For the NHS to take someone off psychiatric medication this means that something they have discovered is wrong. The Drug Paliperidone was prescribed at the following hospitals:

Chase Farm Hospital Enfield

St Pancreas Hospital Ruby Ward

Cygnet Godden Green

Elysium Thornford Park

The Discharge Note points to CNS and all physical health but and no-one wishes to say what it is. The GP Surgery said they were told it was a mistake by Admininistration staff however we know this to be a lie. When I have confronted professionals to say that what they were doing was wrong the response has been one of arrogance. When I called at Chase Farm Hospital’s Foyer and complained that no-one could get through to Elizabeth and that we as a family were concerned. I was shown into an office on ground floor by SE with two others present.

When I complained about the medication Paliperidone (Risperidone Depot) previously found to be allergic to the response from AB was “Are you a Doctor or Nurse?” to which I replied “no” – I am just a mother. Her response then was “I went to University and I have a degree in nursing”. In other words you as a parent/carer are seen as nothing – your concerns are dismissed in that how could a parent/carer have a clue about the prescribed drugs. So I then stated that I had 5/6 drugs charts to indicate allergy to Risperidone. The RC told Elizabeth that “Risperidone is not Paliperidone” however I turned to leading experts for advice on the drugs/drug metabolism.

Take a look at the following:

In conclusion, catatonia could be observed several weeks after titration to a therapeutic dose of paliperidone in a patient without other psychiatric or medical comorbidity. Prompt discontinuation of the implicated drug and giving benzodiazepines are beneficial in patients presenting with catatonic symptoms associated with antipsychotics.

Author: Chao-Ying Tu, Yi-Ling Chien, Wei-Lieh Huang

Risperidone, an atypical antipsychotic, has been reported to induce catatonia in several patients, 1 4 Paliperidone, a major active metabolite of risperidone, was approved by the United States Food and Drug Administration (FDA) in December, 2006, for the treatment of schizophrenia.

Catatonia Associated with Initiating Paliperidone Treatment

Nathanael Mckeown

James H Bryan

Zane Horowitz

Catatonia Associated with Initiating Paliperidone Treatment *Oregon Health & Science University, Department of Emergency Medicine, Oregon Poison Control Center, Portland VA Supervising Section Editor: Eric D. Isaacs, MD Submission history:

Submitted May 1, 2008; Revision Received October 15, 2009; Accepted October 25, 2009 Reprints available through open access at

We present a case of catatonia, which occurred shortly after starting a new antipsychotic, paliperidone, an active metabolite of risperidone.

Catatonia may be caused by a variety of conditions, including metabolic, neurologic, psychiatric and toxic processes.

Interestingly, risperidone, which has been thought to cause several cases of catatonia, has also been recommended as a potential treatment.

We discuss potential mechanisms for causes of drug-induced catatonia as well as potential treatment options. [West J Emerg Med. 2010; 11(2):186-188.]

INTRODUCTION Catatonia can be caused by a variety of metabolic, neurologic, psychiatric, and toxic conditions. Risperidone, an atypical antipsychotic, has been reported to induce catatonia in several patients,1,2 although paradoxically, antipsychotics, including risperidone, have been used successfully to treat catatonia.3,4 Paliperidone, a major active metabolite of risperidone, was approved by the United States Food and Drug Administration (FDA) in December, 2006, for the treatment of schizophrenia.

We report what we believe is the first case of catatonia temporally related to paliperidone, after a single dose.

CASE REPORT An 84-year-old female with history of major depression and anxiety was evaluated by her psychiatrist for worsening anxiety and given a single dose of 3 mg of paliperidone. Eight hours later she became increasingly agitated and, according to her daughter, “looked like she was going to crawl out of her skin.” She then told her daughter “make it go away, make it go away,” and subsequently stopped speaking and responding to any physical or verbal stimuli, although she appeared awake and alert. She had no prior documented episodes of catatonia. Her daughter brought her into the local emergency department (ED). In the ED, she had a temperature of 37.3°C, pulse 80 beats per minute, blood pressure 161/72 mm Hg, respiratory rate 20 breaths per minute and oxygen saturation of 98% on room air. Her medications were citalopram, trazodone, levothyroxine, and paliperidone. She lived with her daughter, who related no recent trauma. The patient previously took risperidone, but it had been discontinued after several months because of mild akathisia, with both restlessness and tremor. Physical exam showed an alert, well appearing elderly female in no acute distress. Her pupils were equal round and reactive to light; she would not comply with extraocular muscle testing. She did open her mouth on request and stuck out her tongue midline; there was no erythema, and mucous membranes were moist. Cardiopulmonary exam was unremarkable; abdominal palpation did not cause any change in her facial expression and was soft without masses. While she complied with several requests for the cranial nerve exam she would not move her fingers or toes when asked, but was noted to turn her head in all directions and roll from side to side, moving all extremities equally. Her brachioradialis and achilles reflexes were equal and Babinski reflexes were downgoing. She exhibited stupor and mutism with fixed postures. Finger-stick glucose was 114 mg/dL. Intravenous diphenhydramine, 25 mg and benztropine, 0.5 mg were given for dystonia without any change. Noncontrast head computed tomography (CT) was performed due to concern for stroke and was unremarkable. Laboratory tests showed white blood cell count of 7.4 K/mm3 with 60% neutrophils, her hematocrit was 37.6%, and platelets were 203 K/mm3 . Electrolytes and renal function showed sodium 135 mmol/L, potassium 3.5 mmol/L, chloride 101 mmol/L, bicarbonate 20 mmol/L, calcium 9.8 mg/dL, blood urea nitrogen 12 mg/dL, and creatinine 1.0 mg/dL. Due to the lack of inpatient psychiatric beds, she was observed in the ED for 12 hours. Psychiatric consultation had no specific recommendations. Sixteen hours after the dose Western Journal of Emergency Medicine 187 Volume XI, no. 2 : May 2010 of paliperidone, without other therapy, she began to talk and interact. More detailed neurological exam showed no focal deficits. Her mood and affect were appropriate. She did not recall the events of the previous evening but remembered her daughter talking, although she was unable to respond. DISCUSSION

Catatonia is a neuropsychiatric syndrome characterized by a combination of mental, motor, vegetative, and behavioral signs and symptoms.

It has been described as a syndrome with prominent motor signs, with positivistic or excitatory symptoms, including mitgehen, in which there are excited movements with light stimulation, even with instructions to the contrary.

Other signs include stupor, immobility, mutism, and negativism, including gegenhalten (increasing resistance to passive movement of the limbs), waxy flexibility, posturing, stereotypic movements, echolalia, and echopraxia.6 Mutism and stupor are generally regarded as principal signs of catatonia, although neither are certainly pathognomonic.

The Diagnostic and Statistical Manual of Mental Disorders, DSM – IV, defines catatonia as the presence of at least two of the following: motoric immobility, excessive motor activity, extreme negativism/mutism, posturing/ stereotyped movements/prominent mannerisms or grimacing, and echolalia or echopraxia.6 Our patient exhibited several of these features, including immobility, with posturing at times, and extreme negativism, including mutism.

While her presenting differential was broad, lack of fever, headache, and a normal white count were inconsistent with infection. A lumbar puncture was not obtained, but complete reversal of symptoms without other therapy would also argue against meningitis or encephalitis. Non-convulsive status epilepticus or partial complex seizures should also be considered, although there was no history of a previous seizure disorder. An electroencephalogram (EEG) should be obtained if clinical suspicion warrants.

Catatonia has been associated with schizophrenia, major depressive disorder, as well as other medical conditions, including alcoholism, bi-frontal tumors, encephalitis, transient ischemic attack, chronic obstructive pulmonary disease, rheumatic heart disease, Alzheimer’s and vascular dementia, central diabetes insipidus, closed head injury, end stage renal disease, and renal tubular acidosis.8 Neuroleptic malignant syndrome, as well as severe extrapyramidal reactions, may also present initially with catatonic features, and has been considered by some to be a subset of catatonia.9 While no studies have specifically evaluated the prevalence of drug-induced catatonia, studies regarding general causes of catatonia suggest that 17-19% of all cases diagnosed as medical catatonia are actually drug-induced catatonia.

Another study found that antipsychotic-induced catatonia accounted for 24% of all catatonic patients referred to the ED of a general hospital.

Drug-induced catatonia has mostly been reported with psychotropic drugs, including fluphenazine, haloperidol, risperidone, and clozapine, non-psychotropic drugs such as steroids, disulfiram, ciprofloxacin, several benzodiazepines, as well as drugs of abuse, including phencyclidine, cannabis, mescaline, LSD, cocaine and ecstasy.

While psychiatric disorders may simply cause catatonia, it does appear that medications themselves can either cause or unmask an underlying predisposition to catatonia. The mechanism by which medications cause catatonia is not known. Mechanisms have been proposed based on animal models: 1) dopamine hypoactivity at the D2 receptor, 2) GABA hypoactivity at the GABAA receptor and hyperactivity at the GABAB receptor, 3) serotonin hyperactivity at 5-HT1A receptor and hypoactivity at 5-HT2A receptor, and 4) glutamate hypoactivity at the NMDA receptor.

Paliperidone is the active major metabolite of risperidone. It was approved by the FDA in December 2006 and released to consumers in the United States in January 2007. Its therapeutic activity is believed to be a result of both central dopamine type 2 and serotonin type 2 receptor antagonism. It is also an antagonist at α1 and α2 adrenergic receptors and H1 histaminergic receptors.

Plasma concentrations are estimated to peak approximately 24 hours after dosing with a terminal half-life of approximately 23 hours. Bioavailability is 28% with apparent volume of distribution of 487 L. Plasma protein binding of paliperidone is 74%. Unlike risperidone, paliperidone is not extensively metabolized by the cytochrome P450 enzymes and is not expected to cause clinically relevant pharmacokinetic drug interactions.10,11 ED evaluation of patients who present with catatonic symptoms requires a comprehensive evaluation and a wide differential and should not be initially attributed to the underlying psychiatric disorder. Treatable common causes of catatonia should be ruled out. Further diagnostic and laboratory studies may include complete blood count, comprehensive metabolic panel, thyroid stimulating hormone, urinalysis, cerebral spinal fluid evaluation, CT, magnetic resonance imaging, EEG, and other studies as clinical history and physical findings dictate.

In most cases of drug-induced catatonia, stopping the implicated drug and supportive care is usually sufficient.

Benzodiazepines and electroconvulsive therapy have also been recommended as potential treatments.5,12

Typical antipsychotics such as haloperidol should be avoided, although a trial of atypical antipsychotics (e.g. risperidone, olanzapine) has been suggested for patients who do not respond to other measures.3,4,13,14

Caution should be taken in considering using paliperidone in patients who have already had previous adverse reaction to risperidone.

Anticonvulsants, valproate,1 and carbamazepine2 have also been reported to be effective but may take longer to work than benzodiazepines. The Naranjo scale of adverse drug reactions15 is a validated score that assesses the probability of a causal relationship between a drug and a clinical event and is Paliperidone-Induced Catatonia McKeown et al. Volume XI, no. 2 : May 2010 188 reported based on several criteria as definite, probable, possible, and doubtful. Although this medication-catatonia relationship was scored as “possible” on the Naranjo scale, there had been no other change in medications or initiation of other medications, which may have been responsible for her condition. Also of note is no previous history of catatonic-like symptoms presented prior to initiation or after discontinuation of the paliperidone.

SUMMARY: A number of medications have been associated with catatonia, including antipsychotics. Providers should consider multiple etiologies when evaluating a patient who presents with catatonia-like symptoms. Paliperidone, similar to risperidone, may be a cause of drug-induced catatonia.

Address for Correspondence: Nathanael J McKeown, DO. Oregon Health & Science University, 3181 SW Sam Jackson Park Rd, Mail Code CB550, Portland, OR 97239. Email:

Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources, and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none. REFERENCES 1. Bahro M, Kampf C, Strnad J. Catatonia under medication with risperidone in a 61-year-old patient. Acta Psychiatry Scand. 1999; 99:222-6 2. Parraga H, Harris K. Catatonia under treatment with risperidone. J Dev Behav Pediatr. 2006; 27:369 3. Cook EH Jr, Olson K, Pliskin N. Response of organic catatonia to risperidone. Arch Gen Psychiatry. 1996; 53:82-3 4. Valevski A, Loebl T, Keren T, et al. Response of catatonia to risperidone: two case reports. Clin Neuropharm 2001; 24:228-31 5. Duggal HS, Singh I. Drug induced catatonia. Drugs of Today. 2005;41:599-607 6. Fink M, Taylor MA. Catatonia: A Clinician’s Guide to Diagnosis and Treatment. Cambridge, UK: Cambridge University Press; 2003 7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th Ed. Washington D.C.: American Psychiatric Association; 1994 8. Huang TL, Ree SC, Huang YC, et al. Catatonic features: Differential diagnosis and treatments at an emergency unit. Psychiatry Clin Neurosci. 1999; 53:63-6 9. Taylor MA, Fink M. Catatonia in psychiatric classification: A home of its own. Am J Psychiatry. 2003; 160:1233-41 10. Paliperidone (Invega) for schizophrenia. Med Lett Drugs Ther. 2007;49:21-3 11. Invega (paliperidone) package insert. Janssen Pharmaceuticals. Issued 12/2006 12. Fricchione GL, Cassem NH, Hooberman D, et al. Intravenous lorazepam in neuroleptic-induced catatonia. J Clin Psychopharmacol. 1983; 3:338-42 13. Duggal HS, Nuñez CY. Risperidone treatment of periodic catatonia. Can J Psychiatry. 2005; 50:241-2 14. Hesslinger B, Walden J, Normann C. Acute and long-term treatment of catatonia with risperidone. Pharmacopsychiatry. 2001; 34:25–6 15. Kruger S, Braunig P. Intravenous valproic acid in the treatment of severe catatonia. J Neuropsychiatry Clin Neurosci. 2001;13:303–4 16. Kritzinger PR, Jordaan GP. Catatonia: an open prospective series with carbamazepine. Int J Neuropsychopharmacol. 2001;4:251–7 17. Naranjo CA, Busto U, Seller EM, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981; 30:239-45

Catatonia and catatonia-type breakdown in autism

Published on 06 December 2016

Author: Dr Amitta Shah

Dr Amitta Shah is a Consultant Clinical Psychologist with over 35 years’ experience in working with autistic children and adults. She has expertise in the diagnosis and management of catatonia in autism and has published papers on the subject with Dr Lorna Wing. Here she shares her insight and expertise of this under-recognised and poorly understood condition.

What is catatonia?

Catatonia is a complex neuro-psychological disorder which refers to a cluster of abnormalities in movement, volition, speech and behaviour. Historically, the term catatonia has been associated with schizophrenia and psychoses, but it is now recognised that it can occur with a range of conditions. 

Catatonia in varying degrees can occur in autistic children and adults. Studies suggest that between 12-18% of autistic people may present with varying levels of catatonia (Wing & Shah, 2000; Billstedt et al. 2005; Ghaziuddin et al, 2012). However, actual prevalence is likely to be higher as there are probably a lot more people with autism and catatonia who do not have a diagnosis and are not known to services.

Clinicians do not generally recognise the gradual presentation which occurs in autistic people rather than the full blown catatonic stupor state which is easy to diagnose and familiar to clinicians. Thus, catatonia type breakdown is rarely picked up at an early stage, and often misdiagnosed and mistreated.  However, if it is picked up early, it is easier to treat and can be reversed. Catatonia type breakdown can progress to full blown catatonia which is extremely difficult to treat and can lead to total immobility, dependence on all aspects of daily living and can become life-threatening. 

Catatonia-like breakdown causes enormous stress to families and affects the quality of life of the individual concerned in extreme ways. It is acknowledged that it is difficult to diagnose and treat especially as the symptoms and severity can fluctuate from day to day and also over time. It is one of the most enigmatic and challenging aspect of autism but the lack of clinical and research interest in this condition is of great concern and needs to be addressed. 

Symptoms of catatonia in autism

As early identification and diagnosis is important, it is crucial for all relevant professionals, clinicians, parents and carers to be aware of early indicators of a catatonia-like breakdown in autistic people. In particular, catatonia-like breakdown should be considered as a possible diagnosis for any autistic individual who shows a marked and obvious deterioration in:

  • movement
  • volition
  • level of activity
  • speech
  • a regression in self-care, practical skills and independence compared to previous levels.

Specific indicators of an onset of catatonia type breakdown may include any of the following:

  • increased slowness 
  • freezing during actions 
  • increase in repetitive movements and hesitations
  • difficulty in crossing thresholds and completing movements
  • marked reduction in speech or complete mutism
  • difficulty in initiating and inhibition of actions
  • increased reliance on physical or verbal prompts for functioning
  • increase in repetitive and ritualistic behaviours
  • getting locked in postures.


There is very little research evidence to guide medical treatment of catatonia in autistic people. The studies which are published on the treatment of catatonia in autism spectrum disorders (ASD) are mainly single case studies using various psychiatric medications or electroconvulsive therapy (ECT) for cases with acute catatonic stupor.

There is a recent paper (De Jong, Bunton and Hare, 2014) which has reported a systematic review of the literature on all interventions used to treat catatonic symptoms in autistic people. The conclusions are that the quality of the studies is poor and there is no convincing evidence that any particular medication or ECT is effective for catatonia type breakdown. The studies also worryingly ignored the side-effects of these treatments and rarely reported long term follow-up of effects.  

In the absence of relevant good quality evidence based research, it is important for professionals and carers to refer to guidelines developed by experienced clinicians. Treatment guidelines based on clinical experience are given for mild, moderate and severe catatonia in Dhossche, Shah and Wing (2006). It is imperative for clinicians not to overlook that psychiatric medications may trigger or worsen Catatonia in autistic individuals. Also, drastic treatments such as ECT and/or high doses of lorazepam should only be tried as a very last resort in cases of severe catatonia which is life-threatening.

We recommend a psychological approach which is based on our finding that stress and anxiety, and side effects of psychiatric medication are the main causes of catatonia-like breakdown (Wing & Shah, 2000). This is an individual approach which investigates the particular stress for the person concerned and addresses this based on a comprehensive psychological assessment and working with carers and local multi-disciplinary teams to implement a holistic plan. This is described in Shah and Wing (2006). The main aspects of this approach include the following:

  • early identification of possible indicators
  • psycho-education to promote understanding of the condition, in particular to carers, professionals and service providers
  • searching for and eliminating any possible causes such as psychiatric medications
  • assessment of the person’s autism and their vulnerability to stress
  • identification of stress factors which may include environmental, lifestyle, and psychological
  • reducing and eliminating stress factors which may include changes in the environment, daily programme, increased staffing and support, etc.
  • providing verbal and physical prompts to overcome movement difficulties
  • maintaining and increasing activities which the person enjoys or has done so previously
  • providing external stimulation and motivation  at appropriate levels to keep the person engaged and responsive and active 
  • increasing structure and predictability and occupation.

Further information

Autistic fatigue – a guide for parents and carers

Exhaustion (fatigue) and then burnout can happen to anybody. Being autistic can make fatigue and burnout more likely, due to the pressures of social situations and sensory overload. If your child or the person you care for is experiencing fatigue or burnout, helping them to manage their energy levels is essential, as this guide explains.  

 What is autistic fatigue and autistic burnout? 

‘Autistic fatigue’ and ‘autistic burnout’ are terms that came from autistic people, and we are learning from the experiences of autistic adults.  

Fatigue, and then subsequent burnout, can happen to anybody. Autistic people, however, can be more susceptible to both, due to the pressures of everyday life, having to navigate social situations and sensory overload.  

Trying to cope with these pressures can lead to exhaustion (autistic fatigue) and over time this can lead to extreme exhaustion or autistic burnout. 

Autistic adults have described various ways that autistic fatigue and burnout have affected them. Autistic fatigue has often been described as exhaustion with additional difficulties such as: 

  • increased meltdowns and sensory sensitivity  
  • physical pain and headaches 
  • physically shutting down, including the loss of speech.   

Autistic burnout affects all aspects of a person’s life, and this makes it different from professional burnout, which is related to work.

What causes autistic fatigue and burnout? 

There are various things that can cause autistic fatigue. Autistic adults suggest several causes, including:  

  • sensory overload  
  • dealing with social situations  
  • masking or camouflaging their autistic traits 
  • suppressing stimming  
  • a sense of not meeting other people’s/society’s expectations of them. 

Changes in your routines or day-to-day life, such as a change of school or job, can increase anxiety and can be additional causes for autistic fatigue and burnout. 

Due to increased sensitivity and stress levels during autistic fatigue, your child may be less able to recover quickly from meltdowns. This exacerbates the exhaustion and stress they experience.

What can I do if the person I care for is experiencing autistic fatigue and burnout? 

Use energy accounting 

Energy accounting is a system used to set manageable limits on your energy levels so you do not deplete yourself to the point of burnout.  

Help your child or the person you care for to set a limit on how much energy they have in a day or week and estimate how much certain activities drain them. Also work out how much certain activities energise them.  

You can then try to plan and balance their activities and energy over a day or week to try and manage stress limits. Make sure you build in time for relaxation and recovery.  

Time off and rest/relaxation 

Whether you use energy accounting or not, time off from work or school and other high-stress activities is key to managing stress levels. Ensuring time for activities/interests that re-energise and promote relaxation is key. This could be connecting with family and friends or enjoying hobbies or interests.  

Time without having to mask 

Autistic people often feel the need to hide or mask their autistic traits in public, for example by suppressing the urge to stim. It can be important to factor times into your child’s day for things like stimming, somewhere they feel comfortable and able to do so.

Useful resources 

Autistic people’s accounts 


Anyway there is no doubt my daughter Elizabeth has had the most horrific time prescribed drugs that all physicians were well aware there was previous allergy recorded yet they continued. The Doctors were well aware because I sent the drugs charts with a line put through Risperidone as being allergic to. Most concerning of all the SOADs provided by the CQC did nothing to protect Elizabeth and allowed maximum levels of drugging to the point she is recorded as being of “high risk of mortality” Mews Score 3.

The rest of the family came to visit Elizabeth yesterday and were in tears at her decline.

Elizabeth spent most of the time asleep in her bed. She also suffers incontinence – there is something wrong with her breathing. They have discharged Elizabeth with Catatonia – now they are having to take her off the antipsychotic drugs which caused this condition. I would accuse Barnet Enfield and Haringey MH Trust of causing injury and all the other hospitals of going along with treatment that clearly was not working resulting in seclusion after seclusion – nothing but punishment.

Elizabeth knows there is something very wrong with her right now. She has spoken that she is too damaged to fix.

Parents/carers like me are left to pick up the pieces and I believe there was a reason why Elizabeth was scheduled to go to the Priory – all of this would have been simply covered up if that had happened.

A big thank you to NAS, Mencap and Access Charities for helping us.


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