Psychiatric Aspects of Movement
Disorders for Nurse Practitioners
1
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
Abstract
2
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.
OBJECTIVES
3
 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
Somatic Symptom Disorders
4
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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
Terminology
5
 Psychogenic considered unsatisfactory
 (Used by clinicians but not usually with pts.)
 More recently “functional”
 Replaces conversion DO, hysteria
PSYCHOGENIC MOVEMENT DISORDERS
(PMD)
6
 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
History
7
 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
Why So Many Changes?
8
 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”
DSM 5
9
 Lack of medical explanation
≠
 Psychiatric Diagnosis
DSM-5: Somatoform DOs Now Somatic
Symptom and Related DO
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 Somatic Symptom Disorder
 Illness Anxiety Disorder
 Conversion Disorder (Functional Neurological
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Symptom Disorder)
Psychological Factors affecting other medical
conditions
Factitious Disorder
Gone: Hypochondrias, somatization disorder, pain
disorder, & undifferentiated somatoform disorder
Epidemiology PMD
11
 Accurate data limited
 ~ 30% of outpatients in neuro settings S&S not caused
by neuro disease
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½ PMD & ½ out of proportion to disease
As distressed and more disabled (Stone & Carson, 2011)
 ~ 1% - 9% neuro unit admissions unexplained motor
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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
Clues A: History
12
 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
Clues A: History
13
 Predisposing factors:
 Low SES, 60%-75% female, hx of abuse and neglect,
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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)
Clues B: Clinical
14
 No single finding will clinch it
 Movements increase with attention and decease with
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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
Clues B: Clinical
15
 PMD don’t usually involve the fingers; MD do
 Functional disability out of proportion to clinical findings
 Multiple symptoms attributable to multiple organ
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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)
Clues C: Pt. Response
16
 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
Pt Challenges
17
 Complicated and difficult diagnostically (can be done)
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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 followup
(Hallett)
Assessment
18
 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
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Helps rapport
 Gradual onset associated with fatigue
 What is pt.'s understanding?
 Irreversibility and damage beliefs prognostic
Caveat
19
 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
PMD Tremor
20
 Common: 35% and 55% of PMDs in two large
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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
PMD Tremor
21
 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
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Usually continuous
 But rarely fingers
 Then head
 Then legs
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Usually not continuous
 Surprisingly little C/O fatigue
PMD: Dystonia
22
 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
PMD Myoclonus
23
 Brief, shock-like muscle contractions or sudden loss
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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)
PMD Myoclonus: Related Culturally-Mediated
Disorders
24
 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
PMD Myoclonus: Related culturally-mediated
Disorders
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 Jumping Frenchmen of Maine: Unusual, extreme
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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
Normal Startle
26
 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
Normal Startle
27
 2nd component
 Begins at latencies overlapping with voluntary reaction
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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
PMD Myoclonus: Related Culturally-Mediated
Disorders
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 Tx: Eliminating intentionally startling and/or
teasing can reduce/end episodes
 Latah in Indonesia
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Most common, middle age women
Often rage, anxiety, fear
 Myriachit in Siberia
 “Ragin’ Cajuns” in Louisiana
 More research needed
Strychnine Poisoning
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 Plant toxin; used by farmers to kill farm pests and by
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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
PMD Chorea/Ballism
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 Changes in definition of chorea have changed over
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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
PMD Tics
31
 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
PMD Facial Spasm Dyskinesia Tics
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 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
PMD Parkinsonism
33
 ~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
PMD Parkinsonism
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 Bizarre movements with mild stimulus of testing
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(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
PMD Parkinsonism
35
 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
PMD Gait Disorders
36
 Long hx in med literature
 ↑ hx of misdx (fx turn out not to be)
 All ages, but caution dx in older people – often have
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(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
PMD Gait Disorders
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 Often exaggerated slowness – “walking through thick
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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)
PMD Gait Disorders
38
 Dragging gait (see next slide)
 Tightrope walker’s gait (arms out)
 Crouching gait- close to ground BC fear falling
(but that requires more strength!)
Example Functional Monoplegic Gait
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Both cases, leg dragged at the hip. External or
internal rotation of the hip or ankle
inversion/eversion is common.
PMD Gait Disorders
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 Astasia-abasia
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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=play
er_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
PMD Gait Disorders
41
 Dx:
 Observe spontaneous gait and tandem heel toe walking
 Wilson’s disease and Huntington's disease most frequent
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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
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White matter disease (some nl in older)
 Dual task walking (Walking and cognitive task)
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Abn in executive fx associated with reduced gait speed
PMD Tourette Syndrome
42
 Tourette: Premonitory urge
 Suppressability-
disappear during voluntary
movements
 Recognized as partially voluntary
 Relief following
 Tics nearly identical
PMD Tourette Syndrome
 Tourette and pseudo tics:
43
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

PMD Weakness
44
 Female, mid-30s
 5/100,000
 Often co-morbid with fatigue & pain
 Most common unilateral > one limb > both LL
 May report limb feels alien
Voluntary S&S: Factitious DO
45
 Factitious: Intentional feigning or producing
physical or psychological symptoms
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Severe form: Munchhausen's syndrome
 Motivation is the sick role
 No external incentives (not for financial, legal, or
other gain)
 Poor prognosis
Voluntary S & S: Malingering
46
 Not a psychiatric DO
 Intentional self-injury motivated by financial gain,
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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
Voluntary S & S: Malingering
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 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
DX PMD: “Here there be dragons”
48
 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)
DX PMD
49
 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
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Legal and ethical issues, impugn autonomy
 Damaging to pt-provider relationship when pt. finds out
 Psychogenic dx should be made by neurology not
psychiatry
Categories of Dx Certainty
50
 Fahn and Williams-accepted standard
 1. Documented: Relieved with therapy, suggestion,
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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
Patient Approach
51
 Empathetic, with certainty, nonjudgmental, that do
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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
Prognosis
52
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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)
Prognosis
53
 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
Talking With Patients About the Dx
54
 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
Presenting the Dx
55
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”)
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Presenting the Dx
56
 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
Presenting the Dx
57
 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
Presenting the Dx
58
 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
Presenting the Dx
59
 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
Presenting the Dx
60
 Resources
 Functional/dissociative neuro symptoms:
 www.neurosymptoms.org
 Non-epileptic seizures
 www.nonepilepticattackes. Org
 British, well-done
Psychotherapy
61
 Psychotherapy seems logical but not enough
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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”
Local MDO Clinics
62
 IU Dept. of Medicine,
http://neurology.medicine.iu.edu/neurologyprograms1/movement-disorders/
 University of Cincinnati Gardner Center for
Parkinson’s Disease and Movement Disorders in the
UC Neuroscience Institute
http://ucgardnercenter.com/
Local MDO Clinics
63
 Kentucky Neuroscience Institute movement
Disorders Clinichttp://ukhealthcare.uky.edu/kyneuro/movement/
Appointments and Info: 859-323-5661
 Frazier Rehab Institute and the University of
Louisville Division of Movement Disorders
http://www.kentuckyonehealth.org/movementdisorders-parkinson-disease-program502-582-7400
TREATMENT INDUCED MOVEMENT
DISORDERS
64
 Acute dystonia
 Akathisia
 Pseudo-Parkinsonism
 Tardive Dyskinesia
 Neuroleptic malignant syndrome
 Punding
 Serotonin syndrome
 Tremor
Pathophysiology
65
 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
EPS
66
 “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”
Tardive Dyskinesia
67
 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

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
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; http://www.cqaimh.org/pdf/tool_aims.pdf
(Stahl)
68
Atypicals Also Risky for TD
69
 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)
Acute Dystonia
70
 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
Acute Dystonia
71
 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)
Anterocillis on upper L, Pisa syndrome on
upper R, Trismus on lower
R,
camptocormia
on
72
lower left, opistotonus middle
Acute Dystonia: DX
73








Earliest EPS; 95% first few days of tx or increase in med
Last hours-days
If med DC, resolves 24-48 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
Acute Dystonia: DX
74
 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)
Acute Dystonia
75
 Pt on L had taken metoclopramide (Reglan) for GI
problems
 Reglan now has a black box warning
Parkinsonism
76
 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
Parkinsonism
77
 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,
Parkinsonism
78
 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
Akathisia
79
 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
Akathisia
80
 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)
Akathisia
81
 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
Catatonia
82
 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
Catatonia
83
 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
Neuroleptic Malignant Syndrome
84
 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
Neuroleptic Malignant Syndrome
85
FEVER mnemonic:
F – Fever
E – Encephalopathy
V – Vitals unstable
E – Elevated enzymes – CPK
R – Rigidity of muscles
Neuroleptic Malignant Syndrome
86
~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
Punding
87
 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
Punding
88
 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
Serotonin Syndrome
89
 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
Serotonin Syndrome Drugs
90
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
Serotonin Syndrome
91
 2002: 7,349 cases serotonin toxicity, 93 deaths
 2005: 118 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
Serotonin Syndrome
92
 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)
Serotonin Syndrome Differential
93
 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
Serotonin Syndrome Management
94
 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
Serotonin Syndrome Management
95
 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
Libby Zion Case
96
 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
Co-occurring Movement Disorders: Tremor
97
 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
Drugs Causing Tremor
98
 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
Drugs Causing Tremor
99
 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)
Drug-Induced Tremor Tx
100
 Lab and imaging studies usually normal
 Stop drug
 Lower dose
 Add propranolol if lowering dose or changing med
not feasible
Drug vs.PD
101
 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
References
102
 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
http://www.nytimes.com/2007/02/27/health/27brody.html?_r=0
 Brown,C. H. (2010). Drug-induced serotonin syndrome. US
Pharmacist, 35(11), HS-16-HS-21.
http://www.uspharmacist.com/content/d/feature/c/23707/
References
103
 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, 387-392.
 Sa, D. S., Galvez-Jimenez, N., & Lang, A. E. (2011).Movement
disorders. (3rd ed.). New York, NY: McGraw Hill.
References
104
 Vorvick, L. J. (2012, July 15). Drug-induced tremor. Retrieved from
http://www.nlm.nih.gov/medlineplus/ency/article/000765.htm
 Watts, R. L., Standaert, D. A., & Obeso, J. A. (2013, March12).
Jumping Frenchmen of Maine. Retrieved from
http://www.rarediseases.org/rare-disease-information/rarediseases/byID/380/viewFullReport
 Wint, C. (2012, July 20). Drug Induced Tremor. Retrieved from
http://www.healthline.com/health/drug-induced-tremor#Symptoms
 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), 463-474.