BACKGROUND: Two million adolescents experience suicidal ideation (SI) or suicide attempt (SA) annually, and they frequently present to emergency departments. Delays in transfer to inpatient psychiatric units increasingly lead to "boarding" in emergency departments and inpatient medical units. We sought to understand adolescents' perspectives during boarding hospitalizations to gain insight into helpful practices and targets for improvement. METHODS: Using convenience sampling, we conducted semistructured interviews with 27 adolescents hospitalized for SI or SA while they were awaiting transfer to an inpatient psychiatric facility. Interviews were recorded and transcribed, and the thematic analysis was organized using NVivo 11. RESULTS: Eight themes emerged: (1) supportive clinical interactions, (2) information needs, (3) repetitive inquiries, (4) safety, (5) previous hospital experiences, (6) activities and boredom, (7) physical comfort, and (8) emotions. Adolescents expressed appreciation for compassionate clinicians and for receiving information about what to expect, experienced the hospital as a safe environment, emphasized the value of staying occupied and of physical comfort, and were relieved to be receiving help to reduce their suicidal thoughts or behaviors. Reports of embarrassment and discomfort about repeated inquiries from the clinical team, comparisons with previous hospital experiences, and unanswered questions about what would occur during the planned inpatient psychiatric hospitalization were common. CONCLUSIONS: The perspectives of adolescents seeking care for SI or SA are an important source of information for health care systems seeking to improve hospital care. Clinicians can relieve distress of adolescents awaiting psychiatric hospitalization by focusing on compassionate connection, minimizing repeated inquiries, and providing complete and concrete information about treatment plans.
Aim: We tested the hypothesis that patients with succinic semialdehyde dehydrogenase (SSADH) deficiency on taurine would have decreased cortical excitability as measured by transcranial magnetic stimulation (TMS) and improved cognition, due to taurine's partial GABA(A and B) receptor agonist effects and rescue in the null mouse model from status epilepticus and premature lethality.Method: Biomarkers including neuropsychological testing, TMS, and CSF metabolites were studied in a cohort of patients on and off three months' taurine treatment.Results: Seven patients (5M/2F; age range 12-33 years) were enrolled in this open-label crossover study. Baseline average full-scale IQ (FSIQ) was 44.1 (range 34-55). Of six who returned at 6-month follow-up, five completed cognitive testing (3M/2F) on therapy; average FSIQ ¼ 43.4 (range 33-51). CSF biomarkers (n ¼ 4 subjects) revealed elevation in taurine levels but no change in free or total GABA. Baseline cortical excitability measured with TMS agreed with previous findings in this population, with a short cortical silent period and lack of long-interval intracortical inhibition. Patients on taurine showed a decrease in cortical silent period and short-interval intracortical inhibition compared to their off taurine study.Interpretation: TMS demonstrated decreased inhibition in patients on taurine, in contrast to the study hypothesis, but consistent with its failure to produce clinical or cognitive improvement. TMS may be a useful biomarker for therapy in pediatric neurotransmitter disorders.Succinic semialdehyde dehydrogenase (SSADH) deficiency is a rare autosomal recessive defect in the catabolic pathway of GABA (gamma-aminobutyric acid), leading to elevated levels of GABA and gamma-hydroxybutyric acid (GHB) in body fluids and brain parenchyma (Pearl et al. 2003a, b). The typical clinical phenotype has been described as a slowly progressive or static encephalopathy. Most patients present with developmental delay noted in the first 2 years of life, as well as hypotonia, hyporeflexia, ataxia, speech disturbance, and intellectual disability, and at least half have seizures.Several lines of evidence indicate that SSADH deficiency results in chronic, overuse-dependent downregulation of GABA(A) and GABA(B) receptors. In the mouse model, decreased binding of the selective GABA(A) receptor antagonist tert-butylbicyclophosphorothionate ([35S]TBPS) was observed in the cerebral cortex, hippocampus, and thalamus of the mutant strain compared to wild type, and reduced GABA(A)-mediated inhibitory postsynaptic potentials and enhanced postsynaptic population spikes were recorded from hippocampal slices of the mutant strain ). There was also significantly decreased binding of a specific GABA(B) receptor antagonist in the mutant strain and attenuated GABA(B)-mediated synaptic potentials . We demonstrated
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