Misdiagnosis of Catatonia

Dear Editor

Catatonia is an enigmatic neuropsychiatric syndrome that may occur in the context of various psychiatric and medical conditions and is characterized by a range of volitional, motor, behavioral and cognitive symptoms.¹ Although catatonia is common among hospitalized patients, its diagnosis may be challenging in the general hospital setting and thus it is likely under-recognized.^2,3 Negativism and gegenhalten may be mistaken for wilful refusal by patients to cooperate with hospital staff,⁴ whereas more serious clinical features such stupor may be misinterpreted as progression of an underlying medical condition potentially resulting in withholding effective interventions.

Rapid, temporary improvement upon the parenteral administration of a single dose of a benzodiazepine may lead to the serendipitous diagnosis of catatonia [for example when administering intravenous midazolam prior to inserting a percutaneous endoscopic gastrostomy (PEG) tube to feed a stuporous patient],² and can be used by clinicians as a diagnostic tool when faced with diagnostic uncertainty.² However, once diagnosed, catatonia is usually highly responsive to benzodiazepines or electroconvulsive therapy (ECT).¹

We report the case of a 62 year old Caucasian woman with recurrent depressive disorder, chronic relapsing alcohol dependence, essential hypertension and insulin dependent diabetes mellitus who was admitted to the local general hospital after she was found unconscious at her home by the community mental health nurse. She had been experiencing major depression [treated with sertraline] and consuming alcohol excessively, and was supported by daily visits from the local mental health service. No prior cognitive or communication impairment was reported.

On admission to the general hospital her Glasgow Coma Scale (GCS) score was 4/15. She was found to be in diabetic ketoacidosis which was managed as per local protocol and was provided with intravenous Pabrinex in view of her alcoholism. A nasogastric (NG) tube was inserted for feeding. Neuroimaging, cerebrospinal fluid examination as well as viral, bacterial and autoimmune screening were all unremarkable. An electroencephalogram revealed slow background activity suggestive of diffuse nonspecific cortical dysfunction.

Her GCS score gradually improved to 14/15 over the following 10 days. However, she was reported to be awake but oblivious to her surroundings and was uncommunicative, emotionally blunted, immobile, and doubly incontinent and was refusing to eat and drink. She was uncooperative and repeatedly pulled out her NG tube necessitating the insertion of a PEG tube. Her upper limbs were noted to be held in a flexed position and they were rigid and resistive to movement. Six weeks into her admission her presentation remained unchanged and the view of the treating medical team was that she may have sustained potentially irreversible hypoxic or alcohol-related encephalopathy and that she would require discharge into nursing care.

At this stage a liaison psychiatric opinion was sought which suggested a probable diagnosis of catatonia. A lorazepam challenge test [2 mg intramuscularly] was negative; yet the patient was commenced [via her PEG tube] on lorazepam 3 mg per day [in 3 divided doses] which was gradually increased to 6 mg per day [in 4 divided doses] over a period of nearly 2 weeks. Additionally, mirtazapine was initiated and titrated up to 45 mg per day over a period of several weeks. One week after commencement of lorazepam therapy the patient started having food and fluids orally and her PEG tube was removed shortly afterwards. She was mobilising with assistance, and she seemed to be more attentive, responsive and engaging. Her speech, however, was minimal and mostly incoherent with a stammering quality.

Over the following few weeks the patient’s verbal communication moderately improved and it became evident that her orientation and anterograde and retrograde memory were impaired. In view of her cognitive impairment a trial of memantine 5 mg per day was commenced which was titrated up to 20 mg per day over 4 weeks.⁵ This was associated with remarkable improvement in the fluency and coherence of her speech but her memory and orientation remained persistently defective which was probably a sequela of the patient’s excessive and chronic alcohol consumption. Six months after admission the patient was discharged from hospital into a rehabilitation unit. Prior to discharge lorazepam was tapered off and stopped while she continued to take mirtazapine 45 mg per day and memantine 20 mg per day.

The misdiagnosis of catatonia in this case was in line with its known under-recognition, and it highlights the important clinical and educational role of liaison psychiatry teams in improving the detection of catatonia in general hospitals. While recognition of some catatonic features may require specialist training, other phenomena such as mutism, immobility and refusal of oral intake are obvious and should prompt an urgent referral for a specialist evaluation. Furthermore, the use of memantine, an NMDA receptor antagonist, was associated with remarkable improvement in the patient’s language disorder, which warrants further research to explore its role in catatonia.