A systematic review of reviews of correctional mental health services using the STAIR Framework

Background: Rising demand for correctional mental health services (CMHS) in recent decades has been a global phenomenon. Despite increasing research, there are major gaps in understanding the best models for CMHS and how to measure their effectiveness, particularly studies that consider the overall care pathways and effectiveness of service responses. The STAIR (Screening, Triage, Assessment, Intervention, and Re-integration) model is an evidence-based framework that defines and measures CMHS as a clinical pathway with a series of measurable, and linked functions. Method: We conducted a systematic review of the reviews of CMHS elements employing PRISMA guidelines, organized according to STAIR pillars. We assessed the quality of included studies using the AMSTAR-2 criteria. Narrative reviews were read and results synthesized. Results: We included 26 review articles of which 12 were systematic, metaanalyses, and 14 narrative reviews. Two systematic reviews and seven narrative reviews addressed screening and triage with strong evidence to support specific screening and triage systems. There was no evidence for standardised assessment approaches. Eight systematic reviews and seven narrative reviews addressed interventions providing some evidence to support specific psychosocial interventions. Three systematic reviews and six narrative reviews addressed reintegration themes finding relatively weak evidence to support reintegration methods, with interventions often being jurisdictionally specific and lacking generalizability. Conclusions: The STAIR framework is a useful way to organize the extant literature. More research is needed on interventions, assessment systems, care pathway evaluations, and reintegration models

Hypoglycemic Seizures in Juvenile Rats: Acute Mortality is Associated with Severe Seizures in Diabetic and Non-diabetic Subjects

Iatrogenic hypoglycemia is a limiting factor for managing diabetes mellitus and can have severe outcomes such as seizures and coma. Although several studies have investigated the central nervous system consequences of hypoglycemia, the effects of seizures, as well as possible treatment strategies, have yet to be elucidated in juvenile animals. The objective of this thesis was to establish an in vivo model of severe hypoglycemia and seizures in juvenile diabetic and non-diabetic rats. In both groups there existed a similar blood glucose threshold for seizures, and mortality only occurred following severe seizures, particularly with repeated seizures that were unresponsive to treatment. While the administration of anticonvulsants temporarily mitigated seizures, glucose administration was required to prevent mortality. Abnormalities in the hippocampal and brainstem electroencephalograms (EEG) were observed in hypoglycemic animals without a clear correlate to convulsive activity.MAS

Severe Hypoglycemia in a Juvenile Diabetic Rat Model: Presence and Severity of Seizures Are Associated with Mortality

<div><p>It is well accepted that insulin-induced hypoglycemia can result in seizures. However, the effects of the seizures, as well as possible treatment strategies, have yet to be elucidated, particularly in juvenile or insulin-dependent diabetes mellitus (IDDM). Here we establish a model of diabetes in young rats, to examine the consequences of severe hypoglycemia in this age group; particularly seizures and mortality. Diabetes was induced in post-weaned 22-day-old Sprague-Dawley rats by streptozotocin (STZ) administered intraperitoneally (IP). Insulin IP (15 U/kg), in rats fasted (14–16 hours), induced hypoglycemia, defined as <3.5 mM blood glucose (BG), in 68% of diabetic (STZ) and 86% of control rats (CON). Seizures occurred in 86% of STZ and all CON rats that reached hypoglycemic levels with mortality only occurring post-seizure. The fasting BG levels were significantly higher in STZ (12.4±1.3 mM) than in CON rodents (6.3±0.3 mM), resulting in earlier onset of hypoglycemia and seizures in the CON group. However, the BG at seizure onset was statistically similar between STZ (1.8±0.2 mM) and CON animals (1.6±0.1 mM) as well as between those that survived (S+S) and those that died (S+M) post-seizure. Despite this, the S+M group underwent a significantly greater number of seizure events than the S+S group. 25% glucose administered at seizure onset and repeated with recurrent seizures was not sufficient to mitigate these continued convulsions. Combining glucose with diazepam and phenytoin significantly decreased post-treatment seizures, but not mortality. Intracranial electroencephalograms (EEGs) were recorded in 10 CON and 9 STZ animals. Predictive EEG changes were not observed in these animals that underwent seizures. Fluorojade staining revealed damaged cells in non-seizing STZ animals and in STZ and CON animals post-seizure. In summary, this model of hypoglycemia and seizures in juvenile diabetic rats provides a paradigm for further study of underlying mechanisms. Our data demonstrate that severe hypoglycemia (<2.0 mM) is a necessary precondition for seizures, and the increased frequency of these seizures is associated with mortality.</p></div

Mean blood glucose level measured hourly related to treatment and survival.

<p>S+S Glu: Seizure + Survival; glucose treated.</p><p>S+S AC+1XGLU: Seizure + Survival; glucose and anticonvulsant treated.</p><p>S+M Glu: Seizure + Mortality; glucose treated.</p><p>S+M AC+1XGLU: Seizure + Mortality; glucose and anticonvulsant treated.</p

EEG abnormalities during hypoglycemia is not associated with seizure behavior.

<p><b>A:</b> Representative EEG recording of hippocampus (CA1) at baseline (post-fasting; prior to insulin IP), 2 hours, 3 hours (slower waves) and 3.5 (EEG suppression) hours after insulin IP <b>B:</b> Electrographic seizure activity observed in CA1 (lower trace) after suppression of EEG activity. No ictal activity in cortex (upper trace) <b>C:</b> EEG recording of hippocampus and contralateral MRF obtained in STZ rat during hypoglycemia. Electrographic seizure activity observed after suppression of EEG activity. Lower trace illustrates magnification of the area in the gray box <b>D:</b> EEG of the rat in (<b>C</b>) during a behavioural seizure; ictal activity may be masked by movement artifact.</p

Seizure score to characterize and quantify the observed seizures.

<p>Seizure score to characterize and quantify the observed seizures.</p

Comparing the association between seizure severity and mortality in CON and STZ rats.

<p><b>A:</b> No significant difference in the mean score of the first seizure treated in CON rats: S+S: 4.3±0.5 (n = 11) and S+M: 6.0±0.4 (n = 5) and STZ rats: S+S: 3.4±0.3 (n = 17) and S+M: 4.7±0.7 (n = 5) <b>B:</b> No significant difference in the mean maximum seizure score observed in CON rats: S+S: 4.9±0.4 (n = 11) and S+M: 6.5±0.3 and STZ rats: S+S: 4.3±0.4 (n = 17) and S+M: 5.5±0.4 (n = 5) <b>C:</b> A statistically significant difference in the mean number of seizures between (*) CON rats: S+S: 1.6±0.3 (n = 11) and S+M: 7.8±2.7 (n = 5; p<0.01) and between (*) STZ rats: S+S: 1.6±0.2 (n = 17) and S+M: 4.4±1.2 (n = 5; p<0.001).</p

Mean blood glucose level measured hourly related to outcome; (±S.E.M).

<p>NS: No Seizure.</p><p>S+M: Seizure + Mortality.</p><p>S+S: Seizure + Survival.</p

Effects of diabetes and seizures on neuronal damage.

<p><b>A:</b> Significant difference in the number of fluorojade (+) cells between CON non-seizing (C+NS: 0±0; n = 5 animals) and STZ non-seizing groups (D+NS; 2.17±1.9 cells; n = 6; p<0.05). No significant difference in the number of cells between CON seizing (C+S: 1.4±1.5; n = 5 cells) and STZ seizing groups (D+S: 4.7±5.8 cells; n = 7) <b>B:</b> Fluorojade (+) cells in the cortical region of (D+S) rat magnified 40X (white arrows).</p