Disease relevance of Frontal Lobe

• Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is a partial epilepsy causing frequent, violent, brief seizures at night, usually beginning in childhood [1].
• The Yo antigen was expressed by the esophageal tumor but not in a frontal lobe cerebral metastasis identified at postmortem [2].
• We studied 8 patients with frontal lobe epilepsy, finding interictal alkalosis in the epileptogenic region compared to the contralateral frontal lobe in all patients (7.10 +/- 0.05 vs 7.00 +/- 0.06, p < 0.001) [3].
• We conclude that striatal dopamine depletion disrupts the normal pattern of basal ganglia outflow in Parkinson's disease and consequently, affects the expression of frontal-lobe functions by interrupting normal transmission of information through frontostriatal circuitry [4].
• Relationship between frontal lobe lesions and Wisconsin Card Sorting Test performance in patients with multiple sclerosis [5].

Psychiatry related information on Frontal Lobe

• MAIN OUTCOME MEASURES: Striatal dopamine D(2) receptor availability estimated with positron emission tomographic imaging and carbon 11 ((11)C)-labeled raclopride, and performance on neuropsychological tests sensitive to frontal lobe functioning and to schizophrenia vulnerability [6].
• Atrophy of the frontal lobe was found in both PSP and dementia with Lewy bodies and correlated with increasing neurofibrillary tangle or Lewy body densities, respectively [7].
• A nocturnal familial form of frontal lobe epilepsy (autosomal dominant nocturnal frontal lobe epilepsy, ADNFLE), often misdiagnosed as parasomnia, has been recently described in some families [8].
• OBJECTIVE: Abnormalities in frontal lobe phosphorous metabolism in patients with bipolar disorder have been reported, but many of the patients studied were receiving lithium [9].
• In addition, vulnerabilities for eating disorders, impulse dyscontrol, and mood disturbances may involve 5-HT and frontal lobe activity [10].

High impact information on Frontal Lobe

• The nicotinic receptor beta 2 subunit is mutant in nocturnal frontal lobe epilepsy [11].
• Clustered attacks of epileptic episodes originating from the frontal lobe during sleep are the main symptoms of autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE, MIM 600513) [11].
• The Wisconsin Card Sorting Test, which probes the ability to shift attention from one category of stimulus attributes to another (shifting cognitive sets), is the most common paradigm used to detect human frontal lobe pathology [12].
• In this issue of Neuron, describe the activity of single neurons in the SEF of monkeys, an oculomotor area of the frontal lobe, during the performance of stereotyped sequences of saccades [13].
• Participants were genotyped for catechol-O-methyltransferase (COMT) at the Val158Met locus, which has been shown to affect executive cognition and frontal lobe function, likely because of genetically determined variation in prefrontal dopamine signaling [14].

Chemical compound and disease context of Frontal Lobe

• Autosomal dominant nocturnal frontal-lobe epilepsy (ADNFLE) is a recently identified partial epilepsy in which two different mutations have been described in the alpha4 subunit of the neuronal nicotinic acetylcholine receptor (CHRNA4) [15].
• A sharply decreased cortical metabolic rate for glucose was obtained in specific gyri, especially in the frontal lobes, where there was extensive gliosis and neuronal loss [16].
• Gene delivery was assessed in C6 gliomas established in the righ frontal lobe of athymic mice [17].
• In 10 patients who had not been treated with neuroleptics for several weeks, we found a dopaminergic hypersensitivity in the frontal lobes, as a weak dose of piribedil restored near-normal frontality [18].
• In three frontotemporal dementia patients, a lactate peak was present in the frontal lobe [19].

Biological context of Frontal Lobe

• CONCLUSIONS: Selective displacement of interstitial WM neurons in the frontal lobe of brains of schizophrenic patients may indicate alteration in the migration of subplate neurons or in the pattern of programmed cell death [20].
• Autosomal dominant nocturnal frontal-lobe epilepsy: genetic heterogeneity and evidence for a second locus at 15q24 [15].
• A new locus for autosomal dominant nocturnal frontal lobe epilepsy maps to chromosome 1 [21].
• Cerebral blood flow tomography, by xenon 133 inhalation or HMPAO (99mTc-d, l-hexamethyl-propylene amine oxime) technetium Tc 99m injection, revealed a severe hypoperfusion in both frontal lobes of a 40-year-old woman with confirmed neuroacanthocytosis [22].
• A missense mutation, leading to the replacement of serine 248 by phenylalanine in the second transmembrane segment, had been detected in patients with autosomal dominant nocturnal frontal lobe epilepsy [23].

Anatomical context of Frontal Lobe

• Pathological studies of two brains from affected members of Family MN obtained at autopsy demonstrate numerous tau-positive inclusions that were most prominent in the frontal lobes, anterior temporal lobes, and brainstem structures, as well as Pick-like bodies and associated granulovacuolar degeneration [24].
• Analysis of individual brain regions revealed significant declines in cerebral glucose utilization in most regions throughout the cerebral cortex, particularly those in the superior half of the frontal lobe [25].
• In schizophrenics, the alterations in expression of NR2 subunit mRNA in prefrontal cortex are potential indicators of deficits in NMDA receptor-mediated neurotransmission accompanying functional hypoactivity of the frontal lobes [26].
• In contrast, 8H9 was nonreactive with normal human tissues including bone marrow, colon, stomach, heart, lung, muscle, thyroid, testes, pancreas, and human brain (frontal lobe, cerebellum, pons, and spinal cord) [27].
• RESULTS: Brain regions that satisfied these criteria were largely left lateralized and included the frontal lobe (medial and middle frontal gyri, bilateral inferior frontal gyrus), parietal lobe (bilateral inferior parietal lobule), insula, and limbic lobe (anterior and posterior cingulate gyrus) [28].

Associations of Frontal Lobe with chemical compounds

• As compared with the values for the controls, normalized glucose metabolism was significantly reduced in six of 60 specific regions of the brain, including an area of the left anterior frontal lobe (P < .05) [29].
• Altered distribution of nicotinamide-adenine dinucleotide phosphate-diaphorase cells in frontal lobe of schizophrenics implies disturbances of cortical development [30].
• CHRNB2 is the second acetylcholine receptor subunit associated with autosomal dominant nocturnal frontal lobe epilepsy [31].
• We studied 8 patients with frontal lobe epilepsy and found mean NA/creatine (Cr) in the epileptogenic frontal lobe decreased by 27% compared with that of the contralateral homologous region (1.81 +/- 0.36 vs 2.49 +/- 0.60, p < 0.008) [32].
• The functional anatomy of frontal lobe neglect in the monkey: behavioral and quantitative 2-deoxyglucose studies [33].

Gene context of Frontal Lobe

• Overall, these findings do not support a major role for COMT in increasing susceptibility for schizophrenia or in mediating frontal lobe function [34].
• Dose dependent effect of APOE epsilon4 on behavioral symptoms in frontal lobe dementia [35].
• Further, we found an association between the A allele of the apolipoprotein C1 (APOC1) polymorphism and poorer memory and frontal lobe function [36].
• A cDNA sequence encoding a putative peptide-specific G-protein-coupled receptor (GPR37) was isolated from a set of human brain frontal lobe expressed sequence tags [37].
• Moreover, a functional Val158Met polymorphism in COMT that alters the activity of the encoded protein has been strongly implicated in frontal lobe function, with the high activity Valine allele being associated with poorer performance, and ADHD is thought to involve fronto-striatal pathways [38].

Analytical, diagnostic and therapeutic context of Frontal Lobe

• EEG predicts surgical outcome in lesional frontal lobe epilepsy [39].
• RESULTS: Based on t-maps, subjects with the PS-1 mutation who were asymptomatic demonstrated reduced perfusion in comparison with the normal control subjects in the hippocampal complex, anterior and posterior cingulate, posterior parietal lobe, and anterior frontal lobe [40].
• DESIGN: Technetium Tc 99m ethyl cysteinate dimer SPECT study using a Patlak plot.Patients Hiroshima University Hospital, Hiroshima, Japan. Ten patients with SCA6 and 9 healthy controls.Main Outcome Measure The rCBF of the cerebellar vermis, cerebellar hemisphere, and frontal lobes [41].
• A MRI scan revealed bilateral calcifications in the basal ganglia and a brain PET showed a massive reduction of glucose metabolism in the basal ganglia and both frontal lobes, but no other brain abnormalities [42].
• Recent technological advances in neuroimaging, electroencephalography, magnetoencephalography and detailed videotape analysis of seizure semiology may enable us to delineate these frontal lobe syndromes with better accuracy, thereby improving outcome after epilepsy surgery [43].

References