Showing posts with label Catatonia. Show all posts
Showing posts with label Catatonia. Show all posts

Thursday, 19 May 2022

The Modified Rogers Scale

The Modified Rogers Scale

It rates abnormalities in movement, volition, speech, and overall behaviour and aids in the distinction of catatonic signs from similar extrapyramidal side effects. It has eleven items, out of which three or more constitute a diagnosis of catatonic syndrome.


The following are the items included in the Modified Rogers Scale.

  1. Stupor
  2. Mutism
  3. Negativism
  4. Opposition
  5. Posturing
  6. Catalepsy
  7. Automatic obedience
  8. Echophenomena
  9. Rigidity
  10. Verbigeration
  11. Withdrawal.
For information on other scales used in catatonia, see Rating Scales for Catatonia

The Bush–Francis Catatonia Rating Scale

The Bush–Francis Catatonia Rating Scale 

The Bush–Francis Catatonia Rating Scale, has been widely recommended for its ease of use and reliability and validity. In this scale, the presence of two or more signs is suggestive of catatonia.

Is the most widely used instrument for catatonia. The Bush–Francis Catatonia Rating Scale has twenty-three items, and there is also a shorter, 14-item screening version. The reliability and validity of the Bush–Francis Catatonia Rating Scale has been established (Bush et al, 1996). The screening section marks items #1-14 as either “absent” or “present.” The full-scale rates items #1-23 on a scale of 0-3. The ratings are made based on the observed behaviours during the examination, except for completing the items for “withdrawal” and “autonomic abnormality,” which may be based upon either observed b behaviours/or chart documentation. Rate items only if well defined. If uncertain, rate the item as “0”.

Using the Bush–Francis Catatonia Rating Scale, 32% of 225 patients with chronic schizophrenia meet the criteria for catatonia. See Ungvari et al., 2005. 

It has two subscales

  1. A screening instrument with fourteen items that are marked as either present or absent.  

  2. The full severity scale with nine extra items scored zero to three.

Ungvari GS, Leung SK, Ng FS, Cheung HK, Leung T. Schizophrenia with prominent catatonic features ('catatonic schizophrenia'): I. Demographic and clinical correlates in the chronic phase. Prog Neuropsychopharmacol Biol Psychiatry. 2005;29(1):27-38. doi: 10.1016/j.pnpbp.2004.08.007

Tuesday, 10 May 2022



Catatonia involves a significant psychomotor disturbance, which can occur as catalepsy, stupor, excessive purposeless motor activity, extreme negativism (seemingly motiveless resistance to movement), mutism, and echolalia (imitating speech), or echopraxia (imitating movements).

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Adapted from Wikipedia. Text is available under the Creative Commons Attribution-ShareAlike License 3.0; additional terms may apply.

Sunday, 10 January 2021

Organic Causes of Stupor and Catatonia

A plethora of medical conditions can cause catatonia and stupor.

(Reviewed by: Serra-Mestres et. al, 2018)  

  • Subarachnoid hemorrhages, Basal ganglia disorders
  • Non‐convulsive status epilepticus 
  • Locked‐in and akinetic mutism states 
  • Endocrine and metabolic disorders, e.g. Wilson’s disease, hypoxia 
  • Down syndrome, Infections, Dementia
  • Drug toxicity and withdrawal states, even clozapine

Thursday, 7 January 2021

Glutamate Antagonists for the Treatment of Catatonia

Because of its N-methyl-d-aspartic acid antagonist properties, amantadine (100–500mg three times a day), and its derivative memantine (5–20mg/day), have been tried in catatonia.

  1. Carroll and coworkers identified 25 cases of amantadine and memantine use in the treatment of catatonia. All cases improved, mostly after 1–7days.

  2. It should be noted, however, that six were unpublished, and that seven other were cases experiencing a “catatonia-parkinsonian syndrome” while under treatment with the high-potency neuroleptic drugs haloperidol or fluphenazine.
  3. The symptoms diminished when neuroleptics were tapered, and they added amantadine. Since then, they have published eleven additional cases describing the successful use of amantadine or memantine in catatonia.
  4. In one case, in an adolescent girl, catatonia that was resistant to ECT improved after the addition of amantadine.
  5. Only in a review of Hawkins and coworkers, they report a case in which the use of amantadine remained without effect. Should acknowledge, however, that negative cases are less likely to be published.
  6. Given these positive signals in the published literature, and evidence of its efficacy in treating the negative and cognitive symptoms of schizophrenia, amantadine should be further studied as a feasible treatment option for catatonia. There is anecdotal evidence from case reports on the use of various other pharmacological agents, such as bromocriptine and biperiden.
  7. Based on the GABA-hypothesis of catatonia, and the GABA-related working mechanism of several anti-convulsive mood stabilizers, these drugs have been proposed as a viable treatment option to treat catatonia in bipolar patients.
  8. Only a few cases have published reports.
  9. They used valproate in several case reports and found not only to have prophylactic effects but also “an improving effect on the catatonic symptoms”.
  10. In a solitary case report, they advocated levetiracetam as a treatment for catatonia in bipolar disorder, given its mood-stabilizing efficacy.
  11. It is of note, however, that levetiracetam has also been described to provoke catatonia.
  12. Using topiramate and carbamazepine have also been reported.
  13. Although lithium has been anecdotally reported to have a beneficial effect on acute catatonic symptoms, they mostly describe it to be of use in the prevention of recurrent catatonia, albeit with sometimes limited results.


  1. Carroll BT, Goforth HW, Thomas C, Ahuja N, McDaniel WW, Kraus MF, et al. Review of adjunctive glutamate antagonist therapy in the treatment of catatonic syndromes. J Neuropsychiatry Clin Neurosci (2007) 19(4):406–12.10.1176/appi.neuropsych.19.4.406  
  2. Gelenberg AJ, Mandel MR. Catatonic reactions to high-potency neuroleptic drugs. Arch Gen Psychiatry (1977) 34(8):947–50.10.1001/archpsyc.1977.01770200085010  
  3. Obregon DF, Velasco RM, Wuerz TP, Catalano MC, Catalano G, Kahn D. Memantine and catatonia: a case report and literature review. J Psychiatr Pract (2011) 17(4):292–9.10.1097/01.pra.0000400268.60537.5e  
  4. Babington PW, Spiegel DR. Treatment of catatonia with olanzapine and amantadine. Psychosomatics (2007) 48(6):534–6.10.1176/appi.psy.48.6.534  
  5. Muneoka K, Shirayama Y, Kon K, Kawabe M, Goto M, Kimura S. Improvement of mutism in a catatonic schizophrenia case by add-on treatment with amantadine. Pharmacopsychiatry (2010) 43(4):151–210.1055/s-0029-1242821  
  6. Hervey WM, Stewart JT, Catalano G. Treatment of catatonia with amantadine. Clin Neuropharmacol (2012) 35(2):86–710.1097/WNF.0b013e318246ad34  
  7. de Lucena DF, Pinto JP, Hallak JE, Crippa JA, Gama CS. Short-term treatment of catatonia with amantadine in schizophrenia and schizoaffective disorder. J Clin Psychopharmacol (2012) 32(4):569–7210.1097/JCP.0b013e31825ebf6e  
  8. Ene-Stroescu V, Nguyen T, Waiblinger BE. Excellent response to amantadine in a patient with bipolar disorder and catatonia. J Neuropsychiatry Clin Neurosci (2014) 26(1):E43.10.1176/appi.neuropsych.13020038  
  9. Mahmood T. Bromocriptine in catatonic stupor. Br J Psychiatry (1991) 158:437–810.1192/bjp.158.3.437  
  10. Franz M, Gallhofer B, Kanzow WT. Treatment of catatonia with intravenous biperidene. Br J Psychiatry (1994) 164(6):847–810.1192/bjp.164.6.847b  
  11. DelBello MP, Foster KD, Strakowski SM. Case report: treatment of catatonia in an adolescent male. J Adolesc Health (2000) 27(1):69–7110.1016/S1054-139X(00)00109-9  
  12. Kruger S, Braunig P. Intravenous valproic acid in the treatment of severe catatonia. J Neuropsychiatry Clin Neurosci (2001) 13(2):303–410.1176/appi.neuropsych.13.2.303  
  13. Bowers R, Ajit SS. Is there a role for valproic acid in the treatment of catatonia? J Neuropsychiatry Clin Neurosci (2007) 19(2):197–810.1176/appi.neuropsych.19.2.197  
  14. Yoshida I, Monji A, Hashioka S, Ito M, Kanba S. Prophylactic effect of valproate in the treatment for siblings with catatonia: a case report. J Clin Psychopharmacol (2005) 25(5):504–510.1097/  
  15. Muneer A. Catatonia in a patient with bipolar disorder type I. J Neurosci Rural Pract (2014) 5(3):314–610.4103/0976-3147.133652 [PMC free article]  
  16. Chouinard MJ, Nguyen DK, Clement JF, Bruneau MA. Catatonia induced by levetiracetam. Epilepsy Behav (2006) 8(1):303–7.10.1016/j.yebeh.2005.04.016  
  17. McDaniel WW, Spiegel DR, Sahota AK. Topiramate effect in catatonia: a case series. J Neuropsychiatry Clin Neurosci (2006) 18(2):234–8.10.1176/appi.neuropsych.18.2.234  
  18. Rankel HW, Rankel LE. Carbamazepine in the treatment of catatonia. Am J Psychiatry (1988) 145(3):361–2.   
  19. Wald D, Lerner J. Lithium in the treatment of periodic catatonia: a case report. Am J Psychiatry (1978) 135(6):751–2.   
  20. Pheterson AD, Estroff TW, Sweeney DR. Severe prolonged catatonia with associated flushing reaction responsive to lithium carbonate. J Am Acad Child Psychiatry (1985) 24(2):235–710.1016/S0002-7138(09)60454-4  
  21. Gjessing LR. Lithium citrate loading of a patient with periodic catatonia. Acta Psychiatr Scand (1967) 43(4):372–510.1111/j.1600-0447.1967.tb05774.x  

Zolpidem for the Treatment of Catatonia

Zolpidem, a positive allosteric modulator of gamma-aminobutyric acid receptors, seems to be a safe and effective treatment alternative. 

Benzodiazepines for the Treatment of Catatonia

Benzodiazepines for the Treatment of Catatonia

Benzodiazepines are the first-choice treatment for catatonia, regardless of the underlying condition. Benzodiazepines are positive allosteric modulators of GABA-A receptors and will correct deficient GABA-ergic function in the orbitofrontal cortex.

Following a positive Lorazepam Challenge Test, repeated doses of benzodiazepines can a treatment. Their use is safe, easy, and effective, with remission rates reported to be as high as 70–80%.

About 65% Rates in a Naturalistic Study

In a naturalistic study of 66 children and adolescents with catatonia, they found that benzodiazepines improved catatonia in 65% of cases, that there was no relation between dose and level of improvement, that the dose was higher sometimes (up to 15 mg of lorazepam) than the dose recommended in pediatric patients, and that side effects were few.

Two-thirds Improved in a Trial of 107 adults

In a recent trial in 107 adult inpatients (49% with a psychotic disorder; 44% with a mood disorder), lower success rates they reported lower success rates: two-thirds responded but only one-third of patients remitted. The authors argue that a delay between illness onset and treatment could explain the lower remission rate) but the doses used in the trial (3–6 mg per day) were inadequately low. As described above, studies have repeatedly shown that chronic catatonia associated with schizophrenia is less responsive to benzodiazepines.

Beckmann and Colleagues Found them Ineffective

Beckmann and colleagues, in a 5-year follow-up study, found benzodiazepines ineffective in the treatment of chronic catatonic schizophrenia. Another study reported a comparable poor response (to lorazepam 6 mg per day); it was a randomized double-blind, placebo-controlled trial in 18 patients with chronic catatonia in schizophrenia.

Efficacy Depends on Dose

Efficacy of benzodiazepines in catatonia depends on dosage, and doses from 8 to 24 mg lorazepam per day are common and are tolerated without ensuing sedation, especially when instituted using daily incremental dosages. Most authors suggest starting at 1–2 mg of lorazepam every 4–12 h and adjusting the dose in order to relieve catatonia without sedating the patient. With an adequate dose, we usually see a response within 3–7 days, but sometimes, the response can be gradual. If we use high dosages of lorazepam, patients should be monitored carefully for excessive sedation and respiratory compromise. Whether some benzodiazepines are more efficacious in catatonia is not clear yet.

Clinicians accept lorazepam to be the first-choice drug, demonstrating a 79% remission rate and the highest frequency of use. Studies have also reported the successful use of diazepam, oxazepam, or clonazepam. There is no consensus on how long benzodiazepines to continue benzodiazepines, and we discontinue them once the underlying illness has remitted. In several cases, however, catatonic symptoms will emerge each time lorazepam is tapered off, urging the clinician to continue benzodiazepines for an extended period.

Evaluation, Differential Diagnosis, and Treatment of Catatonia


Evaluation, Differential Diagnosis, and Treatment


Effective treatment starts with a swift and correct diagnosis. In any patient exhibiting marked deterioration in psychomotor function and overall responsiveness, we should consider catatonia. Any patient that is admitted to a psychiatric ward with a severe psychiatric disorder, such as depression, bipolar disorder, a psychotic disorder, or autism spectrum disorder, should be examined routinely. Some signs and symptoms are clear upon observation of the patient during a psychiatric interview. Other specific symptoms, however, such as automatic obedience, ambitendency, negativism should be elicited during a neuropsychiatric examination.


We can use a rating scale as a screening instrument and aid in the detection and quantification of catatonia. We have found several rating scales reliable, sensitive, and specific:

  1. Rogers Catatonia Scale
  2. Bush-Francis Catatonia Rating Scale
  3. Northoff Catatonia Rating Scale
  4. Braunig Catatonia Rating Scale
Early detection of catatonia is of great importance, since catatonic signs possess significant prognostic and therapeutic value.


Unfortunately, no laboratory test specifically defines catatonia. The “diagnostic weight” of several proposed laboratory and imaging tests is limited. Laboratory tests, primarily to assess various underlying conditions, including a complete blood count and metabolic panel, erythrocyte sedimentation rate, blood urea nitrogen, creatinine, serum iron, and creatinine-phosphokinase, antinuclear antibodies, and urinalysis, and magnetic resonance imaging, electroencephalogram, cerebrospinal fluid analysis. Given the frequent association with anti-NMDAR-encephalitis, detection of IgG antibodies to NMDAR in cerebrospinal fluid or serum is advisable. Since we found serum iron to be reduced in NMS compared to catatonia, some authors see low serum iron as a risk factor for developing NMS after using antipsychotics in a catatonic patient. A drug screen to detect common illicit and prescribed substances is necessary.

An Overview of Catatonia

An overview of Catatonia

Catatonia is a severe motor syndrome with an estimated prevalence among psychiatric inpatients of about 10%. Catatonia can accompany many psychiatric illnesses and somatic diseases. A minority of catatonic patients suffer from schizophrenia, while a majority has a bipolar disorder. They have also linked catatonia to other psychiatric disorders, such as obsessive-compulsive disorder, post-traumatic stress disorder, or withdrawal from alcohol or benzodiazepines. In up to 25% of cases, they relate catatonia with general medical or neurologic conditions. Recent studies show repeatedly that catatonic symptoms are observable in most patients diagnosed with anti-N-methyl-d-aspartate receptor encephalitis. In adolescents and young adults with autism, we find catatonia in 12–17%. Pediatric catatonia also emerges in patients with tic disorders, and a variety of other (developmental) disorders. The same principles of evaluation and treatment seem to apply to pediatric patients as in adult patients.

Lethal Catatonia

A life-threatening situation occurs when catatonia manifests with fever and autonomic abnormalities. Malignant catatonia, as Stauder in 1934 coined “lethal catatonia”, presents as a constellation of catatonia, stuporous exhaustion, autonomic instability, respiratory failure, collapse, coma, and often death if left untreated. This clinical picture is remarkably close to what we observe in neuroleptic malignant syndrome, which several experts consider a drug-induced form of catatonia.

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