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PubMed1999

Change in basal ganglia volume over 2 years in patients with schizophrenia: typical versus atypical neuroleptics.

OBJECTIVE: For many years, it has been assumed that medications affect brain chemistry and physiology but not structure. Recent reports suggest that neuroleptic medication changes basal ganglia volume. To explore this possibility, the authors assessed for basal ganglia volume change in individuals who had their basal ganglia structures delineated and measured on magnetic resonance scans at the beginning and end of a 2-year period and who received neuroleptic medication during this time. METHOD: The basal ganglia volumes of 23 male patients with schizophrenia spectrum disorders were measured from manual traces delineating the caudate and lenticular nucleus on magnetic resonance images at admission and 2 years later. Patients' neuroleptic exposure was calculated over the 2 years by using a dose-year formula. RESULTS: During the 2-year period, mean basal ganglia volume of patients receiving predominantly typical neuroleptics increased, while the opposite was observed for patients receiving mostly atypical neuroleptics. Correlation analysis for the entire group showed a positive relationship between the 2-year exposure to typical neuroleptic medication and change in basal ganglia volume and the reverse for exposure to atypical neuroleptics. CONCLUSIONS: In this group, basal ganglia volume increased following exposure to typical neuroleptics and decreased following exposure to atypical neuroleptics.

Adult↗

PubMed2005

Apathy and the functional anatomy of the prefrontal cortex-basal ganglia circuits.

The clinical signs grouped under the concept of apathy are a common feature of prefrontal and basal ganglia lesions or dysfunctions and can therefore help to improve our understanding of the functional anatomy of the prefrontal-basal ganglia system. Apathy is here defined as a quantitative reduction of voluntary, goal-directed behaviors. The underlying mechanisms responsible for apathy can be divided into three subtypes of disrupted processing: 'emotional-affective', 'cognitive' and 'auto-activation'. Apathy due to the disruption of 'emotional-affective' processing refers to the inability to establish the necessary linkage between emotional-affective signals and the ongoing or forthcoming behavior. It may be related to lesions of the orbital-medial prefrontal cortex or to the related subregions (limbic territory) within the basal ganglia (e.g. ventral striatum, ventral pallidum). Apathy due to the disruption of 'cognitive' processing refers to difficulties in elaborating the plan of actions necessary for the ongoing or forthcoming behavior. It may be related to lesions of the dorsolateral prefrontal cortex and the related subregions (associative territory) within the basal ganglia (e.g. dorsal caudate nucleus). The disruption of 'auto-activation' processing refers to the inability to self-activate thoughts or self-initiate actions contrasting with a relatively spared ability to generate externally driven behavior. It is responsible for the most severe form of apathy and in most cases the lesions affect bilaterally the associative and limbic territories of the internal portion of the globus pallidus. It characterizes the syndrome of 'auto-activation deficit' (also known as 'psychic akinesia' or 'athymormia'). This syndrome implies that direct lesions of the basal ganglia output result in a loss of amplification of the relevant signal, consequently leading to a diminished extraction of this signal within the frontal cortex. Likewise, apathy occurring in Parkinson's disease could be interpreted as secondary to the loss of spatial and temporal focalization of the signals transferred to the frontal cortex. In both situations (direct basal ganglia lesions and nigro-striatal dopaminergic loss), the capacity of the frontal cortex to select, initiate, maintain and shift programs of actions is impaired.

Animals↗

PubMed2002

The control of seizures by the basal ganglia? A review of experimental data.

Over the past few years, the role of the basal ganglia in epilepsy has been widely debated, the debate being mainly based on experimental data obtained from several animal models. In the present review, the possibility that basal ganglia circuits can generate some forms of seizure or participate to their initiation will first be addressed. In the second part of this chapter, recent data suggesting the involvement of the basal ganglia in the control of seizures will be discussed. Although it is clear that basal ganglia circuits cannot generate seizures and are unlikely to be involved in their initiation, numerous experimental data have revealed that seizures modify the activity of this system. More recently, the collection of pharmacological and electrophysiological data in animal models of epilepsy has led to the emergence of the basal ganglia as a possible control circuit for the seizures. These experimental data have already led to initial clinical trials in epileptic patients. The preliminary clinical data encourage the further development of experimental research in chronic models of epilepsy to better determine the exact output circuits involved in seizure interruption, the mechanisms participating in seizure control and whether the same circuits are involved in the control of different types of seizures. These studies may allow the identification of crucial structures and the types of epilepsy likely to benefit from this new therapeutic approach.

Animals↗

PubMed1995

Role of basal ganglia in behavioral learning.

Recent studies on single neuron activity revealed that activities of many basal ganglia neurons are dependent upon the behavioral context. This may give us a reason why observed movement-related activity in the basal ganglia occurred late in relation to prime mover muscle activity. Early onset activity of primate putamen neurons was reported in a study in which animals were required to make a performance of sequential limb movements. This suggests the participation of basal ganglia in the initiation of movement in a behavioral context-dependent manner. The context-dependent activity in the basal ganglia has been shown to be acquired through learning. For instance, midbrain dopamine neurons respond to external sensory stimuli or reward only during early stages of learning motor tasks. Striate neurons acquire task-related activity through learning and the acquired activity almost disappears after selective lesions of nigrostriatal dopamine. In this article, a hypothetical scheme of basal ganglia functioning in behavioral learning is presented. Limbic input conveys information related to 'reinforcement' or 'incentive' either directly to the striatum or indirectly through nigrostriatal dopamine system, and it contributes to the acquisition and expression of learned activity in the striatum. The expression of learned striatal activity would contribute to the initiation of learned motor behavior.

Animals↗

PubMed1991

Differential gene expression for glutamic acid decarboxylase and type II calcium-calmodulin-dependent protein kinase in basal ganglia, thalamus, and hypothalamus of the monkey.

In situ hybridization histochemistry, using cRNA probes, revealed a complementarity in the distributions of cells in the basal ganglia, basal nucleus of Meynert, thalamus, hypothalamus, and rostral part of the midbrain that showed gene expression for glutamic acid decarboxylase (GAD) or the alpha-subunit of type II calcium-calmodulin-dependent protein kinase (CAM II kinase-alpha). Cells in certain nuclei such as the thalamic reticular nucleus, globus pallidus, and pars reticulata of the substantia nigra show GAD gene expression only; others in nuclei such as the basal nucleus of Meynert, medial mamillary nuclei, and ventromedial hypothalamic nuclei show CAM II kinase-alpha gene expression only. A few nuclei, for example, the pars compacta of the substantia nigra and the greater part of the subthalamic nucleus, display gene expression for neither GAD nor CAM II kinase-alpha. In other nuclei, notably those of the dorsal thalamus, and possibly in the striatum, GAD- and CAM II kinase-expressing cells appear to form two separate populations that, in most thalamic nuclei, together account for the total cell population. In situ hybridization reveals large amounts of CAM II kinase-alpha mRNA in the neuropil of most nuclei containing CAM II kinase-alpha-positive cells, suggesting its association with dendritic polyribosomes. The message may thus be translated at those sites, close to the synapses with which the protein is associated. The in situ hybridization results, coupled with those from immunocytochemical staining for CAM II kinase-alpha protein, indicate that CAM II kinase-alpha is commonly found in certain non-GABAergic afferent fiber systems but is not necessarily present in the postsynaptic cells on which they terminate. It appears to be absent from most GABAergic fiber systems but can be present in the cells on which they terminate. This suggests that the kinase may be differentially engaged in pre- and postsynaptic functions at certain synapses.

Animals↗

PubMed2006

Depth perception in cerebellar and basal ganglia disease.

There is increasing evidence that the cerebellum and the basal ganglia serve not only a role in motor control but also in visual perception. Patients with Parkinson's disease (PD) as well as patients with cerebellar lesions exhibit impairments of vision that are not fully explained by ocular motor deficits. It is less clear to which extent these visual deficits contribute to an impaired control of visually guided movements. This study examined whether a dysfunction of the cerebellum or the basal ganglia induces impairments in depth perception, which affect action. We employed an illusionary display, the Ames trapezoidal window, to determine the ability of PD patients (n=10) and patients with spinocerebellar ataxia (SCA) (n=6) to process depth cues when estimating object slant. Participants either pointed to the edges of the window (motor judgement) or verbally indicated the perceived orientation of the display (verbal judgement). To control for ocular and limb motor deficits, participants judged the slant of a non-illusionary display in a second task. Slant estimation of the non-illusionary window was not impaired in either patient group when compared to control subjects (all P>0.2). In contrast, SCA as well as PD patients exhibited significantly greater slant estimation errors than controls when pointing to the illusionary window (P=0.005). In addition, both patient groups made larger errors than controls in their verbal judgements during binocular viewing of the illusion (P=0.005), but not during monocular viewing (P>0.2). In sum, the present findings point towards a role for both the basal ganglia and cerebellum for the processing of visual information about depth. Since the deficits were seen both in the context of action and perception and were only partially reconciled by the availability of binocular depth cues, we conclude that basal ganglia as well as cerebellar disease may affect the visual perception of depth.

Adult↗

PubMed1980

Calcification of the basal ganglia following carbon monoxide poisoning.

Minor calcification of the basal ganglia was demonstrated by computed tomography in a woman, aged 66, who had survived carbon monoxide poisoning 48 years earlier. Extensive neuropathological investigations have demonstrated calcified lesions of the basal ganglia in a number of conditions, but their frequency and topographic distribution in vivo remain to be elucidated, by means of CT.

Adult↗

PubMed2003

Basal Ganglia volumes in patients with Gilles de la Tourette syndrome.

BACKGROUND: Despite strong circumstantial evidence that the pathophysiology of Gilles de la Tourette syndrome (TS) involves structural and functional disturbances of the basal ganglia, inconsistent findings from relatively small in vivo TS imaging studies have supported contradictory conclusions concerning the role of abnormal anatomical characteristics of the basal ganglia in the pathophysiology of TS. METHODS: Basal ganglia volumes were measured on high-resolution magnetic resonance images acquired for 154 children and adults with TS and 130 healthy control subjects. Repeated-measures analyses tested hypotheses concerning regional specificity, age effects, and abnormal asymmetries in the basal ganglia of subjects with TS. Subjects with prior neuroleptic exposure had larger basal ganglia volumes and were excluded from further statistical analyses. RESULTS: Caudate nucleus volumes were significantly (P =.008) smaller in children and adults with TS. Lenticular nucleus volumes also were smaller in adults with TS and in children with TS who were diagnosed as having comorbid obsessive-compulsive disorder. Regional anatomical asymmetries did not differ across groups. Regional volumes did not correlate significantly with the severity of tic, obsessive-compulsive disorder, or attention-deficit/hyperactivity disorder symptoms. CONCLUSIONS: Reduced caudate nucleus volumes may be a good candidate marker for a trait abnormality in the structure of the basal ganglia in persons with TS. Smaller lenticular nucleus volumes may be an additional marker for the presence of comorbid obsessive-compulsive disorder and for the persistence of tic symptoms into adulthood. Brain regions other than the basal ganglia may have greater clinical relevance in determining the severity of tic symptoms.

Adolescent↗

PubMed2006

[Basal ganglia calcification on computed tomography: clinical characteristics in 25 patients].

Twenty-five patients presenting basal ganglia calcification were assessed. This finding comprised 0.68% of all skull CT scan carried out during the period. Two patients were neurologically asymptomatic and 23 presented a variety neurological disorders--headache (7 patients), stroke (5 patients), extrapyramidal syndromes (2 patients), tumor (2 patients), epilepsy (1 patient), mental retardation (1 patient), dementia (1 patient), cranial trauma (1 patient), other neurological conditions (3 patients)--or were asymptomatic from the neurological point of view (2 patients). Findings in the CT scan other than the basal ganglia calcification were observed in 15 (60%) patients. There was a clinical-CT scan correlation in these cases but not in those in which the basal ganglia calcification was an isolated finding. This study highlights the fact that basal ganglia calcification is often a nonspecific finding on CT scan and that it may not be possible to establish a clinical-pathological correlation between them.

Adolescent↗

PubMed2002

Localization and physiological roles of metabotropic glutamate receptors in the direct and indirect pathways of the basal ganglia.

Our current understanding of the circuitry of the basal ganglia, and the pathophysiology of Parkinson's disease has led to major breakthroughs in the treatment of this debilitating movement disorder. Unfortunately, there are significant problems with the currently available pharmacological therapies that focus on dopamine replacement or dopaminergic agonists. Because of this, much effort has been focused on developing novel targets for the treatment of Parkinson's disease. The metabotropic glutamate receptors are a family of G-protein coupled receptors activated by glutamate. These receptors are differentially distributed throughout the basal ganglia in a manner suggesting that they may provide novel targets for the treatment of movement disorders. In this review we summarize anatomical and physiological data from our work and the work of other laboratories describing the distribution and physiological roles of metabotropic glutamate receptors in the basal ganglia with emphasis on possible therapeutic targets.

Afferent Pathways↗

PubMed2001

Interactions between frontal cortex and basal ganglia in working memory: a computational model.

The frontal cortex and the basal ganglia interact via a relatively well understood and elaborate system of interconnections. In the context of motor function, these interconnections can be understood as disinhibiting, or "releasing the brakes," on frontal motor action plans: The basal ganglia detect appropriate contexts for performing motor actions and enable the frontal cortex to execute such actions at the appropriate time. We build on this idea in the domain of working memory through the use of computational neural network models of this circuit. In our model, the frontal cortex exhibits robust active maintenance, whereas the basal ganglia contribute a selective, dynamic gating function that enables frontal memory representations to be rapidly updated in a task-relevant manner. We apply the model to a novel version of the continuous performance task that requires subroutine-like selective working memory updating and compare and contrast our model with other existing models and theories of frontal-cortex-basal-ganglia interactions.

Basal Ganglia↗

PubMed2006

Phenotype of striatofugal medium spiny neurons in parkinsonian and dyskinetic nonhuman primates: a call for a reappraisal of the functional organization of the basal ganglia.

The classic view of anatomofunctional organization of the basal ganglia is that striatopallidal neurons of the "indirect" pathway express D2 dopamine receptors and corelease enkephalin with GABA, whereas striatopallidal neurons of the "direct" pathway bear D1 dopamine receptors and corelease dynorphin and substance P with GABA. Although many studies have investigated the pathophysiology of the basal ganglia after dopamine denervation and subsequent chronic levodopa (L-dopa) treatment, none has ever considered the possibility of plastic changes leading to profound reorganization and/or biochemical phenotype modifications of medium spiny neurons. Therefore, we studied the phenotype of striatal neurons in four groups of nonhuman primates, including the following: normal, parkinsonian, parkinsonian chronically treated with L-dopa without exhibiting dyskinesia, and parkinsonian chronically treated with L-dopa exhibiting overt dyskinesia. To identify striatal cells projecting to external (indirect) or internal (direct) segments of the globus pallidus, the retrograde tracer cholera toxin subunit B (CTb) was injected stereotaxically into the terminal areas. Using immunohistochemistry techniques, brain sections were double labeled for CTb and dopamine receptors, opioid peptides, or the substance P receptor (NK1). We also used HPLC-RIA to assess opioid levels throughout structures of the basal ganglia. Our results suggest that medium spiny neurons retain their phenotype because no variations were observed in any experimental condition. Therefore, it appears unlikely that dyskinesia is related to a phenotype modification of the striatal neurons. However, this study supports the concept of axonal collateralization of striatofugal cells that project to both globus pallidus pars externa and globus pallidus pars interna. Striatofugal pathways are not as segregated in the primate as previously considered.

Animals↗

PubMed1999

Localization of metabotropic glutamate receptor 7 mRNA and mGluR7a protein in the rat basal ganglia.

Metabotropic glutamate receptors (mGluRs) coupled to G-proteins have important roles in the regulation of basal ganglia function. We have examined the localization of the mGluR7 mRNA and mGluR7a protein in the basal ganglia of the rat. Strong mGluR7 hybridization signals are found in cerebral cortex and striatum, but much less intense signals are present in other components of the basal ganglia. Abundant mGluR7a immunoreactivity was found in striatum, globus pallidus (GP), and substantia nigra pars reticulata (SNr). Examination using confocal microscopy together with dendritic and presynaptic markers as well as studies in lesion models provided evidence for the presence of mGluR7a on presynaptic terminals in all three structures. Electron microscopic studies confirmed the presence of mGluR7a in axon terminals in both the striatum and the GP and also revealed the presence of mGluR7a at postsynaptic sites in both of these regions. Our data demonstrate that mGluR7a is located not only on presynaptic glutamatergic terminals of the corticostriatal pathway, where it may serve as an autoreceptor, but also on terminals of striatopallidal and striatonigral projections, where it may modulate the release of gamma-aminobutyric acid (GABA). The presence of mGluR7 at these multiple sites in the basal ganglia suggests that this receptor has a particularly crucial role in modulating neurotransmitter release in major basal ganglia pathways.

Animals↗

PubMed2000

MR volumetric analysis of the human basal ganglia: normative data.

RATIONALE AND OBJECTIVES: The authors undertook this study to identify a precise, semiautomated, reproducible magnetic resonance (MR) imaging technique for measuring the basal ganglia, to establish normative volumetric data, and to verify the presence of previously reported asymmetries. MATERIALS AND METHODS: Twenty-eight healthy adults underwent cranial MR examination. The volumes of the various components of the basal ganglia were measured by means of a combination of thresholding and manual tracing techniques performed with specialized software. The validity of these measurements was assessed by fashioning, imaging, and measuring a practical basal ganglia phantom. Measurement accuracy was also established by means of inter- and intrarater reliability indexes. Normalized volumes were statistically analyzed with analysis of variance and paired t tests. RESULTS: The absolute values of the various components of the basal ganglia varied widely even though the volumes were normalized to differences in intracranial volume. The right caudate nucleus volume was significantly (P < .000001) larger than the left in both men and women and in both right-handed and non-right-handed subjects. This asymmetry led to an increase in the overall volume of the basal ganglia on the right. CONCLUSION: The authors have defined a precise, reproducible technique for measuring various components of the basal ganglia and have established normative data. The basal ganglia, similar to other brain structures, exhibit hemispheric lateralization.

Adult↗

PubMed1994

[Functional significance of calcinosis of the basal ganglia via positron emission tomography].

Four patients with symmetrical basal ganglia calcification of different etiologies detected by cranial computed tomography (CT) were clinically evaluated and underwent positron emission tomography (PET) with (18F)-2-fluoro-2-deoxy-D-glucose (FDG). All patients were subjected to extensive laboratory investigation and neuropsychological testing. In two patients we found typical laboratory signs of hypoparathyroidism, the other two patients had no endocrinological alterations. Changes of glucose metabolism were mainly detected only in calcified tissues. Particularly in two patients with test psychologically confirmed psychomotoric retardation we did not find any cortical dysfunction. In conclusion, basal ganglia calcification in contrast to primary degenerative diseases has no influence on metabolic function in tissue that is not calcified.

Adult↗

PubMed1997

Sensory and cognitive functions of the basal ganglia.

Recent studies have found that the basal ganglia are involved in diverse behavioral activities and suggest that they have executive functions. Highlights from the past year include anatomical and clinical studies that have used sophisticated, novel methods to confirm a role for the basal ganglia in somatosensory discrimination, visual perception, spatial working memory and habit learning.

Animals↗

PubMed1987

Comparative distribution of dopamine D-1 and D-2 receptors in the basal ganglia of turtles, pigeons, rats, cats, and monkeys.

The distribution and density of dopamine D-1 and D-2 receptors were studied in the basal ganglia of adult turtles, pigeons, rats, cats, and monkeys. Dopamine receptors were measured in vitro by quantitative autoradiography in alternate sections processed for D-1 and D-2 receptor subtypes and compared to adjacent sections stained for acetylcholinesterase (AChE) activity. [3H]-SCH 23390 and [3H]-spiroperidol were used to label the D-1 and D-2 dopamine receptor subtypes, respectively. The anatomic distribution of both D-1 and D-2 receptors in the basal ganglia was remarkably similar across all species examined. Whereas the absolute number of D-1 and D-2 receptors in the basal ganglia varied between species, the percentage of D-1 and D-2 receptors in a region was quite similar among species. The pattern of binding to the D-1 and D-2 receptor varied among the different species. The adult turtles, pigeons, and rats demonstrated nonpatchy D-1 and D-2 receptor binding in the striatum and pallidum. The adult cat and monkey caudate nucleus and putamen demonstrated mildly heterogeneous receptor binding in a pattern that differed from that seen with AChE staining, but did occasionally demonstrate similar patterns of the D-1 and D-2 receptor subtypes. The immature cat striatum was characterized by heterogeneous D-1 receptor binding that corresponded to heterogeneous AChE rich patches, whereas D-2 receptor binding was homogeneous. Heterogeneous binding was seen in other basal ganglia structures including the nucleus accumbens, olfactory tubercle, and substantia nigra pars compacta and reticulata. Complementary D-1 and D-2 receptor binding patterns were seen in the pallidum and substantia nigra of the mammals. The results of this study indicate that both D-1 and D-2 dopamine receptors are present in the basal ganglia of five different vertebrates. A common feature of dopamine receptors in the basal ganglia is their heterogeneity in distribution and density. The heterogeneity of dopamine receptors has similarities to and differences from the distribution of presynaptic dopamine and other neurotransmitter markers of the basal ganglia.

Aging↗

PubMed2000

The motor circuit of the human basal ganglia reconsidered.

The standard model of human basal ganglia organization was introduced in the 1980s on the basis of animal experiments and clinical experience of various human motor disorders. This paper reviews evidence from various sources which suggests that this standard model only incompletely accounts for aspects of basal ganglia function, and thus requires modification.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗