From frontal lobe seizures to frontal lobe epilepsies.
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Patients with frontal lobe lesions and control subjects were administered tests of word-stem completion priming. In this implicit memory test, subjects are first presented words (e.g. MOTEL, PARADE) in an incidental learning paradigm. Following word presentation, subjects are shown word stems (e.g. MOT, PAR) and asked to produce the first word that comes to mind. Patients with frontal lobe lesions exhibited normal levels of word-stem completion. These findings indicate that implicit memory can operate normally despite damage to the prefrontal cortex. The present results substantiate previous neuropsychological and positron emission tomography findings which indicate that word priming depends critically on posterior cortical areas.
In patients with frontal lobe tumours the averaged visual evoked responses (AVER) and their dispersion pattern (DP) in visual areas were investigated before and at different periods after operation. Important changes in AVER (in amplitude and latency) were found in the patients with tumours on the midline or in one of the frontal lobes. The DP was abnormal in all the cases. There was no relation to visual acuity, tumour location and existance of intracranial hypertension. After operation, despite the clinical improvement, the alterations of AVERs or DPs were very marked and in some cases became even more important than before. The role of the frontal lobe in the organization of the responses to peripheral stimuli in the visual areas is discussed.
Ictal localization of seizure discharges in the frontal lobe is difficult and not easily resolved by simple translation of techniques that have proved useful for localization within the temporal lobe. There is need for improved interictal localization of functional abnormalities within the frontal lobe utilizing CET and other methods of functional localization including magnetoencephalography, cerebral blood flow, and cerebral metabolism. It is likely that improved localization within the frontal lobe and clarification of clinical syndromes of frontal epilepsy will be obtained through the use of a combination of these interictal methods, aided by the results of intracranial ictal recording and surgical extirpation (7a,b,10a,b,15a-c).
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The corticocortical connections between area 7 and the frontal lobe have been studied in the monkey. Injections of HRP were made into area 7 of the parietal lobe or into area 46 in the walls of the principal sulcus. The two subdivisions of area 7, 7a or PG and 7b or PF, are connected with different parts of the frontal lobe, and each subdivision is connected with two distinct areas. Area 7b, PF, is connected in a well organized and somatotopic manner with the lower premotor area and with the lower part of area 46, below the fundus of the principal sulcus. Area 7a, PG, is connected with area 8a and with the upper part of area 46, above the fundus of the principal sulcus; it is suggested that the lower part of area 8a and the posterior part of area 46 are related to the central visual field, while the medial part of area 8a and the anterior part of area 46 are related to the periphery of the visual field. The corticocortical connections between area 7 and the frontal lobe are reciprocal and those passing from area 7 to the frontal lobe are 'feed-forward' and those to area 7 are 'feed-back'.
We determined the origin of corticospinal neurons in the frontal lobe. These neurons were labeled by retrograde transport of tracers after injections into either the dorsolateral funiculus at the second cervical segment or the gray matter of the spinal cord throughout the cervical enlargement. Using retrograde transport of tracer from the arm area of the primary motor cortex, we defined the arm representation in each premotor area in another set of animals. We found that corticospinal projections to cervical segments of the spinal cord originate from the primary motor cortex and from the 6 premotor areas in the frontal lobe. These are the same premotor areas that project directly to the arm area of the primary motor cortex. The premotor areas are located in parts of cytoarchitectonic area 6 on the lateral surface and medial wall of the hemisphere, as well as in subfields of areas 23 and 24 in the cingulate sulcus. The total number of corticospinal neurons in the arm representations of the premotor areas equals or exceeds the total number in the arm representation of the primary motor cortex. The premotor areas collectively comprise more than 60% of the cortical area in the frontal lobe that projects to the spinal cord. Like the primary motor cortex, each of the premotor areas contains local regions that have a high density of corticospinal neurons. These observations indicate that a substantial component of the corticospinal system originates from the premotor areas in the frontal lobe. Each of the premotor areas has direct access to the spinal cord, and as a consequence, each has the potential to influence the generation and control of movement independently of the primary motor cortex. These findings raise serious questions about the utility of viewing the primary motor cortex as the "upper motoneuron" or "final common pathway" for the central control of movement.
The usefulness of frontal lobe (FL) dysfunction as a conceptual model for Attention Deficit Hyperactivity Disorder (ADHD) was investigated. Twenty-four ADHD and 24 normal control (NC) children were tested using two batteries of tasks. The first was sensitive to FL deficits in motor control and problem solving skills. The second consisted of memory tasks sensitive to temporal lobe dysfunction. ADHD children differed significantly from NCs on measures of FL function, but not on tests of temporal lobe functions. Where norms were available for normal children on the same FL tests, ADHDs performed like 6- to 7-year-olds, despite their mean age of 10 years and minimum age of 8 years. The differential performance of ADHDs on tasks sensitive to FL and temporal lobe dysfunction supports the hypothesis that ADHD deficits are analogous to FL dysfunction and demonstrates that the children's deficits do not reflect generalized cognitive impairment.
Exploratory eye movements in 20 schizophrenics, 18 patients with frontal lobe lesions (9 right-sided and 9 left-sided) and 20 normal controls were examined with an eye mark recorder while they viewed stationary S-shaped figures. The eye movements made during the subject's first 15-s viewing of an original figure were analyzed. Patients with right frontal lobe lesions (RF) and schizophrenics (S) had lower scores than normal controls (NC) for the number of eye fixations, total eye scanning length and mean eye scanning length. Each subject was then shown two other figures slightly different from the original and was requested to compare them with the original. After comparing them, the subject was asked the question, "Are there any other differences?" The eye movements made over the ensuing 5 s in response to this question were scored using the responsive search score (RSS). The RSS was low only in the S group. The subject was also asked to reproduce the original figure before and after making comparisons between the figures. The RF and S groups were poorer at reproduction than the NC group. These findings suggest that there is disordered function of the right frontal lobe in schizophrenia, and that schizophrenia is due not only to localized damage to one part of the brain but to more widespread damage.
A new sorting task designed to isolate and measure specific components of problem-solving ability was administered to four subject groups: patients with focal frontal lobe lesions, patients with both frontal dysfunction and amnesia (Korsakoff's syndrome), patients with circumscribed (non-Korsakoff) amnesia, and normal control subjects. The patients with circumscribed (non-Korsakoff) amnesia, and normal control subjects. The patients with frontal lobe lesions and patients with Korsakoff's syndrome were impaired on eight of the nine components of the task. The findings run counter to theories of a single or primary impairment in patients with frontal lobe dysfunction. Rather, the results suggest that a wide spectrum of deficits in abstract thinking, cognitive flexibility, and use of knowledge to regulate behavior contributes to the problem-solving impairment of these patients. Although the (non-Korsakoff) amnesic patients performed similarly to normal subjects on most measures, a finer analysis suggested that successful performance on this complex sorting task, in addition to being strongly dependent upon frontal lobe function, is mildly dependent upon memory function.
We describe ictal clinical manifestations of frontal lobe epileptic seizures in 22 patients. After examination of all ictal clinical data, 14 catergories of signs and symptoms were established. The validity of the ictal clinical data used was confirmed on the basis of 99 frontal lobe seizures recorded by tele-electroencephalogram or tele-stereo-electroencephalogram. The main conclusion is that the frontal lobe appears to be partially connected with motor acitivity.
The present study examined the sensitivity of the Mini-Mental State Examination (MMSE) in detecting the frontal lobe dysfunction that occurs with normal aging. Eighty normal, independently living older adults in four age groupings from 50 to 89 were administered the MMSE along with three neurocognitive measures sensitive to frontal lobe functioning. Results revealed age-related cognitive decline on frontal lobe tasks that also was detected by the MMSE. These findings are noteworthy because the MMSE was intended as a measure of gross cognitive status rather than of frontal lobe functioning.
This review presents the multiple changes in emotional response and personality that occur after damage to the frontal systems, proposes operational definitions, and analyzes the published reports according to these definitions. Neurological causes of frontal lobe damage and associations of frontal dysfunction with psychiatric disturbances are summarized. It is concluded that symptoms of frontal lobe damage that have been labeled as emotional disturbances may be classified as disorders of drive or motivation, mood (subjective emotional experience), and affect (emotional expression). It is proposed that the primary change after frontal lobe pathology is a disorder of personality, a change in the stable response patterns that define an individual as a unique self. Dysfunction of personality includes cognitive abilities, with a disorder of self-reflective awareness as a key deficit.
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.
We review 22 neuropsychological studies of frontal lobe functions in children with attention deficit disorder with and without hyperactivity (ADD/+H, ADD/-H). Some measures presumed to assess frontal lobe dysfunctions were not reliably sensitive to the deficits occurring in either form of ADD. Tests of response inhibition more reliably distinguished ADD/+H from normal children. Where impairments were found on other tests between ADD and normal subjects, they were highly inconsistent across studies and seemed strongly related to age of the subjects and possibly to the version of the test employed. Other methodological differences across studies further contributed to the discrepant (LD) and conduct problems, with ADD may be an additional confounding factor in some, though not all, of these studies. In a separate reports. The co-morbidity of other disorders, such as learning disabilities (LD) and conduct problems, with ADD may be an additional confounding factor in some, though not all, of these studies. In a separate study, children with ADD/+H (n = 12) were then compared on frontal lobe tests to three other groups: ADD/-H (n = 12), LD but no ADD (n = 11), and normal children (n = 12) statistically covarying for differences in conduct problems across groups. Most measures did not distinguish among these groups. Both ADD groups made more omission errors on a Continuous Performance Test (CPT) than the normal group. All three clinical groups performed more poorly on the word and interference portions of the Stroop Test. Thus, while both types of ADD share some apparent similarities in deficits on a few frontal lobe tests in this study, the totality of existing findings suggests an additional problem with perceptual-motor speed and processing in the ADD/-H group.
Sensorimotor responses to stimulation of the medical frontal and cingulate area were studied in seven unrestrained, unsedated patients who suffered from intractable seizures. Complex postural synergies involving the trunk and proximal extremities appeared contralaterally or occasionally bilaterally. Contraversive turning of head and eyes was not observed. Sensory responses from the supplementary motor area were referred contralaterally and focally; those from the cingulate gyrus were widely referred. Speech impairment from stimulation of the supplementary motor area showed striking similarities with that obtained from stimulation in the frontostriatal region or lateral aspect of the frontal lobe. The observations support the hypothesis that interference with striatal function may be the basis of speech inhibition produced by stimulation of the frontal lobe.
Patient DT was examined 26 years after she acquired focal frontal lobe damage at 7 years of age. This report focused on several aspects of psychological outcome, including the empirical study of social development into early adulthood. Standardized measures of empathy, psychosocial development, and personality were analyzed, along with a moral judgment interview and patterns of adult social behavior. Results indicated that DT has a very limited capacity for empathic understanding, inadequate identity development, difficulties in vocational adjustment, and a concrete level of moral reasoning. Her social behavior and profile of test scores suggest that social development and adaptation have been arrested at early adolescent levels. We conclude that early frontal lobe damage has profound effects on social development, and that the frontal lobes provide a crucial neural substrate for social maturation.
Executive function of frontal lobe systems, like intelligent behavior, appears to demonstrate two major features: it is adaptive and goal-directed. Disruption of executive function following injury to the frontal lobes in childhood might be predicted to impact the trajectory of normal cognitive, behavioral, and social development. Case studies of two children injured at different ages showed the primary developmental impact to involve the behavioral and social realms. While cognitive development may be suspected to also be considerably influenced, assessment of changes in cognitive abilities by traditional psychometric means was found to be problematic. Psychometric changes were found to occur over a prolonged period of time, emphasizing the importance of documenting observations and chronicling postinjury events.