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P J Thompson

Publications and source records attributed to P J Thompson.

At least 19 recordsLinked to original sources
PubMed2001

A study of the relationship between participation in common leisure activities and seizure occurrence.

OBJECTIVE: To investigate whether participation in a structured programme of fairly intensive leisure activities increased seizure occurrence. MATERIAL AND METHODS: 212 adults with medically-intractable epilepsy were closely monitored for seizure occurrence during an "activities day", i.e. a day consisting of various structured sessions of leisure pursuits (video game play, reading, word puzzles, television, physical exercise), and during other days of relative rest, whilst undergoing prolonged video EEG monitoring. RESULTS: The relative risk of seizures did not differ significantly during activities days [0.71 (95% CL: 0.38 to 1.33)] compared with days of relative rest. CONCLUSIONS: These findings fail to provide empirical support for the hypothesis that cognitive exertion has an adverse effect on seizure control.

Activities of Daily Living↗
PubMed2001

The transmembrane protein occludin of epithelial tight junctions is a functional target for serine peptidases from faecal pellets of Dermatophagoides pteronyssinus.

There have been only a few studies of how allergens cross the airway epithelium to cause allergic sensitization. House dust mite fecal pellets (HDMFP) contain several proteolytic enzymes. Group 1 allergens are cysteine peptidases, whilst those of groups 3, 6 and 9 have catalytic sites indicative of enzymes that mechanistically behave as serine peptidases. We have previously shown that the group 1 allergen Der p 1 leads to cleavage of tight junctions (TJs), allowing allergen delivery to antigen presenting cells. In this study we determined whether HDMFP serine peptidases similarly compromise the airway epithelium by attacking TJs, desmosomes and adherens junctions. Experiments were performed in monolayers of MDCK, Calu-3 or 16HBE14o-epithelial cells. Cell junction morphology was examined by 2-photon molecular excitation microscopy and digital image analysis. Barrier function was measured as mannitol permeability. Cleavage of cell adhesion proteins was studied by immunoblotting and mass spectrometry. HDMFP serine peptidases led to a progressive cleavage of TJs and increased epithelial permeability. Desmosomal puncta became more concentrated. Cleavage of TJs involved proteolysis of the TJ proteins, occludin and ZO-1. This was associated with activation of intracellular proteolysis of ZO-1. In contrast to occludin, E-cadherin of adherens junctions was cleaved less extensively. Although Calu-3 and 16HBE14o-cells expressed tethered ligand receptors for serine peptidases, these were not responsible for transducing the changes in TJs. HDMFP serine peptidases cause cleavage of TJs. This study identifies a second general class of HDM peptidase capable of increasing epithelial permeability and thereby creating conditions that would favour transepithelial delivery of allergens.

Amino Acid Sequence↗
PubMed2001

Doctor proactive communication, return-to-work recommendation, and duration of disability after a workers' compensation low back injury.

Although doctors are increasingly evaluated on the basis of return-to-work (RTW) outcomes, the effect of doctor-patient communication about the workplace and RTW after an occupational injury has received little research attention. The effect of patient-reported doctor communication on duration of disability was examined retrospectively in a 3-year cohort of 325 claimants with a lost-time low back injury. Although doctor proactive communication was associated with a greater likelihood of RTW during the acute phase (< 30 days of disability), this effect disappeared when injury and workload characteristics were taken into account. A positive RTW recommendation was associated with about a 60% higher RTW rate during the subacute/chronic phase (> 30 days of disability) only. Prospective studies are needed to confirm this effect. The impact of physician communication on RTW is largely confounded by injury and workplace factors.

Adult↗
PubMed2001

Transforming growth factor beta2 induced pleurodesis is not inhibited by corticosteroids.

BACKGROUND: Talc and tetracyclines induce pleurodesis by directly injuring the pleura. The injury results in intense inflammation which subsequently leads to fibrosis. Corticosteroids can inhibit talc pleurodesis by reducing the inflammatory process. We hypothesised that transforming growth factor beta2 (TGFbeta2), a fibrogenic cytokine with immunomodulatory functions, could induce effective pleurodesis without generating significant pleural inflammation and therefore remain effective despite co-administration of corticosteroids. METHODS: Thirty rabbits were divided into two groups. Rabbits in the steroid group received weekly intramuscular injections of triamcinolone diacetate (0.8 mg/kg). Ten rabbits in each group were given 5.0 microg TGFbeta2 intrapleurally via a chest tube while the remaining five received 1.7 microg TGFbeta2. Pleurodesis was graded macroscopically after 14 days from 1 (none) to 8 (>50% symphysis). RESULTS: TGFbeta2 produced excellent pleurodesis at both 5.0 microg and 1.7 microg doses. The pleural effusions produced after the injection were low in all inflammatory markers. No significant differences were seen between the steroid group and controls in macroscopic pleurodesis scores (7.2 (1.3) v 7.1 (1.2)), levels of inflammatory markers in the pleural fluids (leucocyte 1107 (387)/mm(3) v 1376 (581)/mm(3); protein 3.1 (0.3) mg/dl v 2.9 (0.3) mg/dl, and LDH 478 (232) IU/l v 502 (123) IU/l), and the degree of microscopic pleural fibrosis and pleural inflammation. CONCLUSIONS: TGFbeta2 can induce effective pleurodesis and remains effective in the presence of high dose parenteral corticosteroids.

Animals↗
PubMed2001

Transforming growth factor-beta2 induces pleurodesis significantly faster than talc.

Transforming growth factor-beta2 (TGF-beta2) has recently been shown to produce effective pleurodesis in rabbits. Conventional pleurodesing agents such as talc act by inducing pleural injury, which results in acute inflammation and fibrosis. TGF-beta2 is a profibrotic cytokine capable of producing fibrosis without inducing significant pleural inflammation. We hypothesize that intrapleural administration of TGF-beta2 would (1) produce an effective pleurodesis faster; (2) stimulate more collagen deposition, and (3) induce less inflammation when compared with intrapleural injection of talc. Thirty rabbits were divided into two groups and given either TGF-beta(2) (1.7 microg) or talc slurry (400 mg/kg) via a chest tube. Five rabbits from each group were killed at Days 1, 4, and 7. Gross pleurodesis was graded from 1 (none) to 8 (complete symphysis). The microscopic pleural inflammation and fibrosis were graded from 0 to 4. Pleural thickening and the total area of collagen deposition were compared. Intrapleural injection of TGF-beta2 produced effective pleurodesis within 7 d (median pleurodesis score = 7 at Day 7). At Day 7, TGF-beta2 induced significantly more collagen deposition (19.4 +/- 19.6% versus 4.6 +/- 2.9% of total area of pleura at Day 7), higher pleural fibrosis score (3.0 +/- 1.0 versus 1.8 +/- 0.5), and pleural thickness (286 +/- 191 versus 85 +/- 37 microm) than did talc. There was no difference in the degree of pleural inflammation between the two groups at Day 7 (2.6 +/- 0.9 for TGF-beta2 versus 2.4 +/- 0.6 for talc) or at any other time points. In conclusion, the intrapleural administration of TGF-beta2 produced excellent pleurodesis in rabbits at a rate faster than talc slurry and all other pleurodesing agents investigated before. TGF-beta2 stimulated more collagen deposition without inducing excess inflammation when compared with talc slurry. TGF-beta2 may have advantages over talc slurry in the management of recurrent pleural effusion and pneumothorax.

Animals↗
PubMed2001

Symptomatic persistent post-coronary artery bypass graft pleural effusions requiring operative treatment : clinical and histologic features.

BACKGROUND: More than 85% of patients develop pleural effusions after coronary artery bypass grafting (CABG). Although the majority resolve spontaneously, post-CABG effusions can persist. The cause of these persistent effusions is unknown, and the histology of the pleural changes has seldom been reported. OBJECTIVES: To describe the patient characteristics and pathologic condition of the pleural tissues in patients with persistent post-CABG effusions. SUBJECTS: Eight patients with persistent post-CABG effusions who underwent thoracoscopy or thoracotomy over a 2-year period by one thoracic surgeon. These eight patients were selected as having undergone CABG > 2 months before their thoracic surgery and had no other identifiable causes of effusion. RESULTS: The median time from CABG to pleural surgery was 132 days (range, 74 to 2,258 days). The median left ventricular ejection fraction was 57% (range, 15 to 70%). All patients were dyspneic and had large (> or = 25% of the hemithorax) effusions on chest radiograph. All effusions persisted after two or more thoracenteses. Pleural effusion was left sided in three patients and bilateral in five patients. Pleural fluid was characterized by lymphocytosis (82 to 99%). Four of the eight patients had a visceral peel and trapped lung requiring decortication. Seven of the eight biopsy specimens showed pleural thickening characterized by dense fibrous tissues with associated mononuclear cell infiltration, while the eighth biopsy specimen showed only clotted blood. The degree of inflammation and fibrosis correlated with the interval between CABG and pleural surgery. Early post-CABG patients displayed more inflammation, with abundant lymphocytes in nodular configuration deep in the fibrous tissues away from the surface. Abundant keratin-positive, spindle-shaped cells were present in the fibrous tissues. Late cases showed predominantly mature fibrosis. CONCLUSIONS: Persistent post-CABG effusion can occur. Pleural fluids and pleural tissue in early-stage lesions were characterized by lymphocytosis. With time, the inflammatory changes were replaced by fibrosis that resulted in dyspnea and, at times, trapped lungs requiring surgical intervention.

Aged↗
PubMed2000

Postoperative hippocampal remnant shrinkage and memory decline: a dynamic process.

BACKGROUND: The severity of postoperative memory decline in unilateral temporal lobectomy patients has been associated both with the extent of hippocampal resection and MRI measures of preoperative hippocampal volume. Serial MRI of the hippocampal remnant suggest that further volume loss occurs in the immediate postoperative period. For the majority of patients, this process appears to stabilize within the first 3 months. The authors examined the relationship between the dynamic volume of the hippocampal remnant and postoperative memory decline. METHOD: Seventeen adult temporal lobectomy patients (nine, left; eight, right) underwent a full neuropsychological assessment and a volumetric MRI scan preoperatively and 3 months postoperatively. Examination of the posterior hippocampal remnant on the postoperative scan revealed volume loss in this segment compared to the identical segment preoperatively in 16 of 17 cases. Spearman's correlations were used to examine the relationship between postoperative memory decline (postoperative - preoperative memory scores) and the postoperative/preoperative hippocampal remnant volume ratio. RESULTS: The volume of the hippocampal remnant left in situ was significantly correlated with postoperative memory change. Patients with smaller remnant volumes demonstrated more postoperative memory decline than those with larger remnants. In addition, extensive hippocampal remnant shrinkage was associated with postoperative memory decline in both the right and left temporal lobectomy groups. CONCLUSIONS: The absolute volume and subsequent volume loss in the hippocampal remnant following surgery can influence postoperative memory change. These findings suggest that postoperative processes should be considered in addition to preoperative pathology and surgical factors in the prediction of postoperative memory change.

Adult↗
PubMed2000

Antenatal and postnatal findings in encephalocraniocutaneous lipomatosis.

Encephalocraniocutaneous lipomatosis (ECCL) is a congenital neurocutaneous syndrome that comprises unilateral porencephalic cysts with cortical atrophy; ipsilateral hamartomas of scalp, eyelid, and outer part of the eye; lipomas of the central nervous system (CNS); cranial asymmetry; and characteristic cutaneous lesions. We report on the antenatal and postnatal sonographic and radiologic, and on the postnatal pathologic findings of an infant diagnosed with ECCL at birth. The antenatal sonogram at 28 weeks of gestation showed normal intracranial structures; the sonogram at 38 weeks of gestation showed asymmetry of the cerebral hemispheres and ventriculomegaly. Magnetic resonance imaging at age 6 weeks demonstrated a porencephalic cyst on the left, hemiatrophy of the left cerebrum with cortical dystrophy, and a lipoma in the middle cranial fossa. Histologic findings of the resected cutaneous lesion confirmed the presence of fibrolipoma hamartoma. This case offers a unique insight into the antenatal and postnatal development of the hamartoneoplastic lesions of ECCL, and it highlights the difficulties inherent in the antenatal sonographic diagnosis of hamartoneoplastic syndromes.

Brain Diseases↗
PubMed2000

Nitrite generation and antioxidant effects during neutrophil apoptosis.

Neutrophil apoptosis is important for the resolution of airway inflammation in a number of lung diseases. Inflammatory mediators, endogenous reactive oxygen and nitrogen species, and intracellular and extracellular antioxidants may all influence neutrophil apoptosis. This study investigated the involvement of these factors during apoptosis of neutrophils cultured in vitro. Neutrophils undergoing spontaneous apoptosis in culture as assessed by annexin V binding generated significant amounts of nitrite. Incubation with agonistic anti-Fas monoclonal antibody or tumor necrosis factor-alpha (TNF-alpha) enhanced neutrophil apoptosis at 6 h, although it decreased nitrite accumulation. Although granulocyte-macrophage colony-stimulating factor significantly reduced neutrophil apoptosis, this was also associated with decreased nitrite accumulation. In contrast, inhibition of apoptosis at 16 h by dibutyryl cyclic adenosine monophosphate was associated with increased nitrite accumulation. Exogenous glutathione (GSH) or N-acetylcysteine significantly enhanced neutrophil apoptosis at 6 h and stimulated the production of H(2)O(2), which may mediate apoptosis through intracellular hydroxyl radical production. Intracellular GSH concentrations decreased in neutrophils undergoing apoptosis, and this was more marked in neutrophils treated with anti-Fas or TNF-alpha. These results suggest a causal association between reduced endogenous nitric oxide production, reduced intracellular GSH, and Fas- and TNF-alpha-mediated neutrophil apoptosis, whereas enhanced neutrophil survival mediated by dibutyryl cyclic adenosine monophosphate is associated with increased nitrite generation and maintenance of intracellular GSH. The interaction of endogenous reactive oxygen species with extracellular antioxidants such as GSH could also contribute to the complex processes regulating neutrophil apoptosis and hence the resolution of inflammation in the lung.

Acetylcysteine↗
PubMed2000

Tight junction properties of the immortalized human bronchial epithelial cell lines Calu-3 and 16HBE14o-.

Tight junctions (TJs) make a vital contribution to the barrier properties of the airway lining. Opening of TJs, or their frank cleavage, is suspected as a pathophysiological event in the lung, but research into the cellular and molecular mechanisms involved has been impeded by technical limitations of available experimental models. The authors have compared the properties of two epithelial cell lines derived from bronchial epithelium to explore whether these cell lines could constitute appropriate tools for the study of TJ regulation in bronchial epithelium. Investigations of TJs in 16HBE14o- cells and Calu-3 cells were made by fluorescent antibody labelling in conjunction with wide-field, confocal or 2-photon molecular excitation microscopy (2PMEM). The presence of TJ proteins was confirmed by immunoblotting and functional properties of the monolayers were studied by measurements of transepithelial electrical resistance and mannitol permeability. Cells of both lines formed confluent monolayers in which the cells expressed the TJ proteins occludin and ZO-1 in continuous circumferential patterns suggestive of functional TJs. This interpretation was supported by the development of transepithelial electrical resistances and of low paracellular permeability to solutes. Within the limits of resolution offered by 2PMEM, occludin and ZO-1 appeared to colocalize at TJs. These studies suggest that the 16HBE14o- cells and Calu-3 cell lines are potentially useful in vitro models to study how tight junction opening or cleavage changes the functional barrier properties of bronchial epithelium.

Animals↗
PubMed2000

Leukaemia inhibitory factor (LIF) upregulates excitatory non-adrenergic non-cholinergic and maintains cholinergic neural function in tracheal explants.

The effect of leukaemia inhibitory factor (LIF) in modulating cholinergic and sensory nerve function was examined using guinea-pig tracheal explants. Specific LIF receptors (LIFR) were immunolocalized to both cholinergic and sensory nerves. Release of SP in culture was not influenced by LIF. Similarly, maximum contraction to carbachol (C(max)) was not influenced by LIF. After 3 h, maximum (E(max)) eNANC-induced contraction in controls was 32+/-2. 5% of C(max). In LIF-treated preparations, E(max) was enhanced to 50+/-4.5% C(max) (P<0.05). Cholinergic nerve-induced contractions after 3 h incubation with LIF were similar to control. After 24 h, control E(max) was 25+/-4.5% C(max) (58% smaller than E(max) at 3 h). In contrast, in LIF-treated preparations, E(max) was 37+/-2.5% C(max), (24% smaller than at 3 h, P<0.05). This did not appear to be due to the effect of LIF on muscarinic M(2) receptor expression or function. Thus LIF appears to differentially influence the function of airway nerves and thus may provide an important link between the immune and neural systems.

Animals↗
PubMed2000

Oncostatin M synergises with house dust mite proteases to induce the production of PGE(2) from cultured lung epithelial cells.

The release of PGE(2) and nitric oxide (NO) from the respiratory epithelium may act to dampen inflammation. In other tissues, oncostatin M (OSM), a potent inducer of epithelial antiproteases, has also been shown to interact with IL-1beta to stimulate PGE(2) release. However, whether OSM interacts with pro-inflammatory cytokines and proteases in the production of anti-inflammatory eicosanoids and NO from airway epithelium is unknown. The effect of OSM and the related cytokine leukaemia inhibitory factor (LIF) on PGE(2) and NO production by the respiratory epithelial cell line, A549 in response to pro-inflammatory cytokines as well as protease-rich house dust mite (HDM) fractions and a protease-deficient rye grass pollen extract was examined by immunohistochemistry, cell culture, ELISA and enzyme-immunoassay. Cells treated with a mixture of IL-1beta, IFNgamma and LPS for 48 h produced a 9 fold increase in PGE(2) and a 3 fold increase in NO levels (both P<0.05). Both OSM and LIF were without effect. However, OSM added together with the cytokine mixture synergistically enhanced PGE(2) production (22 fold, P<0.05). OSM also synergistically enhanced PGE(2) production in response to a cysteine protease-enriched, but not serine protease-enriched HDM fraction (P<0.05). Rye grass extract, neither alone nor in combination with OSM, induced PGE(2) or NO production, although it did induce the release of GM-CSF. These observations suggest that OSM is an important co-factor in the release of PGE(2) and NO from respiratory epithelial cells and may play a role in defense against exogenous proteases such as those derived from HDM.

Animals↗
PubMed2000

Quantitative structural and biochemical analyses of tight junction dynamics following exposure of epithelial cells to house dust mite allergen Der p 1.

BACKGROUND: House dust mite allergen Der p 1 is a cysteine peptidase. Previously, we have suggested that the proteolytic activity of this allergen may contribute to asthma by damaging the barrier formed by the airways epithelium. OBJECTIVE: The present study applied novel techniques to compare changes in permeability with quantitative events in tight junctions (TJs) and desmosomes (DMs) of epithelial cells exposed to Der p 1. METHODS: Confluent monolayers of Madin-Darby canine kidney (MDCK) and 16HBE14o-human bronchial epithelial cells were used as experimental models. Permeability was estimated from mannitol clearance. Digital imaging with quantification of TJs and DMs was achieved by fluorescent antibody staining and 2-photon molecular excitation microscopy (2PMEM). Biochemical changes in TJs were studied by immunoblotting, radiolabelling and immunoprecipitation. RESULTS: Der p 1 caused a time-dependent breakage of TJs and reduction in their content of the protein ZO-1. Reduction in ZO-1 immunofluorescence at TJs occurred with a small increase in the amount of diffuse, cytoplasmic immunoreactive ZO-1 staining. Morpho-logical changes in TJs occurred in synchrony with increases in epithelial permeability. DM puncta increased both in size and intensity of staining. Immunoblotting demonstrated that the disruption of TJ morphology was associated with cleavage of ZO-1 and occludin. Cells recovered from allergen exposure by de novo synthesis of occludin. CONCLUSION: Der p 1 could contribute to sensitization and allergic responses by degrading the function of the airway epithelial barrier.

Animals↗
PubMed2000

Alcoholic drinks: important triggers for asthma.

BACKGROUND: Although anecdotally alcoholic drinks seem to be common triggers for asthma, little is known of the prevalence, the characteristics, or the mechanisms underlying these reactions. OBJECTIVES: The primary aim of this study was to determine the frequency and characteristics of asthmatic reactions triggered by alcoholic drinks in a community-based cohort of asthmatic subjects. Investigations of other food sensitivities were also completed to explore some of the possible components of alcoholic drinks that may be responsible for these asthmatic responses. METHODS: A validated food allergy questionnaire was used to assess the characteristics of alcoholic drink-induced asthma in 366 adult patients recruited from the Asthma Foundation of Western Australia. The food allergy questionnaire was sent out by mail and self-administered by recipients. RESULTS: Thirty-three percent of respondents indicated that alcoholic drinks had been associated with the triggering of asthma on at least 2 occasions. Wines were the most frequent triggers, with responses being rapid in onset (<1 hour) and of mild to moderate severity. Logistic regression analysis indicated that wine-induced asthmatic reactions were reported more often by women (P =.032), by those taking oral steroids (P =.021), by individuals who had reported their first asthma attack at a younger age (P <. 001), and by those who had previously visited an alternative health practitioner for asthma (P =.041). A significant association between wine-induced asthma and asthma triggered by sulfite-containing foods (P <.001) and by aspirin and nonsteroidal anti-inflammatory medicines (P =.01) was also observed. CONCLUSION: Alcoholic drinks, and particularly wines, appear to be important triggers for asthmatic responses. Sensitivity to the sulfite additives in wines seems likely to play an important role in many of these reactions. Sensitivities of individuals to salicylates present in wines may also play a role.

Adolescent↗
PubMed2000

Affective aggression in patients with temporal lobe epilepsy: a quantitative MRI study of the amygdala.

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.

Adolescent↗
PubMed2000

Remote memory in epilepsy.

PURPOSE: There is now a considerable amount of research relating to memory functioning in epilepsy. The majority of studies have focused on the retention of new information, and few reports have measured memory for past events. This study aims to redress this and measure the efficiency of remote memory in epilepsy. METHODS: A remote memory questionnaire was prepared and administered to three groups of patients with epilepsy and a control group without epilepsy. The questionnaire assessed knowledge of public events that occurred between 1980 and 1991, inclusive. The epilepsy groups comprised 33 patients with temporal lobe epilepsy (TLE), 33 with extratemporal epilepsy (ExTE), and 10 with primary generalized epilepsy (PGE). Thirty control subjects were tested. RESULTS: Patients with TLE performed significantly less well on the questionnaire than all other groups (p = 0.001), but no effect of laterality was recorded; patients with extratemporal or primary generalised epilepsy did not differ from controls. Performance on the questionnaire was not determined by verbal IQ, educational achievement, social class, or drug treatment, but was related to the number of generalised convulsions that had occurred since 1980. The strongest neuropsychological predictors of performance on this questionnaire were measures of verbal memory. CONCLUSIONS: The study demonstrated weak memory for past events in patients with TLE, thereby providing evidence of a broader memory disturbance in this group than has been previously highlighted. A test of remote memory, such as the one designed for this study, is easy to administer and provides clinically important information not available from conventional neuropsychological tests.

Achievement↗
PubMed2000

Reduction of frontal neocortical grey matter associated with affective aggression in patients with temporal lobe epilepsy: an objective voxel by voxel analysis of automatically segmented MRI.

BACKGROUND: Interictal episodes of aggression are often reported in patients with epilepsy. Some have characteristics of what has been referred to as episodic dyscontrol or intermittent explosive disorder (IED). Although structural brain abnormalities are thought to play a part in the pathophysiology of aggression, there are few in vivo studies of structural cerebral changes in patients with epilepsy and aggression. Using quantitative MRI, subtle structural brain abnormalities can be investigated in subgroups of patients with both epilepsy and episodes of affective aggression. METHODS: After automated segmentation of cerebral grey matter from T1 weighted MRI, the objective technique of statistical parametric mapping (SPM) was applied to the analysis of 35 control subjects, 24 patients with temporal lobe epilepsy (TLE) with a history of repeated, interictal episodes of aggression, and 24 patients with TLE without episodes of aggression. Both TLE patient groups were compared with each other and with the control subjects on a voxel by voxel basis for increases and decreases of grey matter. RESULTS: The patients with TLE with aggressive episodes had a decrease of grey matter, most markedly in the left frontal lobe, compared with the control group and with patients with TLE without aggressive episodes. CONCLUSION: These findings suggest that a reduction of frontal neocortical grey matter might underly the pathophysiology of aggression in TLE. These voxel by voxel comparisons can guide further in vivo studies into aggression.

Adolescent↗