Tag Archives: psychiatry

EM Reflections – June 2020

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Thanks to Dr Joanna Middleton for leading the discussions this month

Edited by Dr David Lewis 

Discussion Topics

  1. Antiviral Toxicity

    • Always adjust dosing in patients with renal impairment

  2. Necrotising Fasciitis

    • Difficult clinical diagnosis
    • Should be on the differential for all soft tissue infections
    • Delayed definitive care always results in poor outcomes

  3. Epidural Abscess

    • Thorough detailed neurological examination required
    • Isolated leg weakness is rare in Stroke
    • Progressive development of symproms and mixed UMN/LMN signs suggests spinal cord compression.

 

Antiviral Toxicity

Case

A 70yr old male presents with a typical zoster rash in the left L1 dermatome. He has a past medical history of chronic renal insufficiency. He is started on Valacyclovir 1000mg TID. He represents 3 days later with hallucinations including a feeling that he was occupying a dead body. What is the differential diagnosis?

 

Varicella Zoster Encephalitis vs Valacyclovir Toxicity

VZV and antiviral toxicity can present with similar symptoms

Two main risk factors increase the risk for VZV

  • age greater than 50 years old
  • immunocompromised due to reduced T cell-mediated immunity

The main risk factor for antiviral toxicity is renal insufficiency

Differentiation

  • Timing
    • Toxicity presents within 1-3 days of starting drug (vs 1-2 weeks)

 

  • Symptoms – both can present with confusion and altered LOC
    • Encephalitis – fever, HA, seizures, more likely with Trigeminal nerve (V1) or disseminated zoster
    • Toxicity – Visual hallucinations, dysphasia, tremor/myoclonus
    • Toxicity – Cotard’s syndrome…

Cotard’s Syndrome

“le délire des négations”

(delirium of negation)

https://en.wikipedia.org/wiki/Cotard_delusion

  • Described in 1880 by neurologist Jules Cotard
    • “patient usually denies their own existence, the existence of a certain body part, or the existence of a portion of their body”
  • Seen in schizophrenia, psychosis and…
  • ….acyclovir toxicity (felt to be due to metabolite CMMB (9-carboxymethoxymethylguanine) crossing BBB)

Further Reading

Varicella Zoster Encephalitis case report and outline

Valacyclovir Toxicity case report and outline

Cotard’s Syndrome

Drug Dosing in Chronic Kidney Disease

 

 

 

Necrotising Soft Tissue Infections (NSTI)

Case

A 28yr old female presents pain, redness and swelling over the right thigh. She has a past medical history of type 2 diabetes. She is managed as an outpatient with intravenous ceftriaxone q24hrs. Her symptoms failed to respond on follow up. What is the concern now? Are there any red flags? What condition needs to be considered in patients with soft tissue infections that fail to respond to antibiotics?

NSTI first described by Hippocrates 5th century BC

“[m]any were attacked by the erysipelas all over the body when the exciting cause was a trivial accident…flesh, sinews, and bones fell away in large quantities…there were many deaths.”

 

Necrotizing fasciitis is characterized by rapid destruction of tissue, systemic toxicity, and, if not treated aggressively, gross morbidity and mortality. Early diagnosis and aggressive surgical treatment reduces risk; however, it is often difficult to diagnose NF, and sometimes patients are treated for simple cellulitis until they rapidly deteriorate.

Infection typically spreads along the muscle fascia due to its relatively poor blood supply; muscle tissue is initially spared because of its generous blood supply.

Infection requires inoculation of the pathogen into the subcutaneous tissue or via hematogenous spread.

Classification

  • Type 1 – polymicrobial – older/diabetics/EtOH/IC/PVD
  • Type 2 – monomicrobial – usually group A beta-hemolytic strep (often hematogenous) – healthy people of all ages

Early signs and symptoms of NSTI are often identical to those seen with cellulitis or abscesses potentially making the correct diagnosis difficult

‘Classic’ Signs / Symptoms

(1) the presence of bullae
(2) skin ecchymosis that precedes skin necrosis
(3) crepitus
(4) cutaneous anesthesia
(5) pain out of proportion to examination
(6) edema that extends beyond the skin erythema
(7) systemic toxicity
(8) progression of infection despite antibiotic therapy or rapid progression

First 4 are “hard” signs

  • Erythema (without sharp margins; 72 percent)
  • Edema that extends beyond the visible erythema (75 percent)
  • Severe pain (out of proportion to exam findings in some cases; 72 percent)
  • Fever (60 percent)
  • Crepitus (50 percent)
  • Skin bullae, necrosis, or ecchymosis (38 percent)

Streaking lymphangitis favours the diagnosis of cellulitis over necrotizing fasciitis

Diagnosis

  • There is no set of clinical findings, lab test results and even imaging that can definitively rule out necrotizing fasciitis
    • “Surgical exploration is the only way to establish the diagnosis of necrotizing infection”.
    • “Surgical exploration should not be delayed when there is clinical suspicion for a necrotizing infection while awaiting results of radiographic imaging other diagnostic information”
  • But what if you really aren’t sure?  Or if you get pushback?
  • CT is probably the best test – esp Type 1 (gas forming)
    • Findings – gas, fluid collections, tissue enhancement, inflammatory fascial changes
  • Finger test…
    • “After local anesthesia, make a 2-3 cm incision in the skin large enough to insert your index finger down to the deep fascia. Lack of bleeding and/or “dishwater pus” in the wound are very suggestive of NSTI. Gently probe the tissues with your finger down to the deep fascia. If the deep tissues dissect easily with minimal resistance, the finger test is + and NSTI can be ruled in.”  (emergencymedicinecases.com)
  • But what about PoCUS????

PoCUS

Diagnosis of Necrotizing Faciitis with Bedside Ultrasound: the STAFF Exam

Findings – “STAFF”

ST – subcutaneous thickening
A – air
FF – fascial fluid

Ultrasound video demonstrating Subcutaneous Thickening, Air, and Fascial Fluid (STAFF).

 

Soft tissue ultrasound findings are significantly different when compared to normal soft tissue ultrasound

Bottom Line: Limited data, but basically PoCUS is not sufficient to rule-in or rule out, but might be helpful in raising suspicion level for necrotising fasciitis for physicians who routinely scan all soft tissue infections.

 

LRINF Score

The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) Score: A Tool for Distinguishing Necrotizing Fasciitis From Other Soft Tissue Infections

Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) Score.  2004, retrospective – score >6 negative predictive value of 96.0% and a positive predictive value of 92%.

 

A validation study looking only at patients with pathology-confirmed necrotizing fasciitis showed that a LRINEC score cutoff of 6 points for necrotizing fasciitis only had a sensitivity of 59.2% and a specificity of 83.8%, yielding a PPV of 37.9% and NPV of 92.5%. However, the study did show that severe cellulitis had a LRINEC Sscore ≥ 6 points only 16.2% of the time.  Therefore, the available evidence suggests that the LRINEC score should not be used to rule-out NSTI.

Bottom Line: Doesn’t rule-out…… or rule-in

 

Suggested Algorithm – UpToDate

 

EM Cases Review

BCE 69 Necrotizing Fasciitis

 

Further Reading

Necrotizing fasciitis – Can Fam Physician. 2009 Oct; 55(10): 981–987.

 

Epidural Abscess

Case

A 40yr old female presents with left leg weakness. She has a complex recent past medical history including recently diagnosed pneumonia, previous renal colic and type 2 diabetes. Could this be a stroke? What are the other causes of leg weakness? How does the examination differentiate UMN from LMN lesions? When considering a diagnosis of epidural abscess what investigation is required? How soon should it be performed?

Only 4% of Strokes present with isolated or predominant leg weakness. (Brain. 1994 Apr;117 ( Pt 2):347-54.
doi: 10.1093/brain/117.2.347)

Common mechanisms of weakness:

  • Upper motor neuron lesions (Stroke, Tumour, Spinal Cord Compression, etc)
  • Lower motor neuron lesions ( Neuropathy, Disc Prolapse, Spinal Cord Compression, etc)
  • Neuromuscular junction lesions (Myasthenia, etc)
  • Neuropathies (Guillain-Barre, etc)
  • Muscle (Myopathies, etc)

Full review on Muscle Weakness from the Merck Manual here

Weakness that becomes severe within minutes or less is usually caused by severe trauma or stroke; in stroke, weakness is usually unilateral and can be mild or severe. Sudden weakness, numbness, and severe pain localized to a limb are more likely caused by local arterial occlusion and limb ischemia, which can be differentiated by vascular assessment (eg, pulse, color, temperature, capillary refill, differences in Doppler-measured limb BPs). Spinal cord compression can also cause paralysis that evolves over minutes (but usually over hours or days) and is readily distinguished by incontinence and clinical findings of a discrete cord sensory and motor level.

Unilateral upper motor neuron signs (spasticity, hyperreflexia, extensor plantar response) and weakness involving an arm and a leg on the same side of the body: A contralateral hemispheric lesion, most often a stroke

Upper or lower motor neuron signs (or both) plus loss of sensation below a segmental spinal cord level and loss of bowel or bladder control (or both): A spinal cord lesion

 

Epidural Abscess

Spinal epidural abscess (SEA) is a severe pyogenic infection of the epidural space that leads to devastating neurological deficits and may be fatal. SEA is usually located in the thoracic and lumbar parts of the vertebral column and injures the spine by direct compression or local ischemia. Spinal injury may be prevented if surgical and medical interventions are implemented early. The diagnosis is difficult, because clinical symptoms are not specific and can mimic many benign conditions. The classical triad of symptoms includes back pain, fever and neurological deterioration.

Spinal Epidural Abscess: Common Symptoms of an Emergency Condition – A Case Report

 

  • 75% are a delayed diagnosis
    • Usually hematogenous spread, usually S. aureus
  • Diagnosis
    • CRP has an sensitivity of 85%, specificity of 50%
    • MRI is gold standard
    • CT with contrast 2nd choice

 

Further Reading

Spinal epidural abscess

Episode 26: Low Back Pain Emergencies

 

 

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EM Reflections – May 2020

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Thanks to Dr Paul Page for leading the discussions this month

Edited by Dr David Lewis 

Discussion Topics

  1. Seizure disorder and safe discharge 

    • Consider risk factors for adverse outcome of discharge for all patients with recurrent seizure disorder
    • Use a checklist

  2. Competency and Capacity

    • Multidisciplinary consultation is paramount in deciding capacity
    • Special circumstances include vulnerable adults and pregnancy

  3. Testicular Torsion

    • Time = Testicle viability
    • Do not delay definitive management

Seizure disorder and safe discharge 

Case

A patient presents with recurrent seizures. They have a past medical history of schizophrenia and mental health delay. Following appropriate ED management with complete resolution of seizures and full recovery of the patient – what is the recommended disposition?

Seizure disorder is a common presentation to the Emergency Department. This EM Cases post provides an excellent summary for the ED approach to resolved seizures:

Ep 132 Emergency Approach to Resolved Seizures

 

ED approach to resolved seizures – Summary pdf

In this study – Ethanol withdrawal or low antiepileptic drug levels were implicated as contributing factors in 177 (49%) of patients. New‐onset seizures were thought to be present in 94 (26%) patients. Status epilepticus occurred in only 21 (6%) patients.

73% of patients were discharged.

 

 

 

Disposition

Most authors recommend admission for patients presenting with FIRST Seizure Episode. Patients with a past medical history of recurrent seizure disorder are more likely to be discharged than admitted.

However – this EBMedicine article cites an incidence of 19% seizure recurrence rate within 24 hours of presentation, which decreased to 9% if patients with alcohol related events or focal lesions on CT were excluded. They suggest, that at present, there is insufficient evidence to guide the decision to admit. They recommend this decision be tailored to the patient, taking into consideration the patient’s access to follow-up care and social risk factors (eg, alcoholism or lack of health insurance). Patients with comorbidities, including age > 60 years, known cardiovascular disease, history of cancer, or history of immunocompromise, should be considered for admission to the hospital.

 

Considerations For Safety On Discharge

Patients and their families should be counseled and instructed on basic safety measures to prevent complications (such as trauma) during seizures. For example, patients should be advised to avoid swimming or cycling following a seizure, at least until they have been reassessed by their neurologist and their antiepileptic therapy optimized, if needed. A particularly important point for seizure patients is education against driving. Although evidence remains controversial on this issue, there is general agreement that uncontrolled epileptic patients who drive are at risk for a motor vehicle crash, with potential injury or death to themselves and others. For this reason, most states do not allow these patients to drive unless they have been seizure-free on medications for 1 year. According to population survey data, 0.01% to 0.1% of all motor vehicle crashes are attributable to seizures

Competency and Capacity

Case

A young female patient with a history of polysubstance drug abuse presents with a psychotic episode. She refuses treatment. What are the competency and capacity implications? She is also pregnant. Does this change the the competency and capacity implications?

This LitFL post provides and excellent outline for Competency and Capacity in the ED:

Capacity and Competence

This article published by the RCPSC provides a useful outline from a Canadian perspective – with the following objectives.

  1. To clarify the role of decisional capacity in informed consent
  2. To discuss problems associated with decisional capacity and addiction

RCPSC – Decisional Capacity

 

 

Capacity in Pregnancy

Recommendations from the American College of Obstetricians and Gynecologists

On the basis of the principles outlined in this Committee Opinion, the American College of Obstetricians and Gynecologists (the College) makes the following recommendations:

  • Pregnancy is not an exception to the principle that a decisionally capable patient has the right to refuse treatment, even treatment needed to maintain life. Therefore, a decisionally capable pregnant woman’s decision to refuse recommended medical or surgical interventions should be respected.
  • The use of coercion is not only ethically impermissible but also medically inadvisable because of the realities of prognostic uncertainty and the limitations of medical knowledge. As such, it is never acceptable for obstetrician–gynecologists to attempt to influence patients toward a clinical decision using coercion. Obstetrician–gynecologists are discouraged in the strongest possible terms from the use of duress, manipulation, coercion, physical force, or threats, including threats to involve the courts or child protective services, to motivate women toward a specific clinical decision.
  • Eliciting the patient’s reasoning, lived experience, and values is critically important when engaging with a pregnant woman who refuses an intervention that the obstetrician–gynecologist judges to be medically indicated for her well-being, her fetus’s well-being, or both. Medical expertise is best applied when the physician strives to understand the context within which the patient is making her decision.
  • When working to reach a resolution with a patient who has refused medically recommended treatment, consideration should be given to the following factors: the reliability and validity of the evidence base, the severity of the prospective outcome, the degree of burden or risk placed on the patient, the extent to which the pregnant woman understands the potential gravity of the situation or the risk involved, and the degree of urgency that the case presents. Ultimately, however, the patient should be reassured that her wishes will be respected when treatment recommendations are refused.
  • Obstetrician–gynecologists are encouraged to resolve differences by using a team approach that recognizes the patient in the context of her life and beliefs and to consider seeking advice from ethics consultants when the clinician or the patient feels that this would help in conflict resolution.
  • The College opposes the use of coerced medical interventions for pregnant women, including the use of the courts to mandate medical interventions for unwilling patients. Principles of medical ethics support obstetrician–gynecologists’ refusal to participate in court-ordered interventions that violate their professional norms or their consciences. However, obstetrician–gynecologists should consider the potential legal or employment-related consequences of their refusal. Although in most cases such court orders give legal permission for but do not require obstetrician–gynecologists’ participation in forced medical interventions, obstetrician–gynecologists who find themselves in this situation should familiarize themselves with the specific circumstances of the case.
  • It is not ethically defensible to evoke conscience as a justification to attempt to coerce a patient into accepting care that she does not desire.
  • The College strongly discourages medical institutions from pursuing court-ordered interventions or taking action against obstetrician–gynecologists who refuse to perform them.
  • Resources and counseling should be made available to patients who experience an adverse outcome after refusing recommended treatment. Resources also should be established to support debriefing and counseling for health care professionals when adverse outcomes occur after a pregnant patient’s refusal of treatment.

Further Reading:

Ethically Justified Clinically Comprehensive Guidelines for the Management of the Depressed Pregnant Patient

How Do I Determine if My Patient has Decision-Making Capacity?

 

Testicular Torsion

Case

A 12 year old boy presents with scrotal discomfort in the early hours of the morning. The department is very busy and the waiting time to be seen is 4 hours. What triage category is this presenting complaint? If a diagnosis of torsion is considered, how quickly should definitive management be initiated?

Ramachandra et al. demonstrated through multivariate analysis of the factors associated with testicular salvage, that duration of symptoms of less than 6 h was a significant predictor of testicular salvage. They found that the median duration of pain was significantly longer in patients who underwent orchiectomy versus orchidopexy. Similar findings were seen with respect to time to operating room from initial presentation. They concluded that time to presentation is in fact the most important factor in determining salvageability of the testicle in testicular torsion. If surgical exploration is delayed, testicular atrophy will occur by 6 to 8 h, with necrosis ensuing within 8 to 10 h of initial presentation. Salvage rates of over 90% are seen when surgical exploration is performed within 6 h of the onset of symptoms, decreasing to 50% when symptoms last beyond 12 h. The chance of testicular salvage is less than 10%, when symptoms have been present for over 24 h

Factors influencing rate of testicular salvage in acute testicular torsion at a tertiary pediatric center.

Ramachandra P, Palazzi KL, Holmes NM, Marietti S

West J Emerg Med. 2015 Jan; 16(1):190-4.

[PubMed]

 

 

This study (Howe et al). confirmed the relationship between duration of torsion and testicle viability and also found a relationship between the degree of torsion

 

 

AAFP Review of Testicular Torsion: Diagnosis, Evaluation, and Management

 

 

 

 

 

 

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Tardive Dyskinesia in an Emergency Setting

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Medical Student Clinical Pearl – October 2019

Faith Moore

Faculty of Medicine
Dalhousie University
CC3
Class of 2021

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual

Case

A 48-year-old female was brought to the emergency department by EMS after developing dystonia that morning, a couple hours earlier, following a restless night. The dystonia had begun affecting her arms, torso and buccal region, but eventually moved to also involve her legs. She had a history of recurrent tardive dyskinesia for the past 20 years since taking stelazine and developing tardive dystonia. She was switched to olanzopine after developing dystonia and stayed on it until two months ago. Her citalopram and clozapam dosing had been increased two weeks ago, and she had also started Gingko biloba extract two weeks ago. She had started Nuplazid 3 days ago.

Upon exam she was diaphoretic with no other abnormal findings other than dystonia affecting the entire body.

Tardive Dyskinesia

Pathophysiology

    • Tardive dyskinesia is a hyperkinetic movement disorder that is associated with the use of dopamine receptor-blocking medications.1 The exact mechanism is under debate, but the main hypotheses include an exaggerated response by dopamine receptors due to a chronic dopamine blockade, oxidative stress, gamma-aminobutyric acid (GABA) depletion, cholinergic deficiency, altered synaptic plasticity, neurotoxicity and defective neuroadaptive signaling. 2 The most accepted theory of the mechanism is that the chronic dopamine blockade caused by the dopamine receptor-blocking medications results in a hypersensitivity of the receptors, specifically at the basal ganglia. 1
    • The medications that are known to have the possibility to cause tardive dyskinesia include antipsychotic drugs, anticholinergic agents (ex. Procyclidine), antidepressants, antiemetics (ex. Metoclopramide), anticonvulsants, antihistamines, decongestants (ex. pseudoephedrine and phenylephrine), antimalarials, antiparkinson agents, anxiolytics, biogenic amines, mood stabilizers and stimulants.1

Who is most at risk?

    • The medications that are the most common culprits are first- and second-generation antipsychotics and metoclopramide. The incidence of tardive dyskinesia from chronic first-generation antipsychotic exposure is 5-6% 3, and is 4% for second generation antipsychotics 4. There is no prospective research on chronic metoclopramide use and the risk for tardive dyskinesia at this point and time5, but a study in the UK in 1985 showed 1 case of tardive dyskinesia for every 35 000 prescriptions6.
      • Most prominent risk factors
        • Old age5
        • Chronic exposure5
        • Patients who develop extrapyramidal symptoms while on antipsychotic drugs.7

Signs and Symptoms

      • Repetitive involuntary body movements that may involve the face, tongue, eyes, arms, torso and legs

Diagnosis

    • The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) classifies tardive dyskinesia as “involuntary movements (lasting at least a few weeks) generally of the tongue, lower face and jaw, and extremities (but sometimes involving the pharyngeal, diaphragmatic, or trunk muscles), developing in association with the use of a neuroleptic medication for at least a few months” and that persists for at least one month after the medication is stopped.8

Differential Diagnosis

    • Acute dyskinesia
    • Akathisia
    • Parkinsonism and tremor
    • Perioral tremor
    • Stereotypies and mannerisms
    • Spontaneous or idiopathic dyskinesias
    • Isolated dystonia
    • Primary movement disorders
    • Chorea from systemic causes 9

Key Questions for History and Physical

    • Are the movements voluntary?
    • Is there an accompanied feeling of restlessness?
      • If yes, might point towards akathisia.
    • When did these movements began?
    • What is the body distribution of the involuntary movements?
    • Are there any extrapyramidal signs and symptoms?
    • Are there any associated features?
    • Have there been any drug changes in the past few months?

 

Management in the Emergency Department

    • First line treatment of tardive dyskinesia generally begins with discontinuation of the offending drug. In the emergency department this should be done after consulting with the treating physician. These patients are often being treated for psychiatric disorder and the treatment of the psychiatric disorder must be balanced with the risk of tardive dyskinesia. It may be appropriate to switch from a first generation antipsychotic medication to a second generation antipsychotic generation medication.
    • If the symptoms of tardive dyskinesia need to be treated, like in our case with this patient, there are various drugs that can be tried.
    • Tetrabenazine is considered first line.10
      • Suggested doses of 12.5-25 mg starting daily dose with a 25-200 mg/day dose range.10
    • Other treatment options
      • Dextromethorphan11
        • In a recent case study patients took under 1mg/kg, not exceeding 42 mg/day.11
        • This was recommended by a local neurologist here at the Saint John Regional Hospital.
      • Valbenazine 12
        • Suggested dose of 40 mg UID, increasing to 80 mg UID after one week.12
      • Amantadine10
        • Suggested dose of 100 mg starting daily dose with a dose range of 100-300 mg/day 10
      • Benzodiazepines12
        • Clonazepam initiated at 0.5 mg and titrated by 0.5 mg increments every 5 days to response up to a maximum dose of 3-4 mg/day. 12
      • Diphenhydramine suggested dose of 25-50 mg IV13
      • Botulinum toxin injections12
    • Commonly used treatments lacking evidence of efficacy
      • Benztropine10
Drug Starting Dose Recommendations Dose Range
1st Line
Tetrabenazine 12.5-25 mg UID 25-200 mg UID
Other options
Dextromethorphan Under 1 mg/kg Not exceeding 42 mg UID
Valbenazine 40 mg UID Increase to 80 mg after 1 week
Amantadine 100 mg UID 100-300 mg UID
Clonazepam 0.5 mg 0.5-4.0 mg UID
Diphenhydramine 25 mg IV 25-50 mg IV
Botulinum toxin injection local injection to treat specific painful dystonia resistant to systemic therapy

 

Case Continued

The patient was given 2mg of Benztropine IV with no effect. Twenty minutes later he was then given 1mg of Ativan SL with no effect. Thirty minutes later the patient was given 150 mg Benadryl IV, and some improvement was then witnessed, the patient was allowed to sleep and was discharged approximately 5 hours after his arrival with no symptoms.

External Resources

Treatment strategies for dystonia

Diagnosis & Treatment of Dystonia

References

  1. Cornett EM, Novitch M, Kaye AD, Kata V, Kaye AM. Medication-Induced Tardive Dyskinesia: A Review and Update.Ochsner J. 2017 Summer;17(2):162-174. Review. PubMed PMID: 28638290; PubMed Central PMCID: PMC5472076.
  2. Kulkarni SK, Naidu PS. Pathophysiology and drug therapy of tardive dyskinesia: current concepts and future perspectives.Drugs Today (Barc). 2003 Jan;39(1):19-49. Review. PubMed PMID: 12669107.
  3. Glazer WM.Review of incidence studies of tardive dyskinesia associated with typical antipsychotics. J Clin Psychiatry. 2000;61 Suppl 4:15-20.  PubMed PMID: 10739326.
  4. Correll CU, Schenk EM.Tardive dyskinesia and new antipsychotics. Curr Opin Psychiatry. 2008 Mar;21(2):151-6. doi: 10.1097/YCO.0b013e3282f53132.  PubMed PMID: 18332662.
  5. Rao AS, Camilleri M.Review article: metoclopramide and tardive dyskinesia.Aliment Pharmacol Ther. 2010 Jan;31(1):11-9. doi: 10.1111/j.1365-2036.2009.04189.x.  PubMed PMID: 19886950.
  6. Bateman DN, Rawlins MD, Simpson JM.Extrapyramidal reactions with metoclopramide. Br Med J (Clin Res Ed). 1985 Oct 5;291(6500):930-2. doi: 10.1136/bmj.291.6500.930. PubMed PMID: 3929968; PubMed Central PMCID: PMC1417247
  7. Novick D, Haro JM, Bertsch J, Haddad PM.Incidence of extrapyramidal symptoms and tardive dyskinesia in schizophrenia: thirty-six-month results from the European schizophrenia outpatient health outcomes study. J Clin Psychopharmacol. 2010 Oct;30(5):531-40. doi: 10.1097/JCP.0b013e3181f14098. PubMed PMID: 20814320.
  1. American Psychiatric Association, Medication-induced movement disorders and other adverse effects of medication, Diagnostic and Statistical Manual of Mental Disorders, fifth edition, American Psychiatric Association, 2013.
  2. Tarsy D, Deik A. Tardive dyskinesia: Etiology, risk factors, clinical features, and diagnosis. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on September 9, 2019.)
  1. DynaMed [Internet]. Ipswich (MA): EBSCO Information Services. 1995 – . Record No.T113751, Tardive Dyskinesia; [updated 2018 Nov 30, cited September 9, 2019]. Available from https://www.dynamed.com/topics/dmp~AN~T113751. Registration and login required.
  1. Kim J. (2014). Dextromethorphan for Tardive Dyskinesia. International Neuropsychiatric Disease Journal. 2. 136-140. 10.9734/INDJ/2014/7970.
  2. Tarsy D, Deik A. Tardive dyskinesia: Prevention, prognosis, and treatment. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on September 9, 2019.)
  1. Buttaravoli P, Leffler SM. Chapter 1 – dystonic drug reaction. 2012:1-3. doi:https://doi.org/10.1016/B978-0-323-07909-9.00001-5 “.
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