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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hippocampal sclerosis: a cause or consequence of epileptic activity? This question has concerned neurologists and pathologists for over 150 years. This paper reviews data from an in vitro model system regarding the consequences of epileptic activity of known origin. Exposure of organotypic hippocampal slice cultures to convulsants, such as bicuculline or picrotoxin for three days leads to pronounced neuronal degeneration and a reversible loss of dendritic spines. A similar pathology has been described in hippocampal tissue removed from patients suffering from severe, drug refractory epilepsy. The consequences of such pathological changes are not self-sustaining epileptic activity, as might be expected if such sclerosis caused epilepsy, but rather a selective decrease in synaptic excitation. Inhibitory synaptic transmission and GABAergic interneurons, in contrast, are preserved. At least two mechanisms contribute to the depression of synaptic excitation: morphological changes in dendritic spines and a decrease in the expression of genes for some glutamatergic receptors. It is hoped that this model will allow the characterization of the mechanisms underlying the pathological consequences of epileptic activity, and lead to useful therapeutic strategies.
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PMID:Consequence of epileptic activity in vitro. 829 97

Recurrent episodes with interictal affective aggression are a rare but well-recognized problem in patients with temporal lobe epilepsy. They are referred to as episodic dyscontrol or, more precisely, as intermittent explosive disorder (IED). The amygdala play a crucial role in the affective evaluation of multimodal sensory input and the neurobiological mediation of aggressive behaviour. With hippocampal sclerosis, in the context of mesial temporal lobe sclerosis, being the most common cause of temporal lobe epilepsy, we hypothesized that the amygdala might be affected by the same pathogenic process in aggressive patients. We investigated 50 patients with temporal lobe epilepsy: 25 with and 25 without a history of IED. Data from clinical, electrophysiological, neuropsychological and psychometric investigations were obtained, as well as MRI scans for the quantitative assessment of possible amygdala pathology. We found no evidence of a higher prevalence of amygdala sclerosis in the aggressive patients. Hippocampal sclerosis was significantly less common in patients with temporal lobe epilepsy and IED. However, a significant subgroup of patients (20%) with temporal lobe epilepsy and aggressive behaviour had severe amygdala atrophy in the context of a history of encephalitis. Another subgroup of aggressive patients (28%) had different left temporal lesions affecting either the amygdala or periamygdaloid structures. IED was associated with left-sided or bilateral EEG and MRI abnormalities, low IQ and high scores in depression and anxiety.
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PMID:Affective aggression in patients with temporal lobe epilepsy: a quantitative MRI study of the amygdala. 1064 32

Hippocampal sclerosis (HS) is one of the most common pathologies in medically intractable temporal lobe intractable epilepsy. Significant hippocampal volume loss has also been found in patients with chronic depression. Depression is common in chronic epilepsy populations, but the effects of this comorbidity on hippocampal volume are unknown. We examined the hippocampal volumes of 87 patients (n=31 right hippocampal sclerosis, RHS; n=56 left hippocampal sclerosis, LHS). Each subject completed the Hospital Anxiety and Depression Scale (HADS). In the group as a whole, 13 subjects (15%) recorded moderate or severe levels of depression. Depression was more common in the LHS group with 1 in 5 scoring in the moderate or severe range on the HADS (n=11). Depression scores were not significantly correlated with quantitative measures of hippocampal volume in the LHS group. However, higher degrees of hippocampal symmetry were associated with higher levels of depression in the RHS group. This suggests that the left hippocampus may be smaller in depressed patients with RHS, although our numbers were too small to confirm this statistically. Our results suggest that the depression may influence left hippocampal volume in patients with right hippocampal sclerosis. We conclude that the neuroradiological characteristics of patients with epilepsy and chronic depression deserve further examination.
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PMID:Epilepsy & depression: the effects of comorbidity on hippocampal volume--a pilot study. 1609 26

Hippocampal sclerosis is defined as selective neuronal loss and gliosis of the hippocampus with heterogeneous etiologies, including neurodegenerative tauopathies. We report a 78-year-old woman who presented with depression, in whom postmortem examination revealed almost complete loss of neurons with gliosis in the subiculum and CA1-3 regions of the hippocampus and abundant neuronal cytoplasmic inclusions in the dentate gyrus. The inclusions were round, slightly basophilic and argyrophilic, resembling Pick bodies. However, they were Gallyas- and 4-repeat tau-positive, and 3-repeat tau- and ubiquitin-negative. To our knowledge, the histopathological features in this case were different from those in hippocampal sclerosis or 4-repeat tauopathies reported previously. It is likely that this case is a new variant of 4-repeat tauopathy presenting with hippocampal sclerosis.
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PMID:Hippocampal sclerosis with four-repeat tau-positive round inclusions in the dentate gyrus: a new type of four-repeat tauopathy. 1936 Apr 25

A putative role of the brain-derived neurotrophic factor (BDNF) in epilepsy has emerged from in vitro and animal models, but few studies have analyzed human samples. We assessed the BDNF expression of transcripts with exons I (BDNFI), II (BDNFII), IV (BDNFIV) and VI (BDNFVI) and methylation levels of promoters 4 and 6 in the hippocampi of patients with pharmaco-resistant temporal lobe epilepsy (TLE) (n=24). Hippocampal sclerosis (HS) and pre-surgical pharmacological treatment were considered as clinical independent variables. A statistical significant increase for the BDNFVI (p<0.05) was observed in TLE patients compared to the autopsy control group (n=8). BDNFVI was also increased in anxiety/depression TLE (N=4) when compared to autopsies or to the remaining group of patients (p<0.05). In contrast, the use of the antiepileptic drug Topiramate (TPM) (N=3) was associated to a decrease in BDNFVI expression (p<0.05) when compared to the remaining group of patients. Methylation levels at the BDNF promoters 4 and 6 were similar between TLE and autopsies and in relation to the use of either Sertraline (SRT) or TPM. These results suggest an up-regulated expression of a specific BDNF transcript in patients with TLE, an effect that seems to be dependent on the use of specific drugs.
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PMID:Increased expression of BDNF transcript with exon VI in hippocampi of patients with pharmaco-resistant temporal lobe epilepsy. 2662 Nov 22