On Catatonia and Dementia: a Case Report

Neurological Bulletin

Volume 2 Issue 1 Article 3

December 2010

On Catatonia and Dementia: A Case Report

Jordan Eisenstock University of Massachusetts Memorial Medical Center

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Neurol. Bull. 2: 12-16, 2010 http://escholarship.umassmed.edu/neurol_bull doi:10.7191/neurol_bull.2010.1019

On Catatonia and Dementia: A Case Report

Jordan Eisenstock

Department of Neurology University of Massachusetts Memorial Medical Center, Worcester, MA

The many pitfalls in the accurate diagnosis of cently passed away about two months prior dementias are well documented. While de- to admission. finitive diagnosis remains the goal, the limits of clinicopathologic knowledge and current With the exception of one prior psychiatric technology oftentimes preclude firm deci- admission about 20 years earlier, also for sions on a specific diagnosis, treatment and worsening depression in the context of a plans. This is particularly pertinent in those family issue, the patient had never consist- cases where the lines between neurology and ently required psychiatric attention. About psychiatry become somewhat blurred. In this two years prior to this admission he had seen report, I present the case of a patient with an outpatient psychiatrist for a couple of probable catatonic depression masquerading months secondary to anxiety and panic initially as frontotemporal dementia. Includ- symptoms and was started on an SSRI and a ed is a brief discussion outlining our current benzodiazepine. At the time of admission knowledge about catatonia: its pertinent his only medications were HCTZ/ signs and symptoms for accurate diagnosis, Triamterene for hypertension and Lumigan its possible pathophysiologic mechanisms, drops for glaucoma. He had been off of all and its relationship to dementia. neuropsychiatric medications for at least one year. His family history was only notable for Case Report question of late-onset dementia in the patient’s mother. The patient is a 56 year old right-handed gentleman who worked for several years in a The neurology service came to be involved supervisory role with the city department of with this patient after the admitting examina- public works and presented to our inpatient tion by the psychiatry resident noted subtle psychiatry unit for one month of worsening perseveration on testing of extraocular move- depression. Neurovegetative symptoms in- ments, brisk reflexes and difficulty changing cluded insomnia, poor appetite and difficulty set despite a MMSE of 30/30. An initial concentrating. There was a potential precipi- neurology consultation yielded a diagnosis of tating event as the patient’s mother had re- Cognitive Symptoms Due to Depression and

Correspondence to Jordan Eisenstock: [email protected] Keywords: catatonia, electroconvulsive therapy, lorazepam, frontotemporal dementia, glutamate, GABA 12 Eisenstock: On Catatonia and Dementia: A Case Report

Neurol. Bull. 2: 12-16, 2010 doi:10.7191/neurol_bull.2010.1019

Figure 1: Left image dated April 2006. Right image dated September 2007.

the brisk reflexes were explained by cervical directly admitted to the inpatient neurology pathology on MRI. The inpatient psychiatry service for a rapidly progressive dementia team resumed the patient’s SSRI and added workup. Of significance, the patient’s MRI an atypical antipsychotic to the regimen and showed minimal nonspecific white matter after two weeks the patient was discharged to changes but no atrophy (Figure 1) and the his home. laboratory findings were not suggestive of any underlying neurologic etiology After continued deterioration despite compli- (summarized in Table 1). An EEG in both ance with medications the patient returned to the awake and asleep states was also normal. the psychiatric emergency room a couple of months later. Again he was admitted to the Over the course of the next four months the inpatient psychiatry unit and trials of new patient continued to decline, his verbal out- SSRI’s and atypical antipsychotic produced put decreased and there were few spontane- little clinical response. Shortly after dis- ous movements. The patient was no longer charge from the psychiatry service he was getting out of bed to toilet himself, and he seen in the outpatient neurology clinic for would not voluntarily eat even if the food follow-up of the original consultation. was delivered to him. Though there was no formal disagreement, the psychiatry service By this time the patient demonstrated mini- suspected a dementia diagnosis and the neu- mal verbal output, most responses being a rology service tended toward a psychiatric rather stereotypic and hesitant “I don’t etiology. Eventually a trial of ECT was or- know” to all variety of questions. His family dered but was unfortunately suspended early noted significant balance problems and he secondary to presumed increased confusion had fallen several times at home. In addition in the setting of a urinary tract infection. to mild rigidity and a grasp reflex, the patient Soon thereafter the patient was sent for a se- was also noted to have startle myoclonus on cond opinion at another large academic med- examination. Subsequently the patient was ical center and returned to our outpatient

13 Eisenstock: On Catatonia and Dementia: A Case Report

Neurol. Bull. 2: 12-16, 2010 doi:10.7191/neurol_bull.2010.1019 Table 1: Laboratory Summary  Basic Metabolic Panel: normal  Drugs of Abuse Screen: negative  Complete Blood Count: normal  Sedimentation Rate: 45 (High, >20)  Liver Function Tests: normal  HbA1C: normal  Fasting Lipid Profile: normal  Serum Protein Electrophoresis: normal  Amylase/Lipase: normal  Anti-Ri/Ma/Ta/Yo/Hu: negative  Porphyrins: normal  VDRL/RPR: non-reactive  TSH: normal  Lyme Serum & CSF: unremarkable  B12: normal  EBV CSF: negative  Folate: normal  Parv B19: negative  CSF: 0 WBC, 0 RBC  VCA-IgM/IgG: negative  CSF: protein, glucose normal  EBNA-IgG: negative  CSF: oligoclonal bands absent  Admark Tau/ABeta42: unremarkable  CSF: 14-3-3 negative

clinic one month later with the opinion of tient’s initial presentation on the psychiatric likely frontotemporal dementia. A decision unit. His current medications include me- had been made at the other institution to de- mantine, topiramate and citalopram. For a fer further ECT treatments, and the family short period of time the patient also required was advised to explore nursing home place- olanzepine secondary to paranoid thoughts ment options. A PET scan at the other insti- about leaving his home; but this medication, tution had apparently demonstrated fronto- along with maintenance lorazepam, has been temporal hypometabolism, which along with successfully discontinued over the past sev- the clinical evaluation had precipitated the eral months. Though he has been unable to above diagnosis. return to his previous work, his sense of hu- mor has returned, his abnormal gait has re- Approximately six months after the first psy- solved and his performance on formal neuro- chiatric hospitalization the patient returned to psychological testing has improved. A re- the inpatient neurology service. On the se- peat PET scan was obtained and was normal, cond evening of admission the patient rather likely indicating that his previous scan was suddenly and unexpectedly shifted from his secondary to severe refractory depression longstanding stuporous state to a verbally rather than frontotemporal dementia. and physically aggressive appearance. Intra- muscular lorazepam was prescribed and Discussion within minutes the patient not only calmed down but voluntarily proceeded to get out of This patient’s case illustrates many of the bed and go to the restroom. Later that even- important teaching points when considering a ing he seemed to enjoy his dinner and con- diagnosis of catatonia. Most experts agree versed with family for the first time in that catatonia is severely under-diagnosed in months. A standing dose of lorazepam was the neuropsychiatric community. Theories initiated, and a previously suggested diagno- exist to explain this phenomenon, such as sis of a catatonic-like, rather than frontotem- lack of teaching about catatonia in medical poral-like, state was supported. school, lack of agreed-upon classifications and guidelines for recognizing catatonia, and It is now two and a half years since the pa- a general lack of understanding of the patho-

14 Eisenstock: On Catatonia and Dementia: A Case Report

Neurol. Bull. 2: 12-16, 2010 doi:10.7191/neurol_bull.2010.1019 Table 2: Phenomenology of Catatonia EXCITEMENT STUPOR

Hyperkinesis Motor Behaviors Stereotypies [repetitive/ritualistic movements, Catalepsy postures or utterances] Rigidity Mannerisms [gestures that become abnormal Waxy Flexibility [maintained immobile posture] with exaggeration] Euphoria Posturing Irritability Psychological Pillow [continued elevation of head as if supported by a pillow] Rigidity Grimacing Autonomic Changes Hypertension Negativism Hyperpyrexia Gegenhalten Diaphoresis Mutism Tachycardia Ambitendency [tendency to act in opposite ways Tachypnea from expected] Mydriasis Automatic Behaviors Obedience [tendency to follow commands even if harmful to self] Echolalia Echopraxia

physiology behind the catatonic state. In- least 50 neurologic conditions have been deed, there is no consensus in the literature identified as direct causes of secondary cata- regarding the phenomenology of catatonia tonia symptomatology. 5 Missing a catatonia (Table 2). As a consequence of unclear treatment opportunity might greatly alter a guidelines, there becomes a relative dispro- patient’s level of functioning. portionate reliance on the art and experience of medical decision-making by an individual Not surprisingly the theories about catatonia physician. Inexperienced physicians become pathophysiology and known dementias over- reluctant and hesitate to make the diagnosis lap considerably. Theories include deficits in and treat the condition. Catatonia is often- cortical development, dopaminergic hypoac- times relegated to “diagnosis by exclusion” tivity, low GABA-A receptor binding, frontal or simply completely avoided. anomalies, dysfunction of norepinephrine and serotonin transmission and of course glu- Delaying the treatment of catatonia negative- tamatergic dysfunction.5,6 A recent article ly impacts patient care, as it significantly re- reviewed adjunctive glutamate antagonist duces the likelihood of traditional (ECT, ben- therapies in the treatment of catatonia and zodiazepine) treatment response.1 Thus, de- noted possible response with medications ferring treatment until tests return to rule out such as amantadine, memantine and topir- known dementias might be detrimental. In amate.6 On the other hand, modalities that fact, catatonia and dementia are not mutually are now viewed with suspicion in the de- exclusive diagnoses.2 The three cardinal cat- mented patient, such as benzodiazepines or atonic features (little or no spontaneous even ECT, might be more welcomed with movement, mutism, refusal to eat or drink) further study. The literature regarding the are hallmark features of advanced dementia.3 possibility of lorazepam-responsive demen- Perhaps treating the catatonic component of tias illustrates this trend.7 As awareness of a patient’s dementing condition may amelio- the catatonic state and its many varieties of rate a reversible or modifying factor.4 At presentation increases, so too might the

15 Eisenstock: On Catatonia and Dementia: A Case Report

Neurol. Bull. 2: 12-16, 2010 doi:10.7191/neurol_bull.2010.1019 available multidimensional forms of treatment for both catatonia and dementia.

References

1. Caroff SN, Ungvari GS, Bhati MT, Datto CJ, O’Reardon JP. Catatonia and predic- tion of response to electroconvulsive therapy. Psychiatr Ann 2007;37:57-63. 2. Alisky JM. Is the immobility of advanced dementia a form of lorazepam-responsive catatonia? Am J of Alzheimers Dis Other Demen 2004;19:213-214. 3. Carroll BT, Kennedy JC, Goforth HW. Catatonic signs in medical and psychiatric catatonias. CNS Spectr 2000;5:66-69. 4. Salam S, Kilzieh N. Lorazepam treatment of psychogenic catatonia: an update. J Clin Psychiatry 1988;49 Suppl:16-21. 5. Northoff G. Brain imaging in catatonia: current findings and a pathophysiologic model. CNS Spectr 2000;5:34-36. 6. Carroll BT, Goforth HW, Thomas C, et al. Review of adjunctive glutamate antagonist therapy in the treatment of catatonic syn- dromes. J Neuropsychiatry Clin Neurosci 2007;19:406-412. 7. Alisky JM. Lorazepam-reversible catatonia in the elderly can mimic dementia, co- ma, and stroke. Age Ageing 2007;36:229.

Disclosure: the authors report no conflicts of interest.

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