What is catatonia

Catatonia is a neuropsychiatric syndrome of apparent unresponsiveness to external stimuli and apparent inability to move normally in a person who is apparently awake ¹. Catatonia is a condition mainly seen in mood disorders, but can also be caused by primary psychiatric, neurologic, medical, metabolic and drug-induced disorders, as well as brain injury ². Catatonia is most commonly characterized by mutism, stupor, posturing, and hypokinesis ³. However, because of catatonia vague presentation, it can be mistaken for a variety of other medical disorders. Most studies on the incidence of catatonia find it to be between 5% – 20% in the acute inpatient psychiatric setting. Most episodes of catatonia can be classified as excited, retarded, or malignant catatonia. Symptoms can wax, wane, or change during these episodes, and patients affected can have periods of withdrawal and periods of excitation ⁴.

Fever and autonomic dysregulation due to malignant catatonia often lead to fatal consequences ⁵, with a mortality rate exceeding 50% ⁶. Evidence suggests that malignant catatonia represents a disturbance of dopaminergic and gamma-aminobutyric acid receptors ⁷, as administration of 1 – 2 mg lorazepam typically leads to rapid resolution of symptoms within two hours ⁸. Such treatment should be used within 24 hours after excluding alternative diagnoses ⁹. Because diagnosis is often difficult and delayed ¹⁰, administration of low-dose benzodiazepines (e.g., five mg diazepam) may be warranted in patients with a history of psychological disorders presenting with malignant catatonia symptoms.

Studies have suggested a connected pathway between the cortex, basal ganglia, and thalamus underpins these different subtypes and results in catatonic symptoms. Recognition and treatment of catatonia can play an important part in both psychiatric and medical treatment as it can inhibit treatment, confusing diagnoses, and be potentially fatal if untreated ¹¹.

Individuals with catatonia often cannot provide a coherent history; however, collateral sources can often relate relevant historical information. Family members can confirm the presence of typical primary features of catatonia, including immobility, stupor, posturing, rigidity, staring, grimacing, and withdrawal.

A history of behavioral responses to others usually includes the presence of the following:

• Mutism (absence of speech)
• Negativism (performing actions contrary to the commands of the examiner)
• Echopraxia (repeating the movements of others)
• Echolalia (repeating the words of others)
• Waxy flexibility (maintaining the physical positions placed on the body of patient by the examiner)
• Withdrawal (absence of responses to the environment)

A history of stereotypies, mannerisms, and verbigeration (uttering gibberish) is often elicited from people who are close to the patient. Priapism was reported in a 20-year-old man with paranoid schizophrenia and catatonia ¹².

The alternative presentation of catatonia is an excited state, possibly with impulsivity, combativeness, and autonomic instability. A history of an excited state should be sought from the family of a person with catatonia, but it is often denied by the family. When excited episodes are present, they are typically short-lived and may precipitate collapse with exhaustion. An excited state of catatonia is usually associated with bipolar disorder.

The history-taking process should include the following:

• During the initial interview of the patient and the family, ask about possible precipitating events, including infection, trauma, and exposure to toxins and other substances
• Inquire about any previous similar episodes of catatonia; determine whether the precipitating events of the earlier episode are present in the current episode, and record any interventions that relieved catatonia previously
• Question the patient and family regarding exposure to neuroleptics and other substances associated with catatonia; catatonia and neuroleptic malignant syndrome (NMS) may follow the administration of neuroleptic medications ¹³
• Identify any comorbid disorders, including schizophrenia, mood disorders, psychological stressors, medical conditions, and obstetric conditions

Catatonia has occurred in patients after treatment with levetiracetam ¹⁴ and levofloxacin ¹⁵. Catatonia developed in a 55-year-old woman with schizophrenia who was treated with rimonabant, a cannabinoid receptor (CB1) antagonist ¹⁶.

Catatonia has the very high morbidity and mortality and is best managed by a multidisciplinary team that includes a mental health nurse, a psychiatrist, a psychologist, an internist, a neurologist, and an ophthalmologist.

In an emergency setting, treatable common causes of catatonia must be rapidly considered and ruled out. The emergency physician must quickly consider the presence of neuroleptic malignant syndrome (NMS) ¹³, encephalitis, including anti-NMDA receptor encephalitis ¹⁷, nonconvulsive status epilepticus, and acute psychosis. Catatonia has occurred in intensive care units (ICUs) ¹⁸. Given that the patients all had serious disorders leading to ICU placement, it is possible that the underlying disorders contributed to the development of catatonia in the units.

A history of exposure to traditional and atypical neuroleptic agents must be sought. Although neuroleptic malignant syndrome often follows the initiation of neuroleptic therapy or an increase in the neuroleptic dosage, exposure to neuroleptics may be minimal in some susceptible individuals. For example, Nielsen and Nielsen report ¹⁹ the occurrence of neuroleptic malignant syndrome after a single dose of neuroleptic medication.

In addition, the patient’s history must be evaluated for the following conditions:

• Encephalitis – Determine whether the patient has had sudden onset of headache, fever, and deterioration in mental functioning
• Nonconvulsive status epilepticus – Determine whether the patient has a history of seizures and whether the patient has been prescribed antiepileptic drugs; determine whether electroencephalography (EEG) has been performed, and if it has, review the findings
• Acute psychosis – Determine whether the patient has exhibited evidence of delusions and hallucinations and whether he or she has exhibited suicidal or homicidal threats or actions; record any history of prior psychiatric hospitalization and treatment

Types of catatonia

There are 3 types of catatonia ²⁰:

1. Catatonia associated with another mental disorder (catatonia specifier),
2. Catatonic disorder due to another medical condition, and
3. Unspecified catatonia.

What causes catatonia?

Catatonia as a syndrome is often secondary to another underlying illness. Psychiatric disorders can present primarily with symptoms of catatonia. Mood disorders such as a bipolar disorder and depression are the most common causes to progress to catatonia. A psychotic disorder such as schizophrenia can also lead to catatonia, and historically schizophrenia recognition and diagnosis included symptoms of catatonia or was subtyped if catatonic symptoms were present. When catatonic symptoms present, the cause is likely psychiatric, but many medical etiologies can lead to catatonia. Neurologic insults such as strokes, neoplasms, or other diseases such as Parkinson Disease can lead to catatonia. Autoimmune, paraneoplastic, infectious, metabolic, and certain drug exposures and poisonings can lead to the development of catatonia. The differential for the cause of catatonia is very broad, and a new case of catatonia without a significant psychiatric history should be a cause for further evaluation for an underlying insult ²¹.

The pathophysiology of catatonia is not fully understood, but as imaging studies have improved more structures and pathways have been implicated in the pathogenesis of this syndrome. Using fMRI imaging, dysfunction has been seen in the right medial orbitofrontal and lateral orbitofrontal prefrontal cortex. The right motor cortex has shown atypical lateralization after patients who were suffering from catatonia were given lorazepam. Dysfunction in GABA, glutamate, serotonin, and dopamine transmissions have been implicated in the initiation and progression of catatonia symptoms through clinical findings of catatonia as a result of agents that disrupt these pathways or agents that affect these pathways relieving the symptoms of catatonia.

Catatonia symptoms

The initial presentation for catatonia can vary greatly due to the different subtypes that this syndrome can present. A lot of causes for catatonia can also make a typical presentation difficult to describe. As most patients with catatonia have a psychiatric illness primarily causing catatonia, a progression of psychiatric illness will be the most likely history.

A patient will often present with worsening depression, mania, or psychosis antecedent to catatonia symptoms beginning. These symptoms can present as excited, withdrawn, or a mixture. A patient presenting with excited catatonia will often have odd mannerisms such as performing actions without purpose or at inappropriate times (e.g., saluting). They may be agitated, hold odd positions against gravity, or have stereotypic and repetitive movements such as picking at their clothes or making odd gestures repeatedly. Their speech may be repetitive or mimic the interviewer’s speech or actions. A patient with withdrawn catatonia will likely be stuporous, hold an odd position, have no response or opposition to outside stimuli, and have very little speech. These symptoms may be present at some times and not at others, may be present in a combination, and vary in intensity throughout the hospital course. If these symptoms begin because of a secondary medical illness that illness may also cause other psychiatric symptoms such as mania or psychosis.

The physical exam for a patient with suspected catatonia can help to diagnose and differentiate it between other conditions such as neuroleptic malignant syndrome. Passive movement of limbs and the type of resistance encountered can reveal what the underlying condition is. If the patient has waxy flexibility and catalepsy (holds a posture against gravity when passively moved into a posture,) catatonia is high on the differential. If there is lead-pipe rigidity, neuroleptic malignant syndrome should be suspected. Spastic rigidity would indicate potential serotonin syndrome. Cogwheel rigidity is more concerning for extrapyramidal symptoms from neuroleptics.

Clinicians must identify comorbid disorders, including schizophrenia, mood disorders, and neurologic and medical conditions. Neuroleptic-induced parkinsonism may also be associated with catatonia. Headache, fever, and a stiff neck in an acutely ill patient suggest encephalitis. The presence of severe muscle rigidity, autonomic dysregulation, and hyperthermia suggests neuroleptic malignant syndrome (NMS). Acute psychosis is suggested by the presence of hallucinations, delusions, and suicidal and homicidal threats and behaviors.

A specific examination for catatonia using the Bush Francis Catatonia Rating Scale consists of:

• Observe the patient during normal conversation.
• Scratch the head in an exaggerated manner while speaking with the patient to see if they will copy the movement.
• Passively move the patient’s arm to examine for cogwheeling, varying the amount of force provided while telling the patient to keep their arm lose.
• Have the patient extend their arm and with one finger apply light pressure on their index finger while telling the patient, “Do not let me raise your arm.”
• Extend your hand for a handshake while telling the patient, “Do not shake my hand.”
• Reach into your pocket and state, “Stick out your tongue; I want to stick a pin in it.”
• Check for grasp reflex.
• Check oral intakes, vital signs, and for any instances of agitation.
• Each day, observe the patient indirectly for other symptoms of catatonia, including their activity level, abnormal movements and speech, echopraxia and echolalia, rigidity, negativism, waxy flexibility, gegenhalten (resistance equal to the amount of pressure applied), mitgehen (the patient raising their hand to the light pressure), ambitendency, automatic obedience, and grasp reflexes.

Catatonia complications

The following complications are associated with catatonia:

• May engage in violence or be involved in trauma as a result of the excited stage. During an excited state, patients with catatonia may cause serious, even fatal, injuries to themselves and others; they may cause marked destruction of property
• Develop autonomic instability. Patients with catatonia may experience autonomic instability manifested by hyperthermia, hypertension, and tachycardia; medical intervention is required
• Refuse to eat. Patients with catatonia may refuse to eat; death may result unless parenteral nutrition and fluids are administered on an involuntary basis
• Develop neuroleptic malignant syndrome
• Risk of DVT and pulmonary embolus. The risk of fatal pulmonary embolism is increased in catatonia; to prevent thromboembolic disease, fibrin D-dimer levels should be checked; if evidence of early coagulation activation is found, hematologic consultation is appropriate ¹⁶.
• Other – Patients with catatonia are at risk of complications from the underlying neurologic, psychiatric, medical, and obstetric causes of catatonia.

Catatonia diagnosis

While the diagnosis of catatonia is a clinical diagnosis that does not require specific lab tests or imaging, certain testing can help determine the underlying cause of the catatonia.

Physical examination

Because patients with catatonia may be unable to cooperate with the requests of the examiner, specific neurologic signs characteristic of catatonia must be quickly elicited, especially in emergency settings. In particular, rigidity, gegenhalten (passive resistance of the patient to the active movement of the patient’s extremities by the examiner), and a grasp reflex are readily apparent signs of catatonia in such settings ²². During the physical examination, it is also important to test for the presence of a grasp reflex, a secondary feature of catatonia.

Commonly observed signs in catatonia include the following:

• Immobility (hypokinesis or akinesis)
• Mutism (absence of speech)
• Stupor (decreased alertness and response to stimuli)
• Negativism (resistance to all instructions or all attempts to be moved)
• Waxy flexibility (slight, even resistance to positioning by examiner)
• Posturing
• Excitement (excessive, purposeless motor activity)
• Staring
• Echophenomena, including echolalia (senseless repetition of another person’s utterances) and echopraxia (senseless repetition of another person’s movements) ²³

Excited and immobile states

The predominant activity level is either markedly slow or extremely high, and the patient’s behavior may shift suddenly and unpredictably from one state to the other.

In the excited state, people with catatonia may injure themselves and assault others. They may also experience autonomic instability manifested by hyperthermia, tachycardia, and hypertension. Individuals in the excited state are at risk for collapse from exhaustion.

In the immobile state, the individual may not move. Akinesia and stupor are synonyms for this state. The patient may appear unresponsive to external stimuli. He or she may be unable to eat and therefore may die unless parenteral nutrition and fluids are administered. People with catatonia may exhibit catalepsy, the persistent maintenance of spontaneous or imposed postures.

Negativistic phenomena

Negativistic phenomena (eg, gegenhalten [“to hold against” in German; the apparent resistance of the movement of the extremities by the examiner], and mitgehen [“to go along with” in German; movement in the direction of a slight push from the examiner in spite of the command to remain still]) are typically observed in catatonia.

Examination should include checking for cogwheeling at the wrist and elbow. Patients should be instructed to keep their arms loose and limp (like a dead fish), and the arms should be moved with varying degrees of force. Rigidity is commonly elicited in the extremities of patients with catatonia.

The particular phenomenon of gegenhalten is characteristic. Patients with gegenhalten demonstrate increasing resistance to passive movement of the limbs. The patient appears to be deliberately opposing the movements of the examiner. Mitgehen is characterized by the patient moving in the direction of a slight push from the examiner in spite of the command to remain still. The physical examination should include tests for these.

Motor persistence (ie, maintenance of a posture when commanded not to maintain it) is a manifestation of catatonia that is associated with right hemispheric strokes. Other negativistic phenomena are withdrawal from all usual activities and refusal to eat.

Automatic obedience

In addition to negativistic phenomena, individuals with catatonia may display other behaviors, indicating inability to appropriately modulate the inhibition of impulses. For example, patients with catatonia may demonstrate automatic obedience, meaning the performance of tasks at the command of the examiner even though the tasks are inappropriate or dangerous.

Stereotypies

Peculiarities of movement are common in catatonia. Stereotypies, in which the patient repetitively performs apparently meaningless activities, are common. These may take the form of repetitive actions or sounds. Verbigeration (verbal stereotypies) refers to the presence of repetitive, apparently meaningless utterances, such as sniffing, clicking, snorting, and nonmeaningful sounds.

Common motor stereotypies include the following:

• Nose wrinkling
• Repetitive movements of the mouth and the jaw
• Repetitive eye movements
• Repetitive tapping of the foot, the finger, or the hand
• Repetitive abdomen patting, shoulder shrugging, or body rocking

Other movements associated with catatonia include mannerisms, postures, gaze fixation, and choreoathetoid movements of the trunk and extremities.

Perseveration

Patients with catatonia may also display perseveration (ie, the inappropriate repetition of acts).

Echophenomena

Echophenomena are typical in catatonia. Echolalia (repetition of the words spoken by the examiner) and echopraxia (repetition of the motor acts performed by the examiner) are common.

Verbal findings

In France, the inappropriately formal use of vous (the formal form of “you”) by the patient to address his or her spouse has been identified as a finding in catatonia. Normally, tu (the informal form of “you”) is used by an individual to address a spouse.

Psychogenic movement disorders

Patients with catatonia exhibit the same general behaviors whether or not the examiner is present. If a patient demonstrates behaviors consistent with catatonia only in the presence of the examiner, then catatonia is unlikely, and conditions characterized by the presence of medical symptoms and signs without physical illness must be considered.

More specifically, catatonia that occurs only when the patient is directly observed by the examiner suggests the presence of somatoform disorders, factitious disorders, or malingering. In the movement disorders literature, somatoform disorders, factitious disorders, and malingering in patients exhibiting abnormal movements are commonly classified as psychogenic movement disorders.

Patients with somatoform disorders (eg, somatization disorder, conversion disorder, and hypochondriasis) report symptoms and signs that they truly believe they have, despite the absence of confirmation on physical examination. Patients with factitious disorders and malingering deliberately report symptoms and signs that they know to be false.

Patients with Munchausen syndrome and other factitious disorders fabricate symptoms and signs because they want to be patients. In Munchausen syndrome by proxy, the parents of the patient (who is typically an infant unable to communicate) fabricate symptoms and signs in the patient.

Unlike patients with factitious disorders, patients with malingering deliberately report false symptoms and signs for specific gain—for example, to obtain disability benefits and to be excused from work.

Laboratory studies

Laboratory studies that may be useful include the following:

• Complete blood count (CBC)
• Electrolyte concentrations
• Chemical analyses of blood
• Fibrin D-dimer. Fibrin D-dimer levels must be obtained to rule out early coagulation activation
• ¹⁶. Patients with catatonia typically have fibrin D-dimer levels higher than 500 ng/mL ¹⁶. Prompt identification and treatment of pulmonary embolism in people with catatonia are crucial for minimizing morbidity and mortality ²⁴.
• Serum creatine kinase level
• Liver function tests
• Serum ceruloplasmin level

To rule out neuroleptic malignant syndrome, immediate evaluation of the serum creatine kinase level, white blood cell (WBC) counts, and liver function test results is warranted. Measurement of serum ceruloplasmin is needed to rule out Wilson disease. In addition, encephalitis must be ruled out.

Imaging studies and electroencephalography

Imaging is mainly useful for ruling out other treatable disorders. Modalities that may be helpful include the following:

• Magnetic resonance imaging (MRI)
• Computed tomography (CT)
• Single-photon emission CT (SPECT)
• Positron emission tomography (PET) with fluorodeoxyglucose (FDG)
• Electroencephalography (EEG) is indicated to rule out a seizure disorder, a space-occupying lesion, and generalized abnormalities.

An EEG in a patient with primary catatonia due to a psychiatric disorder will likely have diffuse slowing on EEG. As a post-ictal state can cause catatonia, an EEG may be helpful in detecting seizure activity driving the syndrome. While an MRI or CT scan cannot show catatonia, brain imaging could show abnormalities which are causing the catatonia. Imaging of the rest of the body may reveal neoplasms causing a paraneoplastic encephalitis. Metabolic screens for illnesses such as diabetic ketoacidosis, glomerulonephritis, hepatic dysfunction, or other abnormalities may reveal a reversible cause. Inflammatory markers and autoantibodies may show autoimmune causes for catatonia. Overall in a patient with new onset catatonia, psychiatric causes should be considered first, but somatic causes should not be ignored, especially if an underlying mental illness does not easily explain the clinical picture ²⁵.

Catatonia treatment

The initial treatment, once potential catatonia causing agents such as neuroleptics, steroids, stimulants, anticonvulsants, dopamine depleters, and others, are stopped, is to provide a lorazepam “challenge.” By giving a dose such as lorazepam 2 mg IV slowly, 60% – 80% of patients with catatonia will have some or significant improvement in catatonia symptoms within 15 min – 30 min. If the patient responds to this lorazepam challenge, lorazepam can be subsequently scheduled at interval doses, often three times a day (though different patients respond at different rates.) The dose of lorazepam can be titrated until catatonia symptoms resolve. Paradoxically catatonic patients do not become sedated on benzodiazepines. Once the dose is titrated for efficacy, patients will be alert and interactive. Throughout this titration, the patient’s underlying cause should also be treated. This lorazepam dose can be slowly tapered as tolerated. If this tapering occurs too quickly, catatonia symptoms may return. Some patients require tapering over months. When the dose makes the patient sedated instead of active, it can likely be reduced ²⁶.

If the patient’s catatonic symptoms do not respond to benzodiazepines, and the underlying cause either cannot be treated or treating it does not improve the symptoms, electroconvulsive therapy (ECT) can be used to reverse the symptoms. Another indication for ECT (electroconvulsive therapy) is malignant catatonia – a catatonic syndrome characterized by fever, hypertension, tachycardia, and tachypnea which can progress to death.

Catatonia prognosis

With treatment, the response rate varies from 50% to 70% and the prognosis is good. However, those who fail to respond to medications have a very poor prognosis. Many of these individuals require continuous mental healthcare and suicides are commonly reported. Further, patients with catatonia are at a very high risk for thrombosis and pulmonary embolism. Finally, those who have catatonia in the presence of schizophrenia have a much worse prognosis than those who do not have schizophrenia ²⁷.

Carroll ²⁸ noted that studies of catatonia have reported recovery rates from 12% to more than 40%, regardless of the treatment administered. A response to benzodiazepines has been reported in more than 70% of patients with catatonia who undergo treatment. Failure to institute treatment early in the course of catatonia is associated with a poor prognosis.

Bonnot et al ²⁹ reported that children with childhood schizophrenia and catatonia have more severe symptoms and a longer duration of illness than do children with childhood schizophrenia without catatonia. They concluded that catatonia has deleterious effects beyond mere motor symptoms in children with schizophrenia.

Catatonia in adolescents also has a poor prognosis. In a prospective follow-up study of 35 people aged 12-18 years with catatonia, 20 of the 31 patients identified for follow-up had schizophrenia, 5 had major depression, 1 had bipolar disorder type 1, and 2 had brief psychiatric episodes ³⁰. At follow-up, 3 deaths were recorded, including 2 suicides. A causal organic disorder was identified for 6 at follow-up. At follow-up, 14 people needed continuous psychiatric care ³⁰.

In Monroe County, New York, the age-adjusted relative risk of death for people with catatonic schizophrenia was 3-fold greater that for the county population during the period 1960-1969. However, the risk of death was no higher than with other forms of schizophrenia or other types of mental illness ³¹.

People with catatonia apparently are at increased risk for death from thromboembolic diseases ¹⁶. Adults with catatonia and schizophrenia have a more prolonged course than those with catatonia without schizophrenia ³².

References

1. Fink M and Taylor MA. The catatonia syndrome: forgotten but not gone. Arch Gen Psychiatry. 2009. 66:1173.
2. James LL. Medical aspects of catatonia. Prim Psychiatry. 2009;16:23–6.
3. Wilcox JA and Reid DP. The syndrome of catatonia. Behav Sci (Basel). 2015;5(4):576-88.
4. Burrow JP, Marwaha R. Catatonia. [Updated 2018 Dec 2]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430842
5. Park J, Tan J, Krzeminski S, et al. Malignant catatonia warrants early psychiatric-critical care collaborative management: two cases and literature review. Case Rep Crit Care. 2017;2017:1951965.
6. Dabrowski M and Parnowski T. Clinical analysis of safety and effectiveness of electroconvulsive therapy. Psychiatr Pol.2012;46(3):345-60.
7. Lang FU, Lang S, Becker T, et al. Neuroleptic malignant syndrome or catatonia? Trying to solve the catatonic dilemma. Psychopharmacology (Berl). 2015;232(14):1-5.
8. Rosebush PI, Hildebrand AM, Furlong BG, et al. Catatonic syndrome in a general psychiatric inpatient population: frequency, clinical presentation, and response to lorazepam. J Clin Psychiatry. 1990;51(9):357-62.
9. Tuerlings JH, van Waarde JA, Verwey B. A retrospective study of 34 catatonic patients: analysis of clinical care and treatment. Gen Hosp Psychiatry. 2010;32(6):631-5
10. Van Waarde JA, Tuerlings JH, Verwey B, et al. Electroconvulsive therapy for catatonia: treatment characteristics and outcomes in 27 patients. J ECT. 2010;26(4):248-52.
11. Tormoehlen LM, Rusyniak DE. Neuroleptic malignant syndrome and serotonin syndrome. Handb Clin Neurol. 2018;157:663-675.
12. Fischel T, Krivoy A, Brenner I, Weizman A. Priapism as an unusual manifestation of catatonia: a case report. Prog Neuropsychopharmacol Biol Psychiatry. 2009 Apr 30. 33(3):570.
13. Vesperini S, Papettia F, Pringuey D. Existe-t-il un lien entre catatonie et syndrome malin des neuroleptiques ? [Are catatonia and neuroleptic malignant syndrome related conditions?]. L’Encéphale. 2009.
14. Chouinard MJ, Nguyen DK, Clement JF, Bruneau MA. Catatonia induced by levetiracetam. Epilepsy Behav. 2006 Feb. 8(1):303-7.
15. Youssef NA, Benazzi F, Desan PH. Levofloxacin-induced catatonia. Prog Neuropsychopharmacol Biol Psychiatry. 2009 Jun 15. 33(4):741-2.
16. Haouzir S, Lemoine X, Desbordes M, Follet M, Meunier C, Baarir Z, et al. The role of coagulation marker fibrin D-dimer in early diagnosis of catatonia. Psychiatry Res. 2009 Jun 30. 168(1):78-85.
17. Pesyna C, Benson L, Lacy M, Cooper J. Excited Catatonia With a Normal Video EEG: a Case of Anti-NMDA Receptor Encephalitis. J Neuropsychiatry Clin Neurosci. 2014. 26:2
18. Rizos DV, Peritogiannis V, Gkogkos C. Catatonia in the intensive care unit. Gen Hosp Psychiatry. 2011 Jan-Feb. 33(1):e1-2.
19. Nielsen N, Nielsen NB. [Malignant neuroleptic syndrome in a 15-year old girl after a single injection of a high-dose neuroleptic]. Ugeskr Laeger. 1991 Aug 5. 153(32):2239-40.
20. Catatonia. https://emedicine.medscape.com/article/1154851-overview
21. Leroy A, Corfiotti C, Nguyen The Tich S, Ferrafiat V, Amad A, Jardri R, Medjkane F. Catatonia Associated With a SCN2A-Related Disorder in a 4-Year-Old Child. Pediatrics. 2018 Nov;142, 5
22. Brasic JR, Barnett JY, Will MV, Nadrich RH, Sheitman BB, Ahmad R, et al. Dyskinesias differentiate autistic disorder from catatonia. CNS Spectr. 2000 Dec. 5(12):19-22.
23. Zisselman MH, Jaffe RL. ECT in the treatment of a patient with catatonia: consent and complications. Am J Psychiatry. 2010 Feb. 167 (2):127-32.
24. Larsen HH, Ritchie JC, McNutt MD, Musselman DL. Pulmonary embolism in a patient with catatonia: an old disease, changing times. Psychosomatics. 2011 Jul-Aug. 52(4):387-91.
25. Sorg EM, Chaney-Catchpole M, Hazen EP. Pediatric Catatonia: A Case Series-Based Review of Presentation, Evaluation, and Management. Psychosomatics. 2018 Nov;59(6):531-538.
26. Mihaljević-Peleš A, Bajs Janović M, Stručić A, Šagud M, Skočić HanŽek M, Živković M, Janović Š. Electroconvulsive therapy – general considerations and experience in Croatia. Psychiatr Danub. 2018 Jun;30(Suppl 4):188-191.
27. Doran E, Sheehan JD. Acute catatonia on medical wards: a case series. J Med Case Rep. 2018 Jul 06;12(1):206.
28. Carroll BT. Kahlbaum’s catatonia revisited. Psychiatry Clin Neurosci. 2001 Oct. 55(5):431-6.
29. Bonnot O, Tanguy ML, Consoli A, Cornic F, Graindorge C, Laurent C, et al. Does catatonia influence the phenomenology of childhood onset schizophrenia beyond motor symptoms?. Psychiatry Res. 2008 Apr 15. 158(3):356-62.
30. Cornic F, Consoli A, Tanguy ML, Bonnot O, Périsse D, Tordjman S, et al. Association of adolescent catatonia with increased mortality and morbidity: evidence from a prospective follow-up study. Schizophr Res. 2009 Sep. 113(2-3):233-40.
31. Guggenheim FG, Babigian HM. Catatonic schizophrenia: epidemiology and clinical course. A 7-year register study of 798 cases. J Nerv Ment Dis. 1974 Apr. 158(4):291-305.
32. Krishna KR, Maniar RC, Harbishettar VS. A comparative study of “idiopathic catatonia’’ with catatonia in schizophrenia. Asian J Psych. 2011. 4:129-33.