Catatonia: What If There’s No Psychiatric Consultant In The House?

I just finished reading the catatonia monograph on the Academy of Psychosomatic Medicine (APM) web site. I wondered if, in a hospital without access to a consulting psychiatrist, if an internist could apply some of the practical recommendations in it, especially since many cases of catatonia arise from medical causes and the presentation is essentially identical to those from psychiatric causes.

If you just read the relatively short section designated as advice for both the psychiatric consultant and the primary medical team, it really doesn’t look so complicated, as long as you remember that diagnosing and even treating the catatonic behaviors is a deceptively simple procedure and only part of the total effort involved in resolving the syndrome. The initial recommendation to the primary team sounds straightforward in terms of tracking down medical causes and what to do first (adapted below):

Suggest medical workup include consideration of the following potential medical causes (and check CPK for rhabdomyolysis):

  • Electroencephalogram to rule out seizure activity
  • Lumbar puncture with cerebrospinal fluid examination, viral serologies, and anti-NMDA-R antibodies.
  • Serum ANA test and other tests for systemic lupus.
  • Paraneoplastic antibody panel
  • CT abdomen/pelvis to rule out ovarian mass which could be causing ANRE
  • MRI brain with contrast to rule out mass, infection, CVA/hemorrhage, autoimmune process, or PRES.
  • Substance use history and urine drug screen
  • Serum B12 level

Suggest consideration of identification and/or discontinuation of the following pro-catatonic agents:

  • Tacrolimus, cyclosporine
  • Fluoroquinolones, cephalosporins
  • Dopamine antagonists (antiemetics, antipsychotics)
  • Corticosteroids
  • Disulfiram
  • Baclofen

Consider withdrawal treatment in connection with the following agents which may be relevant:

  • Alcohol
  • Barbiturates
  • Benzodiazepines
  • Gabapentin or pregabalin
  • Amantadine or memantine
  • Bromocriptine
  • Levodopa/carbidopa

Now what about the actual evaluation; could an internist handle most of it? Probably, although the caveat is that catatonia can look similar to many non-catatonic behaviors that involve withdrawal and resistance to care. However, most of the time catatonia looks bizarre, especially if the patient is posturing or repeating everything you say (called echolalia). Just suppose we give non-psychiatric doctors and nurses enough credit for being able to recognize the basic behaviors, for which you needn’t necessarily try to apply the Bush Francis Catatonia Rating Scale (BFCRS) [1]. You could use a mnemonic, either A SLIME-Posture in the APM monograph or the Wired ‘N Mired in the 2005 online Current Psychiatry article by B. Carroll et al.

In any case, the examination for catatonia isn’t rocket science.

I think many consulting psychiatrists probably get by without using any formal rating scales for diagnosing catatonia, me included. I think what’s really interesting is the differential diagnosis of akinetic mutism, which the APM monograph authors indicate should be distinguished from catatonia, although it can look just like it. I’ve used the telephone effect on patients with catatonia (either from medical or psychiatric causes) and it can be just as strikingly effective as described in C. Miller Fisher’s paper about neurologic diseases with interesting behavioral findings including akinetic mutism [2]. And, in the catatonia treatment section of the APM monograph, the authors describe a case in which the telephone effect was used:

“Amantadine may also be helpful in cases of akinetic mutism. One case report describes a man with akinetic mutism following a traumatic brain injury, wherein his symptoms would dissipate while speaking on the telephone, who improved in the realm of mutism, impulsivity, and disorientation after 2 weeks on amantadine 300mg/day.”

So the telephone effect is little more than putting a telephone receiver up to the patient’s ear, and calling her from outside the room, sometimes only steps away. The mute patient will then sometimes answer questions. It can look almost as impressive as the sudden resolution of catatonia from the lorazepam challenge test. Incidentally, I asked Dr. Andrew Francis ( a catatonia expert who was one of the external reviewers of the APM catatonia monograph) about this at an APM meeting a few years ago. It seemed to puzzle him and he ended up dismissing the whole affair as a “stimulus bound” reaction rather than catatonia per se.

So how difficult is it to conduct the lorazepam challenge test? It’s not beyond the ability of the average internist or emergency room physician. Administering injectable lorazepam is not as potentially hazardous as injecting a barbiturate, which psychiatrists used to do when conducting the so-called Amytal Interview, using sodium amobarbital. You look for the same reaction, which is sometimes a miraculous awakening from the catatonic state, which can occur within minutes or a couple of hours.

In fact, it’s not improbable that internists might have more experience administering drugs listed as alternatives to lorazepam if that drug is ineffective–like NMDA antagonists such as amantadine or memantine, because many psychiatrists might not have used either.

But that’s about as far as an internist could go, I think. If lorazepam or other drugs don’t cure the catatonia, then the safest bet for the patient is to get her to a hospital where electroconvulsive therapy (ECT) can be applied–which can be lifesaving regardless of whether the cause is medical or psychiatric.

"Relegating this work entirely to specialists is futile for it is doubtful whether there will ever be a sufficient number of psychiatrists to respond to all the requests for consultations. There is, therefore, no alternative to educating other physicians in the elements of psychiatric methods."--George W. Henry, MD, 1929

“Relegating this work entirely to specialists is futile for it is doubtful whether there will ever be a sufficient number of psychiatrists to respond to all the requests for consultations. There is, therefore, no alternative to educating other physicians in the elements of psychiatric methods.”–George W. Henry, MD, 1929

 

References:

1. Bush, G., et al. (1996). “Catatonia. I. Rating scale and standardized examination.” Acta Psychiatr Scand 93(2): 129-136.
To facilitate the systematic description of catatonic signs, we developed a catatonia rating examination, rating scale and screening instrument. We constructed a 23-item rating scale and a truncated 14-item screening instrument using operationalized definitions of signs ascribed to catatonia in published sources. Inter-rater reliability was tested in 44 simultaneous ratings of 28 cases defined by the presence of > or = 2 signs on the 14-item screen. Inter-rater reliability for total score on the rating scale was 0.93, and mean agreement of items was 88.2% (SD 9.9). Inter-rater reliability for total score on the screening instrument was 0.95, and mean agreement of items was 92.7% (SD 4.9). Diagnostic agreement was high based on criteria for catatonia put forth by other authors. Seven per cent (15/215) of consecutively admitted patients to an academic psychiatric in-patient facility met criteria for catatonia. It is concluded that catatonia is a distinct, moderately prevalent neuropsychiatric syndrome. The rating scale and screening instrument are reliable and valid. Their use facilitates diagnosis, treatment protocols, and cross-study comparisons.

2. Fisher, C. M. (1983). “Honored guest presentation: abulia minor vs. agitated behavior.” Clinical neurosurgery 31: 9-31.
The neurological analysis of complex behavioral states associated with serious brain disease not infrequently is a difficult task. In many such cases, the signs of minor degrees of akinetic mutism were found when deliberately looked for. Recognition of this feature greatly facilitated interpretation. The ancient term abulia is suggested for the specific neurological syndrome comprising slowness, decreased responsiveness, apathy, etc. Akinetic mutism is its extreme form. A lesser degree of abulia is here termed abulia minor. The attributes of abulia minor are described, and the neurological conditions with which it had been found associated are listed. Preliminary conclusions as to the anatomical localization of the syndrome are presented. The literature on akinetic mutism is reviewed, and a few special observations are commented on–paradoxical activity, the telephone effect, and reflex attention. The application of the newer knowledge of cerebral neurotransmitters to akinetic mutism is illustrated. At the beginning of the study the focus was on abulia, but it was natural that sooner or later the contrasting state of behavioral hyperactivity or agitation would have to come under equal scrutiny. A list of conditions in which psychomotor agitation was a feature has been compiled from personal files. The localization of the disease process in hyperactive states is compared with that in abulia. A few special observations on hyperactive states are presented, along with a note on a unique syndrome termed anideation. There has gradually emerged a concept of a continuum of behavioral activity extending from abulia at one end through eukinesia to hyperactivity at the other end. Involvement of specific fundamental integrative circuits is postulated. This morning we have been enthralled by Computers in Neurosurgery, Neurobiology in Neurosurgery, and Humanism in Neurosurgery. What could be more natural for a neurologist than to talk about Neurology in Neurosurgery. And how best to pay homage to the great lady of Medicine than by offering a modest example of her handiwork. Thus, I am led to discuss a neurological theme which has recently occupied my attention. To anticipate a little, I shall be talking about two somewhat opposite states: on the one hand there is abulia–slowness, apathy, and lack of spontaneity–and on the other hand, agitation and hyperactivity. By way of explanation, this study originated during the bedside examination of patients with brain damage and serious impairment of analysis appeared not only formidable but even impossible.(ABSTRACT TRUNCATED AT 400 WORDS)

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