Disease relevance of Temporal Lobe

• Hypogonadism, hyperprolactinaemia, and temporal lobe epilepsy in hyposexual men [1].
• Herpes simplex viral DNA in temporal lobe epilepsy [2].
• Long-lasting reduction of inhibitory function and gamma-aminobutyric acid type A receptor subunit mRNA expression in a model of temporal lobe epilepsy [3].
• Numerous temporal lobe astrocytes in Alzheimer disease and postnatal Down syndrome were intensely interleukin 1-, S-100-, and glial fibrillary acidic protein-immunoreactive and had reactive structure [4].
• The data indicate that serum prolactin levels always rise after complex partial seizures involving the temporal lobes, and rise after certain simple partial seizures involving limbic structures [5].

Psychiatry related information on Temporal Lobe

• The results of these two studies suggest that previously reported differences between temporal lobe epileptics and normals on these trait variables reflect underlying differences in degree of nonspecific psychopathology and do not necessarily indicate the presence of a specific behavioral syndrome in temporal lobe epilepsy [6].
• Behavioral symptoms in temporal lobe epilepsy [7].
• Remote episodic memory deficits in patients with unilateral temporal lobe epilepsy and excisions [8].
• These scans include the region of the superior surface of the temporal lobe (planum temporale), which is thought to be larger in individuals with left cerebral dominance for speech [9].
• The present study investigated STM and LTM for nonverbal material in three neurological conditions associated with memory impairment: bilateral medial temporal lobe lesions (patient H.M.), Parkinson's disease (PD) and Alzheimer's disease (AD) [10].

High impact information on Temporal Lobe

• We show that the expression pattern of mouse Lgi1 is predominantly neuronal and is consistent with the anatomic regions involved in temporal lobe epilepsy [11].
• A randomized, controlled trial of surgery for temporal-lobe epilepsy [12].
• Positron-emission tomography of four patients showed decreased glucose metabolism in the medial temporal lobes [13].
• Neonatal lesions of the medial temporal lobe disrupt prefrontal cortical regulation of striatal dopamine [14].
• Hippocampal GABA transporter function in temporal-lobe epilepsy [15].

Chemical compound and disease context of Temporal Lobe

• The long-term expression of the proenkephalin mRNA and its peptides in the kainate-treated rat hippocampus also suggests an important role in the recurrent seizures of temporal lobe epilepsy [16].
• Previous magnetic resonance spectroscopy (MRS) studies have shown that N-acetylaspartate (NAA) is reduced not only in the ipsilateral but also in the contralateral hippocampus of many patients with mesial temporal lobe epilepsy (mTLE) [17].
• These data indicate that NMDA-mediated ictal discharges induced by 4AP originate in the entorhinal cortex; such a conclusion is in line with clinical evidence obtained in temporal lobe epilepsy patients [18].
• Autosomal dominant lateral temporal lobe epilepsy previously has been linked to chromosome 10q22-q24, and recently mutations in the LGI1 gene (Leucine-rich gene, Glioma Inactivated) have been found in some autosomal dominant lateral temporal lobe epilepsy families [19].
• 6. There was no edema and no neoplasm in the temporal lobes removed for seizure (n = 2), and their level of leukotriene C4 was 0.4 +/- 0.1 pg/mg tissue [20].

Biological context of Temporal Lobe

• Words elicit a negative event-related potential (ERP) peaking around 400 ms within the anterior mesial temporal lobe (AMTL-N400) [21].
• We conclude that a loss of somatostatin-producing interneurons with an upregulation of dentate somatostatin receptors is a specific and characteristic element in the pathophysiology of human cryptogenic temporal lobe epilepsy [22].
• Experimental and human data suggest programmed (active) cell death may contribute to the progressive hippocampal atrophy seen in patients with refractory temporal lobe epilepsy [23].
• Evidence for digenic inheritance in a family with both febrile convulsions and temporal lobe epilepsy implicating chromosomes 18qter and 1q25-q31 [24].
• A functional polymorphism in the prodynorphin gene promotor is associated with temporal lobe epilepsy [25].

Anatomical context of Temporal Lobe

• The EphA4 receptor tyrosine kinase regulates the formation of the corticospinal tract (CST), a pathway controlling voluntary movements, and of the anterior commissure (AC), connecting the neocortical temporal lobes [26].
• Fluphenazine, but not clozapine, increased metabolic rates in the subcortical and lateral temporal lobes, whereas clozapine, but not fluphenazine, decreased inferior prefrontal cortex activity [27].
• Correlations of metabolic increases in the dorsolateral prefrontal cortex, medial temporal lobe (amygdala), and cerebellum with self-reports of craving suggest that a distributed neural network, which integrates emotional and cognitive aspects of memory, links environmental cues with cocaine craving [28].
• Expression of human epileptic temporal lobe neurotransmitter receptors in Xenopus oocytes: An innovative approach to study epilepsy [29].
• Similar results were observed in 13 specimens of anterolateral temporal neocortex obtained during temporal lobectomies in patients with intractable temporal lobe epilepsy, compared with postmortem human specimen or control brain tissues [30].

Associations of Temporal Lobe with chemical compounds

• These data suggest that temporal-lobe epilepsy is characterized in part by a loss of glutamate-stimulated GABA release that is secondary to a reduction in the number of GABA transporters [15].
• Chlorazepate in temporal lobe epilepsy [31].
• Coronal images focused on the frontal and temporal lobes were acquired using pulse sequences that maximized gray vs white matter contrast [32].
• BACKGROUND: The planum temporale, located on the posterior and superior surface of the temporal lobe, is a brain region thought to be a biological substrate of language and possibly implicated in the pathophysiology of schizophrenia [33].
• Distorted distribution of nicotinamide-adenine dinucleotide phosphate-diaphorase neurons in temporal lobe of schizophrenics implies anomalous cortical development [34].

Gene context of Temporal Lobe

• CONCLUSIONS: Specific alleles of the DISC1 and TRAX genes on 1q42 appear to contribute to genetic risk for schizophrenia through disruptive effects on the structure and function of the prefrontal cortex, medial temporal lobe, and other brain regions [35].
• LGI1, one member of the LGI gene family, encodes a approximately 63 kDa protein, with strong regional expression in neurons within the temporal lobe [36].
• We also show that changes in the expression of other ITFs (Fos, Jun-D and Krox-20) and the BDNF/trkB neurotrophin system may play a central role in the development of hippocampal kindling, an animal model of human temporal lobe epilepsy [37].
• These findings indicate that chronic temporal lobe seizures are associated with differential changes in hippocampal NR1 and NR2A-D hybridization densities that vary by subfield and clinical-pathological category [38].
• Death-associated protein kinase expression in human temporal lobe epilepsy [23].

Analytical, diagnostic and therapeutic context of Temporal Lobe

• This experiment sought to identify neural correlates of memory formation with the use of intracerebral electrodes implanted in the brains of patients with temporal lobe epilepsy [39].
• We analyzed continuous 3- to 14-day intracranial EEG recordings from five patients with mesial temporal lobe epilepsy obtained during evaluation for epilepsy surgery [40].
• Perfusion of the isolated brain with the gamma-aminobutyric acid A receptor antagonist picrotoxin, however, could induce self-sustained temporal lobe epilepsy [41].
• Regional binding of 123I-iododexetimide, a muscarinic acetylcholine receptor antagonist, was measured in vivo in the temporal lobes of 4 patients with complex partial seizures using single-photon emission computed tomography [42].
• Bromodeoxyuridine labeling, in situ hybridization, and immunohistochemistry were used to identify proliferating progenitors and mature DGCs in the adult rat pilocarpine temporal lobe epilepsy model [43].

References