Catatonic Disorder Due to a General Medical or Psychiatric Condition
Abstract
Methods
Subject Identification and Selection
Data Collection
Statistical Analysis
Results
Clinical and Paraclinical Cohort Features
All Patients (N=95) | CD-GMC (N=20) | All Psychiatric (N=75) | OR: CD-GMC (95% CI) | p | |
---|---|---|---|---|---|
Age, years, mean (SD) | 51.9 (20.9) | 44.7 (19.5) | 53.9 (20.9) | 0.8 (0.62–1.02) | 0.08 |
Gender (N [% Men]) | 38 (40%) | 12 (60%) | 26 (34.7%) | 2.83 (1.03–8.06) | 0.04 |
Psychiatric history (N [%]) | 73 (81.1%) | 9 (47.4%) | 64 (90.1%) | 0.09 (0.02–0.31) | 0.0001 |
Family history psychiatric disease (N [%]) | 50 (60.9%) | 9 (47.4%) | 41 (65.1%) | 0.48 (0.17–1.37) | NS |
Neurologic history (N [%]) | 40 (43%) | 13 (68.4%) | 27 (36.5%) | 3.77 (1.32–11.81) | 0.016 |
History of clinical seizure (N [%]) | 18 (19.5%) | 8 (42.1%) | 10 (13.7%) | 4.66 (1.46–14.39) | 0.008 |
Antidepressant use at presentation (N [%]) | 44 (48.8%) | 6 (32.1%) | 38 (53.5%) | 0.4 (0.13–1.13) | 0.1 |
Neuroleptic use at presentation (N [%]) | 41 (44.6%) | 3 (15.8%) | 38 (52%) | 0.17 (0.03–0.57) | 0.01 |
Catatonia improved with benzodiazepines (N [%]) | 39 (76.5%) | 6 (54.5%) | 33 (82.5%) | 0.25 (0.06–1.09) | 0.06 |
Catatonia improved with ECT (N [%]) | 60 (94.1%) | 10 (83.3%) | 50 (96.1%) | 2.16 (0.02–1.82) | NS |
Abnormal MRI (all; N [%]) | 31 (37.8%) | 11 (64.7%) | 20 (30.8%) | 4.12 (1.37–13.47) | 0.01 |
Focal MRI abnormality (N [%]) | 16 (19.5%) | 7 (41.1%) | 9 (13.8%) | 4.36 (1.3–14.63) | 0.02 |
Abnormal EEG (all; N [%]) | 54 (79.4%) | 15 (93.7%) | 39 (75%) | 5 (0.87–94.7) | NS |
Diffuse slowing (all; (N [%]) | 44 (86.3%) | 13 (92.8%) | 31 (83.8%) | 2.51 (0.38–50) | NS |
Focal temporal slowing (N [%]) | 12 (23.5%) | 5 (35.7%) | 7 (19.1%) | 2.4 (0.58–9.44) | NS |
EEG asymmetry (N [%]) | 12 (23.5%) | 6 (42.8%) | 6 (16.2%) | 3.87 (0.98–15.89) | NS |
Maximum creatinine kinasea (median [IQR]) | 138 (59–576) (N=56) | 135 (51–397) (N=13) | 156 (60–653) (N=43) | 0.84 (0.51–1.27) | NS |
Age/Gender | Case Notes | Response to Therapy | Status at Last Follow-Up | |
---|---|---|---|---|
Encephalitis/encephalopathy (N=9) | ||||
Acute encephalitis: #1 | 45/Male | Prodrome of fever, headache, and myalgias; CSF: leukocytes, 18 (96% lymphocytes); protein, 59; glucose normal | Neither Ativan nor ECT attempted. Improved with supportive measures. | Back to normal at 5-month follow-up. |
Acute encephalitis: #2 | 18/Male | Aggressive-disinhibited behavior noted. CSF: Leukocytes, 14 (92% lymphocytes); protein and glucose normal. | Ativan not attempted; catatonia responded well to ECT. | Back to normal at hospital dismissal; no long-term follow-up. |
Acute encephalitis: #3 | 31/Female | CSF: Leukocytes, 53 (98% lymphocytes); protein, 50; glucose normal. | Ativan not attempted; catatonia responded well to ECT. | Full recovery at 5-month follow-up. |
Acute encephalitis: #4 | 29/Male | CSF: Leukocytes, 55 (96% lymphocytes); protein, 40; glucose normal. | Improved initially with Ativan, and then dramatically with ECT. | Improving at hospital dismissal; no long-term follow-up. |
Paraneoplastic limbic encephalitis | 37/Female | History of idiopathic generalized epilepsy, controlled on Phenytoin since age 16. Presented during pregnancy at 9 weeks’ gestation; 10-cm adrenal cortical carcinoma found in evaluation of catatonia. | Catatonic state unchanged after tumor removal; catatonia improved with ECT. | Back to baseline; no relapses at 4-year follow-up. |
Chronic lymphocytic encephalomyelitis of unknown etiology | 23/Male | History of brainstem encephalitis at age 17, with progressive lymphocytic gray- and white-matter inflammatory disorder of unknown etiology. Catatonic syndrome developed after taper of steroids. | ECT was not attempted out of concern for respiratory status. Only minimal improvement noted with high-dose intravenous steroids. | Significant cognitive and motor impairment, without definite catatonia, at 10-year follow-up. |
Hashimoto’s encephalopathy | 52/Female | Presented with relapsing psychotic encephalopathy with catatonia. CSF: 5 monocytes; protein, 235; glucose normal. Antimicrosomal antibodies: 1:6,400; MRI: Nonspecific white-matter hyperintensities. Brain biopsy showed mild, chronic lymphocytic inflammation, without specific diagnosis. | Improvement with both Ativan and ECT. Catatonia noted to worsen after steroid dose decreased. Improvement with pulse doses of IV methylprednisolone. | No recurrence of catatonia at 1-year follow-up; on chronic immunosuppression. |
Steroid-responsive encephalopathy with autoimmune thyroiditis | 65/Female | Presentation with catatonia associated with multifocal myoclonus. EEG showed generalized atypical triphasic waves and multifocal spikes. Brain biopsy showed nonspecific, predominantly subcortical gliosis and microglial activation. CSF: protein, 50; leukocytes normal; NSE: 28.5; serum thyroperoxidase: 89 (normal: <40). | Initial improvement with first three ECT treatments, then declining over subsequent five treatments. Ativan not attempted. Catatonia resolved with high-dose methylprednisolone. | Alive at 5 years, without recurrence of catatonia. |
Relapsing encephalopathy of unknown etiology; suspect metabolic | 44/Male | Familial microcytic anemia and mildly elevated liver enzymes; seizure disorder since age 16. Found on one occasion to have elevated branched chain amino acids, but no diagnosis was made despite extensive evaluation. | Ativan not attempted; improved with ECT. | No long-term follow-up. |
Dementia (N=4) | ||||
Probable bvFTD: 1 (rapidly progressive) | 73/Male | 3-month progression of diminished speech output, obsessive-compulsive symptoms, and behavioral outbursts. PET (18FDG): moderately-to-severely reduced uptake in the fronto-temporal lobes (left > right). | No improvement with either Ativan or ECT. | Not alive 2 years after onset, with catatonic symptoms persisting. |
Probable bvFTD 2 | 68/Male | 5-year progression of aphasic dementia and behavioral dyscontrol. PET (18FDG): marked fronto-temporo-parietal hypometabolism (left > right). | Neither Ativan nor ECT attempted; spontaneous resolution of catatonia with supportive measures. | Not alive 1 year after catatonic episode; managed by hospice with comfort measures only. |
Probable bvFTD 3 (rapidly progressive) | 65/Male | 9-month history of progressive abulia, personality changes, and changes in emotional expression. MRI: bilateral temporal greater than generalized atrophy. | No therapy attempted. | No long-term follow-up. |
Lewy-body dementia | 77/Male | Preceding history of cognitive decline (greatest difficulty with visuospatial functioning), mild parkinsonism, and REM behavior sleep disorder. | No improvement with Ativan; improved with ECT. | Not living at 7-year follow-up; no documented recurrence. |
Developmental (N=3) | ||||
Pervasive developmental disorder | 19/Male | 2-month history of “freezing spells” lasting up to 2 hours, resolving spontaneously, leading to more-protracted episode; had actually developed exposure keratitis as a result of inadequate eye closure. | Ativan not attempted; some improvement noted after 2 ECT treatments; subsequent 13 treatments were not helpful. | No long term follow-up available. |
Asperger’s syndrome | 19/Male | 2-year history of episodic catatonia. | Improvement with both Ativan and ECT. | No long-term follow-up available. |
22q13.3 microdeletion syndrome (periodic catatonia) | 23/Female | Global developmental delay; nonverbal throughout life, but no behavioral problems until age 18, when irritability, aggressive behaviors, and periodic catatonia (every 6–8 weeks) were noted. | Improvement with Ativan; ECT reported not to help in the past. | No long-term follow-up. |
Other (N=4) | ||||
CNS lung cancer metastases | 66/Female | Known metastatic non-small cell lung cancer, to right cerebellum and left parietal lobe; both increased in size along with catatonic presentation. | Improved with Ativan. Documentation insufficient to judge clinical effect of steroids on catatonia. | Not alive at 3-year follow-up; no documented recurrence. |
Postictal psychosis progressing to catatonia | 47/Female | 30-year history of treatment-refractory complex partial epilepsy. | Improved with Ativan; ECT not attempted. | No recurrence at 3-year follow-up. |
Postictal catatonia; simultaneous cannabinoid intoxication. | 51/Female | Distant history of traumatic brain injury and complex partial epilepsy; not on any seizure medicines because of seizure freedom for 10 years. Brought to hospital after an unwitnessed episode of loss of consciousness with urinary incontinence, amnesia. Toxicology positive for cannabinoids. EEG showed bilateral independent temporal sharp waves (left > right). | Improved with Ativan; ECT not attempted. | No recurrence of catatonia at 3-year follow-up. Seizure free on Keppra. |
Treatment-refractory epilepsy s/p left-anterior temporal lobectomy. | 42/Male | Catatonia developed in the setting of epilepsy-monitoring unit evaluation while off seizure medicines (phenytoin and carbamazepine) for 2 days. No epileptiform correlate to catatonia. | Epilepsy medications restarted, without acute load. No improvement with Ativan; dramatic improvement after 2 ECT treatments. | No recurrence at 6-year follow-up. |
Neurodiagnostic Testing in Catatonia
Generalized slowing (N=57) |
Theta (N=26) |
Mixed theta/delta (N=23) |
Delta (N=8) |
Focal slowing (N=26) |
Temporal (N=16), including TIRDA (N=4), and bitemporal slowing (N=7) |
Frontal (N=8), including FIRDA (N=3) |
Occipital (N=2) |
Generalized triphasic waves (N=3) |
Typical (N=1), atypical (N=2) |
Asymmetry (N=9) |
Left > right slowing (N=8) |
Epileptiform activity (N=6) |
Generalized spike and wave (N=2) |
Focal sharp waves and/or spikes (N=4); frontal (N=1), temporal (N=3), parietal (N=1), central (N=2) |
Discussion
Conclusions
Acknowledgments
References
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