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PubMedDate not supplied

Connections from the basal ganglia to the thalamus.

Many data suggest that the basal gnaglia exerts an indirect influence onto the motor cortex through the thalamus which receives pallidal and nigral efferences. According to the anatomical data, the internal segment of globus pallidus projects to the VL-VA and CM of thalamus and the substantia nigra sends axons ending in the VL and VA with an intranuclear organization which did not overlap the pallidal terminations. The electrophysiological records in the VL-VA nucleus demonstrates that pallidal stimulation induces an inhibitory response, mainly on thalamic neurons, which does not receive cerebellar input. If spreading of excitation is avoided, nigral stimulation also induces an inhibition at the thalamic level. This inhibitory effect can be recorded on relay cells with cerebellar input and cortical output as well as on nonrelay cells. The electrophysiological results in the case of the striatopallidal and striatonigral projections are also briefly reported.

Animals↗
PubMed1995

The dorsal thalamus of jawed vertebrates: a comparative viewpoint.

In anamniotes, the dorsal thalamus comprises: (1) a caudal division, the collothalamus, which receives its predominant input from the midbrain roof and projects ipsilaterally to the telencephalon, predominantly to the striatum, and (2) a rostral division, the lemnothalamus, which predominantly receives a direct retinal (lemniscal) input and projects bilaterally to the telencephalon, predominantly to the pallium. In amniotes, collothalamic nuclei relay visual, auditory, and somatosensory-multisensory inputs from the midbrain roof to the ipsilateral telencephalon, terminating in both striatum and pallium. For example, the collothalamic visual nuclei consist of the LP-pulvinar complex in mammals and nucleus rotundus in diapsid reptiles, birds, and turtles. Among amniotes, the latter nuclei are homologous to each other as discrete nuclei, as are the collothalamic auditory and collothalamic somatosensory-multisensory nuclei. Lemnothalamic nuclei (and nuclear groups) in amniotes predominantly (and/or plesiomorphically) receive lemniscal inputs; some project to the telencephalon bilaterally, and most, in contrast to collothalamic nuclei, do not project to the striatum. In mammals, the lemnothalamic nuclei include most of those in the anterior, medial, intralaminar, and ventral nuclear groups and the dorsal lateral geniculate nucleus. In diapsid reptiles, they include the dorsomedial and dorsolateral anterior nuclei and the dorsal lateral optic nucleus; comparable nuclei are present in birds and turtles, with birds additionally having a discrete somatosensory lemniscal relay nucleus. These lemnothalamic nuclei in each amniote radiation are homologous as a field to the lemnothalamus (i.e., nucleus anterior) in anamniotes. Both divisions of the dorsal thalamus were elaborated to some degree in the common ancestral amniote stock. A further major elaboration of the lemnothalamus characterized the ancestral stock of mammals and may have been one of the key events in early mammalian evolution. Birds have independently, to a lesser degree, elaborated the lemnothalamus.

Animals↗
PubMed1981

Organization of projections from the gracile, medial cuneate and lateral nuclei in the North American opossum. Horseradish peroxidase study of the cells projecting to the cerebellum, thalamus and spinal cord.

Using the horseradish peroxidase technique on the North American opossum, we were able to locate the neurons within the dorsal column and lateral cuneate nuclei which innervate the cerebellum and thalamus as well as those within the dorsal column nuclei which project spinalward. The medial and lateral cuneate nuclei supply axons to the anterior lobe, the paramedian lobule and the pyramis of the cerebellum and the lateral nucleus provides an additional projection to the uvula. The cerebellar projections from these nuclei arise from neurons located rostral to the obex. The thalamic projections from the gracile and medial cuneate nuclei originate from neurons throughout their rostral to caudal extent, although most of them are located just rostral to the obex. Neurons within the lateral cuneate nucleus which innervate the thalamus are found at intermediate rostrocaudal levels where most of them approximate the medial cuneate nucleus. The medial cuneate also projects to at least lumbar levels of the spinal cord in the opossum and neurons giving rise to such connections are found at the level of the obex and caudal to it. Neurons within the dorsal part of the dorsal column nuclei were labelled only after thalamic injections. Our results in the opossum are compared with those obtained in several placental mammals.

Animals↗
PubMed2004

Anteromedian, central, and posterolateral infarcts of the thalamus: three variant types.

BACKGROUND AND PURPOSE: Thalamic infarcts have traditionally been classified into 4 territories: anterior, paramedian, inferolateral, and posterior. The purpose of this study was to review this classical versus variant distribution in patients with thalamic stroke. METHODS: We reviewed all patients with a first clinical stroke included in the Lausanne Stroke Registry between 1990 and 2002. Among 71 patients with an acute stroke isolated to the thalamus confirmed by MRI, we selected all patients with lesions outside the classical territories and studied their clinical, etiological, and radiological features. RESULTS: A total of 21 patients (30% of all thalamic stroke patients) showed infarction outside the classical territories, allowing us to delineate 3 variant distributions: (1) Anteromedian territory (9 patients [13%]) involving anterior and paramedian territories, with predominantly cognitive impairment, including executive dysfunction, anterograde amnesia, and aphasia in left-sided or bilateral lesions. The most frequent stroke mechanism was cardiac embolism. (2) Central territory (4 patients [6%]), with lesions on the central part of the thalamus, resulting in a variety of neurological and neuropsychological signs, reflecting the involvement of several adjacent structures. Microangiopathy was the most frequent etiology. (3) Posterolateral territory (8 patients [11%]), involving inferolateral and posterior territories, with hemihypesthesia as the most frequent manifestation, followed by hemiataxia, executive dysfunction, and aphasia in left-sided lesions. Artery-to-artery embolism and microangiopathy were the main stroke mechanisms. CONCLUSIONS: We describe 3 variant topographic patterns of thalamic infarction with distinct manifestations and etiologies. We postulate that these infarcts are the result of a variation in thalamic arterial supply or reflect borderzone ischemia.

Adult↗
PubMedDate not supplied

A model of selective experimental ischaemia in the primate thalamus.

A model for studying changes in local CBF and evoked potentials in selective thalamic ischaemia has been developed. The arterial supply to the posterior thalamus (mainly from the posterior choroidal arteries) was occluded in the baboon using a transorbital approach to the region of prepontine and ambient cisterns. Local CBF was measured by the hydrogen clearance method using electrodes introduced into the nucleus ventralis posterior lateralis of thalamus as well as cortex on both sides. The production of focal ischaemia was demonstrated by a significant decrease in thalamic CBF and confirmed by examination of the brain perfused with carbon particles.

Animals↗
PubMed1990

Progressive shrinkage of the thalamus following middle cerebral artery occlusion in rats.

Permanent middle cerebral artery occlusion in rats results in infarction in the ipsilateral cortex and caudate nucleus-putamen. In this ischemia model, severe shrinkage of the ipsilateral half of the thalamus was observed several months after surgery. We examined the serial profile of this phenomenon in 40 rats at intervals from 2 weeks to 6 months after the operation. The area of the ipsilateral half of the thalamus as a percentage of the area of the contralateral half was 87% at 2 weeks, 77% at 1 month, 54% at 3 months, and 54% at 6 months. Such severe morphologic change distant from the original ischemic focus has not been reported in models of experimental focal ischemia. Retrograde degeneration is thought to play an important role in this phenomenon.

Animals↗
PubMed1990

Neural damage in the rat thalamus after cortical infarcts.

Histopathologic changes in the thalamus of 23 rats after somatosensory cortical infarction produced by middle cerebral artery occlusion were examined using the Fink-Heimer silver staining method, immunohistochemistry with antibodies against glial fibrillary acidic protein and laminin, and conventional stains. Middle cerebral artery occlusion produced cortical infarcts in the lateral parietal region, with variable involvement of the frontoparietal parasagittal sensorimotor cortex. Within 3 days after occlusion, massive terminal degeneration but no neuronal changes were apparent in the ipsilateral thalamus. By 1 week after occlusion, abnormal neurons with darkly stained, shrunken nuclei and atrophic perikarya were present in the ipsilateral thalamic nuclei. These neurons were densely argyrophilic in Fink-Heimer sections. Rats with small lateral parietal cortical lesions had degenerating neurons limited to the medial ventroposteromedial nucleus. Large lesions involving the parasagittal sensorimotor cortex resulted in widespread neuronal damage in the ventroposteromedial, ventroposterolateral, intralaminar, and posterior nuclear regions but nowhere else. Immunoreactivity to laminin antibody decreased, and astrocytic proliferation was abundant in affected thalamic areas. These findings are consistent with retrograde neuronal degeneration due to thalamocortical fiber damage in ischemic cortical regions. Such lesions remote from the infarct may influence functional recovery in patients with stroke.

Animals↗
PubMed1996

PET and MRI of the thalamus in never-medicated patients with schizophrenia.

OBJECTIVE: This study reports the first paired measurements of glucose metabolism and size of thalamic regions in never-medicated schizophrenic patients using coregistered magnetic resonance imaging (MRI) templates. METHOD: Positron emission tomography with [18F]fluorodeoxyglucose and matching MRI scans were obtained in 20 never-medicated patients with schizophrenia and 15 normal volunteers. Methods for thalamic edge finding, statistical testing of shape differences with chi-square maps, and MRI localization of major thalamic subregions were developed. RESULTS: Patients with schizophrenia showed a diminished metabolic rate in the right thalamus, with a loss of the normal pattern of right greater than left asymmetry. Division into anterior/posterior segments revealed that the left anterior and right posterior showed the decrease. Differences were greater for metabolism in the weighted thalamic area (ratexarea) than for rate per unit area, a finding consistent with reported greater decreases in total neuron number than of neuron density in the thalami of schizophrenic patients. The area of the thalamus was smaller in the patients than in the volunteers, and this difference was greatest in the left anterior region. CONCLUSIONS: The reduced thalamic activity observed in this study lends further support to the concept of deficits in sensory filtering in schizophrenia.

Adult↗
PubMed1999

Three-dimensional analysis with MRI and PET of the size, shape, and function of the thalamus in the schizophrenia spectrum.

OBJECTIVE: In an exploration of the schizophrenia spectrum, the authors compared thalamic size, shape, and metabolic activity in unmedicated patients with schizophrenia and schizotypal personality disorder to findings in age- and sex-matched healthy control subjects. METHOD: Coregistered magnetic resonance imaging (MRI) and positron emission tomography scans were obtained in 27 schizophrenic patients, 13 patients with schizotypal personality disorder, and 32 control subjects who performed a serial verbal learning test during tracer uptake. After thalamus edges were outlined on 1.2-mm MRI scans, a radial warping program yielded significance probability mapping in three dimensions. RESULTS: Significance probability mapping (with resampling) identified an area in the region of the mediodorsal nucleus bilaterally with significantly lower relative metabolism in the schizophrenia group than in either the control or schizotypal personality disorder groups, which did not differ from each other. The three groups did not differ significantly in total thalamic volume in square millimeters or thalamic volume relative to brain volume. Shape analyses revealed that schizophrenic patients had significantly fewer pixels in the left anterior region, whereas patients with schizotypal personality disorder had significantly fewer pixels in the region of the right mediodorsal nucleus than did control subjects. CONCLUSIONS: Schizophrenic patients showed significant metabolism and shape differences from control subjects in selective subregions of the thalamus, whereas patients with schizotypal personality disorder showed only a difference in shape. Because the mediodorsal and anterior nuclei have different connections with limbic and prefrontal structures, the anterior thalamic shrinkage and mediodorsal metabolic and shape changes might relate to the different clinical pictures in schizotypal personality disorder and schizophrenia.

Adult↗
PubMed2001

Expression of excitatory amino acid transporter transcripts in the thalamus of subjects with schizophrenia.

OBJECTIVE: Recent investigations of schizophrenia have targeted glutamatergic neurotransmission, since phencyclidine, an N-methyl-D-aspartate (NMDA) receptor antagonist, can induce schizophreniform psychosis. The authors previously reported alterations in thalamic NMDA receptor subunit expression in schizophrenia, consistent with the hypothesis that thalamic glutamatergic hypofunction may contribute to the pathophysiology of this illness. In this study they generalized this hypothesis to include other molecules of the glutamate synapse, specifically excitatory amino acid transporters (EAATs), whose normal expression and regulation in the thalamus may also be disrupted in subjects with schizophrenia. METHOD: In situ hybridization with riboprobes specific for the human excitatory amino acid transporter transcripts EAAT1, EAAT2, and EAAT3 was performed in discrete thalamic nuclei in persons with schizophrenia and comparison subjects. RESULTS: Higher expressions of transcripts encoding EAAT1 and EAAT2, but not EAAT3, were detected in the thalamus of subjects with schizophrenia. CONCLUSIONS: These findings support the hypothesis of glutamatergic dysfunction in schizophrenia and suggest that molecules other than glutamate receptors are abnormally expressed in glutamatergic synapses in this illness.

ATP-Binding Cassette Transporters↗
PubMed2003

Glutamate and glutamine in the anterior cingulate and thalamus of medicated patients with chronic schizophrenia and healthy comparison subjects measured with 4.0-T proton MRS.

OBJECTIVE: This in vivo (1)H magnetic resonance spectroscopy study examined levels of glutamate, glutamine, and N-acetylaspartate in medicated patients with chronic schizophrenia. METHOD: Localized in vivo (1)H spectra were acquired at 4.0 T from the left anterior cingulate and thalamus of 21 patients with schizophrenia and 21 comparable healthy volunteers. RESULTS: Significantly lower levels of glutamine and glutamate were found in the left anterior cingulate cortex of patients with schizophrenia than in the healthy volunteers. For the schizophrenia patients, the glutamine level in the left thalamus was found to be higher than normal, and there was a significant negative correlation between N-acetylaspartate level and duration of positive symptoms. CONCLUSIONS: Since previous studies have found higher than normal levels of glutamine in the left anterior cingulate of never-treated patients, decreased levels of these metabolites in chronic patients could be related to neurodegeneration or the effects of chronic medication.

Adult↗
PubMed2003

Altered transcript expression of NMDA receptor-associated postsynaptic proteins in the thalamus of subjects with schizophrenia.

OBJECTIVE: NMDA receptor dysfunction has been implicated in the pathophysiology of schizophrenia. The NMDA receptor is a multimeric ligand-gated ion channel, and the obligate NR(1) subunit is expressed as one of eight isoforms due to the alternative splicing of exons 5, 21, and 22. Alternative splicing of NR(1) subunits modulates receptor function by influencing the association of NR(1) with other NMDA receptor subunits and myriad intracellular molecules, such as the postsynaptic density family of proteins that target NMDA receptors to the synaptic membrane and couple it to numerous signal transduction enzymes. Recently, the authors reported that the NMDA receptor subunits NR(1) and NR(2C) are abnormally expressed in the thalamus in schizophrenia. They hypothesized that this reduction is associated with specific NR(1) isoforms and that NMDA receptor-related postsynaptic density proteins are abnormally expressed. METHOD: Using in situ hybridization, the authors examined expression of the transcripts encoding NR(1) isoforms containing exons 5, 21, or 22, and the NMDA receptor-related postsynaptic density proteins NF-L, PSD93, PSD95, and SAP102. RESULTS: Reduced NR(1) subunit transcript expression was restricted to exon 22-containing isoforms. Increased expression of the NMDA receptor-associated postsynaptic density proteins NF-L, PSD95, and SAP102 was also detected in the thalamus of subjects with schizophrenia. CONCLUSIONS: These data support the hypothesis of glutamatergic abnormalities in schizophrenia and suggest that glutamatergic dysfunction may occur not only at the level of receptor expression but also within intracellular pathways associated with glutamate receptor-associated signal transduction.

Aged↗
PubMed2004

Low dopamine d(2) receptor binding in subregions of the thalamus in schizophrenia.

OBJECTIVE: Several structural and functional brain imaging studies have pointed to a disturbance of thalamic subnuclei in patients with schizophrenia. The dopamine hypothesis of schizophrenia has, however, not been thoroughly examined in terms of this complex structure, which has connections with most brain regions of central interest in schizophrenia research. The aim of the present study was to examine dopamine D(2) receptor binding in subregions of the thalamus in patients with schizophrenia. METHOD: The authors used positron emission tomography and the radioligand [(11)C]FLB457 to examine dopamine D(2) receptor binding in thalamic subregions of 10 drug-naive patients with schizophrenia. Binding potential was calculated by the reference tissue method and used as an index for dopamine D(2) receptor binding. Comparisons were made with 19 healthy subjects. Subregions of interest were defined on individual magnetic resonance images using a percentage-based operational approach. Clinical symptoms were rated by using the Brief Psychiatric Rating Scale (BPRS). RESULTS: The [(11)C]FLB457 binding potential was lower in the central medial and posterior subregions of the thalamus in patients with schizophrenia. At a functional level, there was a significant negative correlation between binding potential and BPRS positive symptom scores. CONCLUSIONS: The subregions with low D(2) receptor binding comprise primarily the dorsomedial nucleus and pulvinar, two important components in circuitries previously suggested in the pathophysiology of schizophrenia. Aberrant dopaminergic neurotransmission in thalamic subregions might be a mechanism underlying positive symptoms in schizophrenia.

Adult↗
PubMed1997

The role of the thalamus in schizophrenia.

BACKGROUND: Explaining the diversity of symptoms that occur in schizophrenia is a major conceptual challenge. Perhaps the most powerful strategy is to identify a fundamental cognitive process and/or a fundamental neural circuit. METHODS: Convergent data from our research group in Iowa and from investigators in other centres are summarized. RESULTS: The thalamus plays a key role in information processing. A defect in circuitry connecting the thalamus, frontal cortex, and cerebellum could explain a wide range of symptoms. Neuropathology and imaging studies suggest that patients with schizophrenia may have abnormalities in this circuitry. CONCLUSION: The fundamental deficit in schizophrenia may be conceptualized as a "cognitive dysmetria" characterized by impairments in coordinating the perception, encoding, retrieval, and prioritization of experience and information.

Brain Mapping↗
PubMed2001

Prognostic significance of hyperechogenic lesions in the basal ganglia and thalamus in neonates.

Neonatal cranial ultrasonography at times reveals hyperechogenic lesions in the basal ganglia and thalamus. These lesions have been attributed to a wide variety of pathologic states, among them toxoplasmosis, rubella, cytomegalovirus, and herpes simplex (TORCH) infections, chromosomal abnormalities, and asphyxia. The clinical significance in terms of the neurodevelopmental outcome of this radiologic abnormality is unknown. We performed a developmental evaluation on 16 children aged 2 to 6 years in whom neonatal cranial ultrasonography had demonstrated hyperechogenic lesions in the basal ganglia or thalamus and had no other neurodevelopmental risk factors. There was no significant difference between the average Developmental Quotient of the target population and the normal population in regard to developmental status. We conclude that in our population, an isolated finding of hyperechogenic lesions in the basal ganglia is probably not a predictor of poor neurodevelopmental outcome.

Basal Ganglia↗
PubMed2006

Changes in motor cortex excitability with stimulation of anterior thalamus in epilepsy.

BACKGROUND: Deep brain stimulation (DBS) is an effective treatment for movement disorders and pain. Recently, bilateral DBS of the anterior nucleus of thalamus (AN) was performed for the treatment of intractable epilepsy. This surgery reduced seizure frequency in an initial group of patients. However, its physiologic effects on the cortex and mechanisms of action remain poorly understood. Different classes of antiepileptic drugs (AEDs) have distinct effects on the excitatory and inhibitory circuits in the motor cortex, which can be studied noninvasively by transcranial magnetic stimulation (TMS). OBJECTIVE: To examine the effects of bilateral AN DBS on motor cortex excitability in epilepsy and compare these to the known effects of AEDs. METHODS: Cortical excitability was assessed in five medicated epilepsy patients with bilateral stimulators implanted in the anterior thalamus and nine healthy controls. Single and paired TMS were used to examine cortical inhibitory and facilitatory circuits. Electromyography was recorded from the dominant hand, and TMS was applied over the contralateral motor cortex. Patients were studied during DBS turned off (OFF condition), DBS with cycling stimulation mode (1 minute on, 5 minutes off; CYCLE), and DBS with continuous stimulation (CONTINUOUS) in random order on 3 consecutive days. RESULTS: Motor thresholds were increased in the patients regardless of DBS condition. Active short-interval intracortical inhibition (SICI) was significantly reduced in the OFF and CYCLE conditions but returned toward normal levels in the CONTINUOUS condition. Rest SICI, long interval intracortical inhibition, and silent period duration were unchanged. CONCLUSIONS: Increased short-interval intracortical inhibition with continuous deep brain stimulation (DBS) suggests that thalamic DBS might drive cortical inhibitory circuits, similar to antiepileptic drugs that enhance gamma-aminobutyric acid inhibition.

Adult↗
PubMed1997

Late blink reflex changes in lesions of thalamus and internal capsule.

A 60-year-old man suddenly suffered from left hemiplegia with sensory loss on the left side of his face, trunk, and extremities. Brain CT disclosed hemorrhage in the right thalamus and internal capsule. Blink reflex with electrical stimulation on the left supraorbital nerve showed normal early response (R1) on the left side but absent late response (R2) on both sides, while stimulation of the right supraorbital nerve showed normal R1 on the right side and normal R2 on both sides. This observation suggests that the impulses of R2 from stimulation of the supraorbital nerve on the affected side may be blocked by contralateral lesions of the thalamus and internal capsule.

Blinking↗
PubMed1987

Stereotactic resection of juvenile pilocytic astrocytomas of the thalamus and basal ganglia.

Six patients with juvenile pilocytic astrocytomas of the thalamus or basal ganglia underwent seven computer-assisted stereotactic laser craniotomies with complete or nearly complete removal of the tumor in all cases. The tumor was located in the right basal ganglia in one patient, the left basal ganglia in one patient, and the left thalamus in four patients. Postoperative assessment of the completeness of tumor removal was confirmed by contrast-enhanced computed tomographic scanning within the first 2 weeks after operation. None of the patients was neurologically worse after the procedure, and five were improved. The duration of follow-up ranged from 6 months to 3.5 years. In this group of patients, the computer-assisted, stereotactically guided resection of these deeply located, benign tumors was accomplished with no morbidity or mortality.

Adolescent↗