Psychogenic Neurologic Deficits

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Chapter 3 Psychogenic Neurologic Deficits

Classic studies of hysteria, conversion disorders, and related conditions included patients who had only rudimentary physical examinations and minimal, if any, laboratory testing. Studies that re-evaluated the same patients after many years reported that as many as 15% of them eventually had specific neurologic conditions, such as movement disorders, multiple sclerosis (MS), or seizures that had probably been responsible for the original symptoms. In addition, some patients had systemic illnesses, such as anemia or congestive heart failure that might have contributed to their initial symptoms. Another interesting aspect of these studies is that many illnesses assumed to be entirely “psychogenic” in the first two-thirds of the twentieth century are now acknowledged to be “neurologic,” such as Tourette disorder, writer’s cramp, other focal dystonias, erectile dysfunction, migraines, and trigeminal neuralgia. To be fair, the medical community has still not reached a consensus on the etiology of several conditions, such as fibromyalgia, chronic fatigue syndrome, and some aspects of chronic pain. Also unexplained, in many patients, is weakness and disability for more than a decade after their physicians established a psychogenic basis for their symptoms.

Today’s physicians, who still fail to reach 100% accuracy, have at their disposal an arsenal of high-tech tests, including computed tomography (CT), magnetic resonance imaging (MRI), functional MRI (fMRI), electroencephalography (EEG), EEG-video monitoring, and genetic testing, as well as a full array of speciality consultants. In this setting, neurologists use their armamentarium mostly to exclude neurologic illnesses and thereby allow for a diagnosis of a psychogenic deficit. Preliminary reports, however, indicate that fMRI studies may help in establishing a diagnosis of conversion disorder.

The Neurologists’ Role

Even in the face of flagrant psychogenic signs, neurologists generally test for neurologic illness that could explain the patient’s symptoms, particularly those illnesses that would be serious or life-threatening. Although observing the course of the illness regularly proves most informative of its origin, neurologists tend to request extensive testing during the initial evaluation to obtain objective evidence of disease or its absence as soon as possible. They typically disregard the distinction between conscious and unconscious disorders. For example, their examinations do not allow them to differentiate patients with “blindness” due to an unconscious conflict from those deliberately pretending to be blind to gain insurance money. They consider gross exaggerations of a deficit, embellishment, as well as malingering as psychogenic. For various reasons, they bundle all psychiatrically related impairments into “psychogenic neurologic deficits.”

Within the framework of this potential oversimplification, neurologists reliably diagnose psychogenic nonepileptic seizures (PNES) (see Chapter 10), diplopia and other visual problems (see Chapter 12), and tremors and other movement disorders (see Chapter 18). In addition, they acknowledge the psychogenic aspects of headache (see Chapter 9), pain (see Chapter 14), sexual dysfunction (see Chapter 16), posttraumatic headaches and whiplash injuries (see Chapter 22), and many other neurologic disorders.

When consulting on patients who have been shown to have a psychogenic disturbance, neurologists usually offer reassurances, strong suggestions that the deficits will resolve by a certain date, and a referral for psychiatric consultation. Sometimes they provide patients acceptable, face-saving exits by prescribing placebos or nonspecific treatment, such as physical therapy. They avoid ordering invasive diagnostic procedures, surgery, and medications, especially habit-forming or otherwise potentially dangerous ones.

Patients often have mixtures of neurologic and psychogenic deficits, disproportionately severe posttraumatic disabilities, and minor neurologic illnesses that preoccupy them. As long as serious, progressive physical illness has been excluded, physicians can consider some symptoms to be chronic illnesses. For example, chronic low back pain can be treated as a “pain syndrome” with empiric combinations of antidepressant medications, analgesics, rehabilitation, and psychotherapy, without expecting either to cure the pain or determine its exact cause (see Chapter 14).

Psychiatrists, adhering to the preliminary version of the Diagnostic and Statistical Manual of Mental Disorders (DSM), 5th edition, will probably classify deficits that have originated in unconscious processes as a Conversion Disorder (Functional Neurological Symptom Disorder). In contrast, when individuals feign neurologic deficits to obtain “external reward,” psychiatrists would reasonably consider the activity Malingering or the expression a Factitious Disorder.

Psychogenic Signs

What general clues prompt a neurologist to suspect a psychogenic disturbance? When a deficit violates the laws of neuroanatomy, neurologists almost always deduce that it has a psychogenic origin. For example, if temperature sensation is preserved but pain perception is “lost,” the deficit is nonanatomic and therefore likely to be psychogenic. Likewise, tunnel vision, which clearly violates these laws, is a classic psychogenic disturbance (see Fig. 12-8). The caveat is that migraine sufferers sometimes experience tunnel vision as an aura (see Chapter 9).

Another clue to a psychogenic basis is a changing deficit. For example, if someone who appears to have hemiparesis either walks when unaware of being observed or walks despite seeming to have paraparesis while in bed, neurologists conclude that the paresis has a psychogenic basis. Another noted example occurs when someone with a PNES momentarily “awakens” and stops convulsive activity, but resumes it when assured of being observed. The psychogenic nature of a deficit can be confirmed if it is reversed during an interview under hypnosis or barbiturate infusion.

Motor Signs

One indication of psychogenic weakness is a nonanatomic distribution of deficits, such as loss of strength in the arm and leg accompanied by blindness in one eye, and deafness in one ear – all on the same side of the body. Another indication is the absence of functional impairment despite the appearance of profound weakness, such as ability to walk even though manual testing seems to show marked paraparesis.

Deficits that are intermittent also suggest a psychogenic origin. For example, a “give-way” effort, in which the patient offers a brief (several seconds) exertion before returning to an apparent paretic position, indicates an intermittent condition that is probably psychogenic. Similarly, the face–hand test, in which the patient momentarily exerts sufficient strength to deflect her falling hand from hitting her own face (Fig. 3-1), also indicates a psychogenic paresis.

Another indication of unilateral psychogenic leg weakness is Hoover sign (Fig. 3-2). Normally, when someone attempts to raise a genuinely paretic leg, the other leg presses down. The examiner can feel the downward force at the patient’s normal heel and can use the straightened leg, as a lever, to raise the entire leg and lower body. In contrast, Hoover sign consists of the patient unconsciously pressing down with a “paretic” leg when attempting to raise the unaffected leg and failing to press down with the unaffected leg when attempting to raise the “paretic” leg.

A similar test involves abduction (separating) of the legs. Normally, when asked to abduct one leg, a person reflexively and forcefully abducts both of them. Someone with genuine hemiparesis will abduct the normal leg, but will be unable to abduct the paretic one. In contrast, someone with psychogenic weakness will reflexively abduct the “paretic” leg when abducting the normal leg (abductor sign) (Fig. 3-3).

Sensory Deficits

Although the sensory examination is the least reliable portion of the neurologic examination, several sensory abnormalities indicate a psychogenic deficit. For example, loss of sensation to pinprick* that stops abruptly at the middle of the face and body constitutes the classic splitting the midline. This finding suggests a psychogenic loss because the sensory nerve fibers of the skin normally spread across the midline (Fig. 3-5). Likewise, because vibrations naturally spread across bony structures, loss of vibration sensation over half of the forehead, jaw, sternum, or spine strongly suggests a psychogenic disturbance.

A similar abnormality is loss of sensation of the entire face but not of the scalp. This pattern is inconsistent with the anatomic distribution of the trigeminal nerve, which innervates the face and scalp anterior to the vertex but not the angle of the jaw (see Fig. 4-11).

A psychogenic sensory loss, as already mentioned, can be a discrepancy between pain and temperature sensations, which are normally carried together by the peripheral nerves and then the lateral spinothalamic tracts. Discrepancy between pain and position sensations in the fingers, in contrast, is indicative of syringomyelia (see Fig. 2-18). In this condition the central fibers of the spinal cord, which carry pain sensation, are ripped apart by the expanding central canal.

Testing for sensory loss when the arms are twisted, placed out of sight behind the patient’s back, or seen in a mirror may also expose psychogenic sensory deficits.

Finally, because sensory loss impairs function, patients with genuine sensory loss in their feet or hands cannot perform many tasks if their eyes are closed. Also, those with true sensory loss in both feet – from severe peripheral neuropathy or injury of the spinal cord posterior columns, usually from vitamin B12 deficiency, tabes dorsalis, or MS – tend to fall when standing erect with their eyes shut. In other words, they have Romberg sign (see Chapter 2). By contrast, patients with psychogenic sensory loss can still generally button their shirts, walk short distances, and stand with their feet together with their eyes closed.

Special Senses

When cases of blindness, tunnel vision, diplopia, or other disorders of vision violate the laws of neuroanatomy, which are firmly based on the laws of optics, neurologists diagnose them as psychogenic. Neurologists and ophthalmologists can readily separate psychogenic and neurologic visual disorders (see Chapter 12).

A patient with psychogenic deafness usually responds to unexpected noises or words. Unilateral hearing loss in the ear ipsilateral to a hemiparesis is highly suggestive of a psychogenic etiology because extensive auditory tract synapses in the pons ensure that some tracts reach the upper brainstem and cerebrum despite central nervous system lesions (see Fig. 4-16). If doubts about hearing loss remain, neurologists often request audiometry, brainstem auditory-evoked responses, and other technical procedures.

Patients can genuinely lose the sense of smell (anosmia) from head injury (see Chapter 22), neurodegenerative disorders, or advanced age; however, these patients can usually still perceive noxious volatile chemicals, such as ammonia or alcohol, which irritate the nasal mucosa endings of the trigeminal nerve rather than the olfactory nerve. This distinction is usually unknown to individuals with psychogenic anosmia, who typically claim inability to smell any substance.

Other Conditions

A distinct but common psychogenic disturbance, the hyperventilation syndrome, occurs in people with an underlying anxiety disorder, including panic disorder. It leads to lightheadedness and paresthesias around the mouth, fingers, and toes, and, in severe cases, to carpopedal spasm (Fig. 3-6). Although the disorder seems distinctive, physicians should be cautious before diagnosing it because partial complex seizures and transient ischemic attacks (TIAs) produce similar symptoms.

In this syndrome, hyperventilation first causes a fall in carbon dioxide tension that leads to respiratory alkalosis. The rise in blood pH from the alkalosis produces hypocalcemia, which induces the tetany of muscles and paresthesias. To demonstrate the cause of the spasms, physicians may recreate them by having a patient hyperventilate. This procedure may also induce giddiness, anxiety, or confusion. The conventional wisdom dictates that, if hyperventilation causes those symptoms, the physician should abort the demonstration by having the patient continually rebreathe expired air from a paper bag cupped around the mouth. However, that remedy does not stop such attacks and, moreover, physicians employing it might mistakenly put a bag to the face of people breathing rapidly because of an asthma attack or congestive heart failure.

Potential Pitfalls

The examination of a patient suspected of having a psychogenic deficit requires particular sensitivity. It need not follow the conventional format and can be completed in two or more sessions. A threatening, embarrassing, or otherwise inept evaluation may obscure the diagnosis, harden the patient’s resolve, or precipitate a catastrophic reaction.

An unreliable indication of a psychogenic deficit is a patient’s absence of concern or affect, la belle indifférence, concerning it. This emotional posture is now known as a potential manifestation of any neurologic disorder, but particularly hemi-inattention, Anton syndrome, and frontal lobe injury. Physicians should give la belle indifférence no credibility.

Although the neurologic examination itself seems rational and reliable, some findings are potentially misleading. For example, many anxious or “ticklish” individuals, with or without psychogenic hemiparesis, have brisk deep tendon reflexes and extensor plantar reflexes. Another potentially misleading finding is a right hemiparesis unaccompanied by aphasia. In actuality, a stroke might cause this situation if the patient were left-handed, or if the stroke were small and located in the internal capsule or upper brainstem (i.e., a subcortical region). With a suspected psychogenic left hemiparesis, physicians must assure themselves that the problem does not actually represent left-sided inattention or neglect (see Chapter 8).

Neurologists tend to misdiagnose several types of disorders as psychogenic when they are unique or bizarre, or when their severity is greater than expected. This error may simply reflect an individual neurologist’s lack of experience.

They also may misdiagnose disorders as psychogenic when a patient has no accompanying objective physical abnormalities. This determination might be faulty in illnesses where objective signs are often transient or subtle, such as MS, partial complex seizures, and small strokes. If given an incomplete history, neurologists may not appreciate certain disorders, such as transient hemiparesis induced by migraines, postictal paresis, or TIAs, or transient mental status aberrations induced by alcohol, medications, or seizures (see Box 9-3).

Another potential pitfall is dismissing an entire case because a patient is grossly exaggerating a deficit. Patients may feel that they must overstate a genuine medical problem to gain the necessary attention. In addition, the prospect of having developed a neurologic disorder may trigger overwhelming anxiety. For example, patients with a persistent headache may so fear a brain tumor that they embellish their history with additional symptoms to obtain a MRI.

Possibly the single most common error is failure to recognize MS because its early signs tend to be evanescent, exclusively sensory, or so disparate as to appear to violate several laws of neuroanatomy. Neurologists can usually make the correct diagnosis early and reliably – even in ambiguous cases – with MRIs, visual-evoked response testing, and cerebrospinal fluid analysis (see Chapter 15). On the other hand, trivial sensory or motor symptoms accompanied by normal variations in these highly sensitive tests may lead to false-positive diagnoses of MS.

Neurologists are also prone to err in diagnosing involuntary movement disorders as psychogenic. These disorders, in fact, often have some stigmata of psychogenic illness (see Chapter 2). For example, they can appear bizarre, precipitated or exacerbated by anxiety, or apparently relieved by tricks, such as when walking backwards alleviates a dystonic gait. Also, barbiturate infusions usually temporarily reduce or even abolish involuntary movements. Because laboratory tests are not available for many disorders – chorea, tics, tremors, and focal dystonia – the diagnosis rests on the neurologist’s clinical evaluation. As a general rule, physicians should assume, at least initially, that movement disorders are not psychogenic (see Chapter 18).

Physicians often misdiagnose epilepsy and PNES in both directions (see Chapter 10). In general, episodes of PNES are clonic and unaccompanied by incontinence, tongue biting, or loss of body tone (Fig. 3-7). Furthermore, while exceptions occur, patients tend to regain awareness and have no retrograde amnesia immediately after the movements cease. On the other hand, both frontal lobe seizures and mixtures of epileptic and psychogenic seizures notoriously mimic purely psychogenic ones. EEG-video monitoring during and between episodes is the standard diagnostic test.

In the past, individuals with changes in their mental status have often been misdiagnosed – often by default – with a psychogenic disturbance. Some of them were eventually found to be harboring meningiomas or other tumors in the frontal lobe. These tumors notoriously escape early detection because they can produce affective or thought disorders without accompanying physical defects. Now, with the ready availability of CT and MRI, physicians rarely overlook any tumor.

References

Baker GA, Hanley JR, Jackson HF, et al. Detecting the faking of amnesia: Performance differences between simulators and patients with memory impairments. J Clin Exp Neuropsychol. 1993;15:668–684.

Eisendrath SJ, McNiel DE. Factitious disorders in civil litigation: Twenty cases illustrating the spectrum of abnormal illness-affirming behavior. J Am Acad Psychiatry Law. 2002;30:391–399.

Feldman MD, Eisendrath SJ. The Spectrum of Factitious Disorders. Washington, DC: American Psychiatric Press; 1996.

Hayes MW, Graham S, Heldorf P, et al. A video review of the diagnosis of psychogenic gait. Move Disord. 1999;14:914–921.

Hurst LC. What was wrong with Anna O? J R Soc Med. 1982;75:129–131.

Hurwitz TA, Prichard JW. Conversion disorder and fMRI. Neurology. 2006;67:1914–1915.

Kanaan RA, Wessely SC. Factitious disorders in neurology: An analysis of reported cases. Psychosomatics. 2010;51:47–51.

Kanaan RA, Armstrong D, Barnes P, et al. In the psychiatrist’s chair: How neurologists understand conversion disorder. Brain. 2009;132:2889–2896.

Letonoff EJ, Williams TR, Sidhu KS. Hysterical paralysis: a report of three cases and a review of the literature. Spine. 2002;27:E441–E445.

Mace CJ, Trimble MR. Ten-year prognosis of conversion disorder. Br J Psychiatry. 1996;169:282–288.

Richtsmeier AJ. Pitfalls in diagnosis of unexplained symptoms. Psychosomatics. 1984;25:253–255.

Roach ES, Langley RL. Episodic neurological dysfunction due to mass hysteria. Arch Neurol. 2004;61:1269–1272.

Roelofs K, Spinhoven P, Sandijck P, et al. The impact of early trauma and recent life-events on symptom severity in patients with conversion disorder. J Nerv Ment Dis. 2005;193:508–514.

Sonoo M. Abductor sign: a reliable new sign to detect unilateral non-organic paresis of the lower limb. J Neurol Neurosurg Psychiatry. 2004;75:121–125.

Stone J, Carson A. Movement disorders: Psychogenic movement disorders: What do neurologists do? Nat Rev Neurol. 2009;5:415–416.

Stone J, Smyth R, Carson A, et al. La belle indifference in conversion symptoms and hysteria: Systematic review. Br J Psychiatry. 2006;188:204–209.

Stone J, Warlow C, Sharpe M. The symptom of functional weakness: A controlled study of 107 patients. Brain. 2010;133:1537–1551.

Teasell RW, Shapiro AP. Misdiagnosis of conversion disorders. Am J Phys Med Rehabil. 2002;81:236–240.

Voon V, Gallea C, Hattori N, et al. The involuntary nature of conversion disorder. Neurology. 2010;74:223–228.