Crossing State Lines: Ethical and Clinical Considerations in Treating a Child With Catatonia.

Catatonia is a complex constellation of symptoms presenting with abnormalities in movement and behavior and arises from multiple medical, neurologic, and psychiatric conditions. In recent years, there has been a call to move catatonia from a classifier to a diagnosis of its own in the DSM-5.1,2 Catatonia is often underdiagnosed in the hospital and carries with it substantial morbidity and mortality.3 Malignant catatonia, characterized by autonomic instability, hyperactivity, mutism, and stuporous exhaustion, is a medical emergency requiring intensive care.4 Early diagnosis and treatment are imperative, as untreated malignant catatonia may be fatal in up to 10% to 20% of cases, sometimes only days from onset.5 The combination of lorazepam and electroconvulsive therapy (ECT) is a safe and effective treatment for catatonia in both adults and children, although the body of literature pertaining to children remains limited.6,7 In addition, there are multiple case reports of improvement in catatonia with ECT regardless of etiology.8 However, laws in some US states prohibit ECT's use despite evidence of its effectiveness and safety in children and adolescents.9 Here, we describe a case presentation that was both prolonged and complicated by state laws pertaining to the use of ECT in children and adolescents.

Electric field causes volumetric changes in the human brain.

Recent longitudinal neuroimaging studies in patients with electroconvulsive therapy (ECT) suggest local effects of electric stimulation (lateralized) occur in tandem with global seizure activity (generalized). We used electric field (EF) modeling in 151 ECT treated patients with depression to determine the regional relationships between EF, unbiased longitudinal volume change, and antidepressant response across 85 brain regions. The majority of regional volumes increased significantly, and volumetric changes correlated with regional electric field (t = 3.77, df = 83, r = 0.38, p=0.0003). After controlling for nuisance variables (age, treatment number, and study site), we identified two regions (left amygdala and left hippocampus) with a strong relationship between EF and volume change (FDR corrected p<0.01). However, neither structural volume changes nor electric field was associated with antidepressant response. In summary, we showed that high electrical fields are strongly associated with robust volume changes in a dose-dependent fashion.

Catatonia after cerebral hypoxia: do the usual treatments apply?

BACKGROUND: Neurologic deterioration occurring days to weeks after a cerebral hypoxic event accompanied by diffuse white matter demyelination is called delayed posthypoxic leukoencephalopathy (DPHL). Manifestations of DPHL are diverse and include dementia, gait disturbance, incontinence, pyramidal tract signs, parkinsonism, chorea, mood and thought disorders, akinetic mutism, and rarely catatonia. METHODS: We report a case of malignant catatonia in a patient diagnosed with DPHL that was refractory to electroconvulsive therapy (ECT) and review the literature on catatonia in DPHL. RESULTS: The patient was a 56-year-old woman with schizoaffective disorder who was admitted with catatonia 2 weeks after hospitalization for drug overdose and respiratory failure. Her catatonic symptoms did not respond to treatment of lorazepam, amantadine, methylphenidate, or 10 sessions of bilateral ECT at maximum energy. Repeat magnetic resonance imaging revealed extensive periventricular white matter lesions not present on admission scans, and she was diagnosed with DPHL. DISCUSSION: No treatment for DPHL has been proven to be widely effective. Hyperbaric oxygen treatments may reduce the rate of development, and symptom improvement has been reported with stimulants and other psychotropic agents. Review of literature reveals rare success with GABAergic agents for catatonia after cerebral hypoxia and no cases successfully treated with ECT. There are 7 case reports of neurologic decompensation during ECT treatment after a cerebral hypoxic event. CONCLUSION: Caution is advised when considering ECT for catatonia when delayed sequelae of cerebral hypoxia are on the differential diagnosis, as there is a dearth of evidence to support this treatment approach.

Catatonia after deep brain stimulation successfully treated with lorazepam and right unilateral electroconvulsive therapy: a case report.

OBJECTIVES: The presence of a deep brain stimulator (DBS) in a patient who develops neuropsychiatric symptoms poses unique diagnostic challenges and questions for the treating psychiatrist. Catatonia has been described only once, during DBS implantation, but has not been reported in a successfully implanted DBS patient. METHODS: We present a case of a patient with bipolar disorder and renal transplant who developed catatonia after DBS for essential tremor. RESULTS: The patient was successfully treated for catatonia with lorazepam and electroconvulsive therapy after careful diagnostic workup. Electroconvulsive therapy has been successfully used with DBS in a handful of cases, and certain precautions may help reduce potential risk. CONCLUSIONS: Catatonia is a rare occurrence after DBS but when present may be safely treated with standard therapies such as lorazepam and electroconvulsive therapy.

Assembly and processing of an engineered amelogenin proteolytic product (rP148).

The purpose of this study was to express, characterize, and investigate the self-assembly of a recombinant porcine amelogenin lacking the hydrophilic 24 C-terminal amino acids (rP148). To gain further insight into the function of amelogenin processing during enamel mineralization, this protein was also used as a substrate to examine the action of matrix metalloproteinase-20 (MMP-20). The assembly properties of rP148 were monitored by dynamic light scattering (DLS). In general, rP148 molecules assemble into monomers, dimers, oligomers, and some nanosphere-like particles. Depending on the solution conditions, large aggregates were also observed. Matrix metalloproteinase-20 cleaved the rP148 molecule at a few sites, creating a number of different products, including the tyrosine-rich amelogenin polypeptide (TRAP). Our data suggest that although rP148 self-assembles into small particles, its assembly properties are different from those of the full-length rP172, indicating that the C-terminal 24 amino acids play a critical role in nanosphere assembly. We further demonstrate that MMP-20 digests rP148 in a manner that generates a similar proteolytic pattern, as would be expected to occur in vivo.