Catatonia Workup

  • Author: James Robert Brasic, MD, MPH; Chief Editor: Selim R Benbadis, MD   more...
 
Updated: Feb 15, 2012
 

Approach Considerations

Because the treatment of the underlying disorder relieves the catatonia, Lahutte and colleagues recommended the prompt diagnosis and therapy of the comorbid disorders to avoid morbidity and mortality.[65]

Complete blood counts (CBC)s, electrolytes, and chemical analyses of blood are appropriate. In particular, hyponatremia and other metabolic abnormalities must be ruled out. Fibrin D-dimer levels are needed to rule out early coagulation activation.[3] Patients with catatonia typically have fibrin D-dimer levels greater than 500 ng/mL.[3] Prompt identification and treatment of pulmonary embolism in people with catatonia is crucial to minimize morbidity and mortality.[66]

Because elevations of serum creatine kinase, white blood cell (WBC) counts, and liver function test results are common laboratory manifestations of catatonia, it is appropriate to immediately measure the serum creatine kinase level and WBC count and perform liver function tests, to rule out neuroleptic malignant syndrome.

Serum ceruloplasmin is needed to rule out Wilson disease. In addition, encephalitis must be ruled out.

Imaging of the head by means of magnetic resonance imaging (MRI) or computed tomography (CT) scanning 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.

An 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 may quickly confirm the presence of nonconvulsive status epilepticus.

Among the several scales developed to measure catatonia, the Bush-Francis Catatonia Rating Scale (BFCRF) is favored owing to its demonstrated reliability and validity in clinical settings[67, 68]

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CT Scanning

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

Single-photon emission CT (SPECT) scanning 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 scans cannot be used to establish the diagnosis of catatonia. The main value of SPECT scanning in patients with catatonia is to rule out other treatable disorders.

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PET Scanning

Positron emission tomography (PET) scanning 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 scanning cannot be used to establish the diagnosis of catatonia. The main value of PET scanning in patients with catatonia is to rule out other treatable disorders.[7, 8]

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Contributor Information and Disclosures
Author

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

James Robert Brasic, MD, MPH is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Academy of Neurology, and Movement Disorders Society

Disclosure: Taylor and Francis Royalty Independent contractor; Wolters Kluver/Lippincott Williams & Wilkins Royalty Independent contractor; National Alliance for Research on Schizophrenia and Depression Grant/research funds Other; National Institutes of Health Grant/research funds Other

Chief Editor

Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida 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, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Additional Contributors

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.

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Table. Causes of Catatonia by Category
CategoryCauses
Neurologic conditionsNeuroleptic malignant syndrome[15]



Administration of agents that block postsynaptic dopamine receptors*



Administration of sibutramine,[16] withdrawn from US market October 8, 2010



Withdrawal of lorazepam and other sedatives



Akinetic-rigid syndrome



Arachnoid cyst in right parietal region



Astrocytoma



Atrophy of left amygdala[17]



Autistic disorder[6, 7, 8, 18, 19, 20, 21, 22, 23] {{197}



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 (herpes, Trypanosoma cruzi)



Encephalopathy (Borrelia burgdorferi, human immunodeficiency virus [HIV] infection, Wernicke encephalopathy)



Familial fatal insomnia[24]



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[25, 26]



Neurosyphilis



Nonconvulsive status epilepticus



Pervasive developmental disorders[7, 8, 22]



Pallidoluysian atrophy



Paraneoplastic encephalitis[27]



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 encephalitis



Wilson disease



Psychiatric conditionsAcute stress disorder



Anorexia nervosa



Autistic disorder[6]



Brief reactive psychosis with catatonia



Conversion disorder



Hysteria



Major depression, single episode with catatonic features



Mood disorders



Neuroleptic malignant syndrome[15]



Posttraumatic stress disorder



Schizophrenia



Substance intoxication (3,4-methylenedioxymethamphetamine [ie, "ecstasy"], alcohol, amphetamine, phencyclidine, substance withdrawal, hypnotic-sedative, lorazepam)



Psychological factorsImmigration



Experiencing rejection of an expression of love



Feelings of alienation in an unfamiliar country



Medical conditionsAcquired immunodeficiency syndrome (AIDS)



Acute intermittent porphyria



Addison disease



Bacterial septicemia



Bronchorrhea



Carcinoid tumors



Diabetic ketoacidosis



Encephalopathy (hepatic, HIV infection ? related, Wernicke)



Fever of unknown cause



Heat stroke



Hepatic failure



Hereditary coproporphyria



Homocystinuria



Hypercalcemia



Hyperparathyroidism



Hyperthyroidism



Hyponatremia



Hypothermia



Intestinal atony



Malaria



Neuroleptic malignant syndrome[15]



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 encephalitis



Obstetric conditionsHypopituitarism secondary to postpartum hemorrhage
*The administration of agents that block postsynaptic dopamine receptors is associated with the onset of catatonia in some individuals.
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