User login
Stuck in a rut with the wrong diagnosis
CASE Aggressive behaviors, psychosis
Ms. N, age 58, has a long history of bipolar disorder with psychotic features. She presents to our emergency department (ED) after an acute fall and frequent violent behaviors at her nursing home, where she had resided since being diagnosed with an unspecified neurocognitive disorder. For several weeks before her fall, she was physically aggressive, throwing objects at nursing home staff, and was unable to have her behavior redirected.
While in the ED, Ms. N rambles and appears to be responding to internal stimuli. Suddenly, she stops responding and begins to stare.
HISTORY Severe, chronic psychosis and hospitalization
Ms. N is well-known at our inpatient psychiatry and electroconvulsive therapy (ECT) services. During the last 10 years, she has had worsening manic, psychotic, and catatonic (both excited and stuporous subtype) episodes. Three years ago, she had experienced a period of severe, chronic psychosis and excited catatonia that required extended inpatient treatment. While hospitalized, Ms. N had marginal responses to clozapine and benzodiazepines, but improved dramatically with ECT. After Ms. N left the hospital, she went to live with her boyfriend. She remained stable on monthly maintenance ECT treatments (bifrontal) before she was lost to follow-up 14 months prior to the current presentation. Ms. N’s family reports that she needed a cardiac clearance before continuing ECT treatment; however, she was hospitalized at another hospital with pneumonia and subsequent complications that interrupted the maintenance ECT treatments.
Approximately 3 months after medical issues requiring hospitalization began, Ms. N received a diagnosis of neurocognitive disorder due to difficulty with activities of daily living and cognitive decline. She was transferred to a nursing home by the outside hospital. When Ms. N’s symptoms of psychosis returned and she required inpatient psychiatric care, she was transferred to a nearby facility that did not have ECT available or knowledge of her history of catatonia resistant to pharmacologic management. Ms. N had a documented history of catatonia that spanned 10 years. During the last 4 years, Ms. N often required ECT treatment. Her current medication regimen prescribed by an outpatient psychiatrist includes clozapine, 300 mg twice daily, and clonazepam, 0.5 mg twice daily, both for bipolar disorder.
EVALUATION An unusual mix of symptoms
In the ED, Ms. N undergoes a CT of the head, which is found to be nonacute. Laboratory results show that her white blood cell count is 14.3 K/µL, which is mildly elevated. Results from a urinalysis and electrocardiogram (ECG) are unremarkable.
After Ms. N punches a radiology technician, she is administered IV lorazepam, 2 mg once, for her agitation. Twenty minutes after receiving IV lorazepam, she is calm and cooperative. However, approximately 4 hours later, Ms. N is yelling, tearful, and expressing delusions of grandeur—she believes she is God.
After she is admitted to the medical floor, Ms. N is seen by our consultation and liaison psychiatry service. She exhibits several signs of catatonia, including grasp reflex, gegenhalten (oppositional paratonia), waxy flexibility, and echolalia. Ms. N also has an episode of urinary incontinence. At some parts of the day, she is alert and oriented to self and location; at other times, she is somnolent and disoriented. The treatment team continues Ms. N’s previous medication regimen of clozapine, 300 mg twice daily, and clonazepam, 0.5 mg twice daily. Unfortunately, at times Ms. N spits out and hides her administered oral medications, which leads to the decision to discontinue clozapine. Once medically cleared, Ms. N is transferred to the psychiatric floor.
[polldaddy:10869949]
Continue to: TREATMENT
TREATMENT Bifrontal ECT initiated
On hospital Day 3 Ms. N is administered a trial of IM lorazepam, titrated up to 6 mg/d (maximum tolerated dose) while the treatment team initiates the legal process to conduct ECT because she is unable to give consent. Once Ms. N begins tolerating oral medications, amantadine, 100 mg twice daily, is added to treat her catatonia. As in prior hospitalizations, Ms. N is unresponsive to pharmacotherapy alone for her catatonic symptoms. On hospital Day 8, forced ECT is granted, which is 5 days after the process of filing paperwork was started. Bifrontal ECT is utilized with the following settings: frequency 70 Hz, pulse width 1.5 ms, 100% energy dose, 504 mC. Ms. N does not experience a significant improvement until she receives 10 ECT treatments as part of a 3-times-per-week acute series protocol. The Bush-Francis Catatonia Rating Scale (BFCRS) and the KANNER scale are used to monitor her progress. Her initial BFCRS score is 17 and initial KANNER scale, part 2 score is 26.
Ms. N spends a total of 61 days in the hospital, which is significantly longer than her previous hospital admissions on our psychiatric unit; these previous admissions were for treatment of both stuporous and excited subtypes of catatonia. This increased length of stay coincides with a significantly longer duration of untreated catatonia. Knowledge of her history of both the stuporous and excited subtypes of catatonia would have allowed for faster diagnosis and treatment.1
The authors’ observations
Originally conceptualized as a separate syndrome by Karl Kahlbaum, catatonia was considered only as a specifier for neuropsychiatric conditions (primarily schizophrenia) as recently as DSM-IV-TR.2 DSM-5 describes catatonia as a marked psychomotor disturbance and acknowledges its connection to schizophrenia by keeping it in the same chapter.3 DSM-5 includes separate diagnoses for catatonia, catatonia due to a general medical condition, and unspecified catatonia (for catatonia without a known underlying disorder).3 A recent meta-analysis found the prevalence of catatonia is higher in patients with medical/neurologic illness, bipolar disorder, and autism than in those with schizophrenia.4
Table 13 highlights the DSM-5 criteria for catatonia. DSM-5 requires 3 of 12 symptoms to be present, although symptoms may fluctuate with time.3 If a clinician is not specifically looking for catatonia, it can be a difficult syndrome to diagnose. Does rigidity indicate catatonia, or excessive dopamine blockade from an antipsychotic? How can seemingly contradictory symptoms be part of the same syndrome? Many clinicians associate catatonia with the stuporous subtype (immobility, posturing, catalepsy), which is more prevalent, but the excited subtype, which may involve severe agitation, autonomic dysfunction, and impaired consciousness, can be lethal.2 The diversity in presentation of catatonia is not unlike the challenging variety of symptoms of heart attacks.
A retrospective study of all adults admitted to a hospital found that only 41% of patients who met criteria for catatonia received this diagnosis.5 Further complicating the diagnosis, delirium and catatonia can co-exist; one study found this was the case in 1 of 3 critically ill patients.6 DSM-5 criteria for catatonia due to another medical condition exclude the diagnosis if delirium is present, but this study and others suggest this needs to be reconsidered.3
Continue to: A standardized evaluation is key
A standardized evaluation is key
Just as a patient who presents with chest pain requires a standardized evaluation, including a pertinent history, laboratory workup, and ECG, psychiatrists may also use standardized diagnostic instruments to aid in the diagnosis of catatonia. One study of hospitalized patients with schizophrenia found that using a standardized diagnostic procedure for catatonia resulted in a 7-fold increase in the diagnosis.7 The BFCRS is the most common standardized instrument for catatonia, likely due to its high inter-rater reliability.8 Other scales include the KANNER scale and Northoff Catatonia Scale, which emphasize different aspects of the disease or for certain clinical populations (eg, the KANNER scale adjusts for patients who are nonverbal at baseline). One study suggested that BFCRS has lower reliability for less-severe illness.9 These differences emphasize that psychiatry does not have a thorough understanding of the intricacies of catatonia. However, using validated screening tools can lead to more consistent diagnoses and continue important research on this often-misunderstood illness.
Dangers of untreated catatonia
Rapid treatment of catatonia is necessary to prevent mortality. A study of patients in Kentucky’s state psychiatric hospitals found that untreated catatonia with resultant death from pulmonary embolism was the leading cause of preventable death.10 A 17-year retrospective study of patients with schizophrenia admitted to 1 hospital found that those with catatonia were >4 times as likely to die during hospitalization than those without catatonia.11 The significant morbidity and mortality from untreated catatonia are typically attributed to the consequences of poorly controlled movements, immobility, autonomic instability, and poor/no oral intake. Reduced oral intake can result in malnutrition, dehydration, arrhythmias, and increased risk of infections. Furthermore, chronic catatonic episodes are more difficult to treat.12 In addition to the aggressive management of neuropsychiatric symptoms, it is vital to evaluate relevant medical etiologies that may be contributing to the syndrome (Table 213). Tracking vital signs and laboratory values, such as creatine kinase, electrolytes, and complete blood count, is required to ensure the medical condition does not become life-threatening.
Treatment options
Studies and expert opinion suggest that benzodiazepines (specifically lorazepam, because it is the most studied agent) are the first-line treatment for catatonia. A lorazepam challenge test—providing 1 or 2 mg of IV lorazepam—is considered diagnostic and therapeutic given the high rate of response within 10 minutes.14 Patients with limited response to lorazepam or who are medically compromised should undergo ECT. Electroconvulsive therapy is considered the gold-standard treatment for catatonia; estimated response rates range from 59% to 100%, even in patients who fail to respond to pharmacotherapy.15 Although highly effective, ECT is often hindered by the time required to initiate treatment, stigma, lack of access, and other logistical challenges.
Table 314-18 highlights the advantages and disadvantages of treatment options for catatonia. Some researchers have suggested a zolpidem challenge test could augment lorazepam because some patients respond only to zolpidem.14 The efficacy of these medications along with some evidence of anti-N-methyl-
Ms. N was ultimately diagnosed with bipolar disorder, current episode mixed, with psychotic and catatonic features. Ms. N had symptoms of mania including grandiosity, periods of lack of sleep, delusions as well as depressive symptoms of tearfulness and low mood. The treatment team had considered that Ms. N had delirious mania because she had fluctuating sensorium, which included varying degrees of orientation and ability to answer questioning. However, the literature supporting the differentiation between delirious mania and excited catatonia is unclear, and both conditions may respond to ECT.18 A diagnosis of catatonia allowed the team to use rating scales to track Ms. N’s progress by monitoring for specific signs, such as grasp reflex and waxy flexibility.
Continue to: OUTCOME
OUTCOME Return to baseline
Before discharge, Ms. N’s BFCRS score decreases from the initial score of 17 to 0, and her KANNER scale score decreases from the initial score of 26 to 4, which correlates with vast improvement in clinical presentation. Once Ms. N completes the acute ECT treatment, she returns to her baseline level of functioning, and is discharged to live with her boyfriend. She is advised to continue weekly ECT for the first several months to ensure clinical stability. This regimen is later transitioned to biweekly and then monthly. Electroconvulsive therapy protocols from previous research were utilized in Ms. N’s case, but ultimately the lowest number of ECT treatments needed to maintain stability is determined clinically over many years.19 Ms. N is discharged on aripiprazole, 15 mg/d; bupropion ER, 300 mg/d (added after depressive symptoms emerge while catatonia symptoms improve midway through her lengthy hospitalization); and memantine, 10 mg/d. Ideally, clozapine would have been continued; however, due to her history of nonadherence and frequent restarting of the medication at a low dose, clozapine was discontinued and aripiprazole initiated.
More than 1 year later, Ms. N remains stable and continues to receive monthly ECT maintenance treatments.
Bottom Line
Catatonia should always be considered in a patient who presents with acute neuropsychiatric symptoms. Rapid diagnosis with standardized screening instruments and aggressive treatment are vital to prevent morbidity and mortality.
Related Resource
- Freudenreich O, Francis A, Fricchione GL. Chapter 9. Psychosis, mania, and catatonia. In: Levenson, James L, ed. The American Psychiatric Association Publishing textbook of psychosomatic medicine and consultation-liaison psychiatry. 3rd ed. American Psychiatric Association Publishing; 2019.
Drug Brand Names
Amantadine • Symmetrel
Aripiprazole • Abilify
Baclofen • Ozobax
Bupropion ER • Wellbutrin XL
Clonazepam • Klonopin
Clozapine • Clozaril
Lithium • Eskalith, Lithobid
Lorazepam • Ativan
Metoclopramide • Reglan
Memantine • Namenda
Topiramate • Topamax
Zolpidem • Ambien
1. Carroll BT. The universal field hypothesis of catatonia and neuroleptic malignant syndrome. CNS Spectrums. 2000;5(7):26-33.
2. Rasmussen SA, Mazurek MF, Rosebush PI. Catatonia: our current understanding of its diagnosis, treatment and pathophysiology. World J Psychiatry. 2016;6(4):391‐398.
3. Diagnostic and statistical manual of mental disorders, 5th ed. American Psychiatric Association; 2013. 119-121.
4. Solmi M, Pigato GG, Roiter B, et al. Prevalence of catatonia and its moderators in clinical samples: results from a meta-analysis and meta-regression analysis. Schizophrenia Bulletin. 2017;44(5):1133-1150.
5. Llesuy JR, Medina M, Jacobson KC, et al. Catatonia under-diagnosis in the general hospital. J Neuropsychiatry Clin Neurosci. 2018;30(2):145-151.
6. Wilson JE, Carlson R, Duggan MC, et al. Delirium and catatonia in critically ill patients. Crit Care Med. 2017;45(11):1837-1844.
7. Heijden FVD, Tuinier S, Arts N, et al. Catatonia: disappeared or under-diagnosed? Psychopathology. 2005;38(1):3-8.
8. Sarkar S, Sakey S, Mathan K, et al. Assessing catatonia using four different instruments: inter-rater reliability and prevalence in inpatient clinical population. Asian J Psychiatr. 2016;23:27-31.
9. Wilson JE, Niu K, Nicolson SE, et al. The diagnostic criteria and structure of catatonia. Schizophr Res. 2015;164(1-3):256-262.
10. Puentes R, Brenzel A, Leon JD. Pulmonary embolism during stuporous episodes of catatonia was found to be the most frequent cause of preventable death according to a state mortality review: 6 deaths in 15 years. Clin Schizophr Relat Psychoses. 2017; doi:10.3371/csrp.rpab.071317
11. Funayama M, Takata T, Koreki A, et al. Catatonic stupor in schizophrenic disorders and subsequent medical complications and mortality. Psychosomatic Medicine. 2018:80(4):370-376.
12. Perugi G, Medda P, Toni C, et al. The role of electroconvulsive therapy (ECT) in bipolar disorder: effectiveness in 522 patients with bipolar depression, mixed-state, mania and catatonic features. Curr Neuropharmacol. 2017;15(3):359-371.
13. Freudenreich O, Francis A, Fricchione GL. Chapter 9. Psychosis, mania, and catatonia. In: Levenson, James L, ed. The American Psychiatric Association Publishing Textbook of Psychosomatic medicine and Consultation-Liaison Psychiatry. 3rd ed. American Psychiatric Association Publishing; 2019.
14. Sienaert P, Dhossche DM, Vancampfort D, et al. A clinical review of the treatment of catatonia. Front Psychiatry. 2014;5:181.
15. Pelzer A, Heijden FVD, Boer ED. Systematic review of catatonia treatment. Neuropsychiatr Dis Treat. 2018;14:317-326.
16. Carroll BT, Goforth HW, Thomas C, et al. Review of adjunctive glutamate antagonist therapy in the treatment of catatonic syndromes. J Neuropsychiatry and Clin Neurosci. 2007;19(4):406-412.
17. Fink M. Rediscovering catatonia: the biography of a treatable syndrome. Acta Psychiatr Scand Suppl. 2013;(441):1-47.
18. Fink M, Taylor MA. Catatonia: a clinician’s guide to diagnosis and treatment. Cambridge University Press; 2006.
19. Petrides G, Tobias KG, Kellner CH, et al. Continuation and maintenance electroconvulsive therapy for mood disorders: review of the literature. Neuropsychobiology. 2011;64(3):129-140.
CASE Aggressive behaviors, psychosis
Ms. N, age 58, has a long history of bipolar disorder with psychotic features. She presents to our emergency department (ED) after an acute fall and frequent violent behaviors at her nursing home, where she had resided since being diagnosed with an unspecified neurocognitive disorder. For several weeks before her fall, she was physically aggressive, throwing objects at nursing home staff, and was unable to have her behavior redirected.
While in the ED, Ms. N rambles and appears to be responding to internal stimuli. Suddenly, she stops responding and begins to stare.
HISTORY Severe, chronic psychosis and hospitalization
Ms. N is well-known at our inpatient psychiatry and electroconvulsive therapy (ECT) services. During the last 10 years, she has had worsening manic, psychotic, and catatonic (both excited and stuporous subtype) episodes. Three years ago, she had experienced a period of severe, chronic psychosis and excited catatonia that required extended inpatient treatment. While hospitalized, Ms. N had marginal responses to clozapine and benzodiazepines, but improved dramatically with ECT. After Ms. N left the hospital, she went to live with her boyfriend. She remained stable on monthly maintenance ECT treatments (bifrontal) before she was lost to follow-up 14 months prior to the current presentation. Ms. N’s family reports that she needed a cardiac clearance before continuing ECT treatment; however, she was hospitalized at another hospital with pneumonia and subsequent complications that interrupted the maintenance ECT treatments.
Approximately 3 months after medical issues requiring hospitalization began, Ms. N received a diagnosis of neurocognitive disorder due to difficulty with activities of daily living and cognitive decline. She was transferred to a nursing home by the outside hospital. When Ms. N’s symptoms of psychosis returned and she required inpatient psychiatric care, she was transferred to a nearby facility that did not have ECT available or knowledge of her history of catatonia resistant to pharmacologic management. Ms. N had a documented history of catatonia that spanned 10 years. During the last 4 years, Ms. N often required ECT treatment. Her current medication regimen prescribed by an outpatient psychiatrist includes clozapine, 300 mg twice daily, and clonazepam, 0.5 mg twice daily, both for bipolar disorder.
EVALUATION An unusual mix of symptoms
In the ED, Ms. N undergoes a CT of the head, which is found to be nonacute. Laboratory results show that her white blood cell count is 14.3 K/µL, which is mildly elevated. Results from a urinalysis and electrocardiogram (ECG) are unremarkable.
After Ms. N punches a radiology technician, she is administered IV lorazepam, 2 mg once, for her agitation. Twenty minutes after receiving IV lorazepam, she is calm and cooperative. However, approximately 4 hours later, Ms. N is yelling, tearful, and expressing delusions of grandeur—she believes she is God.
After she is admitted to the medical floor, Ms. N is seen by our consultation and liaison psychiatry service. She exhibits several signs of catatonia, including grasp reflex, gegenhalten (oppositional paratonia), waxy flexibility, and echolalia. Ms. N also has an episode of urinary incontinence. At some parts of the day, she is alert and oriented to self and location; at other times, she is somnolent and disoriented. The treatment team continues Ms. N’s previous medication regimen of clozapine, 300 mg twice daily, and clonazepam, 0.5 mg twice daily. Unfortunately, at times Ms. N spits out and hides her administered oral medications, which leads to the decision to discontinue clozapine. Once medically cleared, Ms. N is transferred to the psychiatric floor.
[polldaddy:10869949]
Continue to: TREATMENT
TREATMENT Bifrontal ECT initiated
On hospital Day 3 Ms. N is administered a trial of IM lorazepam, titrated up to 6 mg/d (maximum tolerated dose) while the treatment team initiates the legal process to conduct ECT because she is unable to give consent. Once Ms. N begins tolerating oral medications, amantadine, 100 mg twice daily, is added to treat her catatonia. As in prior hospitalizations, Ms. N is unresponsive to pharmacotherapy alone for her catatonic symptoms. On hospital Day 8, forced ECT is granted, which is 5 days after the process of filing paperwork was started. Bifrontal ECT is utilized with the following settings: frequency 70 Hz, pulse width 1.5 ms, 100% energy dose, 504 mC. Ms. N does not experience a significant improvement until she receives 10 ECT treatments as part of a 3-times-per-week acute series protocol. The Bush-Francis Catatonia Rating Scale (BFCRS) and the KANNER scale are used to monitor her progress. Her initial BFCRS score is 17 and initial KANNER scale, part 2 score is 26.
Ms. N spends a total of 61 days in the hospital, which is significantly longer than her previous hospital admissions on our psychiatric unit; these previous admissions were for treatment of both stuporous and excited subtypes of catatonia. This increased length of stay coincides with a significantly longer duration of untreated catatonia. Knowledge of her history of both the stuporous and excited subtypes of catatonia would have allowed for faster diagnosis and treatment.1
The authors’ observations
Originally conceptualized as a separate syndrome by Karl Kahlbaum, catatonia was considered only as a specifier for neuropsychiatric conditions (primarily schizophrenia) as recently as DSM-IV-TR.2 DSM-5 describes catatonia as a marked psychomotor disturbance and acknowledges its connection to schizophrenia by keeping it in the same chapter.3 DSM-5 includes separate diagnoses for catatonia, catatonia due to a general medical condition, and unspecified catatonia (for catatonia without a known underlying disorder).3 A recent meta-analysis found the prevalence of catatonia is higher in patients with medical/neurologic illness, bipolar disorder, and autism than in those with schizophrenia.4
Table 13 highlights the DSM-5 criteria for catatonia. DSM-5 requires 3 of 12 symptoms to be present, although symptoms may fluctuate with time.3 If a clinician is not specifically looking for catatonia, it can be a difficult syndrome to diagnose. Does rigidity indicate catatonia, or excessive dopamine blockade from an antipsychotic? How can seemingly contradictory symptoms be part of the same syndrome? Many clinicians associate catatonia with the stuporous subtype (immobility, posturing, catalepsy), which is more prevalent, but the excited subtype, which may involve severe agitation, autonomic dysfunction, and impaired consciousness, can be lethal.2 The diversity in presentation of catatonia is not unlike the challenging variety of symptoms of heart attacks.
A retrospective study of all adults admitted to a hospital found that only 41% of patients who met criteria for catatonia received this diagnosis.5 Further complicating the diagnosis, delirium and catatonia can co-exist; one study found this was the case in 1 of 3 critically ill patients.6 DSM-5 criteria for catatonia due to another medical condition exclude the diagnosis if delirium is present, but this study and others suggest this needs to be reconsidered.3
Continue to: A standardized evaluation is key
A standardized evaluation is key
Just as a patient who presents with chest pain requires a standardized evaluation, including a pertinent history, laboratory workup, and ECG, psychiatrists may also use standardized diagnostic instruments to aid in the diagnosis of catatonia. One study of hospitalized patients with schizophrenia found that using a standardized diagnostic procedure for catatonia resulted in a 7-fold increase in the diagnosis.7 The BFCRS is the most common standardized instrument for catatonia, likely due to its high inter-rater reliability.8 Other scales include the KANNER scale and Northoff Catatonia Scale, which emphasize different aspects of the disease or for certain clinical populations (eg, the KANNER scale adjusts for patients who are nonverbal at baseline). One study suggested that BFCRS has lower reliability for less-severe illness.9 These differences emphasize that psychiatry does not have a thorough understanding of the intricacies of catatonia. However, using validated screening tools can lead to more consistent diagnoses and continue important research on this often-misunderstood illness.
Dangers of untreated catatonia
Rapid treatment of catatonia is necessary to prevent mortality. A study of patients in Kentucky’s state psychiatric hospitals found that untreated catatonia with resultant death from pulmonary embolism was the leading cause of preventable death.10 A 17-year retrospective study of patients with schizophrenia admitted to 1 hospital found that those with catatonia were >4 times as likely to die during hospitalization than those without catatonia.11 The significant morbidity and mortality from untreated catatonia are typically attributed to the consequences of poorly controlled movements, immobility, autonomic instability, and poor/no oral intake. Reduced oral intake can result in malnutrition, dehydration, arrhythmias, and increased risk of infections. Furthermore, chronic catatonic episodes are more difficult to treat.12 In addition to the aggressive management of neuropsychiatric symptoms, it is vital to evaluate relevant medical etiologies that may be contributing to the syndrome (Table 213). Tracking vital signs and laboratory values, such as creatine kinase, electrolytes, and complete blood count, is required to ensure the medical condition does not become life-threatening.
Treatment options
Studies and expert opinion suggest that benzodiazepines (specifically lorazepam, because it is the most studied agent) are the first-line treatment for catatonia. A lorazepam challenge test—providing 1 or 2 mg of IV lorazepam—is considered diagnostic and therapeutic given the high rate of response within 10 minutes.14 Patients with limited response to lorazepam or who are medically compromised should undergo ECT. Electroconvulsive therapy is considered the gold-standard treatment for catatonia; estimated response rates range from 59% to 100%, even in patients who fail to respond to pharmacotherapy.15 Although highly effective, ECT is often hindered by the time required to initiate treatment, stigma, lack of access, and other logistical challenges.
Table 314-18 highlights the advantages and disadvantages of treatment options for catatonia. Some researchers have suggested a zolpidem challenge test could augment lorazepam because some patients respond only to zolpidem.14 The efficacy of these medications along with some evidence of anti-N-methyl-
Ms. N was ultimately diagnosed with bipolar disorder, current episode mixed, with psychotic and catatonic features. Ms. N had symptoms of mania including grandiosity, periods of lack of sleep, delusions as well as depressive symptoms of tearfulness and low mood. The treatment team had considered that Ms. N had delirious mania because she had fluctuating sensorium, which included varying degrees of orientation and ability to answer questioning. However, the literature supporting the differentiation between delirious mania and excited catatonia is unclear, and both conditions may respond to ECT.18 A diagnosis of catatonia allowed the team to use rating scales to track Ms. N’s progress by monitoring for specific signs, such as grasp reflex and waxy flexibility.
Continue to: OUTCOME
OUTCOME Return to baseline
Before discharge, Ms. N’s BFCRS score decreases from the initial score of 17 to 0, and her KANNER scale score decreases from the initial score of 26 to 4, which correlates with vast improvement in clinical presentation. Once Ms. N completes the acute ECT treatment, she returns to her baseline level of functioning, and is discharged to live with her boyfriend. She is advised to continue weekly ECT for the first several months to ensure clinical stability. This regimen is later transitioned to biweekly and then monthly. Electroconvulsive therapy protocols from previous research were utilized in Ms. N’s case, but ultimately the lowest number of ECT treatments needed to maintain stability is determined clinically over many years.19 Ms. N is discharged on aripiprazole, 15 mg/d; bupropion ER, 300 mg/d (added after depressive symptoms emerge while catatonia symptoms improve midway through her lengthy hospitalization); and memantine, 10 mg/d. Ideally, clozapine would have been continued; however, due to her history of nonadherence and frequent restarting of the medication at a low dose, clozapine was discontinued and aripiprazole initiated.
More than 1 year later, Ms. N remains stable and continues to receive monthly ECT maintenance treatments.
Bottom Line
Catatonia should always be considered in a patient who presents with acute neuropsychiatric symptoms. Rapid diagnosis with standardized screening instruments and aggressive treatment are vital to prevent morbidity and mortality.
Related Resource
- Freudenreich O, Francis A, Fricchione GL. Chapter 9. Psychosis, mania, and catatonia. In: Levenson, James L, ed. The American Psychiatric Association Publishing textbook of psychosomatic medicine and consultation-liaison psychiatry. 3rd ed. American Psychiatric Association Publishing; 2019.
Drug Brand Names
Amantadine • Symmetrel
Aripiprazole • Abilify
Baclofen • Ozobax
Bupropion ER • Wellbutrin XL
Clonazepam • Klonopin
Clozapine • Clozaril
Lithium • Eskalith, Lithobid
Lorazepam • Ativan
Metoclopramide • Reglan
Memantine • Namenda
Topiramate • Topamax
Zolpidem • Ambien
CASE Aggressive behaviors, psychosis
Ms. N, age 58, has a long history of bipolar disorder with psychotic features. She presents to our emergency department (ED) after an acute fall and frequent violent behaviors at her nursing home, where she had resided since being diagnosed with an unspecified neurocognitive disorder. For several weeks before her fall, she was physically aggressive, throwing objects at nursing home staff, and was unable to have her behavior redirected.
While in the ED, Ms. N rambles and appears to be responding to internal stimuli. Suddenly, she stops responding and begins to stare.
HISTORY Severe, chronic psychosis and hospitalization
Ms. N is well-known at our inpatient psychiatry and electroconvulsive therapy (ECT) services. During the last 10 years, she has had worsening manic, psychotic, and catatonic (both excited and stuporous subtype) episodes. Three years ago, she had experienced a period of severe, chronic psychosis and excited catatonia that required extended inpatient treatment. While hospitalized, Ms. N had marginal responses to clozapine and benzodiazepines, but improved dramatically with ECT. After Ms. N left the hospital, she went to live with her boyfriend. She remained stable on monthly maintenance ECT treatments (bifrontal) before she was lost to follow-up 14 months prior to the current presentation. Ms. N’s family reports that she needed a cardiac clearance before continuing ECT treatment; however, she was hospitalized at another hospital with pneumonia and subsequent complications that interrupted the maintenance ECT treatments.
Approximately 3 months after medical issues requiring hospitalization began, Ms. N received a diagnosis of neurocognitive disorder due to difficulty with activities of daily living and cognitive decline. She was transferred to a nursing home by the outside hospital. When Ms. N’s symptoms of psychosis returned and she required inpatient psychiatric care, she was transferred to a nearby facility that did not have ECT available or knowledge of her history of catatonia resistant to pharmacologic management. Ms. N had a documented history of catatonia that spanned 10 years. During the last 4 years, Ms. N often required ECT treatment. Her current medication regimen prescribed by an outpatient psychiatrist includes clozapine, 300 mg twice daily, and clonazepam, 0.5 mg twice daily, both for bipolar disorder.
EVALUATION An unusual mix of symptoms
In the ED, Ms. N undergoes a CT of the head, which is found to be nonacute. Laboratory results show that her white blood cell count is 14.3 K/µL, which is mildly elevated. Results from a urinalysis and electrocardiogram (ECG) are unremarkable.
After Ms. N punches a radiology technician, she is administered IV lorazepam, 2 mg once, for her agitation. Twenty minutes after receiving IV lorazepam, she is calm and cooperative. However, approximately 4 hours later, Ms. N is yelling, tearful, and expressing delusions of grandeur—she believes she is God.
After she is admitted to the medical floor, Ms. N is seen by our consultation and liaison psychiatry service. She exhibits several signs of catatonia, including grasp reflex, gegenhalten (oppositional paratonia), waxy flexibility, and echolalia. Ms. N also has an episode of urinary incontinence. At some parts of the day, she is alert and oriented to self and location; at other times, she is somnolent and disoriented. The treatment team continues Ms. N’s previous medication regimen of clozapine, 300 mg twice daily, and clonazepam, 0.5 mg twice daily. Unfortunately, at times Ms. N spits out and hides her administered oral medications, which leads to the decision to discontinue clozapine. Once medically cleared, Ms. N is transferred to the psychiatric floor.
[polldaddy:10869949]
Continue to: TREATMENT
TREATMENT Bifrontal ECT initiated
On hospital Day 3 Ms. N is administered a trial of IM lorazepam, titrated up to 6 mg/d (maximum tolerated dose) while the treatment team initiates the legal process to conduct ECT because she is unable to give consent. Once Ms. N begins tolerating oral medications, amantadine, 100 mg twice daily, is added to treat her catatonia. As in prior hospitalizations, Ms. N is unresponsive to pharmacotherapy alone for her catatonic symptoms. On hospital Day 8, forced ECT is granted, which is 5 days after the process of filing paperwork was started. Bifrontal ECT is utilized with the following settings: frequency 70 Hz, pulse width 1.5 ms, 100% energy dose, 504 mC. Ms. N does not experience a significant improvement until she receives 10 ECT treatments as part of a 3-times-per-week acute series protocol. The Bush-Francis Catatonia Rating Scale (BFCRS) and the KANNER scale are used to monitor her progress. Her initial BFCRS score is 17 and initial KANNER scale, part 2 score is 26.
Ms. N spends a total of 61 days in the hospital, which is significantly longer than her previous hospital admissions on our psychiatric unit; these previous admissions were for treatment of both stuporous and excited subtypes of catatonia. This increased length of stay coincides with a significantly longer duration of untreated catatonia. Knowledge of her history of both the stuporous and excited subtypes of catatonia would have allowed for faster diagnosis and treatment.1
The authors’ observations
Originally conceptualized as a separate syndrome by Karl Kahlbaum, catatonia was considered only as a specifier for neuropsychiatric conditions (primarily schizophrenia) as recently as DSM-IV-TR.2 DSM-5 describes catatonia as a marked psychomotor disturbance and acknowledges its connection to schizophrenia by keeping it in the same chapter.3 DSM-5 includes separate diagnoses for catatonia, catatonia due to a general medical condition, and unspecified catatonia (for catatonia without a known underlying disorder).3 A recent meta-analysis found the prevalence of catatonia is higher in patients with medical/neurologic illness, bipolar disorder, and autism than in those with schizophrenia.4
Table 13 highlights the DSM-5 criteria for catatonia. DSM-5 requires 3 of 12 symptoms to be present, although symptoms may fluctuate with time.3 If a clinician is not specifically looking for catatonia, it can be a difficult syndrome to diagnose. Does rigidity indicate catatonia, or excessive dopamine blockade from an antipsychotic? How can seemingly contradictory symptoms be part of the same syndrome? Many clinicians associate catatonia with the stuporous subtype (immobility, posturing, catalepsy), which is more prevalent, but the excited subtype, which may involve severe agitation, autonomic dysfunction, and impaired consciousness, can be lethal.2 The diversity in presentation of catatonia is not unlike the challenging variety of symptoms of heart attacks.
A retrospective study of all adults admitted to a hospital found that only 41% of patients who met criteria for catatonia received this diagnosis.5 Further complicating the diagnosis, delirium and catatonia can co-exist; one study found this was the case in 1 of 3 critically ill patients.6 DSM-5 criteria for catatonia due to another medical condition exclude the diagnosis if delirium is present, but this study and others suggest this needs to be reconsidered.3
Continue to: A standardized evaluation is key
A standardized evaluation is key
Just as a patient who presents with chest pain requires a standardized evaluation, including a pertinent history, laboratory workup, and ECG, psychiatrists may also use standardized diagnostic instruments to aid in the diagnosis of catatonia. One study of hospitalized patients with schizophrenia found that using a standardized diagnostic procedure for catatonia resulted in a 7-fold increase in the diagnosis.7 The BFCRS is the most common standardized instrument for catatonia, likely due to its high inter-rater reliability.8 Other scales include the KANNER scale and Northoff Catatonia Scale, which emphasize different aspects of the disease or for certain clinical populations (eg, the KANNER scale adjusts for patients who are nonverbal at baseline). One study suggested that BFCRS has lower reliability for less-severe illness.9 These differences emphasize that psychiatry does not have a thorough understanding of the intricacies of catatonia. However, using validated screening tools can lead to more consistent diagnoses and continue important research on this often-misunderstood illness.
Dangers of untreated catatonia
Rapid treatment of catatonia is necessary to prevent mortality. A study of patients in Kentucky’s state psychiatric hospitals found that untreated catatonia with resultant death from pulmonary embolism was the leading cause of preventable death.10 A 17-year retrospective study of patients with schizophrenia admitted to 1 hospital found that those with catatonia were >4 times as likely to die during hospitalization than those without catatonia.11 The significant morbidity and mortality from untreated catatonia are typically attributed to the consequences of poorly controlled movements, immobility, autonomic instability, and poor/no oral intake. Reduced oral intake can result in malnutrition, dehydration, arrhythmias, and increased risk of infections. Furthermore, chronic catatonic episodes are more difficult to treat.12 In addition to the aggressive management of neuropsychiatric symptoms, it is vital to evaluate relevant medical etiologies that may be contributing to the syndrome (Table 213). Tracking vital signs and laboratory values, such as creatine kinase, electrolytes, and complete blood count, is required to ensure the medical condition does not become life-threatening.
Treatment options
Studies and expert opinion suggest that benzodiazepines (specifically lorazepam, because it is the most studied agent) are the first-line treatment for catatonia. A lorazepam challenge test—providing 1 or 2 mg of IV lorazepam—is considered diagnostic and therapeutic given the high rate of response within 10 minutes.14 Patients with limited response to lorazepam or who are medically compromised should undergo ECT. Electroconvulsive therapy is considered the gold-standard treatment for catatonia; estimated response rates range from 59% to 100%, even in patients who fail to respond to pharmacotherapy.15 Although highly effective, ECT is often hindered by the time required to initiate treatment, stigma, lack of access, and other logistical challenges.
Table 314-18 highlights the advantages and disadvantages of treatment options for catatonia. Some researchers have suggested a zolpidem challenge test could augment lorazepam because some patients respond only to zolpidem.14 The efficacy of these medications along with some evidence of anti-N-methyl-
Ms. N was ultimately diagnosed with bipolar disorder, current episode mixed, with psychotic and catatonic features. Ms. N had symptoms of mania including grandiosity, periods of lack of sleep, delusions as well as depressive symptoms of tearfulness and low mood. The treatment team had considered that Ms. N had delirious mania because she had fluctuating sensorium, which included varying degrees of orientation and ability to answer questioning. However, the literature supporting the differentiation between delirious mania and excited catatonia is unclear, and both conditions may respond to ECT.18 A diagnosis of catatonia allowed the team to use rating scales to track Ms. N’s progress by monitoring for specific signs, such as grasp reflex and waxy flexibility.
Continue to: OUTCOME
OUTCOME Return to baseline
Before discharge, Ms. N’s BFCRS score decreases from the initial score of 17 to 0, and her KANNER scale score decreases from the initial score of 26 to 4, which correlates with vast improvement in clinical presentation. Once Ms. N completes the acute ECT treatment, she returns to her baseline level of functioning, and is discharged to live with her boyfriend. She is advised to continue weekly ECT for the first several months to ensure clinical stability. This regimen is later transitioned to biweekly and then monthly. Electroconvulsive therapy protocols from previous research were utilized in Ms. N’s case, but ultimately the lowest number of ECT treatments needed to maintain stability is determined clinically over many years.19 Ms. N is discharged on aripiprazole, 15 mg/d; bupropion ER, 300 mg/d (added after depressive symptoms emerge while catatonia symptoms improve midway through her lengthy hospitalization); and memantine, 10 mg/d. Ideally, clozapine would have been continued; however, due to her history of nonadherence and frequent restarting of the medication at a low dose, clozapine was discontinued and aripiprazole initiated.
More than 1 year later, Ms. N remains stable and continues to receive monthly ECT maintenance treatments.
Bottom Line
Catatonia should always be considered in a patient who presents with acute neuropsychiatric symptoms. Rapid diagnosis with standardized screening instruments and aggressive treatment are vital to prevent morbidity and mortality.
Related Resource
- Freudenreich O, Francis A, Fricchione GL. Chapter 9. Psychosis, mania, and catatonia. In: Levenson, James L, ed. The American Psychiatric Association Publishing textbook of psychosomatic medicine and consultation-liaison psychiatry. 3rd ed. American Psychiatric Association Publishing; 2019.
Drug Brand Names
Amantadine • Symmetrel
Aripiprazole • Abilify
Baclofen • Ozobax
Bupropion ER • Wellbutrin XL
Clonazepam • Klonopin
Clozapine • Clozaril
Lithium • Eskalith, Lithobid
Lorazepam • Ativan
Metoclopramide • Reglan
Memantine • Namenda
Topiramate • Topamax
Zolpidem • Ambien
1. Carroll BT. The universal field hypothesis of catatonia and neuroleptic malignant syndrome. CNS Spectrums. 2000;5(7):26-33.
2. Rasmussen SA, Mazurek MF, Rosebush PI. Catatonia: our current understanding of its diagnosis, treatment and pathophysiology. World J Psychiatry. 2016;6(4):391‐398.
3. Diagnostic and statistical manual of mental disorders, 5th ed. American Psychiatric Association; 2013. 119-121.
4. Solmi M, Pigato GG, Roiter B, et al. Prevalence of catatonia and its moderators in clinical samples: results from a meta-analysis and meta-regression analysis. Schizophrenia Bulletin. 2017;44(5):1133-1150.
5. Llesuy JR, Medina M, Jacobson KC, et al. Catatonia under-diagnosis in the general hospital. J Neuropsychiatry Clin Neurosci. 2018;30(2):145-151.
6. Wilson JE, Carlson R, Duggan MC, et al. Delirium and catatonia in critically ill patients. Crit Care Med. 2017;45(11):1837-1844.
7. Heijden FVD, Tuinier S, Arts N, et al. Catatonia: disappeared or under-diagnosed? Psychopathology. 2005;38(1):3-8.
8. Sarkar S, Sakey S, Mathan K, et al. Assessing catatonia using four different instruments: inter-rater reliability and prevalence in inpatient clinical population. Asian J Psychiatr. 2016;23:27-31.
9. Wilson JE, Niu K, Nicolson SE, et al. The diagnostic criteria and structure of catatonia. Schizophr Res. 2015;164(1-3):256-262.
10. Puentes R, Brenzel A, Leon JD. Pulmonary embolism during stuporous episodes of catatonia was found to be the most frequent cause of preventable death according to a state mortality review: 6 deaths in 15 years. Clin Schizophr Relat Psychoses. 2017; doi:10.3371/csrp.rpab.071317
11. Funayama M, Takata T, Koreki A, et al. Catatonic stupor in schizophrenic disorders and subsequent medical complications and mortality. Psychosomatic Medicine. 2018:80(4):370-376.
12. Perugi G, Medda P, Toni C, et al. The role of electroconvulsive therapy (ECT) in bipolar disorder: effectiveness in 522 patients with bipolar depression, mixed-state, mania and catatonic features. Curr Neuropharmacol. 2017;15(3):359-371.
13. Freudenreich O, Francis A, Fricchione GL. Chapter 9. Psychosis, mania, and catatonia. In: Levenson, James L, ed. The American Psychiatric Association Publishing Textbook of Psychosomatic medicine and Consultation-Liaison Psychiatry. 3rd ed. American Psychiatric Association Publishing; 2019.
14. Sienaert P, Dhossche DM, Vancampfort D, et al. A clinical review of the treatment of catatonia. Front Psychiatry. 2014;5:181.
15. Pelzer A, Heijden FVD, Boer ED. Systematic review of catatonia treatment. Neuropsychiatr Dis Treat. 2018;14:317-326.
16. Carroll BT, Goforth HW, Thomas C, et al. Review of adjunctive glutamate antagonist therapy in the treatment of catatonic syndromes. J Neuropsychiatry and Clin Neurosci. 2007;19(4):406-412.
17. Fink M. Rediscovering catatonia: the biography of a treatable syndrome. Acta Psychiatr Scand Suppl. 2013;(441):1-47.
18. Fink M, Taylor MA. Catatonia: a clinician’s guide to diagnosis and treatment. Cambridge University Press; 2006.
19. Petrides G, Tobias KG, Kellner CH, et al. Continuation and maintenance electroconvulsive therapy for mood disorders: review of the literature. Neuropsychobiology. 2011;64(3):129-140.
1. Carroll BT. The universal field hypothesis of catatonia and neuroleptic malignant syndrome. CNS Spectrums. 2000;5(7):26-33.
2. Rasmussen SA, Mazurek MF, Rosebush PI. Catatonia: our current understanding of its diagnosis, treatment and pathophysiology. World J Psychiatry. 2016;6(4):391‐398.
3. Diagnostic and statistical manual of mental disorders, 5th ed. American Psychiatric Association; 2013. 119-121.
4. Solmi M, Pigato GG, Roiter B, et al. Prevalence of catatonia and its moderators in clinical samples: results from a meta-analysis and meta-regression analysis. Schizophrenia Bulletin. 2017;44(5):1133-1150.
5. Llesuy JR, Medina M, Jacobson KC, et al. Catatonia under-diagnosis in the general hospital. J Neuropsychiatry Clin Neurosci. 2018;30(2):145-151.
6. Wilson JE, Carlson R, Duggan MC, et al. Delirium and catatonia in critically ill patients. Crit Care Med. 2017;45(11):1837-1844.
7. Heijden FVD, Tuinier S, Arts N, et al. Catatonia: disappeared or under-diagnosed? Psychopathology. 2005;38(1):3-8.
8. Sarkar S, Sakey S, Mathan K, et al. Assessing catatonia using four different instruments: inter-rater reliability and prevalence in inpatient clinical population. Asian J Psychiatr. 2016;23:27-31.
9. Wilson JE, Niu K, Nicolson SE, et al. The diagnostic criteria and structure of catatonia. Schizophr Res. 2015;164(1-3):256-262.
10. Puentes R, Brenzel A, Leon JD. Pulmonary embolism during stuporous episodes of catatonia was found to be the most frequent cause of preventable death according to a state mortality review: 6 deaths in 15 years. Clin Schizophr Relat Psychoses. 2017; doi:10.3371/csrp.rpab.071317
11. Funayama M, Takata T, Koreki A, et al. Catatonic stupor in schizophrenic disorders and subsequent medical complications and mortality. Psychosomatic Medicine. 2018:80(4):370-376.
12. Perugi G, Medda P, Toni C, et al. The role of electroconvulsive therapy (ECT) in bipolar disorder: effectiveness in 522 patients with bipolar depression, mixed-state, mania and catatonic features. Curr Neuropharmacol. 2017;15(3):359-371.
13. Freudenreich O, Francis A, Fricchione GL. Chapter 9. Psychosis, mania, and catatonia. In: Levenson, James L, ed. The American Psychiatric Association Publishing Textbook of Psychosomatic medicine and Consultation-Liaison Psychiatry. 3rd ed. American Psychiatric Association Publishing; 2019.
14. Sienaert P, Dhossche DM, Vancampfort D, et al. A clinical review of the treatment of catatonia. Front Psychiatry. 2014;5:181.
15. Pelzer A, Heijden FVD, Boer ED. Systematic review of catatonia treatment. Neuropsychiatr Dis Treat. 2018;14:317-326.
16. Carroll BT, Goforth HW, Thomas C, et al. Review of adjunctive glutamate antagonist therapy in the treatment of catatonic syndromes. J Neuropsychiatry and Clin Neurosci. 2007;19(4):406-412.
17. Fink M. Rediscovering catatonia: the biography of a treatable syndrome. Acta Psychiatr Scand Suppl. 2013;(441):1-47.
18. Fink M, Taylor MA. Catatonia: a clinician’s guide to diagnosis and treatment. Cambridge University Press; 2006.
19. Petrides G, Tobias KG, Kellner CH, et al. Continuation and maintenance electroconvulsive therapy for mood disorders: review of the literature. Neuropsychobiology. 2011;64(3):129-140.
