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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-BC Bellarmine University Louisville KY Kentucky 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 (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

51 Patient Approach Empathetic, with certainty, nonjudgmental, that do not believe they are “crazy”, confident of improvement Neurobiological explanation; form of dystonia, myoclonus etc. without severe or permanent brain disease Psych referral to aid in evaluation and coping with burden of illness Psych should be adequately informed-do not want “nothing wrong” dx No controlled trials so empirical approach

52 Prognosis Guarded Many will have persistent disability
Research study, 66 PMD and 704 with PD PMD had more psychiatric DX, more severe psychiatric illness, similarly poor QOL and disability despite younger age and shorter duration of illness 3 years after dx only 4/66 no longer had PMD but two of those had another somatoform DO If no improvement with initial hospital evaluation recovery is rare If legal/compensation issues present, seldom improvement until resolved but resolving many not help (Sa)

53 Prognosis Better prognosis if treated in a psychiatric setting than neuro setting Illness beliefs & financial benefits stronger predictors of recovery than number of symptoms, disability, and distress Better prognosis: Younger age, shorter duration, willing to accept psychological factors, believe reversibility, rapport with clinician, no other symptoms, presence of anxiety and depression, removal of stress, marriage or divorce Poorer prognosis: Believe irreversible, PDO, anger at nonorganic dx, older age, sexual abuse, longer duration

54 Talking With Patients About the Dx
Difficulties: Pts. distress/fear: Implication “on purpose”, wonder if worse dx being missed, convinced do not have a psych problem, shares negative ideas about psychogenic do, confirms worst fears, Clinician: Non psych may be uninterested, may not know what to make of it, may wonder if deliberate, reluctant to make dx and being wrong

55 Presenting the Dx Explain what they have How the dx was made
Explain what they do not have Indicate belief- (“I do not think you are making this up”) Emphasize this is common (“I see many pts. . . “) Emphasize reversibility (“Because there is nothing wrong with your brain, you have the potential to get better”) Emphasize self-help (“This is not your fault but there are things you can do to help yourself get better”) Present the role of depression and anxiety (“Feeling depressed/anxious will tend to make your symptoms worse”)

56 Presenting the Dx Give written information- letter, handout, website
DC meds that indicate a not present disease Suggest antidepressants in context of broader use Psychiatric referral in context of management, not psychiatric illness Involve SO

57 Presenting the Dx Controversy re core explanation
Psychological explanation May improve acceptance, makes connection BT symptoms & emotions, but may negatively affect relationship with pt Functional explanation (“software” problem) Pt less likely to think perceived as “crazy”, better fit with reversal potential but maybe too accommodating, too broad a term, may delay psych. Tx “I don't know” Possibly accurate but creates ↑ doubt about clinician

58 Presenting the Dx If pt hostile to a psych explanation then a functional explanation at start may be advisable If pt taken seriously may be more amenable to a functional explanation first and over time a psych explanation

59 Presenting the Dx Speed acceptance- many pts suspect,
Psychological explanation Speed acceptance- many pts suspect, Helps pt make that link if have not made already No room for confusion May became angry but that may not be a change

60 Presenting the Dx Resources Functional/dissociative neuro symptoms:
Non-epileptic seizures Org British, well-done

61 Psychotherapy Psychotherapy seems logical but not enough research
Tx anxiety and depression if indicated. Meds, CBT Physical therapy “This may be as much as can be done at present – will need to work around it for now”

62 Local MDO Clinics IU Dept. of Medicine, University of Cincinnati Gardner Center for Parkinson’s Disease and Movement Disorders in the UC Neuroscience Institute

63 Local MDO Clinics Kentucky Neuroscience Institute movement Disorders Clinichttp://ukhealthcare.uky.edu/ky-neuro/movement/ Appointments and Info:  Frazier Rehab Institute and the University of Louisville Division of Movement Disorders

64 TREATMENT INDUCED MOVEMENT DISORDERS
Acute dystonia Akathisia Pseudo-Parkinsonism Tardive Dyskinesia Neuroleptic malignant syndrome Punding Serotonin syndrome Tremor

65 Pathophysiology If D2 receptors blocked in nigrostraital pathway get movements resembling PD Since nigostriatal pathway part of EP nervous system called EPS Chronic blockade: Hyperkinetic movement DO known as tardive dyskinesia (TD) D2 receptors upregulate (↑ in number) attempting to overcome drug-induced receptor blockade

66 EPS “Inextricably linked” to antipsychotics Issues:
Mistaken for/worsen psych symptoms Troublesome SE from antiparkisinson meds Sometimes irreversible, even lethal Disfiguring/stigmatizing Negatively affect compliance, relapse, rehospitalization 1988: Clozapine reported to be low on EPS, sets off chain reaction of search for “atypicals”

67 Tardive Dyskinesia Facial and tongue movements
Grimacing, tongue protrusion, constant chewing Limbs: Quick, jerky or choreiform (“dancing”) movements 5% pts. on conventional antipsychotics develop every year Older-25% in first year May reverse if stopped soon enough by “resetting” of D2 receptors (either they decrease in # or become less sensitive) ↓With LT use, no reversibility Vulnerable? Early EPS ~2X risk of TD After 15 years, new risk low Tool: AIMS; (Stahl)

68

69 Atypicals Also Risky for TD
TD study at CT CMHC AIMS & Glazer-Morgenstern criteria for dyskinesia every 6 month for 4 years TD risk with atypicals more than half that of conventional when clozapine excluded or more than two-thirds risk when clozapine included TD risk significantly higher for schizophrenia than affective DO pts Olanzapine may be lower risk (but ziprasidone and aripirazole not included) Clinicians should continue to monitor for tardive dyskinesia, and researchers should continue to pursue efforts to treat or prevent it (Woods et al., 2010)

70 Acute Dystonia Acute, frightening, painful, involuntary MDO
Brief sustained or intermittent contractions of antagonistic muscle groups Twisting and repetitive movements Most common: Head, jaw, eyes, mouth Leads to torticollis, retro/anterocollis, trismus (lockjaw) Blepharospasm (eye spasms), tongue biting, protrusion Not action or sensory dependent More subtle: Muscle cramps, jaw tightness, difficulty speaking/swallowing –may precede or be only S&S

71 Acute Dystonia May get worse: Oculogyric crisis, dysarthria, dysphagia, respiratory stridor (if pharyngeal or laryngeal muscles affected) Less common: Axial, truncal or limb involvement, camptocormia (marked flexion of thoracolumbar spine that abates in recumbent position), pleurothotonus (Pisa syndrome), opistotonus (head and lower limbs to bend backward and the trunk to arch forward)

72 Anterocillis on upper L, Pisa syndrome on upper R, Trismus on lower R, camptocormia on lower left, opistotonus middle

73 Acute Dystonia: DX Olanzapine, quetiapine, ~ clozapine
Earliest EPS; 95% first few days of tx or increase in med Last hours-days If med DC, resolves hours 2%-5% patients overall but can go as high as 90% in young men on IM meds From excessive compensatory dopaminergic activity or dopamine antagonism??? ↑Risk: Young (rare ↑ 45), children ↑risk), male, AA, previous rx, +family hx of dystonia, cocaine use, mood DO, hypocalcemia, hypoparathyroidism, hyperthyroidism, dehydration Dose dependent: Very high/low higher risk; moderate doses OK If have weak dopamine antagonism and strong anticholinergic effects then low dystonia Olanzapine, quetiapine, ~ clozapine

74 Acute Dystonia: DX CATIE study: Older people with chronic schizophrenia given moderate doses of mid-potency FGA (e.g. perphenazine, loxipine) not at increased risk of dystonia Young, high-risk pts., or if paranoid and want to avoid dystonia, then can give anticholinergic prophylactically Respond 10”-20” to benztropine or diphenhydramine (IM, po; IV in emergency) Trilafon loxitane

75 Acute Dystonia Pt on L had taken metoclopramide (Reglan) for GI problems Reglan now has a black box warning

76 Parkinsonism Mimics PD
Bradykinesia, masked facies, reduced arm swing, slowed activity initiation, soft speech, flexed posture, symmetrical resting/action tremors, rabbit syndrome (focal perioral tremor), bilateral & symmetrical rigidity of neck, trunk, limbs with cog-wheeling, ~sialorhea, postural or gait disturbances Compared to dystonia, more common, more difficult to treat, can cause more disability, esp. in older people

77 Parkinsonism Differential: Negative symptoms schizophrenia, psychomotor retardation, idiopathic PD PD usually asymmetric, slow progression, autonomic dysregulation (orthostasis), anosmia; imaging will help 10%-15% pts. on FGAs 50%-75% in a month, 90% in 3 months; also with change/increase meds, WD of anticholinergic Usually reverses in days-weeks but may be months or permanent (real PD?) Risk: Older age, female, family hx of PD, dementia, HIV+, pre-existing extrapyramidal disease,

78 Parkinsonism Tx with anticholinergics not as compelling as for dystonia Risk of atropine toxicity Preferred: Lower dose, switch to lower risk antipsychotic Anticholinergic or amantadine Parkinsonism may worsen if anticholinergic WD

79 Akathisia More often affects lower limbs
Still a problem with SGAs; hard to treat Pts. C/O: Feels tense, anxious, restless, drawing in of legs, feeling fidgety Observe: Complex, semi-purposive, repetitive movements, foot shuffling & tapping, shifting foot to foot, rocking, pacing running Intolerable; associated with suicide and aggression Can be fine within a few days of tx but usually increase with duration; 50% within one month and 90% with 3 mos

80 Akathisia 20%-35% but as much as 75% in some FGA studies
~Risk: Older age, female, negative symptoms, cognitive dysfunction, iron deficiency, Parkinsonism, mood DO SGAs may be less likely Close observation key; once +, discontinue, reduce, or switch to less potent dopamine antagonist TX: Beta-blocker (propranolol), anticholinergic (but ↑ effective if parkinsonism +), benzos, amantadine 5HT2A antagonist: Mirtazepine (equal to propranolol and better tolerated)

81 Akathisia https://outcometracker.org/library/BAS.pdf
Differential: Includes drug intoxication and WD, neurogenerative DOs Meds causing restlessness: SSRIs, CCBs, anti-emetics (metoclopramide), anti-vertigo meds Resembles restless leg syndrome; dopamine agonist will worsen things Need to differentiate from agitation and anxiety Barnes Akathisia Scale https://outcometracker.org/library/BAS.pdf

82 Catatonia Least recognized antipsychotic MDO but also rare
DO of speech, volition, movement S&S: Stupor, akinesia, mutism Must be differentiated from catatonia due to schizophrenia and mood DO, neurodegenerative DOs, other brain DOs Develops within hours-days of drug exposure and resolves as quickly when antipsychotic WD May also develop when benzo or anticholinergic WD

83 Catatonia Risk: Previous catatonia, high potency drugs; SGAs may be lower risk TX: Benzodiazepines and ECT Must TX- can progress to NMS +Hx: Avoid antipsychotics (if possible) Patho may be drugs effects on dopamine pathways in basal ganglia-thalmocortical circuits and GABA/glutamate pathways May be genetic component

84 Neuroleptic Malignant Syndrome
Rare but potentially fatal rx resembling advanced parkinsonism and catatonia Often mistaken for worsening psychosis Differential: Whatever causes fever and encephalopathy (CNS infection, heatstroke, serotonin syndrome, ETOH, sedative, or dopamine agonist WD; dopamine antagonists such as Reglan)) Can have rapid onset but usually within 1-2 weeks of med start Most case resolve in 1-2 weeks

85 Neuroleptic Malignant Syndrome
FEVER mnemonic: F – Fever E – Encephalopathy V – Vitals unstable E – Elevated enzymes – CPK R – Rigidity of muscles

86 Neuroleptic Malignant Syndrome
~0.02% patients, ~15% fatal Death: Renal failure, DIC, PE, pneumonia, cardiac arrest Risk: Dehydration, cathexia, catatonia, previous episode, high IM doses of high potency meds Maybe: Multiple meds (antipsychotics, SSRIs, SNRI, Li) Treatment: Symptom management (cooling, fluids) DC antipsychotic Bromocriptine (Parlodel) - dopamine agonist Dantrolene (Dantrium) - peripheral muscle relaxant

87 Punding From Swedish slang for “block head”- psychostimulant abuse
“Compulsive hobbyism” Repetitive, complex, unproductive, excessive, stereotyped motor behavior Pt has an irresistible urge Often “meaningless” collecting and arranging, may be RT a previous hobby Often co-morbid sleep problems

88 Punding Differential: Motor tics, OCD, impulse control DO, autism spectrum, frontal syndrome (will have lesions in frontotemporal region) Unlike OCD, (a)not instigated by internal tension about whether to do, (b)not driven by fear or anxiety (e.g., locking doors, burglars or washing hands) Dopaminergic drugs, levodopa (L-DOPA Not dose or duration related; idiosyncratic ~8% in PD patients Amphetamine, cocaine abuse

89 Serotonin Syndrome Potentially life-threatening
Associated with ↑ serotonergic activity in CNS Seen with therapeutic med use, increase in dose, drug interactions (combo of two drugs most common reason), OD S&S: Mental status changes (anxiety, agitated delirium, disorientation) Autonomic hyperactivity (diaphoresis, tachycardia, hyperthermia, HTN, V, D), also dry mucous membranes, flushed skin, diaphoresis Neuromuscular abnormalities: Tremor, muscle rigidity, myoclonus, hyperrefelxia, bilateral Babinski sign Hyperrefelxia, *clonus, rigidity common & more pronounced in lower extremities Clonus- involuntary, rhythmic, alternating muscle contraction & relation Myoclonus- quick involuntary muscle jerk- sleep starts, hiccups Clonus cardinal sign

90 Serotonin Syndrome Drugs
SSRIs, SNRIs, TCAs, buspirone, trazodone Triptans for migraine Ecstasy, dextromethorphan, cocaine, hallucinogens (foxy methoxy, Syrian rue, LSD) Carbamazepine, Valproic acid, lithium Fentanyl, *meperidine, methadone, tramodol Herbs: St. John’s wort, ginseng Antiemetic: Metoclopromide Antibiotic: Linezolide (Zyvox) Anti-Parkinson’s drug L-dopa; Pts should be asked for a complete list of drugs regularly taken, including prescriptions, OTC, dietary supplements and recreational drugs before prescribing something new

91 Serotonin Syndrome 2002: 7,349 cases serotonin toxicity, 93 deaths
85% MDs unaware of SS All ages, probably under recognized, many case mild Majority in 24 hours, most within 6 Intentional OD often more toxic (but less reliable) Worse with MAOI use Ask directly; tox screen Clinical dx, no specific labs Complications: DIC, rhabdomyolysis, hemoglobinuria, metabolic acidosis, ARDS, renal failure

92 Serotonin Syndrome Hunter Toxicity Criteria Decision Rules
Hx taking serotoninergic agent Plus ONE of the following: Spontaneous clonus Induced clonus PLUS agitation or diaphoresis Tremor Plus hyperreflexia Hypertonia PLUS temp ↑ & ocular clonus (slow continuous horizontal eye movements)

93 Serotonin Syndrome Differential
NMS: But NMS has slow onset and resolution, SS rapid onset and (usually) rapid resolution; longer with LA agents SS : Neuromuscular hyperactivity, NMS sluggish neuromuscular activity Anticholinergic toxicity: Yes to ↑ temp, agitation, mental status changes, mydriasis, dry mucous membranes, urinary retention, ↓bowel sounds BUT muscle tone and reflexes are normal Malignant hyperthermia: Susceptible, halogenated volatile anesthesia, depolarizing muscle relaxants (e.g., succinylcholine), severe muscle rigidity, tachycardia, ↑ temp, acidosis BUT no neuromuscular activation Ditto for CNS infection Mydriasis pupil dilation

94 Serotonin Syndrome Management
DC serotonin drugs Supportive care: O2, IV fluids, cardiac monitoring, Sedation with benzodiazepines; should not be restrained No butyrophenones (haloperidol, droperidol); anticholinergic effect inhibits sweating Serotonin antagonists in severely ill (Cyprohepadine; histamine receptor antagonist) Hyperthermia: Critical to treat aggressively to avoid complications may require paralysis, intubation Do not use antipyretics; not due to alteration in hypothalamic temp set point

95 Serotonin Syndrome Management
Autonomic instability HTN: short acting agents (e.g., nitroprusside ) not LA (e.g., propranolol) Hypotension- short acting agents (epinephrine, norepinephrine) Avoid indirect agents (e.g., dopamine) bc when monoanimine oxidase is inhibited epi and norepi production not controlled Severe case need ICU

96 Libby Zion Case Libby Zion-18 yo college freshman
New York Hospital ED at night with temp 103.5 “Jerky movements”, rx meperidine, Haldol, and restraints Temp 107 next AM Dies cardiac arrest PGY-2 had 40 patients Accreditation Council Graduate Medical Education

97 Co-occurring Movement Disorders: Tremor
Movement DO with tremor can worse with psychotropic drug tx Essential tremor and ataxias have action type tremors ET any age, equal in MF, autosomal dominant, variable presentation, progressive, often ↓/stop in sleep Many antidepressants, antipsychotics, and mood stabilizers/AEDs Also immunosuppressant's, oncology meds (e.g.., thalidomide and cytarabine), bronchodilators, and caffeine will worsen action tremors and should be used carefully Also alcohol, nicotine, benzo WD

98 Drugs Causing Tremor Cardiac (amiodarone 1/3 pts), procainamide, others) Epinephrine and norepinephrine Weight loss medication (tiratricol) Too much levothyroxine Tetrabenazine, a medicine to treat excessive movement disorder Other: Wilson’s disease(DO copper metabolism) hyperthyroidism, pheochromocytoma

99 Drugs Causing Tremor Bronchodilators (theophylline, albuterol)
Immunosuppressant's (cyclosporine, 40% but mild, tacrolimus- mostly liver transplant and RA pts. can be disabling) Mood stabilizers (lithium-30%, Valproic, 25%, starts after 3 mos. Long acting form may help avoid) Selective serotonin reuptake inhibitors (20%; starts after 2-3 months) Tricyclic antidepressants ↑ 20% Certain antivirals (acyclovir, vidarabine) Weight loss medication (tiratricol) Tetrabenazine (to tx excessive movement disorder)

100 Drug-Induced Tremor Tx
Lab and imaging studies usually normal Stop drug Lower dose Add propranolol if lowering dose or changing med not feasible

101 Drug vs.PD Drug-induced tremors: Both L & R side (but maybe not equally) Usually face, hands, arms, eyelids; rarely lower body Parkinson’s affects primarily one side May have shaky voice, nodding yes or no Symptoms stop when med stopped Usually start within an hour of taking offending med May take months for tremor to subside – up to 18 Parkinson's chronic and progressive No brain degeneration; Parkinson’s causes brain degeneration in a specific area ↑ risk in older people, Hx renal or hepatic disease, medical or neuro disease, women, HIV +, hx of dementia

102 References Bear, M. F., Connors, B. W., Paradiso, M. A. (Eds.). (2007). Neuroscience: Exploring the brain. (3rd ed.). Baltimore: Lippincott. Brady, M. C., Scher, L. M., & Newman, W. (2013). “I just saw Big Bird. He was 100 feet tall!” Malingering in the emergency room. Current Psychiatry, 33(12),33-39. Brody, J. E. (2007. February 27). A mix of medicines that can be lethal. New York Times, Retrieved from Brown,C. H. (2010). Drug-induced serotonin syndrome. US Pharmacist, 35(11), HS-16-HS-21.

103 References Caroff, S.A., Hurford, I.,Lybrand, J. & Campbell, E. C. (2011). Movement disorders induced by antipsychotic drugs: Implications of the CATIE Schizophrenia Trial. Neurologic Clinics, 29(1), 127–viii. Hallett, M., Cloniger, C. R., Fahn, S. Janovic, J., Lang, A. E., & Yudovsky, S. C. (2005). Psychogenic movement disorders. Baltimore, MD: LWW. Peluso, M. J., Lewis, S.W., Barnes T.R.E., & Jones, P. B. (2012). Extrapyramidal motor side-effects of first- and second-generation antipsychotic drugs. British Journal of Psychiatry, 200, Sa, D. S., Galvez-Jimenez, N., & Lang, A. E. (2011).Movement disorders. (3rd ed.). New York, NY: McGraw Hill.

104 References Vorvick, L. J. (2012, July 15). Drug-induced tremor. Retrieved from Watts, R. L., Standaert, D. A., & Obeso, J. A. (2013, March12). Jumping Frenchmen of Maine. Retrieved from Wint, C. (2012, July 20). Drug Induced Tremor. Retrieved from Woods, S.W., Morgenstern, H., Saksa, J. R., Walsh, B. C., Sullivan, M. C., Money, R., Hawkins, K. A.,Ralitza, V, et al. (2010). Incidence of tardive dyskinesia with atypical and conventional antipsychotic medications: Prospective cohort study. Journal of Clinical Psychiatry, 71(4),


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