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Catatonia When Benzodiazepines Fail Neural Circuit Changes Help Explain Syndrome’S Signs, Suggest Potential Therapies

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Catatonia When Benzodiazepines Fail Neural Circuit Changes Help Explain Syndrome’S Signs, Suggest Potential Therapies Current p SYCHIATRY Treating persistent catatonia when benzodiazepines fail Neural circuit changes help explain syndrome’s signs, suggest potential therapies Brendan T. Carroll, MD Associate professor of psychiatry (volunteer) University of Cincinnati, Cincinnati, OH Christopher Thomas, PharmD Clinical pharmacy specialist in psychiatry VA Medical Center, Chillicothe, OH Kameshwari Jayanti, MD Psychiatry service, Mental health care line VA Medical Center, Chillicothe, OH John M. Hawkins, MD Assistant professor of psychiatry (volunteer) University of Cincinnati, Cincinnati, OH Carrie Burbage, BS Physician assistant student Marietta College, Marietta, OH any catatonia cases respond to benzodia- M zepines—especially lorazepam—but up to 30% do not. Electroconvulsive therapy (ECT) can be effective, but what’s the next step when ECT is unavailable or inappropriate for your patient? To help you solve this dilemma, we describe our diagnosis and treatment decisions for a patient we call Mr. C. We explain how our process was guided by recent understandings of an abnormal neural circuit that appears to cause catatonia’s complex motor and behavioral symptoms. © Photolibrary.com / Photonica 56 Current VOL. 4, NO. 3 / MARCH 2005 p SYCHIATRY Current p SYCHIATRY This article describes that neurologic pathol- Table 1 ogy and answers common questions about the Common diagnoses of patients clinical workup and treatment of catatonia. with catatonia CASE: TROUBLE IN TV LAND Psychiatric • Schizophrenia Mr. C, age 69, caused a disturbance at a local TV sta- • Mood disorder (depression, tion, demanding that they broadcast a manuscript he bipolar disorder [manic, mixed, depressed]) had written. Police took him to a local hospital, where • Other psychoses he was stabilized and then transferred to a neuropsy- chiatric hospital for evaluation. • Personality or conversion (somatoform) disorders The psychiatric interview revealed that he had • Developmental disorders (autism) developed insomnia, excessive activity, and delusion- al thinking 2 weeks before admission. His medical his- Organic • Due to a general medical tory included coronary artery disease (CAD), hyper- condition tension, and hypothyroidism. Medications included • Drug-induced thyroid hormone replacement therapy, furosemide, • Idiopathic potassium, ranitidine, simvastatin, metoprolol, and lisinopril. CAD treatment included stent placement and nitroglycerin as needed. prehensive or reliable history.2 They show mutism, He had been hospitalized in his 30s and treated characteristic postures, rigidity, aberrant speech, with ECT for what he called “bad thoughts.” He said negativism, and stereotyped behaviors.1,2 They may he improved after 1 month and had no subsequent present in an excited or retarded state: psychiatric history. He denied drug or alcohol abuse. • Excited patients may injure themselves or oth- Shortly after admission, he refused to eat or drink ers and develop hyperthermia, tachycardia, and and after 1 week became dehydrated. He also elevated blood pressure from excessive motor showed mutism, immobility, and stupor. He was activity. transferred to the medical service for IV rehydration. • Patients in a retarded state may present with bradykinesia and poor self-care. They may be MANY SCENARIOS AND SIGNS unresponsive to external stimuli, develop cata- Mr. C’s symptoms suggest possible catatonia, a tonic stupor, and refuse to eat or drink. neuropsychiatric syndrome of motor dysregulation Mr. C’s earlier insomnia, excessive activity, and found in up to 10% of acutely ill psychiatric inpa- delusional thinking (such as the TV station inci- tients.1,2 A movement disorder,1,2 catatonia occurs dent) may have signaled an excited catatonia. On with general medical conditions and psychiatric admission to the medical service, however, he pre- disorders (Table 1). sented in a retarded state. Pathophysiology. Catatonic signs develop when Signs. Part of the challenge with detecting catato- aberrant signals from neurochemical abnormal- nia’s signs is that there are so many; some rating ities trigger a neural circuit that affects the scales list more than 20. Not all signs need to be pre- medial gyrus of the orbital frontal lobe, the lat- sent to make the diagnosis, however, and if you find eral gyrus, caudate nucleus, globus pallidus, one, others usually turn up in the examination. and thalamus (Box, page 58).3-5 A mnemonic from the Bush-Francis Catatonia Presentation. A focused exam is required because Screening Instrument (Table 2, page 59) represents patients with catatonia often do not provide a com- diagnostic signs in patients with the excited or VOL. 4, NO. 3 / MARCH 2005 57 Catatonia Box Neural loop may explain catatonia’s symptoms and treatment response atatonia is caused by neurochemical abnor- C malities including low GABA activity in Glutamate ➞ the frontal cortex, low dopamine (D2) activity in the basal ganglia, high SMA glutamate—N-methyl-D-aspar- tate (NMDA)—activity in the parietal cortex, or a combina- tion of these.3-5 Catatonic PP signs occur when these CN neurochemical changes GP Thal cause aberrant signals and trigger a neural circuit affect- LG MG ing the medial gyrus of the OFL orbital frontal lobe, the lateral gyrus, caudate nucleus, globus pallidus, and thalamus (Figure). ➞ GABA ➞ Dopamine Posturing occurs when the aberrant signal reaches the posterior parietal lobe. Patients’ bizarre and mundane postures in MG—medial gyrus GP—globus pallidus catatonia are maintained by “anosognosia of OFL—orbital frontal lobe Thal—thalamus LG —lateral gyrus PP—posterior parietal lobe position.” For example, an individual does not CN—caudate nucleus SMA—supplemental motor area know the position of rest for his arm, and it remains in an unusual position as if at rest.3 cause akinetic mutism, and fear is a symptom of AMG recruitment. If the anterior hypothalamus The PP goes on to influence the supplemental is affected, malignant catatonia or neuroleptic motor area (SMA), causing bradykinesia, rigidity, malignant syndrome may occur.3,5 and other motor phenomena that catatonia shares with Parkinson’s disease. The SMA feeds This neural loop demonstrates an integrated back to the medial orbital gyrus, completing the model of psychosis. It may help explain why neural circuit.3 catatonia responds to treatment with lorazepam, ECT, and other agents such as antipsychotics Regions such as the anterior cingulate area (ACA) and NMDA antagonists. and amygdala (AMG) — also may be recruited into the expanded circuit. ACA recruitment may Illustration for CURRENT PSYCHIATRY by Marcia Hartsock, CMI retarded forms.2 We recommend that you review withdrawal (refusal to eat and drink), automatic obe- an authoritative text (see Related resources, page 64) dience, and mitgehen (exaggerated movements in to understand catatonia’s psychopathology.2 response to light finger pressure, despite instruc- tions to stay still). ECT work-up was started, along CASE CONTINUED: MAKING THE DIAGNOSIS with a trial of lorazepam, 1 mg tid. In the medical unit, Mr. C was found to be in a cata- Laboratory studies revealed high BUN/creatinine tonic stupor, with immobility, mutism (monosyllabic (80/2.0) that returned to normal range (BUN 7 to 21 speech), catalepsy, intermittent waxy flexibility, mg/dL; creatinine 0.5 to 1.2 mg/dL) after 3 days of 58 Current VOL. 4, NO. 3 / MARCH 2005 p SYCHIATRY Current p SYCHIATRY hydration. Because of Mr. C’s earlier excited symp- Table 2 toms and delusional thinking, we considered a diag- WIRED `N MIRED: nosis of bipolar disorder with catatonia. However, Mnemonic for detecting catatonia his symptoms did not improve with a trial of valproic acid (serum level 64 mcg/mL). Waxy flexibility/catalepsy Head CT showed generalized atrophy and EEG Immobility/stupor showed delta slowing. Single-photo emission com- Refusal to eat or drink puter tomography (SPECT) showed areas of Excitement decreased perfusion in the cortex, with no perfusion Deadpan staring in the left posterior parietal area (PP). Mental status exam found Mr. C disoriented Negativism/negative symptoms with poor short-term memory and unable to com- Mutism plete the Mini Mental State Examination (MMSE). Impulsivity His Bush-Francis Catatonia Rating Scale score was Rigidity 28 and included many catatonic signs that would Echolalia/echopraxia not be seen a patient with simple dehydration. Direct observation The workup supported a diagnosis of catatonia due to general medical condition (vascular demen- tia) and ruled out schizophrenia with catatonic fea- prolonged stupor or does not respond to initial tures, bipolar disorder, or major depression with drug therapy. catatonia. Psychiatric causes. The clinical setting may sug- gest the most likely primary psychiatric disor- EVALUATION AND DIAGNOSIS ders to consider, such as: Medical causes. A careful history and thorough • bipolar or major depression in acute inpatient physical examination are essential for making an psychiatric units accurate diagnosis and ruling out medical condi- • autism and pervasive developmental disorders tions that could present with or mimic catatonia (PDD) in pediatric or PDD units (Table 3, page 60). Medications that can induce • catatonic schizophrenia in chronic psychotic catatonia include antipsychotics, corticosteroids, patients and disulfiram at therapeutic doses. Drug abuse • somatoform or factitious disorders in forensic (such as with phencyclidine), use of the general settings. anesthetic ketamine, and benzodiazepine with- These generalizations are not clinically
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