A b n o r m a l Mo v e m e n t s a n d

M o v e m e n t D i s o rd e r
Urgencies
Sara Radmard, MD

KEYWORDS
 Movement disorder emergencies  Drug-induced movement disorders
 Movement disorder  Hypokinetic movement  Hyperkinetic movement

KEY POINTS
 History and physical examination delineate the underlying movement disorder and are the
first steps when approaching movement disorder urgencies/emergencies.
 Many movement disorder urgencies are secondary to a drug-induced etiology.
 Movement disorder emergencies may result in organ dysfunction, morbidity, and mortality
if unrecognized and untreated.
 Functional movement disorders have an abrupt onset and fulminant course.

INTRODUCTION

The field of movement disorders encompasses presentations of involuntary excessive

or reduced movements. Although many movement disorders are neurodegenerative
and slowly progressive, acute and urgent presentations do occur. Movement disorder
emergencies are defined as 1 or more movement disorder(s) being the primary clinical
presentation of which failure to recognize may precipitate morbidity or mortality.
Movement disorder urgencies could be intervened upon in the outpatient setting to
prevent hospitalizations; however, some therapies require hospitalization.
Approaching movement disorder urgencies can be a daunting task even for a skilled
neurologist. The first steps in evaluation are carefully obtaining medical and drug his-
tory, noting vital sign abnormalities, examining the patient, and identifying the phe-
nomenology. Once these 4 conditions are established, prompt management is
required. Movement disorder emergencies and urgencies are treatable.

Funding Sources: No specific funding was received for this work.

Department of Neurology, Division of Movement Disorders, Albany Medical Center, 47 New
Scotland Avenue MC70, Albany, NY 12208, USA
E-mail address: sradmard12@gmail.com

Med Clin N Am 109 (2025) 509–528

https://doi.org/10.1016/j.mcna.2024.09.002 medical.theclinics.com
0025-7125/25/ª 2024 Elsevier Inc. All rights are reserved, including those for text and data mining,
AI training, and similar technologies.

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 510 Radmard

DEFINITIONS

When approaching a patient with abnormal, involuntary, or reduced movements,

describing the movements and classifying them is essential for management. The
first examination question is ‘Is this a hypokinetic or a hyperkinetic movement
disorder?’.
Hypokinetic movement disorders result in poverty of spontaneous movements,
slowing of movements, and/or reduction in scaling of movements. Examination ma-
neuvers to bring out bradykinetic and hypokinetic movements include repetitive finger
tapping, hand opening-closing, rapid alternating arm movements, toe tapping, or foot
stomping. Not only is reduced speed typical, but also decrement occurs where each
successive iteration of a repetitive movement results in amplitude and/or cadence
reduction. Other observable signs include reduced facial expression and blink rate
termed hypomimia.
Hyperkinetic movement disorders result in excessive, involuntary movement that
can be present at rest or exacerbated by intentional movements. Several types of hy-
perkinetic movement disorders exist (Table 1). In the acute setting of a movement dis-
order urgency/emergency, multiple types of movement disorders can be present at
one time. The speed of movements can be a clue with athetosis being the slowest
movement and myoclonus, tics, and ballism being the fastest movements. Dystonia
and tremor can be either slow or fast.

Table 1
Phenomenology of movement disorders1–4

Movement
Disorder Description
Dystonia Sustained or intermittent patterned muscle contractions resulting in twisting
or posturing of movements that can be repetitive or tremulous
Athetosis Continuous writhing, slow movements, generally distally in hands or feet
Chorea Non-repetitive, unpredictable, flowing, dance-like movements
Ballism High amplitude flinging of the extremities originating from proximal limb
Tics Patterned, repetitive, semi-involuntary movements or vocalizations often
associated with premonitory urge and sense of relief after the tic is
completed
Myoclonus Brief, sudden muscle jerk or twitch
Tremor Oscillatory and rhythmic movement of a body part

Commonly, movement disorders are associated with changes in tone. Spasticity is

an increase in tone that is direction- and velocity-dependent. Slower passive move-
ment may not elicit increased tone, but faster passive movements will produce a catch
or “clasp-knife” phenomenon. Rigidity is independent of velocity or direction, and
increased tone is felt throughout the passive range of motion. Rigidity is commonly
seen in Parkinsonism.

DISCUSSION
Acute-onset Dystonia
Drug-induced dystonia
Drug-induce dystonia is typically focal (1 body distribution) or segmental (2 contiguous
body distributions); however, generalized dystonia can occur, affecting the trunk and

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 Abnormal Movements and Movement Disorder Urgencies 511

limbs. The most common distributions are the neck, lower face, and eyes. Involuntary
neck movements are usually retrocollis, cervical dystonia of neck extension, and/or
torticollis, cervical dystonia of head rotation to the side (Fig. 1). Lingual-mandibular
movements manifest as jaw pulling, tongue protrusion, or dysarthria. Orbicularis oculi
involvement results in blepharospasm, involuntary closure of the eyelids. Extraocular
muscle involvement may result in oculogyric crisis; unlike gaze deviation associated
with seizure or stroke where the eye movements are horizontally driven, dystonia
has a twisting quality. Thus, eye position is a combination of vertically and horizontally
oriented eye movements.
Acute dystonic reactions generally occur 24 to 48 h after drug exposure and may
arise with 1 single dose. Approximately 50% of cases occur within 48 h and 90%
within 5 d of drug exposure. Dopamine receptor blocking agents (DRBAs) are the
usual culprit, but other medications are implicated (Table 2). Risk factors for devel-
oping an acute dystonic reaction include increased avidity of D2-receptor binding or
blockage, higher dosage, younger age, and male gender.10 Acute dystonic reactions
occur more frequently with first-generation than second-generation antipsychotics
(17% vs 2%).11
Early recognition of an acute dystonic reaction is consequential as it is treatable, re-
actions involving the larynx or pharynx can lead to breathing and swallowing compro-
mise, and forceful sustained contraction can cause joint subluxation.12 Acute dystonic
reactions are sensitive to intravenous (IV) anticholinergics, like diphenhydramine 25 to
50 mg IV in adults, diphenhydramine 1 mg/kg IV (up to 50 mg) in pediatrics, or benz-
tropine 1 to 2 mg IV/IM. Resolution is seen in minutes, but recurrence can occur hours
later for which repeat treatment with oral anticholinergics is indicated for 24 to 48 h
following onset.

Fig. 1. Example of retrcollis seen in drug-induced dystonia.

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 512 Radmard

Table 2
Medications associated with acute dystonic reaction5–9

Drug Class Medications

First-generation antipsychotics Chlorpromazine Pimozide
Fluphenazine Thioridazine
Haloperidol Thiothixene
Perphenazine
Second-generation antipsychotics Aripiprazole Lurasidone
Brexpiprazole Olanzapine
Cariprazine Paliperidone
Clozapine Risperidone
Iloperidone Quetiapine
Lumateperone Ziprazidone
Anti-emetics Metoclopramide Promethazine
Prochlorperazine
Serotonergic medications Citalopram Fluvoxamine
Duloxetine Paroxetine
Escitalopram Sertraline
Fluoxetine Venlafaxine
General anesthetics Propofol
Stimulants Methylphenidate
Cocaine

Paroxysmal sympathetic hyperactivity

Dystonia can manifest as a complex of paroxysmal sympathetic hyperactivity (PSH).
PSH occurs with global brain injuries, including anoxic brain injury, traumatic brain
injury, hydrocephalus, infectious or autoimmune encephalitis, or ischemic or hemor-
rhagic stroke. PSH is due to loss of inhibition on sympathetic centers leading to
excessive sympathetic responses.13 Core clinical features include tachycardia, hy-
perthermia, tachypnea, hypertension, diaphoresis, and dystonia or posturing.13 Dys-
tonia is reported in 40% of cases and tachycardia in nearly all patients.14 Episodes
are transient but repetitive. There are no clear diagnostic criteria.
These attacks of excessive sympathetic tone can be triggered by nursing care or
internal stimuli, like pain.15 Noting vital signs during the posturing or dystonic move-
ments improve diagnostic accuracy in PSH. Although PSH occurs in the acute setting
of brain injury, it can recur later in a patient’s course if systemic complications occur,
such as sepsis.
Prompt institution of treatment is recommended (Table 3). Preventative measures
of bundling care to limit external stimuli and scheduling pharmacotherapy can reduce
the number of attacks.

Status dystonicus
Status dystonicus (SD) is a life-threatening condition that generally presents in child-
hood. The incidence is rare but should be recognized to reduce morbidity and mortal-
ity caused by respiratory failure, bulbar weakness, or metabolic derangements.17 SD
occurs in individuals with known genetic or acquired dystonia disorder, including but
not limited to cerebral palsy, posttraumatic dystonia, postencephalitic dystonia,
monogenic dystonias, and combined inherited dystonias, like pantothenate kinase-
associated neurodegeneration or Wilson disease.17–19 Male gender and younger
age less than 15 y are risk factors.18 SD manifests as increased frequency and severity
of baseline dystonia with painful, sustained, generalized or focal muscle contractions,
or hyperkinetic movements.20

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 Abnormal Movements and Movement Disorder Urgencies 513

Table 3
Treatment of paroxysmal sympathetic hyperactivity16

Abortive Morphine 2–8 mg IV Dual Abortive Propofol

Therapies Hydromorphone 2–6 mg IV and Preventative Abortive: 10–20 mg IV
Fentanyl 50 mcg IV Therapies Preventative:
Diazepam 5–10 mg IV  80 mcg/kg/minute
Lorazepam 2–4 mg IV Dexmedetomidine
Midazolam 1–2 mg IV 0.1–1.5 mcg/kg/hour
Dantrolene 0.25–2 mg/kg IV
Preventative Propranolol 20–80 mg PO q6-8h
Therapies Clonidine 0.1–0.3 mg PO TID
Gabapentin 100–900 mg PO TID
Baclofen 5–10 mg PO TID
Clonazepam 0.5–1 mg PO BID-TID
Bromocriptine 2.5–20 mg PO BID

Abbreviations: IV, intravenous; kg, kilogram; mcg, -microgram; mg, milligram.

Adapted based on Tu JSY, Reeve J, Deane AM, Plummer MP. Pharmacological Management of
Paroxysmal Sympathetic Hyperactivity: A Scoping Review. J Neurotrauma. 2021 Aug 15;38(16):2221-
2237.

SD may be precipitated by infections, adjustment of dystonia medications, surgical

procedures, metabolic derangement, or deep brain stimulation (DBS) battery deple-
tion.18 Recent publications endeavor to standardize treatment.20 Stabilization of circu-
latory or respiratory compromise and end-organ dysfunction is the first step. Prompt
treatment of triggers is necessary. Pain and constipation are exacerbators that should
be recognized. Optimization of the patient’s current medications may prevent hospi-
talization. If that is unsuccessful, targeted IV pharmacologic therapy is required
(Fig. 2).20 Additional doses of the home regimen can be administered, like baclofen
or trihexyphenidyl. If initial pharmacotherapy is unsuccessful, then sedation and intu-
bation are recommended (see Fig. 2). Pharmacotherapy resolves 10% of cases, but
intensive care, intubation, and sedation are usually required.18,20,21 In refractory
cases, DBS should be considered.

Fig. 2. Step-wise approach to treatment of status dystonicus.18,20,21.

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 514 Radmard

Chorea and Ballism

Acute to subacute-onset chorea and ballism
Chorea and ballism are both hyperkinetic movement disorders (see Table 1) of which
ballism is chorea originating from proximal limb muscles and thus causing large, flinging
movements. Causes of acute-to-subacute onset chorea and ballism are listed in Fig. 3.
Abrupt-onset movement disorders occur in 1% of acute strokes located from mul-
tiple brain areas, including basal ganglia, thalamus, subthalamic nucleus, cortex, and
subcortical white matter.25–27 Stroke-induced chorea and ballism are typically self-
limited and do not require treatment unless they interfere with daily activities or gait.
Moyamoya disease is a cerebral vascular angiopathy resulting in terminal internal ca-
rotid aterey (ICA) narrowing and may result in chorea or dystonia in 0.1% to 10% of
pediatric cases.28,29 Post-operative chorea, known as post-pump chorea, occurs in
the setting extracorporeal circulation and is more common in children.
Hyperglycemic- or hypoglycemic-associated chorea can be generalized or unilateral.
Hyperglycemic induced chorea comprises 1% of acquired chorea. Presentation is
commonly in newly diagnosed type 2 diabetes mellitus and elderly women. Average
blood glucose is 300 mg/mL; patients may present in hyperglycemic hyperosmolar
non-ketotic syndrome with blood glucose greater than 600 mg/mL. MRI brain may
demonstrate T1 hyperintensity in the basal ganglia30 (Fig. 4A, B). Resolution occurs after
correction of glycemic changes and may take a few days to, less commonly, months.31

Fig. 3. Diagnostic work-up for acute to subacute-onset chorea and ballism.22–24 APS, anti-
phosopholipid antibody syndrome; CCBs, calcium channel blockers; CRMP5-collapsin,
responsive mediator protein 5; NMDAR, N-methyl-D, aspartate receptor; SSRIs, selective se-
rotonin reuptake inhibitors; TCAs, tricyclic antidepressants.

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 Abnormal Movements and Movement Disorder Urgencies 515

Fig. 4. MRI findings in acute to subacute chorea or ballism. (A, B) demonstrate T1 hyperin-
tensities seen in a patient with type 2 diabetes mellitus presenting with hemichorea and bal-
lism concurrent in the setting of hyperosmolar hyperglycemic nonketotic syndrome. Panel C
shows T1 contrasted study of toxoplasmosis bilaterally in the basal ganglia.

Importantly, other endocrinologic changes causing chorea are also treatable.

Chorea occurring in the first trimester of pregnancy, chorea gravidarum, is generally
self-limiting prior to or after delivery. If therapy is indicated, low-dose haloperidol
can be considered after the first trimester.32 Oral contraceptive pills may cause chorea
within 5 w of initiation. Thyrotoxicosis is rarely associated with chorea. Lastly, hypo-
parathyroidism or pseudohypoparathyroidism can rarely present as chorea and may
be associated with abnormal calcification of the basal ganglia.33
Immune-mediated or paraneoplastic causes of chorea occur in a subacute manner
(<3 months). Chorea is a manifestation of anti-phospholipid syndrome in 1% of cases
and can be unilateral, generalized, acute/subacute, chronic, or episodic.34 Chorea can
precede diagnostic marker positivity in systemic lupus erythematosus.22 The majority
of paraneoplastic causes of subacute-onset chorea include anti-CRMP-5, anti-ANNA-
1 (Hu), and anti-N-methyl D-aspartate receptor autoantibodies.35 These paraneoplas-
tic syndromes are associated with limbic encephalitis, epilepsy, and other movement
disorders in addition to cancer. Whole-body imaging screening with computed to-
mography (CT) chest/abdomen/pelvis with contrast and transvaginal or testicular ul-
trasound is recommended. Immune-mediated causes may respond to IV steroids,
IV immunoglobulin, or plasmapheresis. With high suspicion of autoimmune encepha-
litis, institute treatment before the autoantibodies result from serum and cerebrospinal
fluid (CSF) testing.
Hemiballismus and chorea are one of the most common movement disorder pre-
sentations of human immunodeficiency virus (HIV)-positive persons.36 Opportunistic
infections are the usual etiology. Toxoplasmosis gondii has a predilection for the basal
ganglia causes 60% of hemichorea or dystonia cases in the HIV-affected population.
MRI brain may reveal pathognomonic concentric target sign of alternating concentric
intensities37 (see Fig. 4C). CSF polymerase chain reaction (PCR) testing is required for
diagnosis, and if unrevealing, brain biopsy is necessary. Less common infectious
causes include tuberculosis, syphilis, and progressive multifocal leukoencephalop-
athy (PML).38 CSF testing is required. For tuberculosis meningitis, acid-fast bacilli’s
staining has low sensitivity less than 10%; CSF adenosine deaminase and updated
nucleic acid amplification test have 89% sensitivity.39 Test for CSF venereal disease
research laboratory (VDRL) for syphilis and John Cunningham (JC) virus PCR in sus-
pected PML. With high clinical suspicion for these CNS infections, initiated antimicro-
bials prior to CSF testing.

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 516 Radmard

New-onset chorea in children is most commonly due to Sydenham chorea,40 a

manifestation of rheumatic fever secondary to group A streptococcal infection.
Chorea may manifest months after primary infection. Chorea is generalized or unilat-
eral in 20% of cases. Diagnosis with antistreptolysin O titers and anti-DNAase B are
recommended. A course of oral prednisone 2 mg/kg/day in a small clinical trial
improved remission rate.23
Work-up of acute-onset chorea or ballism should begin with laboratory investigation
followed by imaging (see Fig. 3). MRI brain is preferred; for emergent etiologies, like
stroke, screening CT head and vessel imaging is recommended. Treatment of the un-
derlying cause may result in chorea remission in the majority of cases. In refractory
cases, second-generation antipsychotics, like risperidone, aripiprazole, olanzapine,
or vesicular monoamine transporter type 2 (VMAT2) inhibitors, such as tetrabenazine,
valbenazine, and deutetrabenazine, can be administered.

Tardive dyskinesia
Tardive dyskinesia (TD) is a continuous, repetitive, and stereotyped hyperkinetic
movement disorder that has features of both chorea and dystonia. Oro-buccal-
lingual areas and distal extremities are most affected, manifesting as lip smacking,
lip pursing, jaw opening/closing, appearance of chewing movements, and tongue pro-
trusion. Limb manifestations include “piano playing finger” or repetitive foot tapping.
TD occurs after prolonged exposure of DRBAs (see Table 2). Higher D2-receptor avid-
ity with first-generation antipsychotics and higher dosages are associated with
increased risk of TD. The risk of TD is 3 times lower with second-generation versus
first-generation antipsychotics (7% vs 23%).41
Prognosis for remission is poor; large, randomized control trials are lacking. Prior to
initiation of DRBAs, thoroughly discuss risks of TD. The lowest dose possible should
be administered. Acute withdrawal of the offending agent can cause withdrawal emer-
gent syndrome where hyperkinetic movements become more severe. Location of
choreiform movements is typically in neck, extremities, and trunk, which may differ
from the oro-buccal-lingual movements of TD.
Treatment of TD is listed in Fig. 5. Improvement in TD after switching therapies may
take months, so do not be discouraged if minimal benefit is seen immediately. There is
insufficient evidence that reduction in second-generation antipsychotic dose alone im-
proves TD.42 Quetiapine and clozapine have the lowest rates of drug-induced move-
ment disorders.43 Valbenazine and deutetrabenazine are preferred for directed
treatment due to less adverse effects and higher-quality evidence compared to tetra-
benazine.44 There is a trend to prescribe anticholinergics concurrently with DRBAs in
effort to reduce risks of drug-induced movement disorders; however, there is insuffi-
cient evidence to support anticholinergic usage.45 These may even exacerbate TD.46

Myoclonus
Myoclonus is a rapid, brief muscle jerk that can be generalized, multifocal, hemi-body,
segmental, or focal. Asterixis is negative myoclonus where loss of sustained muscle
posture results in a brief jerk.3 Careful history, including medication evaluation, is
necessary in assessment of myoclonus. The causes of myoclonus are vast. In the
acute to subacute setting, evaluation for secondary causes is advisable (Fig. 6).
If epilepsy, hypoxic brain injury, meningoencephalitis, or immune-mediated causes
are suspected, electroencephalogram is advised. If a readily reversible etiology is
found, like hyperuremia or hyperammonemia, treatment of the underlying cause is
necessary and may result in resolution of myoclonus. Resolution of myoclonus can
take several days after correction of the metabolic derangement.

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 Abnormal Movements and Movement Disorder Urgencies 517

Fig. 5. Treatment algorithm for tardive dyskinesia.41–43

For hypoxic brain injury, epilepsy, or in cases of severe myoclonus that is disruptive,
treatment of myoclonus is recommended. Levetiracetam 500 to 2000 mg twice daily,
valproic acid 15 to 20 mg/kg divided 2 to 3 times daily, and clonazepam 0.25 to 1 mg
twice to 3 times daily are commonly employed as first-line agents. Perampanel 2 to
8 mg is useful in refractory cases of myoclonus, particularly post-hypoxic.48,49 Antiep-
ileptic medications that can exacerbate myoclonus include carbamazepine, oxcarba-
zepine, phenytoin, lamotrigine, gabapentin, and pregabalin.47

Serotonin Syndrome
Serotonin toxicity is a direct result of serotonergic medications leading to increased pe-
ripheral and central serotonin activity. Serotonin syndrome (SS) is likely underrecognized
in mild cases, so the true incidence is unknown. Incidence rate in the United States is
0.07% – 0.19%.50 Increased number of serotonergic mediations result in higher mortality
than a single agent.51 Selective serotonin reuptake inhibitors (SSRIs) as a single agent or
in overdose are the most common cause of SS (Table 4).53 In hospitalized patients, the
author wants to highlight antimicrobials54 and analgesics as causes. Methylene blue55 is
administered intra-operatively and may be missed in post-surgical patients.
SS progresses acutely within hours of inciting drug exposure of which 51% of cases
occur within 6 h.52,56,57 Early recognition is required to reduce the risk of coma, seizure,
circulatory shock, and mortality.57 Signs and symptoms are listed in Table 5. Unified
diagnostic criteria are not established; however, proposed criteria include exposure
to a serotonergic medication plus greater than or equal to 1 below conditions:
1. spontaneous clonus
2. opsoclonus, myoclonus, inducible clonus 1 autonomic system dysfunction (fever,
diaphoresis)
3. hyperreflexia 1 tremor56–58

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 518 Radmard

Fig. 6. Diagnostic work-up for acute to subacute-onset symptomatic myoclonus.47 CBC, com-
plete blood count; CCBs, calcium channel blockers; CJD, Creutzfeldt-Jakob disease; CMP,
comprehensive metabolic panel; CSF, cerebrospinal fluid; MAOI, monoamine oxidase inhib-
itor; PML, Progressive multifocal leukoencephalopathy; SSRIs, selective serotonin reuptake
inhibitors; STREAT, steroid-responsive encephalopathy associated with autoimmune thyroid-
itis; TCAs, tricyclic antidepressants.

Therapeutic intervention includes cessation of the offending agent, symptomatic

treatment, and reversal of serotonin activity if severe (see Table 5). Supportive care
of fluid resuscitation, antipyretics, and antihypertensives should be utilized accord-
ingly. Agitation and severe rigidity can be treated with benzodiazepines. If hyperther-
mia is refractory, consider muscle paralysis.32 The majority of SS occurs from
overstimulation of 5-HT1A/2A receptors.52 Cyproheptadine is a 5-HT1A/2A antagonist
used in more severe and longer-lasting SS cases. Most cases resolve within 24 h of
supportive care after stopping the offending agent. Severe SS is more likely to occur
with exposure to monoamine oxidase inhibitors.59

Acute-onset Parkinsonism
Neuroleptic malignant syndrome
Neuroleptic malignant syndrome (NMS) is a fulminant and life-threatening disorder
related to exposure of DRBAs that also cause acute dystonic reaction (see
Table 2). The incidence of NMS is low at approximately 0.01% to 0.02%60,61 can

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 Abnormal Movements and Movement Disorder Urgencies 519

Table 4
Agents implicated in causing serotonin syndrome52

Drug Class Medications

SSRIs, SNRIs, DNRI Bupropion Fluoxetine
Citalopram Paroxetine
Desvenlafaxine Sertraline
Duloxetine Venlafaxine
Escitalopram
Tricyclic antidepressants Amitriptyline Imipramine
Clomipramine Nortriptyline
MAO-B inhibitors Selegiline
Rasagiline
Other psychiatric Buspirone Phenelzine
Lithium Trazodone
Anti-epileptics Carbamazepine Valproic acid
Lamotrigine
Anti-emetics Metoclopramide
Ondansetron
Antimicrobials Linezolid
Ritonavir
Recreational drugs Amphetamine MDMA
Cocaine Methamphetamine
LSD
Analgesics Cyclobenzaprine Metaxalone
Ergotamine Methadone
Fentanyl Tramadol
Meperidine Triptans
Supplements Ginseng Tryptophan
St. John’s wort
Other Methylene blue

Abbreviations: DNRI, dopamine/norepinephrine reuptake inhibitor; LSD, lysergic acid diethyla-

mide; MDMA, methylenedioxy-methamphetamine; SNRI, selective serotonin and norepinephrine
reuptake inhibitor; SSRI, selective serotonin reuptake inhibitor.
Adapted based on from Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med. 2005 Mar
17;352(11):1112-20.

affect any age group. Male gender, higher potency DRBA, higher dosage, repeated
use of intramuscular injections, use of multiple psychiatric medications, including
SSRIs or Lithium, and are associated with increased risk of NMS.62
NMS presentation is classically a tetrad (Table 6); however, presence of all clinical
manifestations is not generally seen, and partial presentations are more common. The
typical succession is mental status changes first followed by rigidity, hyperthermia,
and then autonomic dysfunction in greater than 70% of patients.62 Evolution arises
over 24 to 72 h. Approximately 66% of cases present within the first week of exposure;
however, NMS can occur on stable medication for months or years.63
Immediate and early recognition is important for reducing morbidity and mortality.
Significant organ damage is associated with NMS, including rhabdomyolysis in
30%, respiratory failure in 16% and renal failure in 18%. The severity of autonomic
symptoms in NMS is more pronounced than what one might see in drug-induced
Parkinsonism, differentiating the 2. Although mortality rates have reduced over time,
they remain 5% to 11%.63,64 Mortality rates are lower with second-generation rather
than first-generation antipsychotics.64

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 520 Radmard

Table 5
Commonalities and distinctions between presentation and management of serotonin
syndrome and neuroleptic malignant syndrome

Serotonin Syndrome Neuroleptic Malignant Syndrome

Onset Acute Gradual
Hyperthermia 1 1
Dysautonomia 1 1
Depressed mentation 1 1
Opsoclonus 1 -
Pupils Dilated Normal
Rigidity 1 1
Tremor 1 -
Hyperreflexia 1 -
Clonus 1 -
Myoclonus 1 -
Diarrhea 1 -
Directed treatment 1. Benzodiazepines: Mild:
Lorazepam 1–2 mg Lorazepam 1–2 mg IV or IM q4-6h
IV or IM q4-6h Moderate:
Diazepam 5–10 g 1. Above therapy
IV or IM q4-6h 2. Bromocriptine 2.5–5 mg PO q8h
2. Cyproheptadine 3. Amantadine 100 mg PO q8h
4–8 mg q6h Severe:
1. Above therapies
2. Dantrolene 1–2.5 mg/kg IV q6h
3. Bilateral electroconvulsive therapy
of 6–10 sessions

Abbreviations: h, hours; IM, intramuscularly; IV, intravenous; kg, kilogram; mg, milligram; PO, per
os, q-every.

Management of NMS requires close attention to multi-organ involvement. Stop the

identifying causative agent. Supportive care and resuscitation to reduce end-organ
damage should be initiated immediately as these are the primary causes of morbidity
and mortality. Directed therapies are listed in Table 5.
SS and NMS can present similarly (see Table 5); however, there are notable differ-
ences to distinguish the 2 syndromes. SS is more acute in onset, associated with eye
findings like opsoclonus and pupillary dilation, and presents with spontaneous or
inducible clonus, myoclonus, and hyperreflexia.

Parkinsonism hyperpyrexia syndrome

Parkinsonism hyperpyrexia syndrome (PHS) falls under the NMS umbrella and is due
to abrupt withholding of dopaminergic medications used to treat Parkinson disease
(PD). This disease is very rare and only case reported.31,65 PHS can occur in the early
or late stages of PD and be associated with withdrawal of low (200 mg) or high
(>2000 mg) dose of levodopa.65 Onset of PHS is 1 d to 1 w after the withdrawal of
dopaminergic medications.
PHS presentation is similar to NMS but is associated with increased parkinsonian
signs. Worsening rigidity is the first sign.66 Dysautonomia, hyperthermia, and changes
in consciousness should signify PHS and not worsening of the underlying parkinso-
nian disease. Management of PHS is congruent with NMS plus adding back

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 Abnormal Movements and Movement Disorder Urgencies 521

Table 6
Clinical tetrad and associated features of neuroleptic malignant syndrome

Clinical Tetrad Associated Features

Hyperthermia Elevated creatine kinase
>38 C (87%) Proteinuria
>40 C (40%) Myoglobinuria
Autonomic Disturbances Leukocytosis with PMN predominance
Tachycardia Transaminitis
Diaphoresis Hypomagnesemia
Labile blood pressure Hypocalcemia
Extrapyramidal Signs Reduced ferritin
Rigidity Severity Scale
Bradykinesia Mild NMS: mild rigidity, confusion,
Dystonia temperature 38 C, and
Tremor tachycardia 100 bpm
Alteration of Mentation Moderate NMS: stupor, catatonia,
Agitation hyperpyrexia 38–40 C, or
Inattention tachycardia 100–120 bmp
Confusion Severe NMS: severe rigidity, catatonia,
Depressed mental status coma, hyperthermia 40 C, or
Catatonia tachycardia 120 bpm
Coma

Abbreviations: PMN, polymorphonuclear leukocyte; bpm, beats per minute.

dopaminergic medications. Metabolic derangements and end-organ failure are less

common, and thus prognosis is more favorable.66

Drug-induced and toxin-induced parkinsonism

Drug-induced parkinsonism (DIP) results from exposure to DRBAs (see Table 2),
VMAT2 inhibitors, valproic acid, and calcium channel blockers, like flunarizine or cin-
narizine. DIP prevalence is 20% to 35%.67 DIP can present asymmetrically, like idio-
pathic PD, but tends to be symmetric in onset. Exposure to DRBAs or depletors can
unmask idiopathic PD signs, making the clinical diagnosis convoluted. A dopamine
transporter scan is normal in DIP (Fig. 7A, B).
DIP is dose-dependent and reversible. Thus, the first step in treatment is reducing or
stopping the offending agent. Increased avidity of D2-receptor binding, higher dosage,
increased length of exposure, older age, and female gender are all risk factors.68 If a
patient requires dopamine antagonism for psychiatric care, then consider switching to
a lower affinity D2-receptor antagonist. Namely, quetiapine and clozapine have less af-
finity for dopamine blockade and induce lower rates of parkinsonism. Resolution of
parkinsonism can take months to approximately 1 y.
In patients with PD or dementia with Lewy body (DLB) who require treatment for
psychosis, avoid higher-affinity DRBAs that increase risk of worsening parkinsonism
and NMS. Quetiapine and clozapine are acceptable therapies. Pimivanserin is a
5-HT2A receptor inverse-agonist and antagonist and is Food and Drug
Administration-approved to treat PD psychosis or psychosis-related DLB.
Lastly, some toxins have a predilection for the basal ganglia and thus can cause
acute-onset parkinsonism. These include carbon monoxide poisoning, 1-methyl-4-
phenyl-1,2,3,6-tetrahydropyridine, and manganese.69 Carbon monoxide causes injury
to the globus pallidus internus (GPi), and parkinsonism can result 2 w to 6 mo after
exposure. MRI brain may show T2 hyperintensities or hemorrhage in the GPi. Manga-
nese targets sites of neuromelanin, including the basal ganglia. Occupational hazards,

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 522 Radmard

Fig. 7. Dopamine transporter scan in drug-induced parkinsonism.Comparison showing loss

of dopaminergic terminals (B) seen in neurodegenerative parkinsonian disorders compared
to normal uptake (A), which is seen in drug-induced parkinsonism.

such as welders, steel workers, or miners are at risk. Notably, liver failure can release
manganese and cause parkinsonism, dystonia, cognitive impairment, and psychosis.
As manganese is paramagnetic, MRI brain reveals T1 hyperintensity in the basal
ganglia in addition to T2 hyperintensity.69

Functional Movement Disorders

Functional neurologic disorder (FND) is a neuropsychiatric disease manifested by
neurologic symptoms or signs that cannot be explained by a structural or
pathologically-known disorder. FND is the second most common diagnosis seen in
neurology outpatient clinics.70 Moreover, functional movement disorders (FMD) ac-
count for 20% to 30% of referrals to movement disorders clinical practice.71 Not un-
commonly, movement disorder clinicians are asked to urgently see acute-onset
movement disorders that progress in a fulminant manner to debility, and many times,
these presentations are FMD.
Primary care physicians are commonly the first providers to manage FND/FMD. The
ability to recognize these disorders is important as positive prognostic signs for recov-
ery are shorter duration of symptoms/time to diagnosis and satisfaction with care or
how the diagnosis is relayed.72 FND/FMD are considered rule-in diagnoses rather
than rule-out diagnoses. Diagnosis is based on phenotypic presentation of cumulative
positive signs (Table 7).
Functional tremor and dystonia are the most common FMDs followed by myoc-
lonus, gait disorder, parkinsonism, and tics.74 Tremor has an inherent pacemaker
or set frequency and direction. Variability of frequency or direction can be clues of
FMD. Entrainment is where the frequency of the functional movement syncs with
the frequency of repetitive movements of another body part when occurring in tan-
dem. Most pathology-defined movement disorders worsen with distraction, whereas
FMDs lessen or cease with distraction. The beginning of the coronavirus disease
2019 pandemic led to a phenomenon in the adolescent and young adult population
of fulminant functional tics.75,76 Functional tics vary from tic disorders, including

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 Abnormal Movements and Movement Disorder Urgencies 523

Table 7
Core diagnostic criteria of functional movement disorder73

Diagnostic
Criteria Description
Variability Presence of inconsistent frequency, duration, or direction of the presenting
abnormal movement
Distractibility Severity of movement disorder lessens or resolves with distraction
maneuvers, like serial sevens, saying the months of the year backwards, or
performing other examinations maneuvers
Entrainment Frequency of the abnormal movement syncs with the frequency of a
repetitive task, like finger taps, hand opening/closing, or toe taps
Suggestibility Direct mention of the abnormal movement or third person presence triggers
the abnormal movement

Adapted from Espay AJ, Aybek S, Carson A, et al. Current Concepts in Diagnosis and Treatment of
Functional Neurological Disorders. JAMA Neurol. 2018 Sep 1;75(9):1132-1141.

Tourette syndrome, by having a female predominance, older age of onset in late

teens to 20’s, absence of rostrocaudal distribution of onset, increased likelihood of
complex movements or vocalizations at onset, and higher severity at onset of
disease.75
The first step in management of FMD is recognition. The author urges restraint in
telling patients the disorder is due to “stress” or psychologic; unlike factitious disor-
der or malingering, FMD is considered involuntary. Explanation of why the neuro-
logic symptoms have occurred can be validating. FND/FMD is miscommunication
disorder due to multi-network dysfunction, resulting in hypoactivation or hyperacti-
vation of neuronal circuits.77 Neurologists routinely use analogies to define FND/
FMD for patients. This author prefers to use the analogy of roads and bridges as
these concepts are easily grasped. Brain areas are connected and communicate
by roads and bridges, and in FND/FMD, a bridge may require repair, or a road could
be flooded, resulting in miscommunication or miswiring of the brain. However, with
appropriate therapy, these roads or bridges can repair themselves and potentially
result in resolution of the abnormal movements. Directed therapies for FND/FMD
include cognitive behavioral therapy and speech, occupational, or physical therapy
when indicated.

SUMMARY

Movement disorders encompass several different phenomenology types that require

correct identification to establish therapy. In the acute and subacute setting, recogni-
tion of the clinical syndrome as a whole can identify potentially life-threatening and
debilitating disorders. Special attention to the history, medication exposure, vital
sign changes, and examination can clarify diagnosis and result in prompt treatment.
Most of these disorders are treatable or reversible.

CLINICS CARE POINTS

 Movement disorder urgencies and emergencies overall lack specified diagnostic criteria and,
thus they rely on clinical presentation and examination for diagnosis.

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 524 Radmard

 Movement disorder urgencies and emergencies are often manifestations of drug-induced or

toxic/metabolic etiologies rather than worsening of underlying neurologic disorder.
 These disorders are mostly treatable or self-resolving with proper therapeutic implementation.

ACKNOWLEDGMENTS

The author would like to acknowledge Julian Agin-Liebes, MD and Steven Shapiro,
MD for their contribution

DISCLOSURE

The author declares consultation for Best In Class MD, which is unrelated to this
article. There are no additional disclosures to report or conflicts of interest related
to the research of this article.

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