Frontal lobe seizures in autism

The set of features that constitute 'autism' has been traced to numerous etiologies. Certain autistic features have been localized to dysfunction in certain neural areas, most notably frontal and temporal regions. The author hypothesizes that many of the symptoms characteristic of autism fit the clinical picture of frontal lobe seizures. Facial, vocal, and other body movements in autism are catalogued in parallel with facial, vocal and body movements that occur during frontal lobe seizures. The variety of etiologies that cause frontal lobe seizures also accounts for the variety of etiologies traced to autism.     

Frontal lobe damage and neuropsychological assessment.

Four cases with neuroradiologically verified frontal lobe damage are reviewed in terms of neuropsychological test performance and behavioral outcome. Frontal damage may result in a wide-spectrum of behavioral and cognitive changes that do not conform to a specific syndrome entity. Many of the traditional neuropsychological measures are insensitive to frontal lobe involvement. Various clinical guidelines are offered.     

Frontal lobe activation during object alternation acquisition

Object alternation (OA) tasks are increasingly used as probes of ventral prefrontal functioning in humans. In the most common variant of the OA task, subjects must deduce the task rule through trial-and-error learning. To examine the neural correlates of OA acquisition, the authors measured regional cerebral blood flow with positron emission tomography while subjects acquired an OA task, performed a sensorimotor control condition, or performed already learned and practiced OA. As expected, activations emerged in the ventral prefrontal cortex. However, activation of the presupplemental motor area was more closely associated with successful task performance. The authors suggest that areas beyond the ventral prefrontal cortex are critically involved in OA acquisition.     

Frontal lobe structure and executive function in migraine patients

Neuroimaging studies have identified frontal lobe brain abnormalities in migraineurs. Neuropsychological investigations highlighted frontal lobe related cognitive impairments in migraineurs, including working memory and executive function deficits. The relationship between brain anatomy and cognitive function in migraine, however, is unclear. The aim of this study was to simultaneously investigated cortex structure and executive function (EF) in patients with migraine and control subjects. Thus, we assessed grey matter (GM) density in 25 adult patients with migraine, compared to age and sex-matched control subjects, using magnetic resonance imaging (MRI) and voxel-based-morphometry (VBM), and we measured EF in the same population, employing three EF tasks of the Maudsley attention and response suppression (MARS) battery. Migraineurs, compared to control subjects, showed decreased frontal and parietal lobe GM density and slower response time to task set-shifting and, the delayed response time correlated significantly with reduced GM density of the frontal lobes in migraineurs. Frontal and parietal lobe abnormalities in migraineurs could be an underlying cause of significantly slower response time during cognitive set-shifting.     

Frontal lobe function and executive skills in children with turner's syndrome

Children with Turner's syndrome (TS), a sex chromosome abnormality in which the second X chromosome is abnormal or deleted, were given a series of tasks that investigated executive skills traditionally considered to be subserved by the frontal lobes. The children with TS showed significant deficits in comparison to controls but the effects were task specific. They were impaired on the Stroop, Verbal Fluency and the abstract version of the Self‐Ordered Pointing task. However, performance was entirely normal on the Wisconsin Card Sorting Test, the Tower of London and the concrete version of the Self‐Ordered Pointing task. These results support the fraction‐ability of executive control processes in development, thereby contradicting Fodor's (1983) conception of the absence of modularity in such systems. The phenotype‐genotype relation for 45,XO TS differed significantly from that of other karyotypes on the Self‐Ordered Pointing task, confirming the distinctive nature of aspects of the cognitive development of children with TS associated with differing etiological genotypes.     

Frontal lobe damage in children and adults: A comparative review

Clinical and experimental studies of focal frontal lobe damage in children and adults are reviewed and analyzed. Although each literature has traditionally been treated separately, we argue that they share many common issues and that comparative analysis reveals both contrasting and complementary, findings that provide the foundation for a life‐span view of frontal lobe maturation and operation. Furthermore, each literature offers unique data regarding frontal lobe damage and recovery. Integration of these diverse findings is important to clinical and theoretical advances, and leads to the common view that the frontal lobes and their connections are critical to the development and maintenance of human adjustment and adaptive behavior throughout life.     

Frontal cognitive impairments and saccadic deficits in low-dose MPTP-treated monkeys

There is considerable overlap between the cognitive deficits observed in humans with frontal lobe damage and those described in patients with Parkinson's disease. Similar frontal impairments have been found in the 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP) primate model of Parkinsonism. Here we provide quantitative documentation of the cognitive, oculomotor, and skeletomotor dysfunctions of monkeys trained on a frontal task and treated with low-doses (LD) of MPTP. Two rhesus monkeys were trained to perform a spatial delayed-response task with frequent alternations between two behavioral modes (GO and NO-GO). After control recordings, the monkeys were treated with one placebo and successive LD MPTP courses. Monkey C developed motor Parkinsonian signs after a fourth course of medium-dose (MD) MPTP and later was treated with combined dopaminergic therapy (CDoT). There were no gross motor changes after the LD MPTP courses, and the average movement time (MT) did not increase. However, reaction time (RT) increased significantly. Both RT and MT were further increased in the symptomatic state, under CDoT. Self-initiated saccades became hypometric after LD MPTP treatments and their frequency decreased. Visually triggered saccades were affected to a lesser extent by the LD MPTP treatments. All saccadic parameters declined further in the symptomatic state and improved partially during CDoT. The number of GO mode (no-response, location, and early release) errors increased after MPTP treatment. The monkeys made more perseverative errors while switching from the GO to the NO-GO mode. Saccadic eye movement patterns suggest that frontal deficits were involved in most observed errors. CDoT had a differential effect on the behavioral errors. It decreased omission errors but did not improve location errors or perseverative errors. Tyrosine hydroxylase immunohistochemistry showed moderate ( approximately 70-80%) reduction in the number of dopaminergic neurons in the substantia nigra pars compacta after MPTP treatment. These results show that cognitive and motor disorders can be dissociated in the LD MPTP model and that cognitive and oculomotor impairments develop before the onset of skeletal motor symptoms. The behavioral and saccadic deficits probably result from the marked reduction of dopaminergic neurons in the midbrain. We suggest that these behavioral changes result from modified neuronal activity in the frontal cortex.     

Frontal and non-frontal lobe neuropsychological test performance and clinical symptomatology in schizophrenia.

Schizophrenic subjects performed significantly worse on neuropsychological tests of frontal lobe function but not on tests of non-frontal lobe function when compared to a matched group of normal subjects. Correlations expected between frontal lobe neuropsychological test performance and negative symptoms were not found.     

Frontal lobe functioning in conduct disordered juveniles: preliminary findings.

This investigation assessed the hypothesis that conduct disordered juveniles may suffer from a maturational lag in the development of behaviors believed associated with the frontal cortex. Twenty conduct disorder (CD) juveniles and 20 normal comparison subjects were compared on nine Lurian tasks that measure behavior attributed to frontal lobe functioning. A three-way ANOVA, with gender, race, and group as factors of interest, revealed significant differences on the verbal conflict task, verbal retroactive inhibition task, and on a measure of receptive vocabulary. Using receptive vocabulary as a covariate, an ANCOVA showed no significant differences between the groups on any of the tasks. These findings appear to support the potential impact that language dysfunction can have in the development of disinhibitory behavior. Other interpretations of the findings are presented.     

Frontal lobe neuronal injury correlates to altered function in FIV-infected cats.

Six cats infected intravenously at 8 weeks of age with feline immunodeficiency virus Maryland isolate (FIV-MD), were evaluated at 8 and 14 months of age (6 months and 12 months postinfection, respectively) with high spatial resolution proton magnetic resonance spectroscopy (MRS) of the frontal cortex. Two separate control cat groups were evaluated at 8 months and 16 months of age. Single voxel two-dimensional high-resolution proton magnetic resonance imaging was performed using the PRESS sequence by selecting a 0.125 ml volume of interest in the medial frontal cortex. A significant reduction in both N-acetylaspartate (NAA) and NAA: choline ratio was found in the FIV 14-month-old group compared with FIV 8-month-old cats, and to the respective age-matched control 16-month-old cats. A negative correlation between NAA and CD4 lymphocyte count was seen in the FIV-14 group only. This group of FIV cats also exhibited a higher proportion of quantitative electroencephalographic relative slow wave activity (RSWA) that correlated to lower NAA content in the frontal cortical voxel. Although peripheral blood proviral load increased over time of infection, no correlation was found between proviral blood or lymph node load and NAA values, CD4 lymphocyte counts, or frontal cortical RSWA. Thus, this study demonstrated that neurologic functional disruption of the frontal cortex correlated strongly with neuronal injury and/or loss in FIV-MD-infected cats independent of peripheral proviral load. The ability to define in vivo neurodegeneration further in this animal model helps in understanding the neuropathogenesis of lentivirus infection, and possibly, a means to follow progression and reversibility during the initial stages of brain infection as therapeutic agents are identified.     

Frontal lobe functioning in geriatric and non-geriatric samples: an argument for multimodal analyses.

The present investigation examines specific aspects of frontal functioning across geriatric and nongeriatric cohorts. Subjects included 193 nongeriatric male pilots (mean age: 48.29 (SD = 6.79); mean education: 15.93 years (SD = 1.86)), and 68 geriatric males and females (mean age: 78.38 (SD = 5.07); mean education: 13.68 (SD = 2.53)). The results of a series of general linear model multivariate one-way analyses revealed poorer performance on frontal measures in the geriatric sample, although no differences were noted between the male and female samples. In contrast, variable interrelations, as assessed by a parametric statistic of betweengroup factor similarity, indicated a noteworthy similarity of factors between the geriatric and nongeriatric groups, and dissimilarities between the factor structures for males and geriatric females. These findings not only support the presence of age-related differences in frontal performance for the domains tested, they suggest the need to examine frontal functioning by multiple methods, as differences in frontal functioning may exist between groups that are undetected by analyses based on intergroup score differences or predictor-criterion correlations alone     

Frontal lobe lesions in man cause difficulties in suppressing reflexive glances and in generating goal-directed saccades

Summary The frontal eye field (FEF) and superior colliculus (SC) are thought to form two parallel systems for generating saccadic eye movements. The SC is thought classically to mediate reflex-like orienting movements. Thus it can be hypothesized that the FEF exerts a higher level control on a visual grasp reflex. To test this hypothesis we have studied the saccades of patients who have had discrete unilateral removals of frontal lobe tissue for the relief of intractable epilepsy. The responses of these patients were compared to those of normal subjects and patients with unilateral temporal lobe removals. Two tasks were used. In the first task the subject was instructed to look in the direction of a visual cue that appeared unexpectedly 12° to the left or right of a central fixation point (FP), in order to identify a patterned target that appeared 200 ms or more later. In the second anti-saccade task the subject was required to look not at the location of the cue but in the opposite direction, an equal distance from FP where after 200 ms or more the patterned target appeared. Three major observations have emerged from the present study. (a) Most frontal patients, with lesions involving both the dorsolateral and mesial cortex had long term difficulties in suppressing disallowed glances to visual stimuli that suddenly appeared in peripheral vision. (b) In such patients, saccades that were eventually directed away from the cue and towards the target were nearly always triggered by the appearance of the target itself irrespective of whether or not the anti-saccade was preceded by a disallowed glance. Those eye movements away from the cue were only rarely generated spontaneously across the blank screen during the cue-target time interval. (c) The latency of these visually-triggered saccades was very short (80–140 ms) compared to that of the correct saccades (170–200 ms) to the cue when the cue and target were on the same side, thereby suggesting that the structures removed in these patients normally trigger saccades after considerable computations have already been performed. The results support the view that the frontal lobes, particularly the dorsolateral region which contains the FEF and possibly the supplementary motor area contribute to the generation of complex saccadic eye-movement behaviour. More specifically, they appear to aid in suppressing unwanted reflex-like oculomotor activity and in triggering the appropriate volitional movements when the goal for the movement is known but not yet visible.     

Neural plasticity and cognitive development

It has been well documented that the effects of early occurring brain injury are often attenuated relative to later occurring injury. The traditional neuropsychological account of these observations is that, although the developing neural system normally proceeds along a well-specified maturational course, it has a transient capacity for plastic reorganization that can be recruited in the wake of injury. This characterization of early neural plasticity is limited and fails to capture the much more pervasive role of plasticity in development. This article examines the role of neural plasticity in development and learning. Data from both animal and human studies show that plasticity plays a central role in the normal development of neural systems allowing for adaptation and response to both exogenous and endogenous input. The capacity for reorganization and change is a critical feature of neural development, particularly in the postnatal period. Subtractive processes play a major role in the shaping and sculpting of neural organization. However, plasticity is neither transient nor unique to developing organisms. With development, neural systems stabilize and optimal patterns of functioning are achieved. Stabilization reduces, but does not eliminate, the capacity of the system to adapt. As the system stabilizes, plasticity becomes a less prominent feature of neural functioning, but it is not absent from the adult system. The implications of this broader view of plasticity for our understanding of development following early brain damage are discussed.