysis vs. rest: activation of putamen bilaterally, left thalamus, right orbitofrontal cortex, left cerebellum, left supplementary motor area
	12	Feigned paralysis (L)		Hypnotic compared to feigned paralysis: right orbitofrontal cortex, right cerebellum, left thalamus and left putamen
fMRI, functional magnetic resonance imaging; PET, positron emission tomography; SPECT, single photon emission computed tomography.

At their best, newer studies based in cognitive neuroscience are leading the way to a more integrated cognitive neuropsychiatric approach to the problem of functional paralysis with a focus on mechanism rather than cause. But although these studies challenge conventional psychogenic models of causation, a purely biologic interpretation of this data is just as unsatisfactory as a purely psychogenic theory of hysterical paralysis.

The Importance of Panic, Dissociation, Physical Injury, or Pain at Onset

Little attention has been paid to the circumstances and symptoms surrounding the onset of functional paralysis. In our experience, the circumstances around onset reported by individual patients provide intriguing clues to the possible mechanisms behind functional paralysis. We tend to think of paralysis, unlike abdominal bloating, as a symptom outside everyday experience and normal physiology. Yet paralysis occurs in all of us during REM sleep, when we are terrified, when we are tired and our limbs feel like lead, or as a very transient protective response when we experience acute pain in a limb. Is it possible that some of these more “everyday” causes of transient paralysis are acting as triggers to more long-lasting symptoms?

Panic and Dissociation

When given in-depth interviews, many patients reluctantly report symptoms of panic just before the onset of functional paralysis. Specifically, they may report that they became dizzy, (by which they often mean the dissociative symptoms of depersonalization or derealization), and autonomic symptoms such as sweating, nausea, and breathing difficulties. Sometimes the patient either refuses to volunteer or genuinely didn’t experience fear in association with other autonomic symptoms—so called “panic without fear” (83). This idea is not new. Savill comments on it in his 1909 book (84) extending the range of attack types at onset to include nonepileptic seizures, something we have also seen:

If the patient is under careful observation at the time of onset, it will generally be found that cases of cerebral paresis, rigidity or tremor are actually initiated, about the time of onset, by a more or less transient hysterical cerebral attack.…

Affirmative evidence on this point is not always forthcoming unless the patient was at the time under observation, or is himself an intelligent observer. I found affirmative evidence of this point in 47/50 cases of hysterical motor disorder which I investigated particularly. Sometimes there was only a “swimming” in the head, or a slight syncopal or vertiginous attack, slight confusion of the mind, or transient loss of speech, but in quite a number there was generalized trepidation or convulsions (84).

Hyperventilation

Hyperventilation may also occur at the onset of symptoms, either alone or in combination with panic and dissociation. The link between hyperventilation and unilateral sensory symptoms is well-established clinically (85,86) and experimentally (87), but the mechanism for this remains in doubt as both central and peripheral factors may be responsible (88).

Physical Injury

Careful reading of the numerous case reports of functional paralysis indicates a large number of cases arising after a physical injury rather than a primarily emotional or psychological shock (although, clearly, physical injury is itself an emotional trauma). The relevance of physical trauma, and its psychological correlates, in precipitating hysteria in vulnerable individuals was well-understood by clinicians, such as Charcot (89), Page (90), Fox (91), and Janet (39), in the late 19th and early 20th century. Subsequently, trauma and shock acquired a much more psychological flavour, and the possibility that simple physical injury, even of a trivial nature, could be enough in itself to produce hysterical symptoms has been lost (although interestingly, similar debate continues with respect to whiplash injury and reflex sympathetic dystrophy).

Pain

A trivial injury could trigger functional paralysis because of panic, dissociation, or hyperventilation as described above. But pain does not have to cause a shock to cause symptoms. It is well-established that pain in itself causes a degree of weakness, which can be overcome only with effort (92). Motor symptoms (predominantly weakness) are prominent in case series of reflex sympathetic dystrophy and complex regional pain. In one case series, 79% of 145 patients described weakness, mostly of the give-way variety, and 88% sensory disturbance (93). When sensory signs and symptoms are sought they seem to be remarkably common in patients with chronic pain (94). Ochoa and Verdugo (95,96) have produced convincing evidence that much of the sensory disturbance and movement disorder seen in complex regional pain is clinically identical to that seen in functional or psychogenic disorders. In one study of 27 patients with complex regional pain syndrome type 1 and sensory symptoms, 50% of the patients had complete reversal of their hypoaesthesia with placebo compared to none out of 13 patients with a nerve injury (95).

Other Pathways

There are many other pathways to the development of functional paralysis. We have seen patients who develop functional paralysis after surgery (who simultaneously experienced intense depersonalization as they came out of the anesthetic), and several whose first experience of paralysis was an episode of undiagnosed sleep paralysis precipitated by depression and insomnia that later snowballed into more permanent nonsleep-related symptoms. Perhaps one of the commonest routes to functional paralysis is that of a patient with mild chronic fatigue or pain who then becomes aware of an asymmetry of symptoms. Either for biologic reasons or for attentional reasons (but probably because of both), this asymmetry escalates over weeks and months until it appears more dramatically unilateral.

These are hypotheses regarding onset and they require testing. They could, however, open a window on the proximal mechanisms of functional paralysis.

Etiology—Conclusions

Functional paralysis is a symptom, like headache or fatigue, which almost certainly has multiple causes. Some predisposing factors, like childhood neglect, are nonspecific and apply to many illnesses; others such as dissociation are perhaps more specific to pseudoneurologic symptoms. Similarly, stress and emotional disorder may be nonspecific precipitating factors, whereas pain or sleep paralysis and the asymmetry of the brain’s functioning in emotional disorder and panic may be more specific triggers. Illness beliefs, such as a belief or fear of stroke, are probably just one of many factors that can play a role in perpetuating the specific symptom of paralysis. Neuroimaging and other biologic approaches may prove helpful in increasing our understanding of the neural mechanisms of functional paralysis. It seems likely that there are a variety of different factors that lead to the development of an apparently identical symptom and that these may differ among patients.

CLINICAL ASSESSMENT

The clinical diagnosis of functional paralysis presents one of the most fascinating and challenging problems in clinical neurology. The neurologist must be able to take a careful and probing history, paying attention to psychologic and social aspects whilst not alienating the patient by appearing too “psychiatric”. The examination remains a crucial element in distinguishing functional paralysis from disease, its importance being to find positive signs of a functional disorder as well as to establish the absence of disease. Finally, the explanation of the diagnosis, perhaps using the examination to do so, is a chance to change the trajectory of a patient’s illness, for good or for bad. In this section, we outline an approach that we find helpful, paying attention specifically to the symptoms of paralysis and sensory loss.

History

Age of Onset and Sex

Functional paralysis can occur in a wide range of ages from children aged 5 up the mid-seventies (97). The average age of onset seems to be in the mid-thirties (8,98, 99, 100), in contrast to patients with pseudoseizures, who characteristically develop attacks in their mid-twenties (only two papers out of 22 in the possession of the author reported a mean age higher than 30 years).

Surprisingly, the literature does not show any gender predominance. An analysis of seven studies of 167 patients with paralysis produced a mean proportion of 48% women (8,44,101, 102, 103, 104). In one further study, 57% of 1,316 patients seen at a Chinese hysterical paralysis treatment center were women (97). A review of the 46 studies of pseudoseizures of which we are aware, with a total of 2,103 patients, indicated that the majority (74%) were women (references available from authors).

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