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Psychiatric Aspects of Movement Disorders for Nurse Practitioners

Psychiatric Aspects of Movement Disorders for Nurse Practitioners . Joan C. Masters, EDD, MBA, APRN, PMHNP-BC Bellarmine University Louisville KY jmasters@bellarmine.edu Kentucky Coalition of Nurse Practitioners and Nurse Midwives Conference Lexington, KY April 15, 2014. A bstract.

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Psychiatric Aspects of Movement Disorders for Nurse Practitioners

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  1. Psychiatric Aspects of Movement Disorders for Nurse Practitioners Joan C. Masters, EDD, MBA, APRN, PMHNP-BCBellarmine UniversityLouisville KYjmasters@bellarmine.eduKentucky Coalition of Nurse Practitioners and Nurse Midwives Conference Lexington, KY April 15, 2014

  2. Abstract Movement abnormalities are often comorbid with psychiatric disorders. A movement disorder may be a manifestation of a psychiatric disorder (i.e. psychogenic disorder), an adverse response to psychiatric treatment (e.g., drug-induced), or a distinct but co-occurring condition with a psychiatric disorder. In this presentation, an overview of the major movement disorders with psychiatric aspects, clinical pearls, and treatment caveats will be presented.

  3. OBJECTIVES At the completion of this presentation, participants will be able to: Differentiate among psychogenic, treatment induced, and co-occurring movement and psychiatric disorders Explain appropriate treatments for psychogenic, treatment induced, and co-occurring movement and psychiatric disorders

  4. Somatic Symptom Disorders Challenging patient population Chronic, difficult to treat High utilizers of the healthcare system Risks Repetitive, unnecessary diagnostic testing Invasive medical/surgical workups Iatrogenic illness Clinical Goals Coordination of care with psychiatric consultation Treat medical illness fully Avoid excess iatrogenic harm

  5. Terminology • Psychogenic considered unsatisfactory • (Used by clinicians but not usually with pts.) • More recently “functional” • Replaces conversion DO, hysteria

  6. PSYCHOGENIC MOVEMENT DISORDERS (PMD) Not caused by structural neuro damage Wide range of symptoms (tremors, bradykinesia, myoclonus, tics, chorea, athetosis, ballism) PMD often (~70%) accompanied by anxiety, depression, PDOs, substance abuse Clinicians (not pts.!) tend to see “stress” as causative but that is overly simplistic

  7. History Somatoform DO Not included in DSM I and II but neurosis was DSM-III: Neurosis too vague and too psychodynamic S&S needed a home: Somatoform DSM-IV: Medical symptoms had to be “unexplained” DSM 5 DX: “Somatic Symptoms and Related Disorders“ replaces old "Somatoform Disorders“ Somatic symptom disorder (subsumes pain DO & somatization DO) New: Illness anxiety disorder and Psychological factors affecting other medical conditions

  8. Why So Many Changes? Overlapping previous diagnoses Difficult for non‐psychiatric clinicians to apply Reduction of stigma ↓ mind‐body dualism Implication that symptoms were not "real” DSM‐5 Changes: Reduction in the number of diagnoses Focus on positive symptoms Removal of “medically unexplained symptoms”

  9. DSM 5 Lack of medical explanation ≠ Psychiatric Diagnosis

  10. DSM-5: Somatoform DOs Now Somatic Symptom and Related DO Somatic Symptom Disorder Illness Anxiety Disorder Conversion Disorder (Functional Neurological Symptom Disorder) Psychological Factors affecting other medical conditions Factitious Disorder Gone: Hypochondrias, somatization disorder, pain disorder, & undifferentiated somatoform disorder

  11. Epidemiology PMD • Accurate data limited • ~ 30% of outpatients in neuro settings S&S not caused by neuro disease • ½ PMD & ½ out of proportion to disease • As distressed and more disabled (Stone & Carson, 2011) • ~ 1% - 9% neuro unit admissions unexplained motor symptoms (Hallett) • ~ 25% MDO pts. some point could be dx with PMDO • Large hospital DC study, 2.6% DC DX somatoform DO • ~3.5% large specialty clinic (Sa) • Tremor, dystonia, myoclonus, gait, Parkinson's, tics • In order of commonality; last two may reverse order

  12. Clues A: History General; DO specific clues with each DO Abrupt onset, static course Inconsistent over time (spontaneous remissions and exacerbations) Multiple somatic C/O Health care worker Onset typically 35 – 50 yoa

  13. Clues A: History Predisposing factors: Low SES, 60%-75% female, hx of abuse and neglect, current mistreatment, modeling, perceived stress; not ↓IQ Precipitating factors: Often a physical injury Perpetuating factors: Illness beliefs, secondary gain; anger at DX, diagnostic uncertainty, involved in litigation/worker’s comp Cluster B traits- low self-directedness and high novelty seeking (Hallett; Sa)

  14. Clues B: Clinical No single finding will clinch it Movements increase with attention and decease with distraction Inconsistent (amplitude, character, distribution, selective disability) Paroxysmal movement DO Abn movements can be triggered or relieved with odd or non physiological tx (e.g., use of tuning fork) False weakness/false sensory CO Deliberate slowness of movements

  15. Clues B: Clinical PMD don’t usually involve the fingers; MD do Functional disability out of proportion to clinical findings Multiple symptoms attributable to multiple organ systems Fixed dystonia (contracted limb) Excessive grimacing or sighing Non-anatomical sensory loss (stocking & glove anesthesia) Movements are bizarre or multiple or hard to classify Self-inflicted injuries (Sa)

  16. Clues C: Pt. Response Responds to placebo Does not respond to appropriate meds Abn movements remit with psychotherapy Pts deny/refuse psychogenic explanation Usually agreeable with pragmatic approach of therapy, meds to treat depression & anxiety, and improving coping skills

  17. Pt Challenges Complicated and difficult diagnostically (can be done) and clinically (because often have other pathology) Inaccurate historians compared to clinicians and to selves One study: Only 22% of self-reported symptoms confirmed Another: Only 61% of med unexplained symptoms and 43% of all symptoms reported by pt a year later Prognosis guarded; Two-thirds same/worse at follow-up (Hallett)

  18. Assessment • Initially should focus on listing all physical S&S • Can wait on depression and anxiety questions- can be alienating • Ask about fatigue, pain, sleep disturbance, dizziness, memory, concentration • Helps rapport • Gradual onset associated with fatigue • What is pt.'s understanding? • Irreversibility and damage beliefs prognostic

  19. Caveat Clues are only that People with organic DO may also have these presentations Up to 30% of people with PMD found to have an organic condition that could explain their S&S Neuro DO can have unusual presentations

  20. PMD Tremor Common: 35% and 55% of PMDs in two large studies More common in middle-age, female Quick onset and rapid progression are clues Variable amplitude and frequency clues Postural more than resting which is more than action Often all three- a clue Organic do not dissipate with distraction

  21. PMD Tremor • Entrainment a clue- pt asked to do a slow rhythmic or complex irregular pattern with uninvolved/other limb the tremor often changes to match contralateral movement • Arm(s) most common • Usually continuous • But rarely fingers • Then head • Then legs • Usually not continuous • Surprisingly little C/O fatigue

  22. PMD: Dystonia • Sustained muscle contractions • Twisting, writhing movements • MD most likely to be dx as psychogenic when not • No bio marker • 39% of PMDO • Young females • Abrupt onset • Lower limb, excessive pain, slowness, non-anatomic sensory dysfunction

  23. PMD Myoclonus Brief, shock-like muscle contractions or sudden loss of tone (negative myoclonus) ~13%, 2 X women, M= 43 yoa Worse with stress and anxiety Most have a precipitating event Electrophysiological testing can differentiate organic from PMD (which is slower, inconsistent, variable)

  24. PMD Myoclonus: Related Culturally-Mediated Disorders • Startle response: Jump, grimace, hunch shoulders, breathe faster • Nl: Habituate and relax on successive exposures • Some people (and dogs, cows, horses, mice, have an exaggerated response; shout, flex arms and legs and fall to ground • Hereditary hyperkplexia • Don’t habituate with repeated exposure • Defect of inhibitory glycine receptors • In humans and one mouse strain one amino acid coded incorrectly- chloride channel opens less frequently when exposed to NT glycine; glycine now ↓ effective in inhibiting neurons in brain stem and sc

  25. PMD Myoclonus: Related culturally-mediated Disorders Jumping Frenchmen of Maine: Unusual, extreme startle response, often followed by echolalia, echopraxia, coprolalia, forced obedience (“Sit!”, “Jump!”) Normal startle habituates, this does not-increasing complexity Late 19th century; isolated lumberjacks Symptoms milder with age More intense with stress, anxiety, and the more frequently startled

  26. Normal Startle Two components 1st abrupt brief blink, grimace, them head & neck movement, with flexion of upper limbs & trunk Involuntary; normally habituates but exaggerates in hereditary hyperekplexia (mutations in glycine receptors) and in acquired hyperekplexia from brainstem disease

  27. Normal Startle 2nd component Begins at latencies overlapping with voluntary reaction times 2nd component longer in duration and subject to voluntary elaboration, “orienting” to the stimulus- look toward, away, raising hands, vocalization (including coprolalia), dropping or throwing objects Presentation varies with intense emotion/pleasure Latah/descendent of JF- startle fall in voluntary reaction times May be linked to frontal lobe dysfunction

  28. PMD Myoclonus: Related Culturally-Mediated Disorders • Tx: Eliminating intentionally startling and/or teasing can reduce/end episodes • Latah in Indonesia • Most common, middle age women • Often rage, anxiety, fear • Myriachit in Siberia • “Ragin’ Cajuns” in Louisiana • More research needed

  29. Strychnine Poisoning Plant toxin; used by farmers to kill farm pests and by psychopaths Antagonizes glycine at its receptor High doses almost eliminates glycine inhibition in sc and brain stem Uncontrollable seizures, unchecked muscle contractions, paralysis of respiratory muscles, asphyxia Agonizing death bc glycine not a NT at higher centers of brain so no cognitive or sensory impairment Low protein binding so enters tissues quickly Death within 1-2 hours Low doses a stimulant; 1992 Olympics

  30. PMD Chorea/Ballism Changes in definition of chorea have changed over time Random fleeting movements that flow from one part of the body to another in an unpredictable way Figidity, antsy Ballism: Involuntary, irregular, violent movements arm and shoulder, rt stroke or tumor, usually one side Again, inconsistent Exceedingly rare

  31. PMD Tics Rare (~3%- 6%) and little written High percentage have an “inner urge” to perform tics In contrast to other organic do (e.g., TD, dystonia) in which no desire

  32. PMD Facial Spasm Dyskinesia Tics • Unusual (~2.4%) • May be overlooked if more dramatic symptoms present • More in women, 30s • Usually found secondary to another PMD • Dx: Abrupt onset, multiple somatization, secondary gain, exacerbation with attention, reduction with distraction

  33. PMD Parkinsonism ~10%-20% of PMDs Slightly more women than men (opposite in PD) Often occurs after injury or accident Tremor present at rest, often of dominant hand, persists with change in posture and action, lack dampening of true PD rest tremor with a new posture or movement Tremor decreases/disappears with distraction Opposite of true resting tremor of PD where mental exercise elicits or intensifies the tremor

  34. PMD Parkinsonism Bizarre movements with mild stimulus of testing (falling backwards but not falling, flailing of arms) Non-anatomical sensory loss “Baby” or foreign accent speech Handwriting irregular but no micrographia Classic abrupt onset, inconsistencies, alteration/ distraction, false neuro signs Rigidity common, often with c/o pain Disability can be severe Can remit with psychotherapy Dx imaging (PET, SPECT) can clarify

  35. PMD Parkinsonism • High resource use, excessive consultation, surgeries, dx tests • Nigrostriatal dopamine system imaging flurodopa PET and betaCIT and I-isoflupane SPECT can dx • Abnormal in even very early PD and not in psychogenic movement DO • Baylor: Placebo test with cariodopa alone and tuning fork test (told vibration will change tremor) • Disclosed after

  36. PMD Gait Disorders Long hx in med literature ↑ hx of misdx (fx turn out not to be) All ages, but caution dx in older people – often have (real) problems in balance with exaggerated compensation RT fear of falling More female Abnormalities often distinctive Psych hx relevant Key: Abrupt onset, inconsistent, incongruent, multiple simultaneous symptoms (e.g., contractions, tremor, voice abnormalities, paralysis), or total remission for day or weeks

  37. PMD Gait Disorders Often exaggerated slowness – “walking through thick soup” Exaggerated effort, exaggerated fatigue Convulsive shaking, scissor walking Uneconomic postures including camptocormia (“bent tree”) Knee bucking, pained affect May have dramatic fluctuations over minutes (rare in neuro DO)

  38. PMD Gait Disorders Dragging gait (see next slide) Tightrope walker’s gait (arms out) Crouching gait- close to ground BC fear falling (but that requires more strength!)

  39. Example Functional Monoplegic Gait Both cases, leg dragged at the hip. External or internal rotation of the hip or ankle inversion/eversion is common.

  40. PMD Gait Disorders • Astasia-abasia • Unstable, staggering way of standing and walking; Uneconomical • Normal limb power in bed but cannot stand or walk • Constantly on the verge of falling, but always saves self • Was most common conversion DO in WW I • Excellent example at http://www.youtube.com/watch?v=tdpvNObwEZo&list=PLz27Rlp3y6Xtfw83z3CfgeHhhuRIOZvBy&feature=player_detailpage (Harrison Video Library of Gait Disorders, # 4) • Observation/distraction may activate/suppress • Prognosis can be good with short duration and acute onset • If ↑ 6 mos and secondary gain sets in prognosis guarded

  41. PMD Gait Disorders • Dx: • Observe spontaneous gait and tandem heel toe walking • Wilson’s disease and Huntington's disease most frequent DO where incorrect dx of PMD made • (Wilson's-autosomal recessive, cannot excrete copper, accumulates liver, brain, kidneys) • In addition to observation: • Lab gait analysis: Software not yet where should be • Imaging • White matter disease (some nl in older) • Dual task walking (Walking and cognitive task) • Abn in executive fx associated with reduced gait speed

  42. PMD Tourette Syndrome • Tourette: Premonitory urge • Suppressability- disappear during voluntary movements • Recognized as partially voluntary • Relief following • Tics nearly identical

  43. PMD Tourette Syndrome • Tourette and pseudo tics: • Abrupt onset • Cessation with distraction • Response to suggestion • Waxing and waning course • Dramatic resolution • Pseudo tics: • Maximum disability at onset • Increase with attention • Variability BT tics • Entrainment • Uncommon

  44. PMD Weakness Female, mid-30s 5/100,000 Often co-morbid with fatigue & pain Most common unilateral > one limb > both LL May report limb feels alien

  45. Voluntary S&S: Factitious DO • Factitious: Intentional feigning or producing physical or psychological symptoms • Severe form: Munchhausen's syndrome • Motivation is the sick role • No external incentives (not for financial, legal, or other gain) • Poor prognosis

  46. Voluntary S & S: Malingering Not a psychiatric DO Intentional self-injury motivated by financial gain, avoiding work, etc. Discrepancy between presentation and findings Rare, absurd, odd symptoms combinations Uncooperative with dx and tx recommendations Antisocial PDO Hx of different names *Possibly rational May clear up spontaneously with settlement or may continue to keep up appearances Clinicians can be reluctant to diagnoses; insurance companies less so

  47. Voluntary S & S: Malingering 13% of patients in ED feign illness Secondary gain most often food, shelter, prescription drugs, financial gain, and avoidance of some responsibility Red flags: Vague answers, professional language, conditional threats, demanding certain meds, eagerly volunteers psychotic S&S, endorses both psychotic and cognitive S&S, overnight illness, no psychotic illness until ~late in life BB article has good tools

  48. DX PMD: “Here there be dragons” • Dx is very difficult and pitfalls abound • Should be done by a movement DO expert, not just a neuro specialist • Differential includes entire spectrum, need wide and deep experience • Incorrect dx of PMD subjects pts. to: • more stress • more, expense • missed opportunity for correct tx • ASE of inappropriate rx • stigma • Only 4% misdiagnosis (PMD incorrectly dx in organic condition)

  49. DX PMD • Hospital admission could be useful • Once correct dx, need to stop searching • Suggestion: Explaining to pt no serious disease along with PT/OT, therapy, biofeedback • Relatively benign approach • Placebo • Legal and ethical issues, impugn autonomy • Damaging to pt-provider relationship when pt. finds out • Psychogenic dx should be made by neurology not psychiatry

  50. Categories of Dx Certainty Fahn and Williams-accepted standard 1. Documented: Relieved with therapy, suggestion, placebo, observed symptom free 2. Clinically established: Inconsistent, incongruent, with definite psychogenic symptoms 1 &2 later “Clinically definite” 3. Probable: Inconsistent/incongruent but that’s all, or high likelihood of organicity but false neuro S&S, or likely organic but plethora of somatic complaints 4. Possible: Obvious emotional issues in someone with a movement DO that appears organic May need revision; many patients have a “functional overlay” to PMDs

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