Approach Considerations

On the grounds that treatment of the underlying disorder relieves the catatonia, Lahutte et al recommended prompt diagnosis and therapy of the comorbid disorders to prevent morbidity and mortality.^[81]This process includes appropriate use of laboratory tests, imaging modalities, and electroencephalography (EEG). EEG is performed to rule out underlying causes.^[82]While an EEG often reveals focal abnormalities or generalized slowing, an EEG may be normal in catatonia.

Lorazepam challenge can also help the diagnosis of catatonia. Patients who respond to the first or two doses of IV lorazepam (1 to 2 mg) are likely to have catatonia. Partial or temporary relief of symptoms and signs of catatonia after 5 to 10 minutes of injection is consistent with catatonia.^{[83, 1]}

An effort should be made to assess the degree of catatonia present. Of the several scales that have been developed to measure catatonia, the Bush-Francis Catatonia Rating Scale (BFCRF) is favored, owing to its demonstrated reliability and validity in clinical settings.^{[84, 85]}

Laboratory Studies

A complete blood count (CBC), measurement of electrolyte concentrations, and chemical analyses of blood are appropriate. In particular, hyponatremia and other metabolic abnormalities must be ruled out.

Fibrin D-dimer levels must be obtained to rule out early coagulation activation.^[61]Patients with catatonia typically have fibrin D-dimer levels higher than 500 ng/mL.^[61]Prompt identification and treatment of pulmonary embolism in people with catatonia are crucial for minimizing morbidity and mortality.^[86]

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

Magnetic Resonance Imaging and Computed Tomography

Imaging of the head by means of magnetic resonance imaging (MRI) or computed tomography (CT) is indicated to rule out treatable mass lesions. If no evidence of increased intracranial pressure is noted on imaging, lumbar puncture is appropriate to rule out encephalitis and other infections, hemorrhages, and tumors.

People with catatonia may exhibit increased ventricle-to-brain ratios on CT scans. However, CT cannot be used to establish the diagnosis of catatonia. The main value of CT in patients with catatonia is to rule out other treatable disorders.

Single-photon emission CT (SPECT) has demonstrated increased cerebral blood flow in the parietal, temporal, and occipital regions of some patients with catatonia secondary to mood disorders after treatment with electroconvulsive treatment (ECT). However, SPECT cannot be used to establish the diagnosis of catatonia. The main value of SPECT in patients with catatonia, like that of CT, is to rule out other treatable disorders.

Positron Emission Tomography

Positron emission tomography (PET) with fluorodeoxyglucose (FDG) reveals bitemporal hypometabolism in catatonia. Patients with various vegetative states have demonstrated decrements in regional cerebral blood flow in the prefrontal and the parietotemporal association areas. However, PET cannot be used to establish the diagnosis of catatonia. The main value of PET in patients with catatonia is to rule out other treatable disorders.^{[10, 11]}

Electroencephalography

EEG is indicated to rule out a seizure disorder. Nonconvulsive status epilepticus can readily be identified on EEG. Obtaining a portable EEG in the emergency department (ED) may quickly confirm the presence of nonconvulsive status epilepticus.

EEG changes in catatonia typically include focal abnormalities or generalized slowing.^[4]However, a normal EEG may occur in a patients with the excited state of catatonia due to anti-NMDA receptor encephalitis.^[4]Therefore, a normal EEG in a patient with catatonia does not rule out the presence of cerebral pathology.

During the psychotic episodes of periodic catatonia, alpha rhythm is characterized by an increase in frequency and a decrease in amplitude. In a patient with periodic catatonia, increased urinary excretion of 4-hydroxy-3-methoxy-mandelic acid (VMA) and of normetadrenaline correlated with increased frequences of alpha rhythm.^{[87, 88]}

Other Tests

Transcranial magnetic stimulation (TMS) is a procedure under investigation for patients with catatonia.

Treatment & Management

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Table. Causes of Catatonia by Category

Table. Causes of Catatonia by Category

Category	Causes
Neurologic conditions	Neuroleptic malignant syndrome^[27] Administration of agents that block postsynaptic dopamine receptors* Administration of sibutramine^[28](withdrawn from US market October 8, 2010) Withdrawal of lorazepam and other sedatives Akinetic-rigid syndrome Anti-NMDA receptor encephalitis^[4] Arachnoid cyst in right parietal region Astrocytoma Atrophy of left amygdala^[29] Autistic disorder^{[17, 10, 11, 30, 31, 32, 33, 34, 35, 12, 13]} Basilar artery thrombosis Bilateral hemorrhagic lesions of temporal lobes Cerebellar catalepsy Cerebral hemorrhage Cerebral infarct Cerebrovascular disease Cortical venous thrombosis Central pontine myelinolysis Cortical basal ganglionic degeneration Dystonia Encephalitis (herpesvirus, Trypanosoma cruzi) Encephalopathy (Borrelia burgdorferi, HIV infection, Wernicke encephalopathy) Familial fatal insomnia^[36] Fibromuscular dysplasia with dissection of basilar artery Frontal lobotomy Head injury Huntington disease Hydrocephalus Hypopituitarism secondary to postpartum hemorrhage Idiopathic recurring stupor Inherited neurometabolic disorders Locked-in syndrome Meningitis, tuberculous Meningoencephalitis Multiple sclerosis^{[37, 38]} Neurosyphilis Nonconvulsive status epilepticus Pervasive developmental disorders^{[10, 11, 34]} Pallidoluysian atrophy Paraneoplastic encephalitis^[39] Parkinsonism Postencephalitic parkinsonism Progressive multifocal leukoencephalopathy Progressive supranuclear palsy Schizencephaly Seizures (complex with partial symptomatology) Stiff-man syndrome Stroke Stupor Subarachnoid hemorrhage Subdural hematoma Substance intoxication (alcohol, disulfiram, organic fluorides, phencyclidine) Subthalamic mesencephalic tumor Surgical removal of cerebellar tumor Tay-Sachs disease Temporal lobe epilepsy Tuberous sclerosis Tumors (corpus callosum, glioma of third ventricle, supraventricular diffuse pinealoma) Vegetative state Von Economo (lethargic) encephalitis Wilson disease
Psychiatric conditions	Acute stress disorder Anorexia nervosa Autistic disorder^[17] Brief reactive psychosis with catatonia Conversion disorder Hysteria Major depression, single episode with catatonic features Mood disorders Neuroleptic malignant syndrome^[27] Posttraumatic stress disorder Schizophrenia Substance intoxication (3,4-methylenedioxymethamphetamine [“ecstasy”], alcohol, amphetamine, phencyclidine, substance withdrawal, hypnotic-sedative, lorazepam)
Psychological factors	Immigration Experiencing rejection of an expression of love Feelings of alienation in an unfamiliar country
Medical conditions	AIDS Acute intermittent porphyria Addison disease Bacterial septicemia Bronchorrhea Carcinoid tumors Diabetic ketoacidosis Encephalopathy (hepatic, HIV infection, Wernicke encephalopathy) Fever of unknown cause Heat stroke Hepatic failure Hereditary coproporphyria Homocystinuria Hypercalcemia Hyperparathyroidism Hyperthyroidism Hyponatremia Hypothermia Intestinal atony Malaria Neuroleptic malignant syndrome^[27] Poisoning (carbon monoxide, tetraethyl lead) Renal failure Substance intoxication (alcohol, cyclosporine, disulfiram, organic fluorides, phencyclidine) Syndrome of inappropriate antidiuretic hormone (SIADH) Syphilis Systemic lupus erythematosus Thermal injury Thrombotic thrombocytopenic purpura Tuberculosis Typhoid fever Uremia Von Economo (lethargic) encephalitis
Obstetric conditions	Hypopituitarism secondary to postpartum hemorrhage
*Administration of agents that block postsynaptic dopamine receptors is associated with the onset of catatonia in some individuals.

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Author

James Robert Brasic, MD, MPH, MS, MA Assistant Professor, Russell H Morgan Department of Radiology and Radiological Science and Neurology, Division of Nuclear Medicine and Molecular Imaging, Assistant Professor, Department of Neurology, Johns Hopkins University School of Medicine

James Robert Brasic, MD, MPH, MS, MA is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Academy of Neurology, International Parkinson and Movement Disorder Society, Society for Neuroscience, Society of Nuclear Medicine and Molecular Imaging

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Johns Hopkins University School of Medicine Serve(d) as a speaker or a member of a speakers bureau for: Society of Nuclear Medicine and Molecular Imaging, Maryland Regional Council of Child and Adolescent Psychiatry Received research grant from: National Institutes of Health, Johns Hopkins University School of Medicine, Intellectual & Developmental Disabilities Research Center (U54 HD079123) at the Kennedy Krieger Institute Received income in an amount equal to or greater than $250 from: Gerson Lehrman Group; Guidepost Received royalty from Medscape for other.

Coauthor(s)

Farzaneh Farhadi, MD Postdoctoral Research Fellow, Johns Hopkins Hospital

Disclosure: Nothing to disclose.

Chief Editor

Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida Morsani College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, American Medical Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Bioserenity, Ceribell, Eisai, Jazz, LivaNova, Neurelis, Neuropace, SK life science, Sunovion, Takeda, UCB Serve(d) as a speaker or a member of a speakers bureau for: Aquestive, Bioserenity, Eisai, Jazz, LivaNova, Neurelis, SK life science, Stratus, Sunovion, UCB Received research grant from: Cerevel Therapeutics, Ovid Therapeutics, Neuropace, Greenwich Jazz, SK Life Science, Xenon Pharmaceuticals, UCB, Marinus, Neuroelectrics Corporation, Longboard, Janssen, Equilibre Biopharmaceuticals.

Acknowledgements

Nestor Galvez-Jimenez, MD, MSc, MHA Chairman, Department of Neurology, Program Director, Movement Disorders, Department of Neurology, Division of Medicine, Cleveland Clinic Florida

Nestor Galvez-Jimenez, MD, MSc, MHA is a member of the following medical societies: American Academy of Neurology, American College of Physicians, and Movement Disorders Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Acknowledgments

The research for this article was supported by the Essel Foundation; the National Alliance for Research on Schizophrenia and Depression (NARSAD); the Tourette Syndrome Association, Inc; the National Institutes of Health; and the Department of Psychiatry of Bellevue Hospital Center and the New York University School of Medicine, New York, New York. The cooperation of the Health and Hospitals Corporation of the City of New York is gratefully acknowledged.