Psychogenic Symptoms Are Not Only for the Epileptologist: All Physicians Be Aware!

PSYCHOGENIC SYMPTOMS ARE NOT ONLY FOR THE EPILEPTOLOGIST: ALL PHYSICIANS BE AWARE!

Selim R.Benbadis, MD

University of South Florida

2 Tampa General Circle

Tampa, FL

Phone: 813-259-8577

Fax: obsolete; do not use

Email:

RichardSutton

National Heart & Lung Institute

Imperial College

London, UK

Character count for title: 82

Word count: 938

Search terms: seizures, syncope, psychogenic

Psychogenic symptoms are pervasive in medicine and are likely under-diagnosed and under-reported for two reasons: 1) Their psychological origin, while often suspected,is usually difficult, and sometimes impossible, to prove; 2) It is safer, at least initially, for both the patient and the doctor to err on theside of organic illness.

Among all psychogenic symptoms, psychogenic nonepilepticseizures events (PNEES)are by far the best studied. (We will use the term “events” in order to avoid the confusing term “seizures” here [1, 2]) Within neurology, movement disorders are also relatively well documented and studied. In cardiology, common psychogenic symptoms are non-cardiac chest pain and psychogenic pseudosyncope (PPS). The pathophysiology, or rather psychopathology, is similar for psychogenic symptoms regardless of the presenting symptoms. For patients with spells or fits, whether they are labeled PPS or PNES dependsmostly on what they resemble more (shaking = seizure, limp = syncope) and to which specialist theypresent.

In this issue of Neurology, Blad et al [31] report a sizeable group of patients with both vasovagal syncope (VVS) and psychogenic pseudosyncope (PPS). The two were coexisted more than they should by chance. Not surprisingly, the “red flags“ that suggested a psychogenic origin were similar to those that are well established for PNES [42](see Table 1).

This study is an important illustration of embellishment, or exaggeration of organic symptoms. Thus, the symptoms here can be viewed as partially psychogenic. The tilt-table procedure, like any medical procedure, acts like a provocative technique both in suggestible patients, those with PPS [42], andin those constitutionallyvulnerable to vasodepression[53]. “Embellishment” is similar to subconsciously learning from VVSsymptoms and signs to manifest PPS.

The findings of Blad et al have important practical implications. Internists and cardiologists who evaluate syncope should consider the diagnosis of PPS more often and earlier, just like most neurologists have learned to consider the diagnosis of PNES in patients withrefractory seizures. Early consideration of the diagnosis of PPS is rare among cardiologists, and only thosewith a special interest in syncopewill currently make thisdiagnosis.It is likely that PPS accounts for a proportion of thegroup labeled “syncope of unknown origin”, although this group has decreased in numbers in recent years [64]. Because of this, the diagnostic delay for PPS is likely to be longand possibly longer than the 7-10 year diagnostic delay of PNEES [42].

Another important lesson is that tilt-table testswould offer enhanced diagnostic capability by being performed routinely with EEG monitoring. “Ictal” recording easily distinguishes organic syncope(of any cause) and PPS, due to a predictable and sensitive series of changes [75]. For routine EEG monitoring during tilt to be achieved, close cooperation between neurologist and cardiologist is necessary and, unfortunately, is usually lacking. A potential limitation of the benefit of EEG monitoring is that EEG changes may not be present (“false negative”) in incomplete or “pre” syncope (e.g., dizziness, lightheadedness), but this is no different from ictal EEG being “negative” in very mild or limited “simple” partial seizures.

The authors show that VVS and PPS often concur, suggesting that VVS plays an etiological role in PPS: an interesting hypothesis, but there is no proof that this is the case. Historically, the very first attack is often the most typical of VVS in a PPS patient. Those patients who come to tilt-table testing rather obviously are those where the coincidence is seen, although these persons represent a small minority of patients with syncope.

If a standing provocation test were performed on all patients with syncope unexplained by history, physical and 12-lead ECG, a notable and larger proportion with PPS might be found and coincidence with VVS may be less. In parallel, most patients with PNES do not have coexisting epilepsy [86].

While psychogenic symptoms or signs exist in all specialties, PNEESare the most provable of all psychogenic symptoms, so they havebeen well studied. Since the advent of EEG-video monitoring, a consistent finding at epilepsy centers is that about 30% of patients with refractory seizures actually have PNEES.

All specialties have their equivalent psychogenic symptoms: shortness of breath and cough in pulmonary medicine, constipation and abdominal pain in gastroenterology, blindness in ophthalmology, dysphonia orglobus in otolaryngology, etc.Interestingly, pain is the least provable psychogenic symptom, so much so that the diagnosis of “psychogenic pain” is no longer accepted. Chronic pain conditions, such as fibromyalgia, continue to be controversial as to whether they are organic or psychogenic [42, 97]. Common features of psychogenic symptoms exist,whichever the specialty. They are first diagnosed as, and may coexist with, the ‘mimicked’ organic illness. In general, most patients with psychogenic symptoms are not consciously faking (factitious, malingering) but rather fall under the unconscious category (formerly somatoform disorders, now somatic symptom disorders). It then follows that if 30% of refractory seizures are psychogenic, it islikely {honestly I prefer “likely” to “possible” here  } that 30% of refractory unexplained syncope is psychogenic, orpartly embellished by a psychogenic component.

The last, and rather sad, common featureof psychogenic symptoms across all specialtiesis that it is difficult to find good treatment. At least for PNES, there is recent evidence that SSRIs and CBT can be effective [108, 119]. This may not be the case for PPS, but successful treatment depends on rarely encountered mental health professionals, most of whom pay little attention and show little interest in this category of disorders [42, 1210].

Table 1. Clinical features of psychogenic pseudosyncope

• Prolonged duration or delayed recovery,
• Atypical triggers
• High attack frequency
• Eye closure during attack
• Lack of prodrome
• Attacks refractory to accepted methods in VVS (explanation, fluid, salt, and counter-pressure maneuvers)
• An attack occurring in office or waiting room
• Active collapse in contrast to crumpling in VVS
• Increased heart rate in attack

REFERENCES

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