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Apa workshop 05.20.15 what every psychiatrist needs to know about epilepsy
- 1. 5/20/15 1 New Anti-Seizure Medications Elia M Pestana Knight, MD Cleveland Clinic Epilepsy Center Nothing to disclose
- 2. 5/20/15 2 Topics for this lecture Antiepileptic Drugs What are antiepileptic drugs? Historical development of the drugs How doctors select the drugs to treat the seizures? Common side effect Drug interactions A case for the need of Epilepsy and Psychiatry team interaction Antiepileptic Drugs
- 3. 5/20/15 3 What are antiepileptic drugs? Antiepileptic drugs (AEDs) Anticonvulsant medications Antiseizure medications
- 4. 5/20/15 4 Antiseizure medications Drugs that decrease the frequency and/or severity of seizures in people with epilepsy Treat the symptom of seizures, not the underlying epileptic condition They don’t change the course of the disease Antiepileptic drugs Drugs that prevent the development of recurrent seizures in people at risk Drugs that reduce seizure frequency and severity outlasting the treatment period Example: after head trauma, stroke, brain tumors, etc. Animal studies suggest that Levetiracetam and Ethosuximide are potential antiepileptic drugs BUT there are no studies in humans to support this
- 5. 5/20/15 5 Use of antiseizure medications Epilepsy Pain treatment Neuralgias, neuropathic pain, etc. Migraine prophylaxis Treatment of bipolar disorder, mood disorder and anxiety Historical development of the drugs
- 6. 5/20/15 6 History of AEDs in the U.S. 1857 – Bromides 1882 – Paraldehyde (not longer in use in USA) 1912 – Phenobarbital (PB) 1937 – Phenytoin (PHT) 1944 – Trimethodione 1953 – Acetazolamide 1954 - Primidone 1960 – Ethosuximide 1963 - Diazepam 1974 – Carbamazepine (CBZ) 1972 – Clorazepate and Lorazepam 1975 – Clonazepam (CZP) 1978 – Valproate (VPA) New AEDs in the U.S. 1993 – Felbamate (FBM), gabapentin (GBP) 1995 – Lamotrigine (LTG) 1996 – Fosphenytoin 1997 – Topiramate (TPM), tiagabine (TGB) 1999 – Levetiracetam (LEV) 2000 – Oxcarbazepine (OXCBZ), zonisamide (ZNS) 2005 - Pregabalin (PGB)
- 7. 5/20/15 7 Newer Drugs 2008 – Lacosamide (Vimpat) 2008 – Rufinamide (Banzel) 2009 – Vigabatrin (Sabril) 2011 – Ezogabine (Potiga) and Clobazam (Onfi) 2012 – Perampanel (Fycompa) When? – CBD oil – IF ….. No FDA approved AEDs Bromides (1857) Sulthiame Stiripentol (2001)
- 8. 5/20/15 8 Other treatments, diet and devices Sex hormones: Progesterone Diets: Ketogenic diet, Low glycemic diet, modified Atkins diet Devices: Vagus Nerve Stimulator (VNS) and Neuropace Epilepsy Surgery How doctors select the drugs to treat the seizures?
- 9. 5/20/15 9 Selecting the AEDs Seizure types or syndrome Rational polytherapy Age of the patient (oral suspension, chewable, sprinkles for children) Dosing schedule Comorbidities and other medical conditions Potential side effects and toxicity Interaction with other drugs Cost-effectiveness Goals of treatment Reduced number of seizures Minimal adverse events or side effects Best quality of life possible
- 10. 5/20/15 10 Common side effects Adverse Effects Acute dose-related: reversible Idiosyncratic Uncommon - rare Potentially serious or life threatening Chronic: reversibility and seriousness vary
- 11. 5/20/15 11 Acute - Dose-Related Adverse Effects of AEDs Neurologic/psychiatric: most common • Sedation, fatigue - All AEDs, except unusual with LTG and FBM - More pronounced with traditional AED • Unsteadiness, poor coordination, dizziness - Mainly traditional AEDs - May be sign of toxicity with many AEDs • Tremor – valproate • Depression ???? Acute, Dose-Related Adverse Effects of AEDs (cont.) • Parenthesis (topiramate, zonisamide) • Diplopia, blurred vision, visual distortion (carbamazepine, lamotrigine) • Mental/motor slowing or impairment (topiramate at higher doses) • Mood or behavioral changes (levetiracetam) • Changes in libido or sexual function (carbamazepine, phenytoin, phenobarbital)
- 12. 5/20/15 12 Acute, Dose-Related Adverse Effects of AEDs (cont.) Gastrointestinal (nausea, heartburn) Mild to moderate laboratory changes • Hyponatremia: carbamazepine, oxcarbazepine • Increases in ALT or AST: valproate • Leukopenia: • Thrombocytopenia: valproate P-Slide 23 Acute, Dose-Related Adverse Effects of AEDs (cont.) Weight gain/appetite changes Valproic acid Gabapentin Pregabalin Weight loss Topiramate Zonisamide Felbamate P-Slide 24
- 13. 5/20/15 13 Idiosyncratic Adverse Effects of AEDs Toxic Epidermal necrolysis Stevens-Johnson syndrome More common in lamotrigine, patients receiving valproate and/ or aggressively titrated. Signs of potential Stevens-Johnson syndrome Hepatic damage Early symptoms: abdominal pain, vomiting, jaundice Laboratory monitoring probably not helpful in early detection Patient education Fever and mucus membrane involvement HLA-B 1502 and AED induced rash Racial groups: Han Chinese and other South East Asian groups Drugs: Carbamazepine, Oxcarbazepine, Phenytoin, Fosphenytoin US FDA recommendations: Genotypic all Asian descend patients before therapy (Ferrell and McLeod. Pharmacogenomics 2008)
- 14. 5/20/15 14 AED Hypersensitivity Syndrome Characterized by rash, systemic involvement hydrolase Cross-reactivity Phenytoin Carbamazepine Phenobarbital Oxcarbazepine Relative cross reactivity - lamotrigine Idiosyncratic Adverse Effects of AEDs Hematologic damage Marrow aplasia, agranulocytosis, aplastic anemia Early symptoms: abnormal bleeding, acute onset of fever, symptoms of anemia Laboratory monitoring probably not helpful in early detection Felbamate aplastic anemia approx. 1:5,000 treated patients Patient education
- 15. 5/20/15 15 Other idiosyncratic reactions Serum sickness Pancreatitis Long-Term Adverse Effects of AEDs Endocrine/Metabolic Effects • Osteomalacia, osteoporosis • Carbamazepine • Phenobarbital • Phenytoin • Oxcarbazepine • Topiramate • Valproate • Zonisamide • Folate (anemia, teratogenesis) • Phenobarbital • Phenytoin • Carbamazepine • Valproate • Lamotrigine • Topiramate • Altered connective tissue metabolism or growth (facial coarsening, hirsutism, gingival hyperplasia or contractures) • Phenytoin • Phenobarbital Neurologic • Neuropathy • Cerebellar syndrome - phenytoin Sexual Dysfunction - 30-60% • Phenytoin • Carbamazepine • Phenobarbital • Primidone
- 16. 5/20/15 16 Drug interactions Pharmacokinetic Interactions Be aware that drug interactions may occur when there is the: Addition of a new medication when an inducer/ inhibitor is present. Addition of inducer/inhibitor to an existing medication regimen. Removal of an inducer/inhibitor from chronic medication regimen.
- 17. 5/20/15 17 Hepatic Drug Metabolizing Enzymes and Specific AED Interactions Phenytoin: CYP2C9/CYP2C19 Inhibitors: valproate, ticlopidine, fluoxetine, topiramate, fluconazole Carbamazepine: CYP3A4/CYP2C8/CYP1A2 Inhibitors: ketoconazole, fluconazole, erythromycin, diltiazem Lamotrigine: UGT 1A4 Inhibitor: valproate Important note about oral contraceptives (OCPs): OCP efficacy is decreased by inducers, including: phenytoin, phenobarbital, primidone, carbamazepine; and higher doses of topiramate and oxcarbazepine OCPs and pregnancy significantly decrease serum levels of lamotrigine. Potent inducers Carbamazepine, Phenobarbital, Phenytoin Effect of induction is seen within the first 3 weeks of treatment Caution when prescribing Bupropion, Quetiapine, etc Definitively have a significant effect over the metabolism of Sex hormones Vitamin D Thyroid hormones Lipid metabolism Folic acid
- 18. 5/20/15 18 Mild inducers Clobazam, eslicarbazepine, felbamate, lamotrigine, oxcarbazepine, rufinamide, topiramate, vigabatrin, and vaproic acid Can be inducers at higher doses Sometime have combined inhibitor effects It can take months before the maximum effect is seen Effect on systemic metabolism is present at a lesser degree AEDs and Drug Interactions Although many AEDs can cause pharmacokinetic interactions, several agents appear to be less problematic. AEDs that do not appear to be either inducers or inhibitors of the CYP system include: Gabapentin Lamotrigine (low dose) Pregabalin Tiagabine Levetiracetam Zonisamide P-Slide 36
- 19. 5/20/15 19 AEDs and Foods Grapefruit juice A case for the need of Epilepsy and Psychiatry team interaction
- 20. 5/20/15 20 Case 1. Marcella 15 years old left handed female refractory right parieto-occipital epilepsy status post partial right occipital cortical resection at age 13 years seizure-free for a month Seizures recurred Past Antiepileptic Medications Carbamazepine, Lamotrigine, Zonisamide Current Antiepileptic Medications • Keppra 2,000 mg bid • Trileptal 1,200 mg bid • Other Meds: Prozac, Folic acid, multivitamin, Vitamin D
- 21. 5/20/15 21 Seizure onset T8P8 P8O2 Fp1F3 F3C3 C3P3 P3O1 Fp2F4 F4C4 C4P4 P4O2 Ictal onset : P8, O2 Pre-op MRI
- 22. 5/20/15 22 Pre-op PET Pre-op Neuropsychological Evaluation Report : Full scale IQ=77(6th%-borderline) Verbal scale=78(7th%-borderline) Performance scale=81(10th%-borderline) Visual immediate memory=109(73rd%-high average) Visual delayed memory=103(58th%average to high average) Verbal immediate memory=69(2nd%-low average to poor) Verbal delayed memory=72(3rd%-low average to poor)
- 23. 5/20/15 23 Her Medical Comorbidities Morbid Obesity Weight = 145 kg = 319 lbs Mild to Moderate Asthma Obstructive Sleep Apnea Her Neuropsychiatric Comorbidities Depression treated with Prozac 10mg suicidal ideation Anxiety not treated Migraine without aura chronic daily headaches Learning disability in need of IEP home schooled Epilepsy stigma bullying at school poor peer acceptance
- 24. 5/20/15 24 Anesthesiologist Sleep Medicine Pulmonologist Endocrinologist Neurosurgeon Epileptologist Psychiatrist Pediatrician Child and Family The Knowledge Program Developed at the Cleveland Clinic Screening tool for neuropsychiatry comorbidities Katzan I et al. 2011
- 25. 5/20/15 25 Take home points Antiseizure medications are prescribed taking into account a number of factors Keep in mind drug drug interaction when prescribing antiseizure medications A multidisciplinary team, that includes a Psychiatrist, is a very important part of the care for patients with epilepsy QUESTIONS
- 26. 5/20/15 26 Jana E. Jones, PhD Associate Professor Department of Neurology University of Wisconsin School of Medicine & Public Health May 20, 2015 Anxiety Disorders in Epilepsy Outline 1. Anxiety & Adults with Epilepsy 2. Anxiety & Children with Epilepsy 3. Anxiety & Quality of Life 3. Treatment Options 4. Conclusions
- 27. 5/20/15 27 • 15% to 25% Community prevalence. • 16% to 25% Hospital prevalence. • 11% to 32% prevalence among surgery candidates. Vazquez & Devinsky, 2003 DSM/ICD Based Diagnoses Victoroff (1994) 32% Manachanda et al. (1996) 11% Perini et al. (1996) 16% Altschuler et al. (1999) 5% Glosser et al. (2000) 22% Swinkles et al. (2001) 25% Jones et al. (2007) 35% Tellez-‐Zenteno et al. (2007) 22% Brandt et al. (2010) 20% Kanner et al. (2010) 15% Mean = 20% Median = 21%
- 28. 5/20/15 28
- 29. 5/20/15 29 • A large number of participants have more than one diagnosis (n=59). (Jones et al., 2005)
- 30. 5/20/15 30 Anxiety in Pediatric Epilepsy Observational Studies Authors Measure Outcome in epilepsy __________________________________________________________ Ettinger et al. (1998) RCMAS 16% elevated anxiety Williams et al. (2003) RCMAS 23% elevated anxiety Baki et al. (2004) STAI 49% mild to mod. Anxiety Vega et al. (2011) BASC 30% elevated anxiety __________________________________________________________
- 31. 5/20/15 31 Controlled Studies Authors Measure Outcome _____________________________________________________ Oguz et al. (2002) STAI High state & trait anxiety Baker et al. (2005) SADS/LOI High social anxiety & obsessive symptoms Loney et al. (2008) RCMAS Elevated anxiety _____________________________________________________ DSM based studies Anxiety Disorders Alwash et al. (2000) 48.5% OM et al. (2001) 13.0% Adewuya & Ola (2005) 31.4% Caplan et al. (2005) 36.0% Jones et al. (2007) 35.8%
- 32. 5/20/15 32 New Onset Sample • Children with new-‐onset epilepsy (n = 180) and healthy first-‐degree cousin controls (n = 107). • Study parVcipants were recruited from pediatric neurology clinics at two large Midwestern medical centers. • Children with epilepsy were included: (1) diagnosis of epilepsy within the past 12 months (2) chronological age between 8–18 years (3) no other developmental disabiliVes (e.g. auVsm, intellectual disability) (4) no other neurological disorder and normal clinical MRI. • Children and parents parVcipated in a structured psychiatric interview (K-‐SADS) at baseline. Prevalence of Current Anxiety Disorders at Baseline Epilepsy (n=180) Control (n=107) Any Axis I Disorder 113 (62.8%) 28 (26.2%) Any Anxiety Disorder 70 (38.9%) 19 (17.8%) Specific Phobia 36 (20.0%) 11 (10.3%) Social Phobia 16 (8.9%) 1 (1.0%) SeparaTon Anxiety 13 (7.2%) 0 Generalized Anxiety Disorder 15 (8.3%) 5 (4.7%) Anxiety NOS 15 (8.3%) 6 (5.6%) Number of Anxiety Disorders Single Anxiety Disorder 48 (68.6%) 15 (78.9%) Two or More Anxiety Disorders 22 (31.4%) 4 (21.1%) 1 No cases of Agoraphobia and Panic Disorders
- 33. 5/20/15 33 0 2 4 6 8 10 12 14 16 18 20 22 24 Specific Phobia Social Phobia SeparaVon Anxiety Prevalence (percent) Median Age of Onset (years) Common anxiety disorders in childhood: Prevalence and age of onset (Kessler et al., 2012) New Onset Epilepsy with & without Anxiety
- 34. 5/20/15 34 Jones et al., 2015 Jones et al., 2015
- 35. 5/20/15 35 Jones et al., 2015 Jones et al., 2015
- 36. 5/20/15 36 MRI Findings • Anxiety is a common psychiatric comorbidity in children with recent-onset epilepsy. • Potential neuroanatomical substrate consisting of volumetric enlargement of the amygdala. Daley et al. (2008) reported a similar finding. • Thinner cortex in orbital and other regions of prefrontal cortex. MRI findings • There are abnormalities in brain structures that are involved in the networks found in individuals with anxiety disorders in the general population. • These anatomic findings: – are evident early in the course of epilepsy. – are not related to chronicity of seizures. – are linked to a family history of anxiety and depressive disorders.
- 37. 5/20/15 37 2 Year Follow-up • Children with epilepsy returned for follow- up 2 years after their baseline evaluation. • Healthy controls also returned. • The KSADS was repeated with child and parent separately. Jones et al. (2015) Jones et al., in progress
- 38. 5/20/15 38 In epilepsy, suicide aMempters had elevated anxiety compared to those with no history of suicide aMempts. Batzell & Dodrill (1986) • At Baseline: – 42% children with epilepsy and anxiety had suicidal thoughts. – 45% children with epilepsy and no anxiety. • At Follow-‐up: – 21% children with epilepsy and anxiety had suicidal thoughts. – 34% children with epilepsy and no anxiety. • Suicidal thoughts are common in children with epilepsy and anxiety. • Suicidal thoughts are also quite common in children with epilepsy without anxiety.
- 39. 5/20/15 39 Poorer HRQOL is significantly associated with increased symptoms of anxiety. Proportion of variance in HRQOL accounted for by demographic, clinical epilepsy and anxiety variables.
- 40. 5/20/15 40 Treatment Recommendations • No randomized controlled trials for the treatment of anxiety disorders in children or adults with epilepsy, including pharmacological and nonpharmacological intervenVons. • Very lidle evidence regarding specific pracVce parameters for the treatment anxiety disorders in adults or children. Baseline: KSADS interview Questionnaires 3-month follow up: Booster session Parent Meeting Questionnaires Level 7: Begin Exposure Tasks Parent Meeting Questionnaires Level 2: Physical signs of anxiety Level 1: CBT & anxiety Parent Meeting Level 12: Exposure Tasks Parent Meeting Questionnaires Levels 8-11: Exposure Tasks Level 3: Relaxation Parent Meeting Levels 4-6: Anxious thoughts, coping thoughts, problem solving, & self-reward Skill Building Phase Skill Practice Phase Camp Cope-A-Lot Intervention Outline (Khanna & Kendall, 2008)
- 41. 5/20/15 41 (Blocher et al., 2013)r (Jones et al., 2014) al Piers-Harris-2 at baseline, week 7, 12 and 3 months
- 42. 5/20/15 42 Pharmacological Treatment • There are no randomized controlled trials of the use of SSRIs in the treatment of anxiety disorders in adults or children with epilepsy. • There is evidence to suggest that seizure frequency is not adversely impacted by the introduction of SSRIs. • Anxiety is common in adults and children with epilepsy. • There are potenTal neuroanatomical substrates idenTfied in children with epilepsy similar to those reported in the general populaTon. • Anxiety has a negaTve impact on overall QOL. • Anxiety is frequently under recognized and under treated.
- 43. 5/20/15 43 • Only 1/3 of children with epilepsy and mental health problems receive treatment (OM et al., 2001). • Parents report that emoTonal and behavioral problems are very concerning to them (Wu et al., 2008). • Neurologists & pediatricians who treat children with epilepsy feel there is a resistance on the part of mental health providers to treat children with epilepsy (Smith et al., 2007). Acknowledgements University of Wisconsin UCLA Bruce P. Hermann, PhD Rochelle Caplan, MD Carl Stafstrom, MD, PhD David Hsu, MD, PhD Mayo/Nemours Children’s Hospital Fred Edelman, MD Raj Sheth, MD Lucy Zawadzki, MD Chris Ikonomidou, MD Rosalind Franklin University Daren Jackson, PhD Michael Seidenberg, PhD Kevin Dabbs, MS Jacque Blocher Funding: Connie Sung, MPh RO1 NINDS 4435-‐06-‐07 Mayu Fujikawa, MS People Against Childhood Epilepsy Michelle Szomi (PACE) Dace Almane, MS 1KL2RR025012-‐01 Kelly Darby, MS Kate Young, MS
- 44. 5/20/15 44 Gaston Baslet, M.D. Division of Neuropsychiatry Department of Psychiatry Brigham and Women’s Hospital Harvard Medical School I have no conflicts of interest to disclose I will be discussing off label use of medications
- 45. 5/20/15 45 Psychogenic Non Epileptic Seizures are paroxysmal episodes of altered consciousness, movement, sensation or experience resembling epileptic seizures, but not associated with ictal electrical discharges in the brain or other recognized physiological paroxysms Most common condition misdiagnosed as epilepsy. Average of 7 years until correct diagnosis is made. 25-‐33% of EMU admissions diagnosed as PNES.1 12% in outpatient Neurology Clinics.2 Annual incidence in Scotland is 3-‐5 per 100,000 but this is an underestimate.3 1. Reuber et al, Neurology, 2002; 2. Reuber, Epilepsy and Behavior, 2008; 3. Duncan et al, Epilepsy and Behavior, 2011.
- 46. 5/20/15 46 Neurologist Psychiatrist Symptom Presentation Engagement Acute treatment Phase Long-‐term Follow-‐up Baslet et al, Clin EEG Neurosci, 2014
- 47. 5/20/15 47 A. One or more symptoms of altered voluntary motor or sensory function. B. Clinical findings provide evidence of incompatibility between the symptom and recognized neurological or medical conditions. C. The symptom or deficit is not explained by another medical or mental disorder. D. The symptom or deficit causes clinically significant distress or impairment in social, occupational, or other important areas of functioning or warrants medical evaluation Specifier: with weakness or paralysis, with abnormal movement (PMD), with swallowing symptoms, with speech symptom, with attacks or seizures (PNES), with anesthesia or sensory loss, with special sensory symptom, with mixed symptom. Specifier: acute episode (< 6 months), persistent (> 6 months). Specifier: with psychological stressor, without psychological stressor. American Psychiatric Association, 2013 PNES: Psychogenic Non-Epileptic Seizures; PMD: Psychogenic Movement Disorder. Levels of Diagnostic Certainty History Witnessed event EEG Possible + By witness or self-‐report/ description No epileptiform activity in routine or sleep deprived interictal EEG Probable + By clinician who reviewed video recording in person, showing semiology typical of PNES No epileptiform activity in routine or sleep deprived interictal EEG Clinically established + By clinician experienced in diagnosis of sz disorders (on video or in person) showing semiology typical of PNES No epileptiform activity in routine or ambulatory EEG during a typical ictus/ event in which the semiology would make ictal epileptiform EEG expectable during equivalent epileptic sz Documented + By clinician experienced in diagnosis of sz disorders, showing semiology typical of PNES, on video EEG No epileptiform activity immediately before, during or after ictus captured on ictal video EEG with typical PNES semiology La France et al, Epilepsia, 2013
- 48. 5/20/15 48 Signs that favor PNES Evidence from primary studies Sensitivity (%) for PNES Specificity (%) for ES Long duration Fluctuating course Asynchronous movements Pelvic thrusting Side-‐to-‐side head or body movements Closed eyes Ictal crying Memory recall Good Good Good (FLS excluded) Good (FLS excluded) Good (convulsive events only) Good Good Good 69 (events) 47-‐88 (patients) 44-‐96 (events) 9-‐56 (patients) 1-‐31 (events) 7.4-‐44 (patients) 25-‐63 (events) 15-‐36 (patients) 34-‐88 (events) 52-‐96 (patients) 13-‐14 (events) 3.7-‐37 (patients) 63 (events) 77-‐88 (patients) 96 96-‐100 93-‐96 93-‐100 96-‐100 92-‐100 96-‐100 92-‐100 74-‐100 97 100 100 96 90 Signs that favor ES Evidence from primary studies Sensitivity for ES Specificity for ES Occurrence from EEG-‐confirmed sleep Post-‐ictal confusion Stertorous breathing Good Good Good (convulsive events only) 31-‐59 (events) -‐ 61-‐100 (events) 67 (patients) 61-‐91 (events) 100 -‐ 88 84 100 Other signs Evidence from primary studies Gradual onset Non-‐stereotyped events Flailing or thrashing movements Opisthotonus Tongue biting Urinary incontinence Insufficient Insufficient Insufficient Insufficient Insufficient Insufficient La France et al, Epilepsia, 2013 PNES: psychogenic non-‐epileptic seizures ES: epileptic seizures Psychosocial Factors Child/Adult Trauma Family Dysfunction Interpersonal communication Adverse life events Psychiatric Conditions Depression, Anxiety, PTSD Somatoform Disorders Dissociative Disorders Personality Disorders Substance Abuse Eating Disorders Neurological Conditions Epilepsy Migraine Chronic pain Head Trauma Neuropsychological Deficits/ Vulnerability Traits Avoidance Impulsivity Somatic preoccupation Alexithymia Emotion regulation styles Limited effort Suggestibility ? PNES
- 49. 5/20/15 49 As a psychiatrist, you can establish the diagnosis of PNES after carefully reviewing the exam and tests that confirm incompatibility between the symptom and the preserved physiological functioning. Always confer with a neurologist. Early screening for risk factors can help you formulate an explanatory model for the patient. There is growing evidence of effective treatments for PNES, mostly based on psychotherapeutic interventions.
- 50. 5/20/15 50 Symptom Presentation Engagement Acute treatment Phase Long-‐term Follow-‐up Baslet et al, Clin EEG Neurosci, 2014 MDD: Major Depressive Disorder; Kanner et al, Neurology, 1999 Class I, n = 13 Class II, n = 12 Class III, n = 20 Psychiatric variable n (%) n (%) n (%) Recurrent MDD 1 (8) 2 (17) 14 (70) Personality disorder 1 (8) 3 (25) 16 (80) Chronic abuse 3 (23) 1 (8) 16 (80) Denial of psychosocial problems 0 8 (75) 1 (5) What happens after an acute intervention in PNES?
- 51. 5/20/15 51 Patient filled postal questionnaire (n=164) 4.1 years post-‐PNES diagnosis 71% of patients continue to be symptomatic.1 Complaint at doctor’s visit over 6 months (n=167) 5-‐10 years post-‐PNES diagnosis 26% of patients continue to complain of seizures. Significant reduction in ED visits and AED prescription, but not in employment rates.2 1. Reuber et al, Annals of Neurology, 2003 2. Duncan et al, JNNP, 2014 There is a variety of outcome patterns in PNES patients. Identifying subgroups of patients with different outcomes may help customize treatment protocols for subpopulations and improve overall functional outcomes.
- 52. 5/20/15 52 APA 2015
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- 55. 5/20/15 55 Falcone et al Psychiatric comorbidities in patients undergoing epilepsy surgery- AES 2009
- 56. 5/20/15 56 EXAMPLE OF SEIZURE DRAWING THAT DEPICTS THE THEME OF HELPLESSNESS OR DEPRESSION 10-year-old boy with complex partial seizures depicts himself inside a coffin, screaming, ‘‘Let me out!’’
- 57. 5/20/15 57 16-year-old boy with left temporal lobe epilepsy and generalized tonic–clonic seizures.
- 58. 5/20/15 58 Make sure that you listen, make sure that you care, make sure you are watching — something’s always there. Adwoa Boakye Release Emily Good
- 59. 5/20/15 59 QOL Seizures Ability to Think And Remember Neuro and Physical Limitations Inattention and Mood