Andrew Francis, PhD, MD

Catatonia is a neuropsychiatric syndrome in which the cluster of psychomotor signs and symptoms results in aberrations of movement and behavior. DSM-IV included new criteria for mood disorders with catatonic features, and for catatonic disorder secondary to a general medical condition. In DSM-5, catatonia is recognized as due to a medical or psychiatric condition, or unspecified, as, for example, in recurrent idiopathic catatonia. Mood disorders such as MDD and bipolar disorder are now recognized as more commonly associated with catatonia.

The diagnosis of catatonia relies on the recognition of its sometimes unusual symptoms. Three subtypes of catatonia are conceptualized in 

: stuporous, excited, and malignant. Catatonic withdrawal or stuporous catatonia, includes motoric immobility, staring, mutism, rigidity, withdrawal and refusal to eat, along with more bizarre features such as posturing, grimacing, negativism, waxy flexibility, echophenomena, stereotypy, verbigeration, and automatic obedience. Excited catatonia is characterized by purposeless and excessive motor activity that includes disorganized pressured speech, flight of ideas, verbigeration, disorientation and/or confusion, and confabulation.

Catatonic signs of malignant subtype are accompanied by fever and dysautonomia. Malignant catatonia is associated with increased morbidity and mortality. A specific example of malignant catatonia is neuroleptic malignant syndrome, induced by dopamine-blocking agents or withdrawal of a dopamine or gamma-aminobutyric acid

) agonist. Another variant, known as manic delirium or delirious mania, exists with features of both excited and malignant catatonia. Periodic catatonia can present with alternating stuporous and excited forms.

The prevalence of catatonia among psychiatric patients ranges from 7.6% to 38%.

Catatonia has attracted neuroscientists interested in brain mediation of motivation and movement, leading to attention on neurotransmitters and circuits. Several models for the neuropathophysiology of catatonia focus on neurotransmitters. In 1985, it was hypothesized that pharmacotherapies for catatonia act on dopamine- GABA connections in the mesostriatal and mesocorticolimbic systems and in the hypothalamus.

 A restitutive dopamine system seeks rebalance through GABA

–mediated up- and down-regulation of dopamine.

When the restitutive system is dysfunctional, a vulnerability to catatonia emerges from dopamine antagonists. Carroll3 has described a “universal field theory” encompassing diverse neurotransmitter changes for catatonia. Their model postulates a reduced GABA activity in the frontal cortex, increased 

-methyl-D-aspartate glutamatergic activity in the posterior parietal cortex, and a dampening of dopaminergic action in the basal ganglia.

Approaching catatonia from a circuits perspective, C. Miller Fisher

 proposed that catatonic depression emerged from connection disturbances in the same mesoencephalofrontal system (brainstem to basal ganglia to limbic system and cerebral cortex) that also leads to akinetic mutism. Northoff

 used neuroimaging in patients recovering from catatonia to uncover trait features through provocative testing of response to fearful faces and situations. He described a region of interest in the orbitofrontal cortex that overreacts in these provocative situations, which suggests dysfunctional responsiveness.

Other functional imaging studies have shown altered activity in orbitofrontal, prefrontal, parietal, and motor cortical regions.

 Recently, T1-weighted MRI imaging in catatonia secondary to schizophrenia spectrum disorders showed reduced cortical thickness in frontoparietal regions as well as hypergyrification in the anterior cingulate cortex and medial orbitofrontal cortex compared with controls.

 The basal-ganglia-thalamo-cortical loop system has been implicated in the pathophysiology of catatonia, with interruption at various nodes leading to specific symptoms of catatonia.

 For example, disruption to the anterior cingulate cortex circuit may contribute to akinesia and mutism; to the lateral orbitofrontal circuit, echophenomena; and to the supplementary motor area circuit, increased tone. Integration of these hypotheses comes closest to offering a putative pathophysiological understanding of the mystery of catatonia.

Catatonia as a syndrome may arise from multiple etiologies and can lead to medical complications that result in significant morbidity and mortality, making rapid diagnosis and treatment a priority. Medical complications abound, and the mortality rate for malignant catatonia despite better recognition and treatment is still 9% to 10%.

 For a list of potential medical complications, see 

Catatonia has several mimics, which must be ruled out before making a diagnosis. Locked-in syndrome, linked to pontine lesions, can be distinguished from catatonia because patients will generally attempt to communicate with their eyes. Patients in a persistent vegetative state may also appear to be catatonic. Stiff person syndrome is an autoimmune disorder that presents during severe stress with intense lower extremity spasmodic stiffness that may appear like catatonic posturing, but these patients speak and complain about their pain.

Some patients suspected of being in a catatonic state may have an extrapyramidal parkinsonism. These can have a distinctive tremor but are not negativistic and lack bizarre catatonic psychomotor symptoms. Nonconvulsive status epilepticus can also produce a catatonic-like state; electroencephalography is essential for accurate diagnosis and prompt management may minimize cognitive damage.

Several additional syndromes show clinical overlap with catatonia. Like Fisher,

 we believe akinetic mutism, an extreme form of the abulic syndrome caused by neurological injury, to be a neurologic version of catatonia. Hypoactive delirium may overlap or coexist with catatonia. It is extremely important to confirm a delirious patient is not also suffering from a catatonic episode, because neuroleptics can worsen simple catatonia, resulting in malignant catatonia. Decreased eyeblink and resistance to eye and mouth opening may hint at a catatonia nested in delirium.

To assess catatonia, a few steps can be routinely followed (

). Once the diagnosis of catatonia is made, a definable etiology must be sought. In addition to mood disorders and schizophrenia-spectrum disorders, catatonia can be seen in up to 20% of patients with autism-spectrum disorders. Case reports have described catatonia secondary to obsessive compulsive disorder, PTSD, and personality disorders.

Up to 50% of cases of catatonia may be due to a host of neuromedical syndromes. These include paraneoplastic and limbic encephalitidies (especially anti-NMDA receptor antibody encephalitis), ictal and post-ictal states, posterior reversible encephalopathy syndrome, and lupus. Substances associated with catatonia include dopamine-blocking agents, tacrolimus, disulfiram, and phencyclidine, among others. Finally, catatonia can occur as an isolated clinical syndrome without an obvious underlying cause; this phenomenon is known as recurrent idiopathic catatonia.

With severe threat, challenges to brain function can emerge via circuit disconnection or modulatory dysfunction and result in catatonia. This view may underlie the effectiveness of benzodiazepine GABAA agonism, of NMDA-R antagonism, and of electroconvulsive therapy (ECT). These treatments show effects on GABA, dopamine, acetylcholine, and glutamate within cortico-striato-thalamo-cortical loops. (For an outline of a proposed catatonia treatment algorithm, please see 

All treatments for catatonia are off-label uses, as there is no FDA-approved drug indicated for catatonia. In 1983, lorazepam was described as a successful treatment for catatonia and later became the first-line treatment for the catatonic syndrome.

 A lorazepam challenge (using 2-mg intravenous [IV] lorazepam) can be a helpful diagnostic test. Although a negative response does not rule out catatonia, many patients will show improvement with a single dose. Following the challenge, a standing dose of 2 mg every 4 to 6 hours is typical; some patients may require titration to as much as 30 mg daily, especially in cases with malignant features.

Doses should be held only for respiratory depression due to oversedation and not for sedation alone, as the regularity of dosing is important for full lysis. IV lorazepam is preferred over other routes or benzodiazepine types because of its quick onset, preference for the GABA-A receptor, and long duration of effect.

Approximately two-thirds of patients will respond to treatment with benzodiazepines, although those with catatonic schizophrenia show reduced responsiveness. Catatonia sometimes re-emerges during transition from IV lorazepam to oral dosing. This may require reinstitution of IV lorazepam and an eventual higher oral dosing. There is no established guideline for how long benzodiazepine responders will require maintenance. We have had patients on benzodiazepines for weeks and even months, necessitating careful eventual taper. If decreased tolerance to benzodiazepines emerges (via increasing sedation), it is safe to gradually taper the benzodiazepine. After discontinuation, lorazepam may again be needed in cases of catatonic rebound.

If catatonia persists for more than 2 to 3 days or if malignant features are present, ECT remains the definitive treatment. ECT works synergistically with benzodiazepines and demonstrates response rates of up to 80%.

 Bitemporal placement is recommended, at a frequency of 3 times per week for at least 6 sessions. ECT may work by increasing cerebral blood flow to the orbitofrontal and parietal cortices, increasing GABA activity and GABA receptor expression, and by increasing dopamine release and modulation of dopamine receptors.

When benzodiazepines are ineffective or contraindicated and ECT is unavailable or refused, second-line treatments include glutamatergic agents, such as memantine (5-10 mg twice daily) or amantadine (400-600 mg daily in divided doses). These agents appear to be safe, well-tolerated, and effective in case reports, as monotherapy or in combination with a benzodiazepine. Other options include valproate or carbamazepine, which may be particularly useful if the catatonia is related to underlying mania. Valproic acid has demonstrated some effectiveness in excited catatonia.

A final option to consider is an atypical antipsychotic. These agents are the last step in the algorithm because of their potential to worsen catatonia or cause conversion to a malignant catatonia. Antipsychotics should be given in combination with a benzodiazepine, and low-potency atypical agents are preferred. Among antipsychotic agents, aripiprazole may be the safest choice given its partial-agonist activity. If the catatonia occurs in the setting of clozapine cessation, re-initiation of clozapine should be a first-line strategy. High-potency typical antipsychotics should generally be avoided in catatonic patients.

Supportive management is essential in cases of catatonia. In addition to treatment of the catatonic symptoms, full resolution often requires treatment of the underlying disorder. This can be challenging in cases of psychosis, which may require a careful balance of antipsychotics and benzodiazepines.

As a neuropsychiatric and general medical syndrome, catatonia represents an important diagnostic and treatment challenge for all clinicians given its morbidity and mortality. By examining the nature of cortico-striato-thalamo-cortical circuits and the effects of transmitters and modulating systems, we can better understand why such a wide array of etiologies can present with the catatonic syndrome and why the pharmacologic and electroconvulsive treatments can be very effective when provided expeditiously.

Dr Beach is Assistant Professor of Psychiatry and Residency Training Director, Massachusetts General Hospital, Harvard Medical School; Dr Francis is Professor of Psychiatry, Associate Director of Residency Training, and Director of Neuromodulation Services, Penn State Medical School, Hershey Medical Center, Hershey, PA; Dr Fricchione is Professor of Psychiatry, Mind Body Medical Institute and Associate Chief of Psychiatry, Massachusettes General Hospital, Harvard Medical School, Boston, MA. Drs Fricchione and Beach have received funding through the David Judah Fund for catatonia research.

 Taylor MA, Fink M. Catatonia in psychiatric classification: a home of its own. 

 Fricchione GL. Neuroleptic catatonia and its relationship to psychogenic catatonia. 

 Carroll BT. The universal field hypothesis of catatonia and neuroleptic malignant syndrome. 

 Fisher CM. Honored guest presentation: abulia minor vs. agitated behavior. 

 Northoff G. What catatonia can tell us about “top-down modulation”: a neuropsychiatric hypothesis. 

 Northoff G. Catatonia and neuroleptic malignant syndrome: psychopathology and pathophysiology. 

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 Tuerlings JH, van Waarde JA, Verwey B. A retrospective study of 34 catatonic patients: analysis of clinical care and treatment. 

 Fisher CM. “Catatonia” secondary to disulfiram toxicity. 

 Fricchione GL, Cassem NH, Hooberman D, Hobson D. Intravenous lorazepam in neuroleptic-induced catatonia.

 Bush G, Fink M, Petrides G, Dowling F, Francis A. Catatonia. II. Treatment with lorazepam and electroconvulsive therapy. 

 Petrides G, Divadeenam KM, Bush G, Francis A. Synergism of lorazepam and electroconvulsive therapy in the treatment of catatonia. 

Catatonia: A Clinician’s Guide to Diagnosis and Treatment

. New York, NY: Cambridge University Press; 2003.

 Levenson JL. Medical aspects of catatonia. 

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Articles

As a neuropsychiatric and general medical syndrome, catatonia represents an important diagnostic and treatment challenge for all clinicians given its morbidity and mortality.

Neuropsychiatry of Catatonia: Clinical Implications

 is admitted to the hospital with rash, arthralgias, and altered mental status. On examination, the patient displays stupor, mutism, posturing, and echopraxia while vital signs, creatine kinase, and brain MRI are all normal. Lorazepam 2mg IV q6 partially improves her symptoms, but higher doses cause more sedation. How would you proceed?

B. Switching from lorazepam to oral diazepam

A variety of medical conditions can produce stupor, which is a decreased awareness and interaction with the external environment. Stupor can occur with preserved alertness, more often seen in catatonia, or with lethargy, more often seen in delirium. Differences between etiologies (psychiatric vs medical) do not appear to alter the general treatment approach for catatonia. Removal of suspected offending agents, treatment of the underlying medical condition, or management of drug withdrawal are essential.

Potential adverse effects of high-dose intravenous lorazepam include anion gap acidosis from its solvent, propylene glycol. This risk increases with higher doses and in renal impairment, but toxicity has been reported with as little as 2 mg per hour. The osmolar gap (a marker for glycol toxicity) should be monitored every other day if the lorazepam infusion reaches 1 mg/kg daily.

Augmentation with memantine or amantadine may be helpful. Their hypothesized mechanism is N-methyl-d-aspartic acid (NMDA) receptor antagonism, which may be linked to GABA hypofunction. Memantine can be started at 5 to 10 mg daily and titrated based on medical status with monitoring of the QT interval. Improvement from memantine seems slower than with lorazepam, but both can be co-administered. Amantadine is started at 100 to 200 mg daily and titrated, but it should be used with caution if renal impairment or seizure risk is present. Mania, suicidal ideation, and withdrawal-emergent NMS have also been reported with administration of amantadine.

Update on Medical Catatonia: Highlight on Delirium

, by Jo Ellen Wilson, MD, MPH, Lex Denysenko, MD, and Andrew Francis, PhD, MD, on which this quiz is based.

Poll

A patient with lupus presents with rash, arthralgias, and altered mental status. Various symptoms, including stupor and mutism, improve with treatment but higher doses of the drug cause more sedation. How would you proceed?

Mini Quiz: Medical Catatonia

Catatonia, described in 1874 by K. L. Kahlbaum, is a distinct and heterogeneous neuropsychiatric syndrome, with both motoric and behavioral signs. It may be hypokinetic, hyperkinetic, or mixed and includes volitional signs, such as mutism, negativism, and automatic obedience. It was formerly relegated to a schizophrenia subtype, or considered extinct after the advent of modern psychopharmacology. Renewed interest and emerging systematic data have highlighted the frequency and pattern of catatonic presentations in psychiatric and medical settings, including in critical illness.

Historically, up to 40 signs were recognized, and most are now included in the published scales for detecting and rating the severity of catatonia. The Bush-Francis Catatonia Rating Scale (BFCRS) is widely used in both clinical and research settings, shows high inter-rater reliability and favorable sensitivity and specificity, and was validated in a mixed medical and psychiatric sample.

 The 23-item BFCRS was derived from classic descriptions of catatonia and modern diagnostic criteria. Cases are defined by the presence of 2 or more of the first 14 signs.

DSM-5 criteria require 3 or more from a similar list of 12 common catatonic signs. The BFCRS or DSM-5 items identify diverse clinical features, including motoric, behavioral, volitional, and autonomic signs. Statistical analyses identified subtypes of catatonia, including a retarded and an excited form. Malignant catatonia-a severe form with fever and autonomic instability-is uncommon but is important to identify as it may be fatal if not recognized and aggressively treated.

Despite effective treatments, patients with any form of catatonia remain at risk from serious complications such as dehydration, muscle breakdown, aspiration, or embolic phenomena. Once catatonia is recognized, these risks can be mitigated by effective treatments. Among the most studied treatment modalities, regardless of the underling etiology, prompt administration of gamma-aminobutyric acid (GABA) receptor agonists or ECT for severe or resistant cases usually relieves the symptoms and may be lifesaving.

Pathology of catatonia in the context of medical illness

The exact pathogenesis of catatonia remains unknown. Systematic examination of catatonia with genetic and brain imaging studies has been slow to develop. Familial aggregation has been reported for periodic catatonia, and preliminary evidence associated this with 15q15 chromosome.

 Single photon emission CT studies using a GABA-A ligand revealed reduced binding in areas of the frontal lobe.

 More recent studies showed increased cerebral blood flow in the supplementary motor cortex, which correlated with BFCRS severity scores, and apparent loss of frontal and insular gray matter in catatonic schizophrenia.

For catatonia in medical populations, the pattern or frequency of catatonic signs does not distinguish psychiatric from medical catatonia. A review of case reports on catatonia associated with brain lesions found an association with frontal and basal ganglia damage. The most recent systematic reports of medical catatonia confirm that non-localizing encephalopathies were the most common primary diagnoses associated with catatonia; a variety of non-specific EEG findings were also seen.

 Catatonia is generally thought to be under-recognized in the medically ill.

Of particular interest and potentially of great clinical significance is the relationship between catatonia and delirium. Delirium is the classic syndrome of acute brain dysfunction-with disturbed attention, awareness, and cognition-and is predictive of excess mortality, longer hospitalization, costlier care, and long-term cognitive impairment. While delirium is often assessed in critical settings such as the ICU, catatonia is not. Recognition and study of ICU catatonia have until recently been hindered by recent editions of DSM, which consistently hold that catatonia cannot be diagnosed in the presence of delirium. However, there is no clear evidence to support the exclusion.

Despite the DSM exclusion, delirium might coexist with catatonia, perhaps most prominently in the hypoactive motoric subtype of delirium. Hypoactive delirium includes decreased motor activity, decreased speech, and behavioral withdrawal-all of which map to catatonic features.

The first prospective report of catatonia with delirium was published in 2014.

 The data showed that 13% of 205 consecutive delirium cases met DSM-5 criteria for catatonia, and 32% met BFCRS criteria for catatonia. However, no treatment or outcome data were presented.

The many implications of more clinical attention and systematic study of comorbid delirium and catatonia include prognosis and management. For catatonia, active treatment consists of benzodiazepines (typically lorazepam) and/or ECT; antipsychotics are generally avoided because they may worsen catatonia or precipitate a lethal or malignant form similar to neuroleptic malignant syndrome (NMS). Conversely, treatment of delirium addresses the underlying medical condition and environmental factors, and antipsychotics are often used; however, benzodiazepines are generally avoided (except for known substance-withdrawal delirium).

There are no prospective data on the management or outcome of catatonia with delirium that address this apparent dilemma. However, a recent study of medical inpatients identified 54 cases of catatonia of whom 43% had a prior psychiatric history, while 54% had suspected delirium.

 When medical catatonia was compared to that attributed to psychiatric disorders, there was no statistical difference in the rates of treatment attempts using lorazepam nor in response, which was greater than 80%. However, cases of catatonia comorbid with suspected delirium were less likely to respond to lorazepam (71%) than cases without delirium (100%), regardless of etiology. While this was a retrospective study, it supports the assertion that catatonia and delirium can be comorbid and suggests that in many cases the treatment of catatonia with benzodiazepines may be successful in the presence of a delirium.

A variety of medical conditions can produce stupor, which is a decreased awareness and interaction with the external environment. Stupor can occur with preserved alertness, more often seen in catatonia, or with lethargy, more often seen in delirium. Stupor that is associated with a metabolic disorder or that is associated with delirium may present with catatonic features. The 

 presents examples of medical conditions associated with catatonia.

NMS, serotonin syndrome, and non-convulsive status epilepticus are other examples of stuporous states associated with catatonia. It may be that NMS and serotonin syndrome are actually medication-induced malignant catatonia.

Delirious mania is a rare syndrome linked to bipolar disorder characterized by the rapid onset of delirium, mania, and psychosis, with prominent hyperactive catatonia. Delirious mania can be construed as a malignant hyperactive form of catatonia, as well as a hyperactive delirium. Delirious mania has been associated with medical disorders. The newly characterized excited delirium syndrome, induced by cocaine or other stimulants, has been likened to delirious mania. Delirious mania was reported after cerebellar/pontine stroke, which produced delirium that was treated with antipsychotics that led to a catatonic state; this ultimately resolved with continuation of valproate, removal of antipsychotics, and administration of lorazepam.

Differences between etiologies (psychiatric vs medical) do not appear to alter the general treatment approach for catatonia. Removal of suspected offending agents, treatment of the underlying medical condition, or management of drug withdrawal are essential for both forms of catatonia.

For persistent catatonia, rapid initiation of lorazepam or a related benzodiazepine, which may require cautious titration to higher dosages (eg, 8 mg/d or more of lorazepam), usually leads to improvement of symptoms. Benzodiazepines (and related agents such as amobarbital and zolpidem) may counteract hypothesized GABA-receptor hypofunction in catatonia. Intravenous lorazepam has more assured absorption and may exert more prolonged clinical effects than the oral form based on differing drug distribution.

Augmentation with memantine or amantadine may also be helpful. Their hypothesized mechanism is N-methyl-d-aspartic acid (NMDA) receptor antagonism, which may be linked to GABA hypofunction. Memantine can be started at 5 to 10 mg daily and titrated based on medical status with monitoring of the QT interval. Improvement from memantine seems slower than with lorazepam, but both can be co-administered. Amantadine is started at 100 to 200 mg daily and titrated, but it should be used with caution if renal impairment or seizure risk is present. Mania, suicidal ideation, and withdrawal-emergent NMS have also been reported with administration of amantadine.

ECT can be considered for inadequate medication response for persistent and severe catatonia and may be used more emergently for malignant features (autonomic instability and hyperthermia). Use of ECT for catatonia in medical settings or with uncertain CNS pathology should be approached cautiously, and the potential benefit weighed against the known adverse risk of severe and prolonged catatonia. Some reports show a benefit of ECT for catatonia for various acute neurological illnesses.

 However, no benefit was seen with the use of ECT in catatonia after cerebral hypoxia; in this setting, it may worsen neurological status.

Atypical antipsychotics were reported to benefit some cases of non-medical catatonia after other treatments had failed, or for coexistent catatonia and psychosis when ECT was not feasible.

 Serum iron should be measured, since low levels may be predictive of conversion to malignant catatonia. Benzodiazepines should be continued concurrently with the antipsychotic, with monitoring for extrapyramidal or autonomic symptoms that portend malignant catatonia or NMS. Antipsychotics in medical catatonia or delirium with catatonia have not been studied, and caution is advised with their use.

When medical catatonia is identified, the primary hospital service may initially resist lorazepam treatment, particularly when the patient is medically compromised. Under-dosing of lorazepam and treatment failure may result if the rationale for its use is not clearly expanded. Inviting the primary care team to witness a lorazepam or zolpidem challenge may help medical specialists appreciate that a sedating agent can improve catatonic stupor.

Frequent vital sign assessments, monitoring of the osmolar gap, and pulse oximetry can improve safety, along with ready access to flumazenil for reversal of potential adverse effects of benzodiazepines. If sedation is a concern, adding non-sedating memantine or amantadine may allow for lower benzodiazepine dosing.

When multiple hospital consultants are involved in complex cases, interdisciplinary meetings are strongly recommended. In such situations, we encourage a clear consensus that identifies specific targets for defining both treatment response and adverse effects.

Dr. Wilson is Instructor in the Department of Psychiatry and Behavioral Sciences at Vanderbilt University Medical Center, Nashville, TN. Dr. Denysenko is Assistant Professor in the Department of Psychiatry at Rowan University School of Osteopathic Medicine, Cherry Hill, NJ. Dr. Francis is Professor of Psychiatry at Penn State Medical School, Hershey, PA.

The authors report no conflicts of interest concerning the subject matter of this article.

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. November 30, 2016; Epub ahead of print.

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http://www.apm.org/library/monographs/catatonia/Catatonia_APM-EAPM_2015-04-17.pdf

Renewed interest and emerging systematic data have highlighted the frequency and pattern of catatonic presentations in psychiatric and medical settings, including in critical illness.

Author | Andrew Francis, PhD, MD

Articles

Neuropsychiatry of Catatonia: Clinical Implications

Mini Quiz: Medical Catatonia

Update on Medical Catatonia: Highlight on Delirium