Psychogenic non-epileptic seizures

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Historical Perspective

Initially, the disease was observed in 1900 BCE by the Egyptians and the condition was named hysteria, at the rise of Christianity at that time it was considered a demon possession. Later a similar condition was observed and it was described as major hysteria by French neurologist Jean-Martin Charcot it was believed that the disease might be caused by the dynamic lesion that affects the motor pathway however according to Sigmund Freud, the founder of psychoanalysis, the condition may occur due to psychiatric conflict that converts into physical symptoms.[1]

Classification[2]

Numerous classification systems have been proposed based on age, semiology, and video EEG analysis to categorize PNES, classification for the disease was put forward in 2016 and it was better to understand and manage the diverse manifestations of the disease based on the concept that all the sub type of PNES resemble to the subtype of seizures it was categorized into four categories including.

  • Hypermotor
  • Akinetic
  • Focal motor
  • PNES with “Subjective symptom

Pathophysiology

PNES also known as Pseudoseizures and functional neurological disorder (FND), resembles epileptic seizures but the etiology of the seizures varies. Two of these diseases are different based on the abnormal epileptic form of discharge which is observed in seizures related to epilepsy but not in PNES, psychotic epilepsy is associated with mental symptoms and psychological issues such as stress or trauma[3]except those major difference the condition is also distinguished based on various factors like duration of episodes, postictal phase, number of episodes, patients history of mental health, lactate level, presence of brain structural pathology and other physical symptoms also help to differentiate between two conditions including tongue biting,vomit and incontinence[4],PNES shows EEG normal and the treatment of this condition is not same as epilepsy.Traditional epileptic drugs(AEDs) are not good for the treatment of PNES.[5]

To advance the treatment and decrease the burden of the common disease understanding of the etiology is necessary but it is still unknown some recent Investigations suggest that the diseases may occur due to abnormal brain activity in the limbic system and prefrontal cortex. The limbic system that is involved in emotional and memory processes shows abnormalities [6], and functional white matters such as uncinate fasciculus (UF) fibers increase connectivity in PNES[7], decrease in gray matter and cortical thickness in the prefrontal area observed including cingulate gyrus, middle frontal gyrus, and superior frontal gyrus[8]. Except above mansion brain regions abnormalities are also observed in the insular cortex and supplementary motor area (SMA) this region of the brain is mostly reported in the structural and functional image of the brain it is involved in the sensory emotion and cognitive processes of the brain and also control heart rate and blood pressure. And SMA is associated with the coordination moment of the body[9].

All above mansion studies suggest that the development and maintenance of the disease occur due to abnormalities in the region that controls cognition, emotion, heart rate, and coordination muscles of the body.

Causes[10]

The underlying causes of the disease are complex and can be understood through the biopsychosocial model of PNES that highlights predisposing, precipitating, and perpetuating factors in the disorder.

Predisposing factors:

It makes a person susceptible to the condition includes genetic, temperamental, and other neurological problems that exist along with PNES and childhood trauma

Precipitating factors:

It involves stressful events that trigger the onset of the disease.

Perpetuating factors:

It can maintain or worsen the condition such as lack of social support and avoidance behaviors.

Psychiatric disorders other factors:

They also contribute to diseases like anxiety, mood disorders, alcohol use disorder, post-traumatic stress disorder, trauma history, and family history of epilepsy are recognized as risk factors for PNES.

Epidemiology and Demographics

Annually, the reported incidence of PNES is ranging between 1.4 to 4.9 individuals per 100,000 with the prevalence estimated to be between 2 and 33 per 100,000 individuals. These figures emphasize the significance of PNES as a relatively common condition within the spectrum of neurological disorders.[11]

Age

The disease is reported in the age of 30-40 years.

Gender

PNES is two to three times more common in teenagers, children, and women were in higher number as compared to the male population.

Diagnosis

Diagnosis of the disease is difficult due to seizures in the present or past, therefore, it is mostly misdiagnosed and treated as epilepsy, early correct diagnosis is necessary before treatment it can save the patient's quality of life decrease the disease burden, and reduce the cost of the disease diagnosis of the condition involve gathering and analyzing data from multiple sources like Patients history, home video recording, direct seizures observation, Peri-ictal ictal ECG changes, Video-EEG, Provocation techniques, Showing seizure videos to patients and witnesses, Biomarkers.

Home video recording:

The initial diagnosis by using home video recording when combined with clinical data these videos can make the confident diagnosis.[12]

Direct seizures observation:

The diagnosis can be made by direct observation of seizures but not always the sign that suggests the PNES are tightly closed eyes, respond to environmental stimuli like light touch, no sign of bluish skin, normal pupil reaction to light, self-protective moments that are not observed in epileptic seizures.[13]

Peri-ictal Ictal ECG changes:

ECG machine recording is synchronized with EEG recording it provides valuable diagnostic information because the heart rate of Epileptic seizure and PNES vary, the heart rate is sudden in epileptic seizure whereas it is not the same in PNES.

Video-EEG:

To confirm the diagnosis Video EEG plays an important role it is important to take multiple recordings on EEG to ensure that all seizures are recorded properly and analyzed, providing a comprehensive basis for an accurate diagnosis and effective treatment planning.[14]

Provocation techniques:

Techniques include any method that focuses patients' attention on their seizures this technique is required to reduce the time of monitoring and it enhances the results of EEG recordings this method is employed by the task force at times when the seizures are not recorded, a method that is employed for the technique are included detail history of the seizures, routine activation method like photic stimulation, nocebo technique can provoke seizure in a patient having PNES. This technique does not differentiate the disease from epilepsy.[13]

Showing seizure videos to patients and witnesses:

To correctly diagnose the disease it is necessary to interview the witness the perspective of the witness is also important and it helps to diagnose the disease presence of the witness is necessary at the time of EEG recording.[13]

Laboratory test:

Although blood tests do not help to detect the disease time they provide hints that blood oxygen level is high in patients with PNES whereas it is lower in tonic-clonic seizures and creatine phosphokinase level (CPK) do not arise in PNES as increases after tonic-clonic seizures.[15]

MRI

MRI is used to detect abnormal neural activities in the area of the prefrontal cortex abnormal connectivity and neural activity is observed in the structure of the limbic system including the hippocampus and amygdala.[16]

Treatment

The delay in diagnosis of PNES has been estimated to be about 8 years during this period patients are often treated with anti-epileptic drugs they exposed to potential adverse drug side effects. Among the later adverse effects that are of remarkable clinical importance is the possible teratogenic risk for women of childbearing age. Moreover, patients with ES/PNES can mistakenly be classified as drug-resistant epilepsy and treated with complex combinations of anti-epileptic compounds or even referred to epilepsy surgery.

In 2013, the International League against Epilepsy (ILAE) Neuropsychobiology Commission gave health professionals guidelines on how to treat patients with psychogenic non-epileptic seizures (PNES). They outlined three key stages in managing the disease PNES diagnosis, the communication of the diagnosis, and the treatment. Treatment strategies for PNES include cognitive behavioral therapy (CBT) as an effective intervention (CBT), when combined with standard medical care, has shown promise in reducing dissociative seizure frequency[17]

References

  1. ↑ Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMID https://doi.org/10.1007/978-3-030-44507-2_11 Check |pmid= value (help).
  2. ↑ Magaudda A, Laganà A, Calamuneri A, Brizzi T, Scalera C, Beghi M; et al. (2016). "Validation of a novel classification model of psychogenic nonepileptic seizures by video-EEG analysis and a machine learning approach". Epilepsy Behav. 60: 197–201. doi:10.1016/j.yebeh.2016.03.031. PMID 27208925.
  3. ↑ Fredwall M, Terry D, Enciso L, Burch MM, Trott K, Albert DVF (2021). "Outcomes of children and adolescents 1 year after being seen in a multidisciplinary psychogenic nonepileptic seizures clinic". Epilepsia. 62 (10): 2528–2538. doi:10.1111/epi.17031. PMID 34339046 Check |pmid= value (help).
  4. ↑ Lehn A, Watson E, Ryan EG, Jones M, Cheah V, Dionisio S (2021). "Psychogenic nonepileptic seizures treated as epileptic seizures in the emergency department". Epilepsia. 62 (10): 2416–2425. doi:10.1111/epi.17038. PMID 34396517 Check |pmid= value (help).
  5. ↑ Sharma AA, Goodman AM, Allendorfer JB, Philip NS, Correia S, LaFrance WC; et al. (2022). "Regional brain atrophy and aberrant cortical folding relate to anxiety and depression in patients with traumatic brain injury and psychogenic nonepileptic seizures". Epilepsia. 63 (1): 222–236. doi:10.1111/epi.17109. PMC 8742780 Check |pmc= value (help). PMID 34730239 Check |pmid= value (help).
  6. ↑ Mcsweeney M, Reuber M, Levita L (2017). "Neuroimaging studies in patients with psychogenic non-epileptic seizures: A systematic meta-review". Neuroimage Clin. 16: 210–221. doi:10.1016/j.nicl.2017.07.025. PMC 5544493. PMID 28808618.
  7. ↑ Hernando KA, Szaflarski JP, Ver Hoef LW, Lee S, Allendorfer JB (2015). "Uncinate fasciculus connectivity in patients with psychogenic nonepileptic seizures: A preliminary diffusion tensor tractography study". Epilepsy Behav. 45: 68–73. doi:10.1016/j.yebeh.2015.02.022. PMID 25868002.
  8. ↑ Perez DL, Matin N, Williams B, Tanev K, Makris N, LaFrance WC; et al. (2018). "Cortical thickness alterations linked to somatoform and psychological dissociation in functional neurological disorders". Hum Brain Mapp. 39 (1): 428–439. doi:10.1002/hbm.23853. PMC 5747307. PMID 29080235.
  9. ↑ Diez I, Ortiz-Terán L, Williams B, Jalilianhasanpour R, Ospina JP, Dickerson BC; et al. (2019). "Corticolimbic fast-tracking: enhanced multimodal integration in functional neurological disorder". J Neurol Neurosurg Psychiatry. 90 (8): 929–938. doi:10.1136/jnnp-2018-319657. PMC 6625895 Check |pmc= value (help). PMID 30850473.
  10. ↑ Gibson D, Watters A, Bauschka M (2023). "Seizures in eating disorders". Int J Eat Disord. 56 (8): 1650–1660. doi:10.1002/eat.23969. PMID 37092766 Check |pmid= value (help).
  11. ↑ Peköz MT, Aslan-Kara K, Demir T, Aktan G, Balal M, Cakmak S; et al. (2022). "Frequency and economic burden of psychogenic non-epileptic seizures in patients applying for disability benefits due to epilepsy". Arq Neuropsiquiatr. 80 (11): 1112–1118. doi:10.1055/s-0042-1759759. PMC 9797265 Check |pmc= value (help). PMID 36577410 Check |pmid= value (help).
  12. ↑ Dash D, Sharma A, Yuvraj K, Renjith A, Mehta S, Vasantha PM; et al. (2016). "Can home video facilitate diagnosis of epilepsy type in a developing country?". Epilepsy Res. 125: 19–23. doi:10.1016/j.eplepsyres.2016.04.004. PMID 27328162.
  13. ↑ 13.0 13.1 13.2 Whitehead K, Kane N, Wardrope A, Kandler R, Reuber M (2017). "Proposal for best practice in the use of video-EEG when psychogenic non-epileptic seizures are a possible diagnosis". Clin Neurophysiol Pract. 2: 130–139. doi:10.1016/j.cnp.2017.06.002. PMC 6123876. PMID 30214985.
  14. ↑ Chen-Block S, Abou-Khalil BW, Arain A, Haas KF, Lagrange AH, Gallagher MJ; et al. (2016). "Video-EEG results and clinical characteristics in patients with psychogenic nonepileptic spells: The effect of a coexistent epilepsy". Epilepsy Behav. 62: 62–5. doi:10.1016/j.yebeh.2016.06.018. PMID 27450307.
  15. ↑ Javali M, Acharya P, Shah S, Mahale R, Shetty P, Rangasetty S (2017). "Role of Biomarkers in Differentiating New-onset Seizures from Psychogenic Nonepileptic Seizures". J Neurosci Rural Pract. 8 (4): 581–584. doi:10.4103/jnrp.jnrp_139_17. PMC 5709881. PMID 29204018.
  16. ↑ Balachandran N, Goodman AM, Allendorfer JB, Martin AN, Tocco K, Vogel V; et al. (2021). "Relationship between neural responses to stress and mental health symptoms in psychogenic nonepileptic seizures after traumatic brain injury". Epilepsia. 62 (1): 107–119. doi:10.1111/epi.16758. PMID 33238045 Check |pmid= value (help).
  17. ↑ Goldstein LH, Robinson EJ, Pilecka I, Perdue I, Mosweu I, Read J; et al. (2021). "Cognitive-behavioural therapy compared with standardized medical care for adults with dissociative non-epileptic seizures: the CODES RCT". Health Technol Assess. 25 (43): 1–144. doi:10.3310/hta25430. PMC 8273679 Check |pmc= value (help). PMID 34196269 Check |pmid= value (help).
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