Objective This study aimed to describe and compare the proportion of patients classified as an emergency department (ED) mental health presentation under different definitions, including the Australian Institute of Health and Welfare (AIHW) definition. Methods This retrospective cohort study enrolled all patients that presented to the EDs of a multi-centre Victorian health service between 1 January 2020 and 30 June 2023. Varying definitions of a mental health presentation were applied to each ED attendance, applying the current AIHW definition (using selected diagnosis codes), broader diagnosis-based coding, the presenting complaint recorded at triage and whether the patient was seen by or referred to the emergency psychiatric service (EPS).
View Article and Find Full Text PDFRationale: Altered expression of glutamate transporter EAAT2 protein has been reported in the hippocampus of patients with temporal lobe epilepsy (TLE). Two alternative EAAT2 mRNA splice forms, one resulting from a partial retention of intron 7 (I7R), the other from a deletion of exon 9 (E9S), were previously implicated in the loss of EAAT2 protein in patients with amyotrophic lateral sclerosis.
Methods: By RT-PCR we studied the occurrence of I7R and E9S in neocortical and hippocampal specimens from TLE patients and non-neurological controls.
Molecular misreading of the ubiquitin-B (UBB) gene results in a dinucleotide deletion in UBB mRNA. The resulting mutant protein, UBB+1, accumulates in the neuropathological hallmarks of Alzheimer disease. In vitro, UBB+1 inhibits proteasomal proteolysis, although it is also an ubiquitin fusion degradation substrate for the proteasome.
View Article and Find Full Text PDFGlial fibrillary acidic protein (GFAP) is considered to be a highly specific marker for glia. Here, we report on the expression of GFAP in neurons in the human hippocampus. Intriguingly, this neuronal GFAP is coded by out-of-frame splice variants and its expression is associated with Alzheimer pathology.
View Article and Find Full Text PDFIn patients suffering from temporal lobe epilepsy (TLE), increased extracellular glutamate levels in the epileptogenic hippocampus both during and after clinical seizures have been reported. These increased glutamate levels could be the result of malfunctioning and/or downregulation of glutamate transporters (also known as EAATs; excitatory amino acid transporters). In this study, the distribution of protein and mRNA of EAAT subtypes was examined in the hippocampus of TLE patients with hippocampal sclerosis (HS group) and without hippocampal sclerosis (non-HS group), and in autopsy controls without neurological disorders.
View Article and Find Full Text PDFThe expression of glial and neuronal glutamate transporter proteins was investigated in the hippocampal region at different time points after electrically induced status epilepticus (SE) in the rat. This experimental rat model for mesial temporal lobe epilepsy is characterized by cell loss, gliosis, synaptic reorganization, and chronic seizures after a latent period. Despite extensive gliosis, immunocytochemistry revealed only an up-regulation of both glial transporters localized at the outer aspect of the inner molecular layer (iml) in chronic epileptic rats.
View Article and Find Full Text PDFIn patients suffering from temporal lobe epilepsy (TLE) a highly variable degree of hippocampal sclerosis (HS) can be observed. For standard neuropathological evaluation after hippocampal resection, neuronal cell loss in the hippocampal subareas is assessed (Wyler score 0-4) [Wyler et al. (1992) J Epilepsy 5: 220-225].
View Article and Find Full Text PDFHippocampal sclerosis (HS) is a common derangement in many patients with temporal lobe epilepsy. As a result of neuronal cell loss in the hilar region of the hippocampus, it is proposed that mossy fibres sprout and re-innervate new regions of the dentate gyrus. This sprouting may cause recurrent excitation that may lead to the generation of seizures.
View Article and Find Full Text PDF