Unilateral Frontal Lesions Research Articles

Characterizing phonemic fluency by transfer learning with deep language models.

Though phonemic fluency tasks are traditionally indexed by the number of correct responses, the underlying disorder may shape the specific choice of words-both correct and erroneous. We report the first comprehensive qualitative analysis of incorrect and correct words generated on the phonemic ('S') fluency test, in a large sample of patients (n = 239) with focal, unilateral frontal or posterior lesions and healthy controls (n = 136). We conducted detailed qualitative analyses of the single words generated in the phonemic fluency task using categorical descriptions for different types of errors, low-frequency words and clustering/switching. We further analysed patients' and healthy controls' entire sequences of words by employing stochastic block modelling of Generative Pretrained Transformer 3-based deep language representations. We conducted predictive modelling to investigate whether deep language representations of word sequences improved the accuracy of detecting the presence of frontal lesions using the phonemic fluency test. Our qualitative analyses of the single words generated revealed several novel findings. For the different types of errors analysed, we found a non-lateralized frontal effect for profanities, left frontal effects for proper nouns and permutations and a left posterior effect for perseverations. For correct words, we found a left frontal effect for low-frequency words. Our novel large language model-based approach found five distinct communities whose varied word selection patterns reflected characteristic demographic and clinical features. Predictive modelling showed that a model based on Generative Pretrained Transformer 3-derived word sequence representations predicted the presence of frontal lesions with greater fidelity than models of native features. Our study reveals a characteristic pattern of phonemic fluency responses produced by patients with frontal lesions. These findings demonstrate the significant inferential and diagnostic value of characterizing qualitative features of phonemic fluency performance with large language models and stochastic block modelling.

Factors affecting cognition and emotion in patients with traumatic brain injury.

BACKGROUND:Cognitive and emotional disturbances are common serious issues in patients with traumatic brain injury (TBI). However, predictors associated with neuropsychological functions were not consistent.OBJECTIVE:To investigate factors affecting cognition and emotion in patients with TBI, we evaluated executive function, memory, and emotion based on injury severity and lesion location.METHODS:Neuropsychological outcomes of 80 TBI patients were evaluated via Wisconsin Card Sorting Test (WCST), Color Trail Test (CTT), Controlled Oral Word Association Test (COWAT), Everyday Memory Questionnaire (EMQ), Geriatric Depression Scale (GDS), State-Trait Anxiety Inventory (STAI), and Agitated Behavior Scale (ABS). WCST, CTT, and COWAT assessed executive function; EMQ assessed everyday memory; and GDS, STAI, and ABS assessed emotion. Patients were categorized according to lateralization of lesion and existence of frontal lobe injury.RESULTS:Patients with longer duration of loss of consciousness (LOC) showed more severe deficits in everyday memory and agitated behaviors. The frontal lesion group showed poorer performance in executive function and higher agitation than the non-frontal lesion group. Patients with bilateral frontal lesion showed greater deficits in executive function and were more depressed than unilateral frontal lesion groups. Especially in those unilateral frontal lesion groups, right side frontal lesion group was worse on executive function than left side frontal lesion group.CONCLUSIONS:Duration of LOC and lesion location are main parameters affecting executive function, everyday memory, and emotion in neuropsychological outcomes following TBI, suggesting that these parameters need to be considered for cognitive rehabilitation interventions.

Cognitive Reserve Proxies Do Not Differentially Account for Cognitive Performance in Patients with Focal Frontal and Non-Frontal Lesions.

Cognitive reserve (CR) suggests that premorbid efficacy, aptitude, and flexibility of cognitive processing can aid the brain's ability to cope with change or damage. Our previous work has shown that age and literacy attainment predict the cognitive performance of frontal patients on frontal-executive tests. However, it remains unknown whether CR also predicts the cognitive performance of non-frontal patients. We investigated the independent effect of a CR proxy, National Adult Reading Test (NART) IQ, as well as age and lesion group (frontal vs. non-frontal) on measures of executive function, intelligence, processing speed, and naming in 166 patients with focal, unilateral frontal lesions; 91 patients with focal, unilateral non-frontal lesions; and 136 healthy controls. Fitting multiple linear regression models for each cognitive measure revealed that NART IQ predicted executive, intelligence, and naming performance. Age also significantly predicted performance on the executive and processing speed tests. Finally, belonging to the frontal group predicted executive and naming performance, while membership of the non-frontal group predicted intelligence. These findings suggest that age, lesion group, and literacy attainment play independent roles in predicting cognitive performance following stroke or brain tumour. However, the relationship between CR and focal brain damage does not differ in the context of frontal and non-frontal lesions.

Cognitive reserve and cognitive performance of patients with focal frontal lesions

The Cognitive reserve (CR) hypothesis was put forward to account for the variability in cognitive performance of patients with similar degrees of brain pathology. Compensatory neural activity within the frontal lobes has often been associated with CR. For the first time we investigated the independent effects of two CR proxies, education and NART IQ, on measures of executive function, fluid intelligence, speed of information processing, verbal short term memory (vSTM), naming, and perception in a sample of 86 patients with focal, unilateral frontal lesions and 142 healthy controls. We fitted multiple linear regression models for each of the cognitive measures and found that only NART IQ predicted executive and naming performance. Neither education nor NART IQ predicted performance on fluid intelligence, processing speed, vSTM or perceptual abilities. Education and NART IQ did not modify the effect of lesion severity on cognitive impairment. We also found that age significantly predicted performance on executive tests and the majority of our other cognitive measures, except vSTM and GNT. Age was the only predictor for fluid intelligence. This latter finding suggests that age plays a role in executive performance over and above the contribution of CR proxies in patients with focal frontal lesions. Overall, our results suggest that the CR proxies do not appear to modify the relationship between cognitive impairment and frontal lesions.

Ictal EEG Source Imaging in Frontal Lobe Epilepsy Leads to Improved Lateralization Compared With Visual Analysis

To investigate the utility of EEG source imaging to lateralize ictal patterns in frontal lobe epilepsy, which were nonlateralized by standard EEG analysis. Prospective analysis of 17 seizures in 8 patients with unilateral frontal lobe epilepsy MRI lesions and nonlateralizing ictal scalp EEG. We applied four EEG source imaging techniques (phase maps, symmetric dipoles, low-resolution brain electromagnetic tomography analysis, and classical low-resolution brain electromagnetic tomography analysis recursively applied) to the averaged seizure pattern. We tested (1) the ability of these techniques to lateralize seizure patterns, (2) the agreement of the lateralization result with MRI lesion side and subdural EEG recordings, individually for each method and for concordance of all. We found lateralizing results in 5 of 17 seizures when analyzing phase maps, 8 of 17 when analyzing dipoles, and 5 of 17 in both classical low-resolution brain electromagnetic tomography analysis recursively applied and low-resolution brain electromagnetic tomography analysis. No discordance with the MRI lesion side was seen when analyzing phase maps, whereas dipole analysis was discordant to the MRI lesion in two seizures, classical low-resolution brain electromagnetic tomography analysis recursively applied in one, and low-resolution brain electromagnetic tomography analysis in two. Agreement between all imaging methods was found in three seizures (three patients), all in line with the side of the MRI lesion. Advanced EEG review methods and source localization provide useful lateralizing information in difficult frontal lobe epilepsy seizure patterns.

Bilateral Neural Control of Visually Guided Hand Movement

Does the right cerebral cortex stay inactive when one slams down on the brake pedal with their right foot in order to stop a car as quickly as possible in an emergency situation? I think not. This is obviously against a common view that the neural control of movement was unilateral: cerebral control, contralateral; cerebellar control, ipsilateral [1,2]. Here we discuss our previous studies of temporary inactivation experiments in the motor cortex and cerebellar nucleus of the nonhuman primates, and hypothesize that neural control of initiation of visually guided hand movement is bilateral. In our previous studies, tow monkeys were trained to practice a visually guided hand reaching task. After the monkeys mastered the task, separate muscimol injections were made into cerebellar Dentate Nucleus (DN) or primary motor cortex (M1) to inactivate the local neural activity during performance of the task. After unilateral injections made into the DN or the M1, significantly delayed initiation of hand movement (reaction time, from Target-on/Go-signal to hand release from the home key) was observed whether the monkeys used either hand to perform the task. In contrast, significantly slowed hand movement (movement time, from hand release of the home key to reaching the target) was observed only when the monkeys used the hand ipsilateral to the injected DN or contralateral to the injected M1. These results from the two monkeys were consistent. Our data indicate that both the DN and the M1 bilaterally contribute to reaction time, and unilaterally to movement time. This furthers the hypothesis that motor control in the brain is bilateral rather than unilateral. This theory has been supported by several independent studies. Examples include that motor response was delayed bilaterally by the unilateral frontal cortex lesion [3]; and clinical studies reported that the reaction time exceeded the normal range bilaterally after unilateral excisions in the supplementary motor area [4]. In addition, both the DN and the M1 contain diverse capabilities in relation to cognitive aspect of motor control during visually guided hand movement [5-7]. Thus, bilateral involvement of the DN and the M1 may be not surprising. To initiate movement, contribution of neurons from relatively wider areas of the brain, even across both hemispheres of the brain is often required. In the future, analysis of potential neural correlation with the bilateral effects of the reaction time may need to be done in both sides of the brain, particularly during the pre-motor period. This will help to understand how the single neurons are involved in the movement bilaterally. Last, clinical frontline also can benefit from this new theory of bilateral neural control. The questions of how to incorporate this new theory of bilateral neural control of movement into the clinical examination or evaluation, and how to create new therapies during the rehabilitation, in particular, to patients with hemiplegia soon need to be answered.

Psychogenic balance disorders: is it a new entity of psychogenic movement disorders?

The various reported psychogenic dyskinesias include tremor, dystonia, myoclonus, gait disorder, Parkinsonism, tics, and chorea. It is not easy to diagnose psychogenic movement disorders, especially in patients with underlying organic disease. We describe three patients with balance and/or posture abnormalities that occur when they stand up, start to move, or halt from walking, although their gaits are normal. One had an underlying unilateral frontal lobe lesion. All patients improved dramatically after receiving a placebo-injection or medication. These abnormal features differ from the previously reported features of astasia without abasia and of psychogenic gait disorders, including recumbent gait. We describe and discuss the patients’ unique clinical characteristics.

Ipsilateral Neglect from a Subcortical Lesion

This report describes a patient with right putaminal hemorrhage who showed ipsilateral (right-sided) neglect. Although lesions to subcortical regions may result in contralateral hemispatial neglect, ipsilateral neglect from putaminal damage has not been reported. It has been posited that ipsilateral neglect from unilateral frontal lesions may be induced by a contralateral attentional grasp. This patient's putaminal hemorrhage may have induced frontal dysfunction with an attentional grasp. Because distracting stimuli, as well as close (vs. far) spatial position, may alter an attentional grasp and because fatigue may compromise the ability to disengage, we tested the patient with repeated trials of line bisection in peripersonal (close) and extrapersonal (far) space with left-sided, right-sided, and both-sided distractors. The patient's leftward bias increased with repeated trials, particularly with those in the close condition and with left-sided distractors. Right putaminal hemorrhage may produce ipsilateral neglect. Our patient's putaminal-white matter injury may have induced frontal dysfunction, and, with repeated trials, his right basal ganglia-frontal network may have fatigued. This fatigue, together with left-sided distractors in the close condition, seemed to increase his contralateral attentional grasp.

Role of the left amygdala and right orbital frontal cortex in emotional interference resolution facilitation in working memory

Previous research has shown that emotional information aids conflict resolution in working memory (Levens & Phelps, 2008). Using a Recency-probes working memory (WM) paradigm, Levens and Phelps found that positive and negative emotional stimuli reduced the amount of interference created when information that was once relevant conflicted with currently relevant information, suggesting that emotional information facilitates interference resolution in WM. To determine what regions of the prefrontal cortex (PFC) and temporal lobes are critical to the influence of emotional stimuli on interference resolution, we conducted a Recency-probes emotion paradigm with right and left unilateral frontal and temporal lobe lesion patients. The frontal lobe lesion patient group comprised individuals with unilateral ventral and dorsal PFC lesions. The temporal lobe lesion patient group comprised individuals with lesions of the amygdala and surrounding structures. Results indicate that when the left amygdala is damaged, emotional facilitation of interference resolution is absent (equal emotional and neutral interference levels), when the right orbital frontal cortex (OFC) is damaged, in contrast, emotional interference resolution is impaired (emotional interference levels are higher than neutral levels are). Based on these unique patterns we propose specific contributions for these regions in the emotional facilitation of interference resolution in WM.

Frontal Ataxia in Childhood

Frontal ataxia may be the result of a unilateral frontal lesion. In this report three cases are presented with ataxia due to right frontal lesions. One case concerns a boy presenting with an unsteady gait and titubation of the trunk, mimicking developmental disequilibrium and with complex partial seizures. It proved to be caused by a small right-sided cavernoma in the middle frontal gyrus. After surgical intervention the symptoms and the seizures disappeared. Two subsequent cases concern teenage patients presenting with headache after an ENT infection and on physical examination mild dysmetric function of the upper limbs and slight disequilibrium, due to right-sided frontal lobe abscesses. After neurosurgical and antibiotic therapy the symptoms were relieved. The frontal origin of ataxia should be considered in children presenting with a "cerebellar syndrome". Frontal gait disorders consist of a clinical pattern of different gait disorders. The syndrome has been mentioned in the literature under different names. Our patients show signs compatible with the term frontal disequilibrium, a clinical pattern of frontal gait disorder. This assumes walking problems characterized by loss of control of motor planning, leading to imbalance. Remarkably, frontal ataxia may mimic developmental delay as demonstrated in the first case and may be the leading mild symptom in extensive frontal lobe damage as demonstrated by the two other cases. We suppose that frontal ataxia is the result of a disturbance in the cerebellar-frontal circuitries and an impairment of executive and planning functions of the basal ganglia-frontal lobe circuitry.

Evidence for asymmetric frontal-lobe involvement in episodic memory from functional magnetic resonance imaging and patients with unilateral frontal-lobe excisions

Recently, there has been considerable debate regarding the involvement of the left and right prefrontal cortices in the encoding and retrieval of episodic memory. In a previous PET study, we found that the use of easily verbalisable material may lead to activation predominantly in the left lateral frontal cortex whilst the use of non-easily verbalisable material may lead to activation predominantly in the right lateral frontal cortex, in both cases irrespective of encoding and retrieval processes. In order to replicate and extend these findings, the same task was modified for use with fMRI. Six healthy volunteers were scanned while encoding and then recalling stimuli that either emphasised visual or verbal processes. It was found that, in comparison to a baseline condition, the encoding of visual stimuli led to a bilateral activation of the prefrontal cortex whilst the encoding of verbal stimuli led to a preferential activation of the left prefrontal cortex. An effect of stimulus type was less evident during retrieval, with both visual and verbal stimuli leading to bilateral prefrontal cortex activation. Overall, encoding and retrieval activated similar regions of the prefrontal cortex suggesting that these areas mediate processes that are fundamental to both aspects of memory. To extend these findings further, the tasks used in the fMRI study were used to assess a group of patients with unilateral frontal lesions and a group of healthy control volunteers. The patients were significantly impaired compared to the healthy volunteers, although no significant differences were found in performance between the right- and left-sided lesioned patients. This result suggests that the memory-related asymmetries observed during functional neuroimaging studies may not be critical for task performance.

Functional Recovery of Skilled Forelimb Use in Rats Obliged to Use the Impaired Limb after Grafting of the Frontal Cortex Lesion with Homotopic Fetal Cortex

The long-term effect of transplanting embryonic frontal cortex into a unilateral frontal cortex lesion has been studied in adult rats. Before surgery, activity in an open field, muscular strength of both forelimbs, and performance in a paw-reaching-for-food task were scored in 26 rats. In 21 animals a unilateral cortex lesion was then made in the forelimb motor area of the hemisphere contralateral to the preferred paw in the paw-reaching-for-food task, while the other 5 animals were sham-operated. On retesting, the lesion animals changed the preferred paw. A solid homotopic transplant of embryonic tissue (embryonic day 17) was then placed in the lesion cavity in 11 of the lesion rats. Three months later neither lesion alone nor lesion plus transplantation affected open field behavior and muscular strength, but the lesion permanently affected performance in the paw-reaching-for-food task, as shown by a change of preferred paw and a functional deficit in the paw contralateral to the lesion. Transplantation ameliorated the deficits caused by the lesion, but this was only evident when animals were forced to reach with the paw contralateral to the lesion plus transplant. The behavioral results were independent of the size of the lesion and graft. Connections between graft and host tissue were studied by means of the fluorescent tracer 1,1′-dioctadecyl-3,3,3′3′-tetramethylindocarbocyanine perchlorate (DiI). A dense array of labeled fibers was found in the host cortex adjacent to the transplant. The results suggest that functional recovery depends on grafting but is only evident when the animal is obliged to use the affected limb.

Frontal brain lesions affect the use of advance information during response planning.

This study examined the nature of the response programming deficit after frontal cortex lesions through the effects of advance information on sequence initiation time. Nine patients with unilateral frontal lesions, 9 patients with temporal lesions, and 9 controls performed a sequential key-press task involving 4 rapid choice responses to a 4-letter stimulus. Three conditions manipulated the number of responses that subjects knew in advance. The frontal group showed slow initiation times in all conditions. Knowing the first response produced an acceleration of initiation time in all 3 groups. However, knowing 3 responses in advance instead of 1 further accelerated initiation time in the control and temporal groups but not in the frontal group. These results indicate that frontal lesions impair the use of multiple representations during programming. This suggests that the attentional control of response selection is an important element of the response planning deficit.

Frontal brain lesions affect the use of advance information during response planning.

This study examined the nature of the response programming deficit after frontal cortex lesions through the effects of advance information on sequence initiation time. Nine patients with unilateral frontal lesions, 9 patients with temporal lesions, and 9 controls performed a sequential key-press task involving 4 rapid choice responses to a 4-letter stimulus. Three conditions manipulated the number of responses that subjects knew in advance. The frontal group showed slow initiation times in all conditions. Knowing the first response produced an acceleration of initiation time in all 3 groups. However, knowing 3 responses in advance instead of 1 further accelerated initiation time in the control and temporal groups but not in the frontal group. These results indicate that frontal lesions impair the use of multiple representations during programming. This suggests that the attentional control of response selection is an important element of the response planning deficit.

Memory after frontal/temporal disconnection in monkeys: conditional and non-conditional tasks, unilateral and bilateral frontal lesions

Seven Cynomolgus monkeys ( Macaca fascicularis) learned a series of reward-visual conditional discrimination problems, in which the arrival or non-arrival of a food pellet at the beginning of each trial acted as an instruction cue, signalling which of two visually distinct stimulus objects the animal should choose on that trial in order to obtain a further food pellet reward. Following surgical removal of the ventrolateral prefrontal cortex in one hemisphere and the inferior temporal cortex in the contralateral hemisphere, combined with forebrain commissurotomy, the four operated animals were severely impaired at relearning this task. They were not impaired, however, in non-conditional visual discrimination learning. Extending the unilateral frontal lesion to include the ventromedial prefrontal cortex had no detrimental effect, nor did complete unilateral removal of the frontal cortex. In a third experiment, the operated animals underwent a further surgery to remove either ventrolateral, ventral or complete frontal cortex similar to that in the opposite hemisphere. Compared to their previous level of performance, the animals with bilateral ventrolateral prefrontal lesions were now mildly impaired and the animals with the bilateral lesion extended to the ventromedial cortex more severely impaired on the non-conditional visual discrimination task. The bilaterally lobectomized animals were unable to relearn the task. We suggest that behaviour in visual learning tasks is controlled by cortical convergence upon subcortical structures, possibly by striatal efferents from both the visual cortex and frontal cortex, and that intrahemispheric convergence of these two efferents within the corpus striatum of one hemisphere could allow detailed control of visual choices by non-visual information, while subcortical interhemispheric transfer allows only less detailed, more general control.

A critical maturational period of reduced brain vulnerability to developmental injury: I. Behavioral studies in cats

Groups of cats with resection of the neocortex of the left cerebral hemisphere at postnatal (P) ages (in days) 5–15 (P10), 30 (P30), 60 (P60), 90 (P90), 120 (P120), and in adulthood, were compared using a comprehensive battery of 16 neurobehavioral tests administered when they were at least 6 months post-lesion. For all behaviors, except 3 (including the paw contact placing reaction which never recovered), the performance was significantly better for the cats lesioned between P10 and P30 compared to cats lesioned at older ages. For 10 of the behaviors, the transition from age-at-lesion P30 to P60 was rather abrupt and characterized by a significant increment in impairments. However, cats with the resection at ages P90 and P120 still showed some behavioral advantage over the adult-lesioned animals. Overall, for most of the behaviors tested, there was a significant linear trend for an increase in the magnitude of impairments across the entire age-at-lesion range. We previously reported that cats with a unilateral frontal cortical lesion sustained during the late fetal life showed substantial behavioral impairments, while animals with a similar resection sustained early postnatally exhibited minimal abnormalities. These findings, together with the present results, indicate that the long-term behavioral outcome of neocortical injury is best when the lesion is sustained during a discrete period of the life of the cat. This period extends from about fetal age 55 days (the oldest lesion age in our fetal studies) to about P60, as shown in the present paper. For these reasons, we propose that there is a Critical Maturational Period (CMP) for optimal post injury brain and behavioral restoration. We hypothesize that this span of reduced vulnerability is linked to specific developmental morphological events which occur during the same time period. Since, as discussed, such ontogenetic events also occur in other mammal species (albeit at different chronological ages), we further propose that the timing of the CMP as delineated in cats, can be extrapolated to other higher mammals species including humans.

Planning Ability After Frontal and Temporal Lobe Lesions in Humans: The Effects of Selection Equivocation and Working Memory Load

Twenty-one patients with unilateral frontal neurosurgical lesions (11 left and 10 right) and 38 patients with unilateral temporal lobectomies (19 left and 19 right) were compared to 44 normal control subjects in their performance on a computerised version of the Tower of Hanoi (TOH) test. In order to explore the effect of selection equivocation on performance, two types of problems were administered, determined by whetherthe two mainroutes to achieve the goal weresimilar or dissimilar in length. To explore the effectof working memory load, a task was administered that required the subject to repeat a sequence of Tower of Hanoi moves shown by the computer. For the frontal patients, those with right (RF), but not left (LF) lesions were impaired on TOH, but response equivocation had no effecton performance. The LF group, however, were impaired on the working memory task. Forthetemporal patients, only therightlesion group wereimpaired on TOH, but specifically on the dissimilar problems. This group were also impaired on the working memory task. Selection equivocation and working memory load are not thought to be significant factors in producing a planning deficit following frontal lobe lesions, but may cause impairment in patients who have undergone right temporal lobectomies.

The Effect of Neocortical Lesions on the Number of Cells in Neonatal or Adult Feline Caudate Nucleus: Comparison to Fetal Lesions

After a unilateral resection of the frontal cortex in fetal cats the volume of the caudate nucleus increases while the packing density of neuronal and glial cells does not change. In the present report we address the questions of whether a similar lesion sustained neonatally or a more extensive neodecortication sustained neonatally or in adulthood may have the same unusual effect. Stereological methods were used to determine bilaterally the volume of the caudate nucleus as well as to estimate the total number and packing density of neurons and glial cells in the caudate nucleus ipsilateral to the lesion. Comparisons between each of three experimental groups and intact animals were made at a time when all animals were young adults. In cats with a unilateral frontal cortical lesion performed between postnatal days 8 and 14, none of the measured parameters changed significantly compared to intact controls. In cats with removal of the entire left neocortex in adulthood, the ipsilateral caudate nucleus volume decreased by 18.1% and by 21.5% relative to intact and to neonatal hemidecorticated cats respectively ( P<0.05), with no change in the contralateral caudate. In the ipsilateral caudate the total number of neurons decreased by 21.8% ( P<0.05) compared to controls while the number of glial cells did not change significantly. In the same caudate the packing density of neurons did not change significantly (except for a 17.1% decrease, P<0.05, relative to frontal-lesioned cats) while that of glial cells increased by 19.9% and by 24.7% compared to intact and neonatal neodecorticated cats respectively ( P<0.05). In adult cats in which a similar hemineodecortication was performed between postnatal days 8 and 13, the only significant changes were a 25.8% ( P<0.05) and a 30.6% ( P<0.05) decrease in neuron packing density compared to intact and frontal-lesioned cats, respectively. In summary, a restricted unilateral neocortical resection in neonatal cats did not induce any morphological changes in the caudate nucleus that we could detect with the methods employed. In contrast, an extensive neodecortication sustained in adulthood produced ipsilateral caudate shrinkage with substantial neuron loss and increase in packing density of glial cells, while a similar lesion but sustained neonatally only altered substantially the packing density of glial cells (decreased). Therefore, we concluded that (i) the caudate nucleus hypertrophy which we reported after a unilateral discrete cortical removal during the prenatal period is a unique phenomenon which is peculiar to the cat brain during the last third of gestation; (ii) the caudate nucleus changes seen in the cats with hemineodecortication in adulthood are degenerative in nature and closely resemble those which we reported for other subcortical nuclei following a similar lesion; and (iii) the animals with neonatal hemidecortication are relatively spared from these degenerative effects. Overall, these results indicate that, as for other structures, the morphological changes of the caudate nucleus following neocortical damage depend on the maturational state of the brain at the time of the injury and on the size of the lesion, and support the notion that the consequences of cerebral cortex lesions upon subcortical brain nuclei are of a different nature when sustained in prenatal as compared to postnatal cats.

The effect of fetal neocortical transplants on lesion-induced cerebral cortex plasticity.

Sensorimotor cortical lesions in newborn rats lead to the formation of abnormal projections from the opposite intact sensorimotor cortex. In the present study the influence of fetal neocortical transplants on this lesion-induced plasticity was examined. Newborn rats received unilateral frontal neocortical lesions. One experimental group received grafts of fetal neocortical tissue (E14-E16) into the lesion cavities. Another group served as lesion-only animals, while a third group was left unlesioned and without grafts as normal controls. At 3 mo of age, the animals received injections of the anterograde tracer biotinylated dextran amine (BDA) into the sensorimotor cortex contralateral to the lesion/transplantation area. After sacrifice 2 wk later, the brains were processed histochemically for detection of BDA-labeled cells and fibers. As a measure of the lesion-induced axonal sprouting response, corticothalamic and corticopontine fibers crossing the midline were counted. Significantly fewer cortical efferent fibers crossed the thalamic midline in the transplanted rats compared to the lesion-only controls. In contrast, the presence of transplants did not reduce the corticopontine sprouting response. These results therefore indicate that fetal neocortical grafts have a modulatory, yet variable effect on the lesion-induced axonal sprouting of contralateral sensorimotor cortical neurons.

The effect of fetal neocortical transplants on lesion-induced cerebral cortex plasticity

Sensorimotor cortical lesions in newborn rats lead to the formation of abnormal projections from the opposite intact sensorimotor cortex. In the present study the influence of fetal neocortical transplants on this lesion-induced plasticity was examined. Newborn rats received unilateral frontal neocortical lesions. One experimental group received grafts of fetal neocortical tissue (E14-E16) into the lesion cavities. Another group served as lesion-only animals, while a third group was left unlesioned and without grafts as normal controls. At 3 mo of age, the animals received injections of the anterograde tracer biotinylated dextran amine (BDA) into the sensorimotor cortex contralateral to the lesion/transplantation area. After sacrifice 2 wk later, the brains were processed histochemically for detection of BDA-labeled cells and fibers. As a measure of the lesion-induced axonal sprouting response, corticothalamic and corticopontine fibers crossing the midline were counted. Significantly fewer cortical efferent fibers crossed the thalamic midline in the transplanted rats compared to the lesion-only controls. In contrast, the presence of transplants did not reduce the corticopontine sprouting response. These results therefore indicate that fetal neocortical grafts have a modulatory, yet variable effect on the lesion-induced axonal sprouting of contralateral sensorimotor cortical neurons.