Dissociable contributions of thalamic nuclei to recognition memory: novel evidence from a case of medial dorsal thalamic damage.

The thalamic nuclei are thought to play a critical role in recognition memory. Specifically, the anterior thalamic nuclei and medial dorsal nuclei may serve as critical output structures in distinct hippocampal and perirhinal cortex systems, respectively. Existing evidence indicates that damage to the anterior thalamic nuclei leads to impairments in hippocampal-dependent tasks. However, evidence for the opposite pattern following medial dorsal nuclei damage has not yet been identified. In the present study, we investigated recognition memory in NC, a patient with relatively selective medial dorsal nuclei damage, using two object recognition tests with similar foils: a yes/no (YN) test that requires the hippocampus, and a forced choice corresponding test (FCC) that is supported by perirhinal cortex. NC performed normally in the YN test, but was impaired in the FCC test. Critically, FCC performance was impaired only when the study-test delay period was filled with interference. We interpret these results in the context of the representational-hierarchical model, which predicts that memory deficits following damage to the perirhinal system arise due to increased vulnerability to interference. These data provide the first evidence for selective deficits in a task that relies on perirhinal output following damage to the medial dorsal nuclei, providing critical evidence for dissociable thalamic contributions to recognition memory.

Severe Neonatal Anaemia, MRI Findings and Neurodevelopmental Outcome.

BACKGROUND AND OBJECTIVE: Severe neonatal anaemia can impair cerebral oxygen supply. Data on long-term outcomes following severe neonatal anaemia are scarce. METHODS: Clinical data and neurodevelopmental outcome of 49 (near) term infants with haemoglobin concentration after birth <6.0 mmol/l were retrospectively collected and analysed. In a subgroup of 28 patients, amplitude-integrated EEG was available and in 25 infants cerebral MRI was obtained. Infants were followed up at 14-35 months of age and assessed with the Griffiths Scale of Mental Development or Bayley Scale of Infant Development. RESULTS: Eighteen patients (37%) died during the neonatal period. In 25 patients MRI was performed. A predominant pattern of injury on MRI was seen in the basal ganglia and thalami in 7 patients (28%), whereas some form of white matter injury was present in 16 (64%) and a combination in 3 (12%). Follow-up data were available for 26 patients (84% of survivors). Formal assessment of neurodevelopmental outcome was performed in 20 of 31 (65%) infants who survived (median age: 19 months, range: 14-35). Sixteen infants (80%) had a developmental quotient appropriate for age in the first 2 years after birth. On motor outcome, 1 patient (5%) scored below average (Z-score -1.10). One patient developed cerebral palsy. CONCLUSION: Early neurodevelopmental outcome in surviving patients with severe neonatal anaemia was within the normal range in the majority of the survivors. MRI showed mild-to-moderate white matter injury in two thirds of the infants. Prospectively collected data with a longer follow-up period are needed.

Role of thalamic nuclei in the modulation of Fos expression within the cerebral cortex during hypertonic saline-induced muscle nociception.

It has been proposed that thalamic mediodorsal (MD) and ventromedial (VM) nuclei form thalamic 'nociceptive discriminators' in discrimination of nociceptive afferents, and specifically govern endogenous descending facilitation and inhibition. The present study conducted in rats was to explore the role of thalamic MD and VM nuclei in modulation of cerebral neuronal activities by means of detection of spatiotemporal variations of Fos expression within the cerebral cortex. Following a unilateral intramuscular injection of 5.8% saline into the gastrocnemius muscle, Fos expression within the bilateral, different areas of the cerebral cortex except S2 was significantly increased (P<0.05). Particularly, the increases in Fos expression within the cingulate cortex and the insular cortex occurred at 0.5h, 4h and reached the peak level at 4h, 16h, respectively. Electrolytic lesion of the contralateral thalamic MD and VM nuclei significantly blocked the 5.8% saline intramuscularly induced increases in Fos expression within the bilateral cingulate and insular cortices, respectively. Additionally, the 5.8% saline-induced Fos expression in the cingulate cortex and the insular cortex were dose-dependently attenuated by microinjection of µ-opioid antagonist ß-funaltrexamine hydrochloride into the thalamic MD and VM nuclei. It is suggested that (1) the neural circuits of 'thalamic MD nucleus - cingulate cortex' and 'thalamic VM nucleus - insular cortex' form two distinct pathways in the endogenous control of nociception, (2) mirror or contralateral pain is hypothesized to be related to cross-talk of neuronal activities within the bilateral cerebral cortices modulated by µ-opioid receptors within the thalamic MD and VM nuclei.

Dendritic morphology changes in neurons from the prefrontal cortex, hippocampus and nucleus accumbens in rats after lesion of the thalamic reticular nucleus.

Several studies in rodents have shown that dysfunctions of the thalamic reticular nucleus (TRN) result in deficits of sensory gating and attentional processes, two core features of schizophrenia. TRN receives inputs from the prefrontal cortex (PFC) and hippocampal formation, two structures which send excitatory projections to the nucleus accumbens (NAcc) and are interconnected with the basolateral amygdala (BLA). Here we determined whether (and which) changes occurred four weeks after a TRN lesion in the dendritic morphology of pyramidal neurons of layers 3 and 5 of the PFC, neurons of ventral and dorsal hippocampus, BLA, and the medium spiny neurons of the NAcc. Dendritic morphology and characteristics were measured by using Golgi-Cox procedure followed by Sholl analysis. We also evaluated the effects of TRN lesion on exploratory behavior assessed by hole-board test and locomotor activity induced by a novel environment. We found that TRN damage induced a reduction in the exploratory behavior measured by hole-board test with neuronal hypotrophy in PFC (layer 5), CA1 ventral hippocampus and NAcc neurons. Taken together, these data suggest that the behavioral and morphological effects of TRN lesion are, at least partially, mediated by limbic subregions with possible consequences for schizophrenia-related behaviors.

Abnormal anterior pretectal nucleus activity contributes to central pain syndrome.

Central pain syndrome (CPS) is a debilitating condition that affects a large number of patients with a primary lesion or dysfunction in the CNS, most commonly due to spinal cord injury, stroke, and multiple sclerosis lesions. The pathophysiological processes underlying the development and maintenance of CPS are poorly understood. We have recently shown, in an animal model of CPS, that neurons in the posterior thalamic nucleus (PO) have increased spontaneous and evoked activity. We also demonstrated that these changes are due to suppressed inhibitory inputs from the zona incerta (ZI). The anterior pretectal nucleus (APT) is a diencephalic nucleus that projects on both the PO and ZI, suggesting that it might be involved in the pathophysiology of CPS. Here we test the hypothesis that CPS is associated with abnormal APT activity by recording single units from APT in anesthetized rats with CPS resulting from spinal cord lesions. The firing rate of APT neurons was increased in spinal-lesioned animals, compared with sham-operated controls. This increase was due to a selective increase in firing of tonic neurons that project to and inhibit ZI and an increase in bursts in fast bursting and slow rhythmic neurons. We also show that, in normal animals, suppressing APT results in increased PO spontaneous activity and evoked responses in a subpopulation of PO neurons. Taken together, these findings suggest that APT regulates ZI inputs to PO and that enhanced APT activity during CPS contributes to the abnormally high activity of PO neurons in CPS.

Arousal by stimulation of deep-brain nuclei.

Schiff et al. show that deep-brain stimulation of the unspecific thalamocortical system through certain midline thalamic nuclei produces an alerting effect in a patient in a minimally conscious state. Such nuclei include the central lateral nucleus, paralaminar regions of the median dorsalis, and the posterior-medial aspect of the centromedian/parafascicularis nucleus complex.

Demencia talámica secundaria a infarto agudo paramediano talámico bilateral por oclusión de la arteria de Percheron / Thalamic dementia secondary to acute bilateral paramedian thalamic infarcts after occlusion of the artery of percheron

La parte anterior y medial del tálamo se encarga de múltiples funciones cognitivas por las conexionestalamocorticales. Un infarto talámico bilateral puede provocar una demencia secundaria por desaferentación talamocortical con cierto grado de reversibilidad. Presentamos el caso de una demencia de inicio aguda por lesiones talámicas bilaterales. Caso clínico. Varón de 42 años, fumador y con estrés laboral, que de forma brusca presentó un síndrome confusionalagudo con alteración del lenguaje, bradipsiquia y hemiparesia e hemihipoestesia derecha. En la resonancia magnética craneal se apreció una afectación bilateral de ambos tálamos compatibles con un infarto agudo a estos niveles por probable irrigación del tálamo a través de la variante de Percheron tipo 2. A partir de esta fecha, a los tres meses el paciente presentó faltade atención, alteraciones en la memoria de retención, apatía, falta de iniciativa, síndrome depresivo y cambios de humor, y mejoró parcialmente en los siguientes seis meses. Conclusiones. La demencia talámica se suele producir por afectación bilateralde ambos tálamos y, preferentemente, en la zona anterior y medial. En nuestro caso, mediante SPECT cerebral se pone de manifiesto la hipocaptación frontal por un fenómeno de diasquisis

The anterior and medial part of the thalamus is the responsible of multiples cognitive functions throughthe thalamus-cortical connections. A bilateral thalamic infarction can cause a secondary dementia and these are related to a thalamocortical deafferentation with a partial recovery. We report a case of sudden onset dementia caused by bilateral thalamus lesions. Case report. A 42 smoker male, that suddenly had an acute confusional syndrome with altered language,bradypsychia, right hemiparesis and right hemisensory loss. Cranial magnetic resonance imaging showed a bilateral thalamic stroke probably due to a variant talamus irrigation (artery of Percheron type 2). From this date, in three months, the patienthad attention deficit, impairment of memory retention, apathy, initiative deficit, depressive syndrome and mood changes. All these symptoms improving partially in the following six months. Conclusions. The thalamic stroke can cause a thalamic dementia, commonly bilateral and preferable located in the anterior and medial nuclei. In our case, cranial SPECT showed frontal hypocaptation for diaschisis phenomenon

Behavioural effects of parafascicular thalamic lesions in an animal model of parkinsonism.

We recently reported that the centromedian-parafascicular thalamic complex (CM-Pf) degenerates in Parkinson's disease and progressive supranuclear palsy. The contribution of such thalamic pathology to disease symptoms has not yet been established. The present study therefore investigated the behavioural impact of lesioning the corresponding thalamic region (termed Pf) on a range of behaviours present in rodents. There were four surgical groups: (1) sham medial forebrain bundle (mfb)+sham Pf, (2) 6-OHDA mfb lesion+sham Pf, (3) sham mfb+NMDA Pf lesion, (4) 6-OHDA+NMDA Pf lesions. Posture, sensory functions and apomorphine-induced rotational asymmetry were assessed before and after each surgery. Other assessments performed including a timed motivational task, grooming behaviours and piloerection. 6-OHDA lesions induced postural (ipsilateral curling and head position biases), sensorimotor (increased latency to respond to tactile stimulation of the contralateral side when eating or grooming) and rotational abnormalities (contralateral circling after apomorphine). The main effects of combined 6-OHDA+Pf lesions were improved performance in a motivational task (decreased latency to retrieve reward) but worsened piloerection, relative to animals with either 6-OHDA or Pf lesions alone. The thalamic zone common to all lesioned animals involved the posterior Pf. Our data suggests that the posterior CM-Pf may be involved in motivational responses and autonomic dysfunction in parkinsonian disorders.

Effects of excitotoxic thalamic intralaminar nuclei lesions on attention and working memory.

In rats, lesions of the thalamic intralaminar nuclei (ILn) impair measures of working memory, but it is unclear whether alterations of attention contribute to the mnemonic deficits. The present experiment tested the effects of ILn lesions on a two-lever attention task that required discrimination of visual signals and non-signals. Rats were trained presurgically in the task and then received sham surgery or infusions of n-methyl-d-aspartate (NMDA) into the ILn to induce excitotoxic lesions. ILn lesions transiently decreased accurate detection of signals. ILn lesions also increased omissions. Compared to sham-lesioned rats, ILn-lesioned animals were not differentially affected when task demands were increased by presenting a visual distracter. Finally, a retention interval was incorporated into the task to assess whether the lesions affected acquisition of a working memory version of this behavioral paradigm. Unlike sham-lesioned animals, ILn-lesioned rats did not demonstrate a significant improvement in signal detection when a retention interval was introduced. The transient lesion-induced deficits in the attention task suggest that, in rats, the ILn may contribute to aspects of attentional processing, but through neural re-organization or activity in other regions, there is compensation for the loss of ILn functioning. The ILn appear to be necessary for maintaining performance when working memory demands are increased.

Distribution and binding parameters of GABAA receptors in the thalamic nuclei of Macaca mulatta and changes caused by lesioning in the globus pallidus and reticular thalamic nucleus.

Ascending output from the basal ganglia to the primate motor thalamus is carried by GABAergic nigro- and pallido-thalamic pathways, which interact with intrinsic thalamic GABAergic systems represented in primates by local circuit neurons and axons of the reticular thalamic nucleus. Disease-triggered pathological processes in the basal ganglia can compromise any of these pathways either directly or indirectly, yet the effects of basal ganglia lesioning on its thalamic afferent-receiving territories has not been studied in primates. Two GABA(A) receptor ligands, [(3)H]muscimol and [(3)H]flunitrazepam, were used to study the distribution and binding properties of the receptor in intact monkeys, those with kainic acid lesions in the globus pallidus, and those with ibotenic acid lesions in the reticular nucleus using quantitative autoradiographic technique on cryostat sections of fresh frozen brain tissue. In control monkeys the binding affinities for [(3)H]muscimol averaged 50 nM in the thalamic nuclei and 86 nM in the basal ganglia while the binding densities varied (maximum density of binding sites [Bmax] range of 99.4-1000.1 fmol/mg of tissue). Binding affinities and Bmax values for [(3)H]flunitrazepam averaged 2.02 nM and 81-113 fmol/mg of tissue, respectively. Addition of 100-microM GABA increased average affinity to 1.35 nM whereas Bmax values increased anywhere from 1-50% in different nuclei. Zolpidem (100 nM) decreased binding by 68-80%. Bmax values for both ligands were decreased at the two survival times in both medial and lateral globus pallidus implying involvement of both nuclei in the lesion. Statistically significant, 40% decrease (P=0.055) of Bmax for [(3)H]muscimol was observed in the ventral anterior nucleus pars densicellularis (VAdc, the main pallidal projection territory in the thalamus) 1 week after globus pallidus lesioning and a 36% decrease (P=0.017) 4 months post-lesioning. In contrast, [(3)H]flunitrazepam Bmax values in the VAdc of the same animals were increased by 23% (P=0.021) at 1 week and 28% (P=0.005) 4 months postlesion, respectively. One week after the reticular nucleus lesioning, the binding densities of [(3)H]muscimol and [(3)H]flunitrazepam were decreased in the thalamic nuclei receiving projections from the lesioned reticular nucleus sector by approximately 50% (P<0.05) and 10-33% (P<0.05), respectively. The results suggest that different GABA(A) receptor subtypes are associated with different GABAergic systems in the thalamus which react differently to deafferentation.

Performance of different synchronization measures in real data: a case study on electroencephalographic signals.

We study the synchronization between left and right hemisphere rat electroencephalographic (EEG) channels by using various synchronization measures, namely nonlinear interdependences, phase synchronizations, mutual information, cross correlation, and the coherence function. In passing we show a close relation between two recently proposed phase synchronization measures and we extend the definition of one of them. In three typical examples we observe that except mutual information, all these measures give a useful quantification that is hard to be guessed beforehand from the raw data. Despite their differences, results are qualitatively the same. Therefore, we claim that the applied measures are valuable for the study of synchronization in real data. Moreover, in the particular case of EEG signals their use as complementary variables could be of clinical relevance.

Progressive ratio performance in rats with gustatory thalamus lesions.

To determine whether damage of the gustatory thalamus (the parvicellular region of the ventroposteromedial nucleus) disrupts the perceived value of reinforcing stimuli, the performance of rats with bilateral, electrophysiologically guided, electrolytic lesions of the area was examined in Experiment 1 with a progressive-ratio schedule of reinforcement. Lesioned rats showed normal concentration-dependent changes in break point (an index of the amount of effort a subject will expend to obtain reinforcement) and in consummatory responding (licking) for the sucrose reward. In the reward comparison procedure of Experiment 2, however, the same lesioned rats failed to show morphine-induced suppression of alanine consumption. The results provide no support for the view that the thalamic taste area is involved in the perception of the absolute reinforcing value of gustatory stimuli.

Medullo adrenal response to lesion of anterodorsal thalamic nuclei in rats.

Anterodorsal thalamic nuclei (ADTN) exert an inhibitory influence on hypophyso-adrenal system (HAS) in rats. With the purpose of evaluating if ADTN are also involved in the control of medullo adrenal activity, experiments were conducted on female rats with bilateral lesion of these nuclei. Thirty days after lesion, plasma epinephrine (E) concentration in lesioned rats was higher than that in sham-lesioned control group (P < 0.02). Meanwhile, adrenal E content was significantly lower in lesioned animals than that found in the control group (P < 0.005). Plasma norepinephrine (NE) values in lesioned rats were not significantly different from those in the control ones, however, there was a significant decrease in adrenal NE when compared to the control one (P < 0.02). Basal values of plasma ACTH and plasma and adrenal corticosterone (C) were signicantly higher than those in sham lesioned rats (P < 0.05; P < 0. 001; P < 0.001 respectively). These findings demonstrate that the ADTN in rats are involved in the regulation of both cortico and medullo adrenal activity.

Interaction between the postsubiculum and anterior thalamus in the generation of head direction cell activity.

Previous research has identified neurons in the postsubiculum (PoS) and anterior dorsal thalamic nucleus (AD) of the rat that discharge as a function of the animal's head direction. In addition, anatomical studies have shown that the AD and PoS are reciprocally connected with one another. The current study examined whether head direction (HD) cells in each of the two areas is dependent on input from the other structure. After both electrolytic or neurotoxic lesions of the AD, no cells were identified with direction-specific discharge in the PoS. In contrast, AD HD cell activity was still present after neurotoxic lesions to the PoS. However, AD HD cells in PoS-lesioned rats exhibited three important differences compared with AD HD cells in intact animals: (1) their directional firing range was significantly larger, (2) their firing predicted the animal's future head direction by a larger amount, and (3) their preferred firing direction was substantially less influenced by a prominent visual landmark within the recording environment. These results indicate that information critical for HD cell activity is conveyed in both directions between the AD and the PoS; whereas the AD is necessary for the presence of HD cell activity in the PoS, the PoS appears important in allowing visual landmarks to exert control over the preferred firing direction of AD HD cells. These findings have implications for several computational models that propose to account for the generation of the HD cell signal.

The role of somatosensory information in a constrained locomotor task.

The purpose of this project was to study the role of somatosensory information in the performance of a constrained locomotor task by rats and to further examine the influence of structural recovery in the somatosensory thalamus, specifically the ventral posterolateral nucleus (VPL). Groups of rats were trained to traverse an elevated, one inch bar for a reward. The time taken to run across the bar (run time) was used as a measure of the success of the goal-directed behavior. The movement pattern of the hindlimb during the swing phase of the locomotor task was quantified from videotape on Preoperative (PRE) Day 15 and during the 46-day postoperative period. The movement pattern was characterized using six different parameters: the area, the X and Y values of the centroid under the normalized curve of the hindlimb trajectory, the vertical displacement of the hindlimb in the flexion and extension phases of the swing cycle, the maximum instantaneous hindlimb velocity, and the proportion of time spent in the acceleration versus deceleration phases of the swing cycle. In order to disrupt the central pathways for somatosensory information, lesions were made in (i) the right gracile nucleus (GN) (n = 18), (ii) bilateral GN (n = 7), (iii) the right GN and the left VPL (n = 6), and (iv) bilateral VPL (n = 8), and (v) sham-operated animals (n = 5). The run time and the pattern of the hindlimb swing cycle were used as measures of loss and recovery of function. Only the bilateral VPL group showed an impairment in run time and they recovered by Postoperative (POST) Week 4. All groups demonstrated an impairment in initial flexion of the hindlimb during the swing cycle that recovered in the right GN group only. On POST Day 49, the right GN, bilateral GN, and the sham groups received injections of 5% WGA-HRP into both CN to determine the location of these projections in VPL. The CN projections were not redistributed into the gracile area of VPL after GN lesions. Since our previous study (24) had shown the number of synapses in VPL returned to normal after dorsal column nuclei (DCN) lesions by POST Day 50, the recovery of the number of synapses alone was not sufficient to restore the normal gait pattern, while the recovery of the run time preceded the complete recovery of the number of synapses.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal function response to chronic stress in rats with anterodorsal thalami nuclei lesions.

The effects of chronic stress (forced immobilization, 15 min/day during 12 days), on the plasma corticosterone and the adrenal catecholamines response in rats with anterodorsal thalami nuclei (ADTN) lesions were studied. In sham lesioned rats, chronic stress produced a significant increase in plasma corticosterone (C), as compared to unstressed animals (p < 0.05). The adrenal C was, however, similar in both groups. There were no differences in plasma C values between unstressed and stressed lesioned rats. The adrenal C content, was significantly lower (P < 0.005) in stressed lesioned rats when compared with unstressed lesioned animals. Adrenal norepinephrine (NE) values, in sham lesioned rats after forced immobilization, were significantly below those found in unstressed sham lesioned ones (P < 0.05). There were no changes in adrenal epinephrine (E) response after forced immobilization. In lesioned rats, NE response to chronic stress showed the opposite pattern to that in sham lesioned ones; the adrenal glands of these animals showed a significant increase in NE content as compared to unstressed lesioned rats (P < 0.01). Similar alterations in the adrenal E concentration were found, post stress values were significantly higher (P < 0.01).

[Long-term rearrangements of the processing of kinesthetic afferentation at the neuronal level of the cat motor cortex after damage to the ventrolateral thalamic nucleus]. / Dlitel'no tekushchie perestroiki protsessov obrabotki kinesteticheskoi afferentatsii na urovne neironov motornoi kory koshek posle povrezhdeniia ventrolateral'nogo iadra talamusa.

Single-unit recordings from motor cortex (area 4) were obtained in cats and under semichronic experimental conditions before and within various periods (from a week to five months) after the lesion in thalamic nucleus ventralis lateralis (n. VL). Neuronal responses to tactile stimulation of the contralateral forelimb and its passive movement in the wrist joint with the mean speed 170 degrees/s were studied. As it had been already reported by others, the magnitude and time course of averaged response histograms for some neurons, which were evoked by imposed displacements of the forelimb, were related to the velocity and/or acceleration components of the movements. Spontaneous firing and kinematic processing capabilities of motor cortical cells were affected by the lesion. The findings are in agreement with a hypothesis that n. VL is essential for encoding specific kinematic features of angular joint movements. Restoration of kinematic processing by cortical neurons in the course of post-traumatic period was characterized by facilitation of activatory reactions of the area 4 cortical cells to peripheral cutaneous stimulation. Some suggestions are made on the nature of plastic changes which develop in neuronal nets of the motor cortex after the lesion of n. VL.

Development of akinetic mutism and hyperphagia after left thalamic and right hypothalamic lesions.

A case of childhood post-traumatic akinetic mutism is presented. The patient showed a hyperphagic condition while recovering from akinetic mutism. He had lesions in the left interlaminal nucleus of the thalamus, right globus pallidus, and right dorsomedial nucleus of the hypothalamus. Laboratory data indicated slightly disturbed hypothalamic functions. In general, akinetic mutism can be seen with bilateral destructive lesions, while hyperphagia may occur after destruction of dorsomedial hypothalamic nucleus, but it is very rare. This is the first reported case of akinetic mutism caused by a unilateral lesion.

Selective loss of neurons from the thalamic reticular nucleus following severe human head injury.

The GABAergic neurons of the thalamic reticular nucleus, or nucleus reticularis thalami (RT), have been implicated as important components in attentional processing systems. Neurons in the RT are exquisitely sensitive to degeneration following kainic and domoic acid toxicity, experimental global ischemia, human cardiac arrest, and experimental closed head injury in nonhuman primates. The present study was performed to establish whether the selective loss of human RT neurons occurred following severe head injury. Brains from 37 human nonsurvivors of head injury were examined for evidence of RT neuronal loss. RT lesions in were found in 36 of 37 cases, representing 65 of 73 (89%) of the reticular nuclei examined. The incidence of RT lesions was similar in all age groups: 13 of 14 cases (92.9%) in the pediatric (< or = 16 years) group, 33 of 37 (89.2%) in the young adult (18-45 years) group, and 19 of 22 (86.4%) in the older adult (> 45 years) group. RT lesions were characterized by loss of one fourth to three fourths of the neurons from the region of the nucleus associated with the frontal cortex and thalamic mediodorsal (MD) and ventrolateral (VL) nuclei. Sparing of RT neurons correlated highly with the presence of extensive frontal cortical lesions, suggesting that an intact corticothalamic projection was necessary for RT degeneration following head injury. A pathologic cascade with a prominent excitotoxic component is proposed. The loss of these inhibitory thalamic reticular neurons and the resultant thalamic and neocortical neuronal dysfunctions may underlie some forms of attentional deficits that persist following head injury.

Auditory neglect after right frontal lobe and right pulvinar thalamic lesions.

Auditory unilateral neglect or extinction to simultaneous stimulation is reported in a right-handed male with a lesion in the right frontal lobe and in the right thalamic pulvinar area. The patient was submitted to stereotactic thalamotomy for a post-traumatic intentional ataxia in the left extremities. He was subjected to repeated tests with dichotic listening to consonant-vowel syllables under three different attentional instructions. He was also tested monaurally with the same stimulus materials as used in the dichotic test. The results showed almost complete extinction of the left ear input during dichotic presentations, despite normal hearing when tested with audiometer screening. The left ear extinction effect was independent of instructions to attend to the left or right ear input. However, during monaural presentation, correct left ear reports increased to about 85%. The results are interpreted as showing an auditory attentional neglect caused by the right frontal and pulvinar lesions.