SEARCH · PubMed Health

Results for “Frontal Lobe”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources

PubMed2002

Neuropsychological performance in frontal lobe epilepsy.

The search for a special neuropsychological profile of frontal lobe epilepsy subjects (FLE) has so far led to inconclusive results. In this paper we compared the preoperative neuropsychological performance of FLE and temporal lobe epilepsy (TLE) subjects. We further investigated whether frontal lobe lesions of epileptogenic cause produce the same type of cognitive dysfunction as do tumours of the frontal lobe. Sixteen FLE subjects were compared to 16 TLE subjects as well as to a group of 10 subjects after the removal of frontal lobe tumors (TUM) and a healthy control group. A set of neuropsychological test measures routinely used for presurgical evaluation, an emotional conceptualization task and two associative learning tasks were administered. We found that subjects with frontal lobe damage were significantly impaired relative to controls on a wide range of cognitive functions independent of neurological cause. FLE subjects could hardly be discriminated from TLE subjects as both groups showed a similarly reduced level of neuropsychological performance. Our results demonstrate the devastating effect that frontal lobe epilepsy can have on cognitive functioning. Routinely used neuropsychological test measures lack the specificity to distinguish between frontal and temporal lobe epilepsy. Highly specialized measures are necessary to reveal differences.

Adult↗

PubMed2004

Age differences in veridical and false recall are not inevitable: the role of frontal lobe function.

The relationship of neuropsychological measures of frontal lobe function to age differences in false recall was assessed using the Deese/Roediger-McDermott associative false memory paradigm (Deese, 1959; Roediger & McDermott, 1995). As other studies have found, older adults were less likely to correctly recall studied items and more likely to falsely recall highly related but nonpresented items than were younger adults. When older adults were divided based on a composite measure of frontal lobe functioning, this age difference was found only for low frontal lobe functioning individuals. High frontal lobe functioning older adults and young adults had equivalent levels of false recall, as well as equivalent levels of veridical recall. These results suggest that age differences in memory may be due to declines in frontal lobe function. More important, our findings indicate that declines in veridical recall and increases in false recall are not an inevitable consequence of aging.

Adult↗

PubMed1996

Frontal lobe dementia and motor neuron disease.

Frontal lobe dementia (FLD) (syn. frontotemporal dementia and dementia of frontal type) is a generic term that describes a clinical syndrome in which patients manifest a profound breakdown in personality and social conduct, together with adynamic spontaneous speech, culminating in mutism. This pattern of cognitive impairment implicates bilateral frontal lobe dysfunction, an assumption supported by functional neuroimaging findings of anterior cerebral abnormality. Patients with FLD can go on to develop motor neuron disease (FLD-MND), although the clinical features of MND may accompany or occasionally precede the onset of dementia. The emergence of MND is responsible for death within 3 years of onset. Frontotemporal lobar pathology in FLD-MND is characterized by loss of large cortical neurons, spongiform change and mild astrocytic gliosis. Ubiquitinated (but not tau-positive) inclusions are present within the frontal cortex. There is severe nigral cell loss (without Lewy bodies), and marked hypoglossal and spinal motor neuron degeneration, together with ubiquitinated (but not tau-positive) inclusions within the spinal neurons. Some authors suggest that FLD-MND is a separate disease entity, whereas others suggest it represents an interface between FLD and "classic" (non-dementing) motor neuron disease (CMND). An association with CMND is supported by findings in these patients of failure in tasks sensitive to "frontal lobe" dysfunction, and patterns of functional neuroimaging abnormality which are identical in distribution, but less severe than those encountered in FLD-MND. However, the nosological status of FLD-MND remains enigmatic in the absence of defined pathological and molecular markers.

Dementia↗

PubMedDate not supplied

Confused and disturbed behavior in the elderly following silent frontal lobe infarction.

It is unclear whether silent frontal lobe infarction is truly asymptomatic; frontal behavioral syndromes following strokes have rarely been reported. We studied 12 elderly patients with silent frontal lobe infarction who were exhibiting confused and disturbed behavior. Ten were male and two female; their ages ranged from 68 to 79 (mean 78). Three groups of symptom clusters emerged: changes in mood and emotional behavior, cognitive deterioration with minor psychiatric symptoms, and a confusional state. When related to the CT scan location, three regions were identified: predominantly orbitofrontal, deep white matter and caudate, and border-zones, respectively. These findings were related to what is known about the neuroanatomic location of the lesions and the role of the frontal subcortical circuitry in relation to behavior. The different manifestations could be explained by damage to the frontal lobe or interruption of the complex frontal subcortical circuits.

Aged↗

PubMedDate not supplied

Assessment of neuropsychological dysfunction in frontal lobe degeneration.

The quality of the neuropsychological investigation of behavioural changes in frontal dementias is dependent on the specificity of the behavioural analyses. A review of methodological issues and published findings identifies possible potential reasons for misinterpretation of research neuropsychological data in these studies. The areas reviewed include the operational definitions of terms such as 'frontal lobes' and 'frontal functions'; identification of experimental limitations in frontal lobe research; and highlights of neuropsychological investigations of frontal lobe functions. These deliberations suggest a practical approach to the behavioural assessment of frontal dementias.

Dementia↗

PubMed1989

Frontal lobe connections of the superior temporal sulcus in the rhesus monkey.

The frontal lobe connections of different architectonic areas of the superior temporal sulcus (STS) in the rhesus monkey were investigated with the aid of both anterograde and retrograde tracing techniques. The proisocortical area in the rostralmost STS connects with proisocortical regions on the ventral and medial surfaces of the frontal lobe. The frontal lobe projections of polymodal cortex (area TPO) in the upper bank of the STS are organized according to the rostral-to-caudal topography of the sulcus. Rostral TPO interconnects with ventral (areas 13, 12, 11, and 14), medial (areas 24, 32, 14, and 9), and lateral (areas 10, 12, and 46) sectors of the frontal lobe. The mid-portion of polymodal cortex projects to, and receives fibers from, rostral subdivisions of lateral prefrontal cortex, viz. dorsal area 46, areas 9 and 10, whereas the caudal segment of TPO has reciprocal connections with caudal subdivisions (areas 46, 8, and 6) of the lateral frontal lobe. Visual-related zones (areas TEa and TEm) in the rostral lower bank of the STS have connectional relationships with orbitofrontal areas 11 and 12 and lateral frontal areas 46 and 8. A presumed somatic sensory-related area in the rostral depth of the STS (area IPa) projects to orbital (areas 11 and 14) and lateral (areas 46, 10, and 12) sectors of the frontal lobe.

Amino Acids↗

PubMed2004

[MRI findings in schizophrenic patient with frontal lobe atrophy].

In schizophrenic patients, cognitive and behavioral deficits are often associated with frontal lobe dysfunction. By functional neuroimaging studies, abnormalities of the frontal lobe (especially the prefrontal lobe) have been detected in schizophrenic patients. As for morphological changes on neuroimaging, lateral lobe atrophy and enlargement of the lateral ventricles or third ventricle are often reported, but there is no consensus as to whether frontal lobe atrophy is seen more frequently in schizophrenic patients compared with normal controls. The reasons for this disagreement include variations in the precision of measurement on MRI, differences in the methods of MRI among studies, and biases in the subjects being evaluated. Here we present a patient with schizophrenia and frontal lobe atrophy, which was clearly recognized on MRI and showed no progress in the 2 years following its detection. The patient was a 26-year-old woman with a 4.5-year history of schizophrenia when she was referred to us for the treatment of persistent auditory hallucinations and delusions. She showed no neurological findings apart from her psychiatric symptoms. Head MRI showed mild atrophy of the frontal lobe, and the extent of atrophy did not change over the following two years. On resting SPECT 99mTc-HMPAO, hypoperfusion of the bilateral frontal regions was demonstrated. There were no significant findings in the temporal lobe on either MRI or SPECT. She achieved low scores in neuropsychological tests of intelligence, memory, and frontal lobe-associated functions, and showed almost the same degrees of impairment in all of the tests in 2 years of follow-up. The possibility of degenerative diseases, such as young-onset frontotemporal dementia, was ruled out. She had a low intelligence quotient in the WAIS-R and her answers showed the specific pattern which is commonly seen in schizophrenic patients. There is a possibility that hypoperfusion on resting SPECT reflected not only frontal lobe atrophy, but also frontal lobe dysfunction in this patient. Frontal lobe dysfunction in schizophrenics is generally considered to be a secondary effect of meso-limbic system pathology. In this patient, however, the dysfunction seemed to arise from an intrinsic disorder of the frontal lobe, because frontal lobe abnormalities were conspicuous, whereas the temporal lobe was almost normal on both MRI and SPECT.

Adult↗

PubMed2000

The Frontal Lobe Score: part II: evaluation of its clinical validity.

OBJECTIVE: To evaluate the ability of the Frontal Lobe Score (FLS) to differentiate patients with frontal lobe lesions from those with nonfrontal lesions and normal controls. DESIGN: In a prospective, blind setup, the sensitivity and specificity of the Frontal Lobe Score was compared with the Wisconsin Card Sorting Test (WCST) and the Stroop Test. PATIENTS: A sample of 108 subjects (26 patients with cerebral lesions confined to the frontal lobes, 28 patients with cerebral lesions without involvement of the frontal lobes, 31 patients with mixed frontal/nonfrontal lesions, 23 controls without cerebral lesions) was examined. MEASURES: Frontal Lobe Score, Wisconsin Card Sorting Test, Stroop Test. RESULTS: The Frontal Lobe Score detected pure frontal lesions with a sensitivity of 92.3%. It discriminated patients with frontal lesions from normal controls with a specificity of 100%; differentiation from patients with nonfrontal lesions was obtained with a specificity of 75.0%. For the WCST, sensitivity for detection of pure frontal lesions was 65.4%, while specificity was 60.9% compared with normal controls and 53.6% compared with nonfrontal lesions. The Stroop Test showed a sensitivity of 30.8%, a specificity compared with normal controls of 95.7% and compared with nonfrontal lesions of 92.9%. CONCLUSION: The Frontal Lobe Score has clinical usefulness for screening of effects of frontal lobe damage superior to that of the WCST and the Stroop Test.

Adult↗

PubMed1998

Frontal lobe volume in patients with Huntington's disease.

Neuropathologic and neuroimaging studies have suggested that frontal lobes are affected in Huntington's disease (HD), and that atrophy in this region may be associated with some of the cognitive impairment and clinical decline observed in patients with HD. We measured gray and white matter volumes within the frontal lobes on MRI for 20 patients with HD (10 mildly affected and 10 moderately affected) and 20 age- and sex-matched control subjects. We also correlated frontal lobe measurements with measures of symptom severity and cognitive function. Patients who were mildly affected had frontal lobe volumes (both gray and white matter) essentially identical to those of control subjects, despite clearly abnormal basal ganglia. Patients who were moderately affected demonstrated significant reductions in total frontal lobe volume (17%) and frontal white matter volume (28%). Frontal lobe white matter volume reductions, but not total frontal lobe volume reductions, were disproportionately greater than overall brain volume reductions (17%). Frontal lobe volume correlated with symptom severity and general cognitive function, but these correlations did not remain significant after taking into account total brain volume. We conclude that cognitive impairment and symptom severity are associated with frontal lobe atrophy, but this association is not specific to the frontal lobes. Frontal lobe atrophy (like total brain atrophy) occurs in later stages of increasing HD symptom severity and this atrophy primarily involves white matter.

Adult↗

PubMed1997

Clinical characteristics of complex partial seizures: a temporal versus a frontal lobe onset.

The site of origin of complex partial seizures (CPS) is predominantly in the temporal lobe, but frontal, parietal, and occipital lobes may also be involved. In order to correlate clinical behaviours with either a temporal or frontal site of origin, we analysed 211 seizures occurring during invasive monitoring in 26 patients with temporal lobe epilepsy (TLE) and in eight patients with frontal lobe epilepsy (FLE). Although leg movements, defined as thrashing, pedalling and kicking, hand posturing, facial twitching, sitting up, and tonic-clonic movements occurred more frequently in FLE, and hand automatisms were more frequent in TLE, no statistically significant difference was found between the two groups. When analysing only electrographic seizures that did not spread or propagated only to homologous controlateral lobes, leg movements and hand posturing were seen only with FLE, and oral automatisms only in TLE. Seizures of temporal lobe origin were longer in duration and had a higher frequency of auras. We therefore conclude that the reliability of clinical behaviour alone to predict the site of origin of an epileptic discharge is limited when the surface EEG is equivocal or the neuroradiologic evidence of a focus is not clear.

Adolescent↗

PubMed1998

Frontal lobe hypometabolism and depression in Alzheimer's disease.

Depression is common in Alzheimer's disease (AD). Clinicoanatomic studies in focal brain injuries and functional imaging studies both in primary depression and in depression secondary to neurologic diseases have demonstrated involvement of the frontal lobe. Frontal involvement has not been established in the depression of AD. We studied the correlation between focal brain metabolic abnormalities and depression in AD. In 53 patients with probable AD of minimal to moderate disability, we assessed the severity of depression using the Neuropsychiatric Inventory and correlated the depression score with regional cerebral glucose metabolism determined by 18F-fluorodeoxyglucose and PET. Depression was present in 19 patients (36%). The depression score correlated significantly with normalized glucose metabolic rates in the bilateral superior frontal and left anterior cingulate cortices. These results indicated an association between depression and decreased activity in the frontal lobe in AD and support frontal involvement, especially in the left side, in depression, irrespective of disease etiology.

Aged↗

PubMed2004

Cognitive and emotional components of frontal lobe functioning in childhood and adolescence.

Frontal lobe functions include a range of cognitive, emotional, and social abilities that enable goal-directed behavior. Although a number of studies have plotted the development of frontal lobe functions in childhood, few have extended into the adolescent years. There is also little information on which cognitive and emotional components of frontal functioning may be correlated. The aims of this study were to identify and compare age effects on different components of frontal functioning in childhood and adolescence and to examine whether abstract reasoning skills were associated with levels of emotional intelligence and social sensitivity. Twenty children (ages 9-18) were recruited from the local community for a study of normal adolescent brain development. All subjects were free of psychiatric or developmental disorders, as determined by a structured interview. Subjects completed a comprehensive neuropsychological test battery, as well as self-report measures of social sensitivity (anxiety) and emotional intelligence. Significant age effects were found for measures of abstract reasoning, response inhibition, and attentional set shifting. Levels of social anxiety increased moderately with age, although not significantly at this sample size. Abstract reasoning skills correlated positively with levels of social anxiety but not emotional intelligence. The pattern of results suggests differential developmental trajectories across various cognitive and emotional domains of frontal lobe functioning in childhood and adolescence. Increased abstract reasoning ability may be associated with increased vulnerability to social anxiety during this period.

Adolescent↗

PubMed1998

Neuropsychological consequences of epilepsy surgery in frontal lobe epilepsy.

The present study investigated the effect of frontal lobe surgery on "cognitive functions", which have previously been shown to be discriminative in the evaluation of non-resected patients with frontal lobe epilepsy (FLE). The cognitive outcome was evaluated with particular consideration of the side (left/right), the site (lateral, orbital, mesial, premotor/SMA), the type of surgery (resections vs. resections plus multiple subpial transections; MST), and seizure outcome. The evaluation is based on 33 patients with left (n = 17) or right (n = 16) frontal surgery. Forty-five patients who underwent successful left (n = 21) or right (n = 24) temporal lobectomy served as controls. The neuropsychological examination covered speed/attention, motor sequencing/coordination, response maintenance/inhibition, short-term memory, and language. With the exception of short-term memory, the chosen tests were discriminative in determining preoperative frontal lobe dysfunctions but they did not differentiate patients with a different lateralization or localization of the frontal focus. At the 3 month follow-up examination, patients with temporal lobectomy had improved frontal functions, whereas patients with frontal lobe surgery showed a mild deterioration. Within the frontally resected group, completely seizure-free patients had significantly improved short-term memory. Further consideration of the side, site and the type of the frontal resection indicated that patients with premotor/SMA surgery and patients with precentral/central MST had additional impairment after surgery. Premotor/SMA resections led to a deterioration in response maintenance/inhibition and if performed left sided also to deteriorated language functions. The latter impairment could be clearly related to transient aphasia directly after surgery. Irrespective of pareses observed immediately after surgery, patients with MSTs of the precentral/central areas displayed additional problems in motor coordination at the follow-up examination. In this group the seizure outcome was also less favourable. In summing up, frontal lobe surgery does not cause any considerable additional impairment in the short-term follow-up. However, caution is recommended when surgery or MST affect functional relevant cortex (here the prefrontal/SMA and precentral/central area). Finally, a release of functions associated with frontal areas not affected by surgery is suggested, when seizures are successfully controlled by surgery.

Adult↗

PubMed1994

Unilateral spatial neglect due to right frontal lobe haematoma.

Two patients with unilateral spatial neglect caused by right frontal lobe lesions underwent cerebral blood flow studies. A 54-year-old, right-handed woman developed left hemiplegia and frontal lobe neglect associated with cerebral haemorrhage after surgical excision of a frontal tumour. A 66-year-old, right-handed woman developed a haemorrhage in the right frontal lobe caused by rupture of an aneurysm. This was followed by left hemiplegia and frontal lobe neglect. In both cases, 123I-iodoamphetamine single photon emission CT disclosed a reduction in regional cerebral blood flow localised along the circumference of the haematoma in the frontal lobe, but did not reveal any lesions in the parieto-occipital junction. These findings suggest that, in these two cases, the frontal lobe neglect was caused by lesions confined to the frontal lobe.

Cerebral Hemorrhage↗

PubMed2000

Absence seizures and the frontal lobe.

There is no doubt that the frontal lobe plays a major role in the 3/sec spike-wave absence seizure. It is pointed out initially that the controversies of cortical vs. thalamic origin of the spike-waves and the associated absence can be laid at rest as far as human absence seizures and human primary generalized epilepsy (PGE) are concerned: their origin is cortical with maximal frontal lobe involvement. Experimentally-induced spike-wave bursts or spontaneous spike-waves in animals pertain to other forms of epileptic seizure disorder. The frontal maximum of the 3/sec spike-wave pattern indeed indicates maximal frontal lobe involvement including both prefrontal and frontomotor portions. The absence as such is presumed to be a suspension of the working memory--an eminently frontal lobe function. This explains the immediate restoration of ictally-impaired neurocognitive functions right at the termination of the seizures. This concept can be applied not only to the classical absence occurring in PGE but also to the rare cases of secondary bilateral synchrony with a primary frontal epileptogenic focus leading to true (though very slightly different) absences.

Animals↗

PubMed1998

Individual differences in P3 scalp distribution in older adults, and their relationship to frontal lobe function.

There is evidence that frontal lobe function may diminish in normal aging. The P3 component of the event-related brain potential (ERP) elicited by target events in an oddball paradigm becomes more frontally oriented in elderly subjects. It was hypothesized that the extent to which the P3 distribution is frontally oriented in old subjects may index less efficient frontal lobe function. In this study, bootstrapping methods were used to establish the reliability of the locations of maxima of surface brain activity obtained with ERP recordings from young and old subjects. The results indicated that brain activity maxima are reliable for a given individual. However, among the elderly only, there were also clear individual differences in the distribution of the P3 component elicited by target stimuli in an oddball paradigm. On the basis of these differences, the old subjects were divided into two groups. In line with predictions, those elderly subjects who showed frontal-maximal P3 scalp distributions had lower performance on standardized neuropsychological tests of frontal lobe function than those elderly subjects who showed posterior-maximal scalp topographies.

Adult↗

PubMed1999

Associative learning impairments in patients with frontal lobe damage.

The performance of 18 frontal lobe lesion (FL) and 10 frontal lobe dementia (FLD) patients on an associative memory test was compared with the performance of their matched normal controls. The FL group was severely impaired on cued and free recall and was moderately impaired on a recognition condition. Left FL patients performed the poorest on the cued and free recall conditions. The FLD patients were moderately impaired on the free recall condition only but there was a subgroup of FLD patients with additional left temporal atrophy who appeared severely impaired on both cued and free recall. These findings indicate that both left frontal and temporal lobe damage can impair associative learning and that this impairment is more strikingly seen with free rather than cued recall.

Adult↗

PubMed1996

Autosomal dominant nocturnal frontal lobe epilepsy: electroclinical picture.

PURPOSE: Nocturnal frontal lobe epilepsy is a disorder that is difficult to diagnose because its clinical presentation is often limited to motor behavior during sleep. For this reason, a misleading diagnosis of benign nocturnal parasomnias might be possible. Recently, an inherited form of nocturnal frontal lobe epilepsy was described in some families. The aim of our work was to describe the electroclinical pattern of a sample of familial cases with this syndrome. METHODS: We observed 33 patients, all complaining of frequent nocturnal motor attacks, from eight Italian families. The family trees were strongly supportive of autosomal dominant inheritance. We performed a full-night video-polysomnographic monitoring in 12 patients. RESULTS: The recordings showed attacks in all patients, there being a widespread pattern of motor activity. Ictal and interictal EEG abnormalities were often hidden and, unless associated with a video recording, were of no use for the final diagnosis. Intraindividual stereotypy, abrupt onset, and semiology of attacks allowed differentiation from healthy subjects' nocturnal motor behavior. CONCLUSIONS: Autosomal dominant nocturnal frontal lobe epilepsy is probably not uncommon. Full-night video-polysomnographic monitoring is fundamental for the differential diagnosis of benign parasomnias and, consequently, for appropriate therapy.

Adolescent↗