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PubMed2003

Dopamine transporter density of basal ganglia assessed with [123I]IPT SPET in obsessive-compulsive disorder.

It has been suggested that dopamine, as well as serotonin, is associated with the pathophysiology of obsessive-compulsive disorder (OCD). Thus, many studies have been performed on brain regions associated with dopamine in patients with OCD. In the present study, we investigated the DAT density of the basal ganglia using iodine-123 labelled N-(3-iodopropen-2-yl)-2beta-carbomethoxy-3beta-(4-chlorophenyl) tropane ([123I]IPT) single-photon emission tomography (SPET) and evaluated the activity of the presynaptic dopamine function in patients with OCD. Fifteen patients with OCD and 19 normal control adults were included in the study. We performed brain SPET 2 h after the intravenous administration of [123I]IPT and carried out both quantitative and qualitative analyses using the obtained SPET data, which were reconstructed for the assessment of the specific/non-specific dopamine transporter (DAT) binding ratio in the basal ganglia. We then investigated the correlation between the severity scores of OCD symptoms assessed with the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) and the specific/non-specific DAT binding ratio of the basal ganglia. Compared with normal control adults, patients with OCD showed a significantly increased specific/non-specific DAT binding ratio in the right basal ganglia and a tendency towards an increased specific/non-specific DAT binding ratio in the left basal ganglia. No significant correlation was found between the total scores on the Y-BOCS and the specific/non-specific DAT binding ratio of the basal ganglia. These findings suggest that the dopaminergic neurotransmitter system of the basal ganglia in patients with OCD could be involved in the pathophysiology of OCD.

Adolescent↗
PubMed2004

Redefining functional models of basal ganglia organization: role for the posteroventral pallidum in linguistic processing?

Traditionally the basal ganglia have been implicated in motor behavior, as they are involved in both the execution of automatic actions and the modification of ongoing actions in novel contexts. Corresponding to cognition, the role of the basal ganglia has not been defined as explicitly. Relative to linguistic processes, contemporary theories of subcortical participation in language have endorsed a role for the globus pallidus internus (GPi) in the control of lexical-semantic operations. However, attempts to empirically validate these postulates have been largely limited to neuropsychological investigations of verbal fluency abilities subsequent to pallidotomy. We evaluated the impact of bilateral posteroventral pallidotomy (BPVP) on language function across a range of general and high-level linguistic abilities, and validated/extended working theories of pallidal participation in language. Comprehensive linguistic profiles were compiled up to 1 month before and 3 months after BPVP in 6 subjects with Parkinson's disease (PD). Commensurate linguistic profiles were also gathered over a 3-month period for a nonsurgical control cohort of 16 subjects with PD and a group of 16 non-neurologically impaired controls (NC). Nonparametric between-groups comparisons were conducted and reliable change indices calculated, relative to baseline/3-month follow-up difference scores. Group-wise statistical comparisons between the three groups failed to reveal significant postoperative changes in language performance. Case-by-case data analysis relative to clinically consequential change indices revealed reliable alterations in performance across several language variables as a consequence of BPVP. These findings lend support to models of subcortical participation in language, which promote a role for the GPi in lexical-semantic manipulation mechanisms. Concomitant improvements and decrements in postoperative performance were interpreted within the context of additive and subtractive postlesional effects. Relative to parkinsonian cohorts, clinically reliable versus statistically significant changes on a case by case basis may provide the most accurate method of characterizing the way in which pathophysiologically divergent basal ganglia linguistic circuits respond to BPVP.

Aged↗
PubMed2006

Predictive and reactive control of grasping forces: on the role of the basal ganglia and sensory feedback.

We comparatively investigated predictive and reactive grip force behaviour in 12 subjects with basal ganglia dysfunction (six subjects with Parkinson's disease, six subjects with writer's cramp), two subjects chronically lacking all tactile and proprioceptive sensory feedback and 16 sex- and age-matched control subjects. Subjects held an instrumented receptacle between the index finger and thumb. A weight was dropped into the receptacle either unexpectedly from the experimenter's hand with the subject being blindfolded or expectedly from the subject's opposite hand. This paradigm allowed us to study predictive and reactive modes of grip force control. All patients generated an overshoot in grip force, irrespective of whether the weight was dropped expectedly or unexpectedly. When the weight was dropped from the experimenter's hand, a reactive grip force response lagged behind the load perturbation at impact in patients with basal ganglia dysfunction and healthy controls. When the weight was dropped expectedly from the subject's opposite hand, patients with basal ganglia dysfunction and healthy subjects started to increase grip force prior to the release of the weight, indicating a predictive mode of control. We interpret these data to support the notion that the motor dysfunction in basal ganglia disorders is associated with deficits of sensorimotor integration. Both deafferented subjects did not show a reactive mode of force control when the weight was dropped unexpectedly, underlining the importance of sensory feedback to initiate reactive force responses. Also in the predictive mode, grip force processing was severely impaired in deafferented subjects. Thus, at least intermittent sensory information is necessary to establish and update predictive modes of grasping force control.

Adult↗
PubMed2007

The basal ganglia and cortex implement optimal decision making between alternative actions.

Neurophysiological studies have identified a number of brain regions critically involved in solving the problem of action selection or decision making. In the case of highly practiced tasks, these regions include cortical areas hypothesized to integrate evidence supporting alternative actions and the basal ganglia, hypothesized to act as a central switch in gating behavioral requests. However, despite our relatively detailed knowledge of basal ganglia biology and its connectivity with the cortex and numerical simulation studies demonstrating selective function, no formal theoretical framework exists that supplies an algorithmic description of these circuits. This article shows how many aspects of the anatomy and physiology of the circuit involving the cortex and basal ganglia are exactly those required to implement the computation defined by an asymptotically optimal statistical test for decision making: the multihypothesis sequential probability ratio test (MSPRT). The resulting model of basal ganglia provides a new framework for understanding the computation in the basal ganglia during decision making in highly practiced tasks. The predictions of the theory concerning the properties of particular neuronal populations are validated in existing experimental data. Further, we show that this neurobiologically grounded implementation of MSPRT outperforms other candidates for neural decision making, that it is structurally and parametrically robust, and that it can accommodate cortical mechanisms for decision making in a way that complements those in basal ganglia.

Algorithms↗
PubMed1991

[Basal ganglia germinoma treated with interstitial brachytherapy; case report].

A case of primary intracranial germinoma in the left basal ganglia treated with interstitial brachytherapy was reported. A 15-year-old boy was referred to our hospital for evaluation of right hemiparesis. A CT scan showed a slightly hyperdense mass with multiple cystic low density in the left basal ganglia. The mass was heterogeneously enhanced after intravenous administration of contrast material. T1 weighted image showed a slightly hyperintense mass with cystic components and the mass was heterogeneously enhanced with Gd-DTPA. T2 weighted MR image showed a mixed intensity mass and peritumoral edema. Stereotactic needle biopsy and implantation of 3 catheters for interstitial brachytherapy were performed simultaneously using BRW CT guided stereotactic apparatus. After the histological diagnosis was confirmed to be two cell pattern germinoma, 9 iridium-192 seeds were inserted into the catheters and maintained for 10 days to give 35Gy of irradiation at the tumor periphery. Subsequent CT scans showed marked tumor regression and the clinical symptoms were improved. Germinoma originating in the basal ganglia is rare and hard to diagnose previous to biopsy. Histological confirmation is essential before initiation of treatment because germinoma is commonly thought to be radiosensitive tumor. The interstitial brachytherapy enables selective irradiation of the tumor and actually causes no complications such as bone marrow suppression or cerebral atrophy. The neuroradiological findings, especially of CT scan and MRI, were presented and the strategy for treatment of germinoma in basal ganglia was discussed.

Adolescent↗
PubMed1996

Evolution of high-intensity basal ganglia lesions on T1-weighted MR in neurofibromatosis type 1.

PURPOSE: To characterize the temporal evolution of the foci of T1 shortening in basal ganglia lesions in patients with neurofibromatosis type 1 (NF-1). METHODS: A retrospective review of MR images of 37 patients with NF-1 revealed 8 patients in whom regions of T1 shortening were noted in the basal ganglia. We reviewed sequential images obtained in these selected patients with special attention to chronological changes in the foci of T1 shortening and their relationship to changes on T2-weighted images. RESULTS: Regions of short T1 in the globus pallidus were observed in 8 patients. In 2 of 3 patients in whom foci of T1 shortening were not identified on the initial imaging study, T1 shortening developed and T2 prolongation diminished after an initial increase. In the third patient, T1 and T2 prolongation appeared simultaneously. Sequential scans in the other 5 patients, in whom areas of increased signal intensity in the globus pallidus were present on both T1-weighted and T2-weighted images on the initial MR examination, showed a diminution in the size of the region of T2 prolongation in 2 patients, an increase in the size of the region of T2 prolongation in 1 patient, a mixed pattern of change in the size of the region of T2 prolongation in 1 patient, and no change in the region of T2 prolongation in 1 patient. During the periods of these T2 changes, the areas of T1 shortening showed no significant interval change. CONCLUSION: The foci of prolonged T2 relaxation in the basal ganglia appear to evolve in a manner similar to the foci of T2 prolongation in the white matter of the posterior fossa. However, the corresponding foci of short T1 in the basal ganglia may evolve with a different time course. In some patients, the foci of short T1 develop at a later time than the T2 prolongation and progress; these foci of short T1 do not appear to regress over periods as long as 90 months. Possible causes of the T1 shortening are remyelination and calcification.

Adolescent↗
PubMed1994

Characterization and localization of D1 dopamine receptors in the sexually dimorphic vocal control nucleus, area X, and the basal ganglia of European starlings.

D1 dopamine receptors were pharmacologically characterized and localized by quantitative autoradiography in the basal ganglia of male and female European starlings (Sturnus vulgaris). The D1 selective antagonist SCH 23390 was used to label this receptor subtype. Starlings are songbirds and possess a neural circuit implicated in the learning and production of song. This circuit includes a sexually dimorphic nucleus, area X, that is a subregion of the parolfactory lobe of the basal ganglia and is known from work on zebra finches to receive dopaminergic input from the area ventralis of Tsai. We focused our investigation on the D1-like receptor subtype because they are abundant in the basal ganglia. Competition studies indicate that a variety of dopaminergic ligands compete with [3H] SCH 23390 for the binding site in an order of potency characteristic of a D1-like receptor. Autoradiographic studies of the basal ganglia revealed high D1 receptor densities in the avian homologues of the caudate-putamen and relatively low-receptor densities were observed in the avian homologue of the globus pallidus. In male starlings, area X could be reliably discerned on the autoradiograms by the higher density of D1 receptors compared to the surrounding parolfactory lobe (LPO). This was also true for females, though not as reliably as in males. When we compared the mean D1 receptor density in area X for males and females we did not find a significant sex difference. However, we also analyzed the data by comparing sex differences in the degree to which area X has a higher receptor density in comparison with the surrounding LPO. When we normalized D1 receptor density in area X relative to the LPO, we did find a significant sex difference. This sex difference in relative receptor density represents another neural sex difference in the song circuit that may mediate sex differences in the learning and production of song in starlings and other songbirds.

Animals↗
PubMed2003

Basal ganglia injury as a complication of the ketogenic diet.

Movement disorders or basal ganglia injury have not been reported as complications of the ketogenic diet, an alternative treatment for intractable epilepsy. We report on a novel complication of the ketogenic diet manifesting as a severe extrapyramidal movement disorder and bilateral putaminal lesions. A single case is described. A video demonstrating the movement disorder is included. A 5-year-old girl with a cryptogenic epileptic encephalopathy developed focal dystonia, diffuse chorea, and ataxia after starting the ketogenic diet. Cranial magnetic resonance imaging (MRI) demonstrated bilateral putaminal lesions that were not present before starting the diet. MR spectroscopy showed a lactate peak in the basal ganglia, suggesting a failure of mitochondrial energy metabolism as the mechanism of cerebral injury. The radiographic abnormalities resolved after stopping the diet, although the movement disorder persisted. Basal ganglia injury and extrapyramidal movement abnormalities are potential complications of the ketogenic diet. Concomitant use of valproate or a latent inborn error of metabolism may be risk factors for these rare complications.

Ataxia↗
PubMed1996

Basal ganglia and movement disorders: an update.

A model of basal ganglia functioning proposed a few years ago suggests that increased and decreased activity in basal ganglia output to the thalamus underlies akinesia, as seen in Parkinson's disease, and dyskinetic movements as seen in Huntington's disease or after treatment with L-dopa and neuroleptics, respectively. Although the basic features of this model have stood the test of time, patterns of electrophysiological activity and changes in indices of GABA-dependent transmission in the external pallidum lead to a reconsideration of the mechanisms responsible for these changes in output activity.

Basal Ganglia↗
PubMed1980

Injuries of basal ganglia following head trauma in children.

7 pediatric patients with injuries of basal ganglia following head trauma were reported. They ranged in age from 10 months to 10 years. 5 boys and 2 girls comprised the patients. Cases 1--4 are mild cases in which the children fell down backward while playing, followed by a minimum loss of consciousness. In every case there was hemiparesis, but all of them showed remarkable recovery. CT findings are that of unilateral basal ganglia infarction. In cases 5--7, patients suffered from symptoms of brain contusion after running out in front of an oncoming car, and they developed hemiparesis. CT findings in cases 5 and 6 showed unilateral infarction. CT of case 7 showed a massive unilateral hemorrhage of the basal ganglia. All 7 cases sustained only slight scalp wounds and no skull fracture in spite of the severity of injuries signs and CT findings. This discrepancy seems to be explained only by the so-called shearing strain theory. But we have hypothesized that anterior stretch of the lateral branch of the perforator of the middle cerebral artery plays a major role in its pathogenesis.

Basal Ganglia↗
PubMed1991

Movement disorders--limb movement and the basal ganglia.

The primary concern of this article is to review experimental methods that may lead to a better understanding of the functional role of the basal ganglia in the control of movement. Two models of basal ganglia impairment are considered: Parkinson's disease and Huntington's disease. The review focuses primarily on akinesia and bradykinesia because they are key abnormalities of basal ganglia dysfunction. In general, through electromyography and kinematic analysis of movement, it may be possible to characterize specific movement disorders. Specifically, if damage sustained by the central nervous system is traced to a certain structure, it may provide insight on the extent of involvement and functional role of that structure in the control of movement. Much of the data reviewed suggests that the basal ganglia may play a specific role in the initiation and regulation of force control.

Basal Ganglia↗
PubMed2001

Distribution of the major gamma-aminobutyric acid(A) receptor subunits in the basal ganglia and associated limbic brain areas of the adult rat.

Within the basal ganglia, gamma-aminobutyric acid (GABA) exerts a fundamental role as neurotransmitter of local circuit and projection neurons. Its fast hyperpolarizing action is mediated through GABA(A) receptors. These ligand-gated chloride channels are assembled from five subunits, which derive from multiple genes. Using immunocytochemistry, we investigated the distribution of 12 major GABA(A) receptor subunits (alpha1-5, beta1-3, gamma1-3, and delta) in the basal ganglia and associated limbic brain areas of the rat. Immunoreactivity for an additional subunit (subunit alpha6) was not observed. The striatum, the nucleus accumbens, and the olfactory tubercle displayed strong, diffuse staining for the subunits alpha2, alpha4, beta3, and delta presumably located on dendrites of the principal medium spiny neurons. Subunit alpha1-, beta2-, and gamma2-immunoreactivities were apparently mostly restricted to interneurons of these areas. In contrast, the globus pallidus, the entopeduncular nucleus, the ventral pallidum, the subthalamic nucleus, and the substantia nigra pars reticulata revealed dense networks of presumable dendrites of resident projection neurons, which were darkly labeled for subunit alpha1-, beta2-, and gamma2-immunoreactivities. The globus pallidus, ventral pallidum, entopeduncular nucleus, and substantia nigra pars reticulata, all areas receiving innervations from the striatum, displayed strong subunit gamma1-immunoreactivity compared to other brain areas. In the substantia nigra pars compacta and in the ventral tegmental area, numerous presumptive dopaminergic neurons were labeled for subunits alpha3, gamma3, and/or delta. This highly heterogeneous distribution of individual GABA(A) receptor subunits suggests the existence of differently assembled, and presumably also functionally different, GABA(A) receptors within individual nuclei of the basal ganglia and associated limbic brain areas.

Animals↗
PubMed1989

Encephalopathy with calcifications of the basal ganglia in children. A reappraisal of Fahr's syndrome with respect to 14 new cases.

Calcifications of the basal ganglia are described under the heading of "Fahr's syndrome". The clinical pattern is variable and the syndrome may be sporadic or familial. This study describes a personal series of 14 cases of encephalopathy with calcification of the basal ganglia and reviews the literature cases. A four-group classification is proposed. The first group includes encephalopathy, microcephaly, dwarfism, retinal degeneration or optic atrophy, symmetrical patchy demyelination with calcifications and probable autosomal recessive inheritance. Some cases have an early onset, a rapid evolution. Others have a later onset, longer course and retinal degeneration. In the second group, the children suffer from a congenital encephalopathy or a cerebral palsy without clear deterioration, without short stature, ocular impairment or persistent CSF abnormalities. This group has not been reported in the literature. The cases do not seem to be genetic. The precise cause in unknown but a sporadic non progressive anoxo-ischemic, or viral prenatal disease is suggested. In the third group, the association of encephalopathy, microcephaly, and persistent CSF lymphocytosis, has a high recurrence rate. The pathogenesis is still a matter of dispute. The fourth group is characterized by autosomal dominant calcifications of the basal ganglia with or without neurological abnormalities. Finally calcium metabolism disorders and mitochondrial encephalomyopathy may be associated with calcifications of the basal ganglia.

Basal Ganglia Diseases↗
PubMed1994

The distribution of excitatory amino acid receptors in the normal human midbrain and basal ganglia with implications for Parkinson's disease: a quantitative autoradiographic study using [3H]MK-801, [3H]glycine, [3H]CNQX and [3H]kainate.

Quantitative receptor autoradiography using [3H]MK-801, [3H]glycine, [3H]CNQX and [3H]kainate was employed to determine the distribution and density of excitatory amino acid (EAA) binding sites in the midbrain and basal ganglia of the normal human nervous system. Detailed knowledge of the anatomy and subtype specificity of glutamate receptors is important both in understanding the normal physiology of basal ganglia neurotransmission and the pathophysiological changes occurring in diseases affecting the basal ganglia such as Parkinson's disease (PD). In PD, glutamate receptor activation may contribute to cell death of dopaminergic neurones in the substantia nigra. In addition, perturbation of glutamate neurotransmission resulting from dopamine depletion in the basal ganglia is likely to contribute to the clinical manifestations of motor dysfunction. The distribution and density of ligand binding representing N-methyl-D-aspartate (NMDA), AMPA (2-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) and kainate receptors has a heterogeneous distribution in the human midbrain and basal ganglia. In the substantia nigra relatively high densities of [3H]MK-801 and strychnine-insensitive [3H]glycine binding sites representing NMDA receptors were present, whereas only moderate densities of [3H]CNQX and [3H]kainate binding sites were present, compared to other regions. In both the medial globus pallidus and subthalamic nucleus, binding sites representing NMDA, AMPA and kainate receptors were all present at low density. These findings suggest that the clinical usefulness of modifying glutamatergic neurotransmission in these basal ganglia nuclei may be limited by the relatively low density of EAA binding sites present.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1997

Longitudinal change in basal ganglia volume in patients with Huntington's disease.

Cross-sectional MRI studies demonstrating an association between caudate atrophy and symptom severity and duration of symptoms in patients with Huntington's disease (HD) have been assumed to reflect longitudinal changes in basal ganglia, but such neuropathologic progression has never been directly demonstrated. Subjects in the current study were 23 HD patients at various stages of the disorder who had two MRI images at least 10 months apart (mean interimage interval = 20.8 months). We measured volumes of caudate, putamen, and globus pallidus blind to the order of the images. For each structure, we calculated a change score by subtracting the volume obtained on the follow-up imaging from that obtained on the initial imaging. Results indicated significant decreases over time in caudate, putamen, and total basal ganglia volume. Age at onset and length of trinucleotide repeat correlated significantly with amount of volume change in caudate and total basal ganglia, even after controlling for length of interimage interval, duration of disease, and measures of symptom severity. Amount of change in basal ganglia structures was not significantly correlated with neurologic symptom severity at the time of the initial imaging or duration of symptoms. This is the first longitudinal MRI study to document progressive basal ganglia atrophy in HD, and suggests that quantitative neuroimaging with serial MRI may be useful in monitoring effectiveness of potential treatments. In addition, demonstration of greater rate of basal ganglia atrophy in patients with earlier symptom onset suggests that treatment effects may be more quickly observed in this subgroup of patients than in the general HD population.

Adult↗
PubMed2005

Basal ganglia volumetric studies in affective disorder: what did we learn in the last 15 years?

Until today, morphometric neuroimaging studies on affective disorders concentrate on the limbic system, especially the hippocampus, amygdala, and anterior cingulate. In most of the studies and reviews available today, the basal ganglia are of secondary interest. It seems that the basal ganglia are interest of neurologist, whereas the limbic system is reserved for psychiatric neuroimaging studies. We follow a different approach in this review, studying all available papers on MRI research of the basal ganglia in unipolar depression and bipolar disorder. We found a possibly larger neostriatum in bipolar and possibly smaller one in unipolar patients. None of the unipolar studies found any larger basal ganglion, and only one out of 12 bipolar studies found smaller basal ganglia. Both findings seemed to depend on age (tendency toward smaller volumes in unipolar and bipolar with older age), sex (men tending to pathology in both disorders) and bipolar patients show a possible influence of medication, which is not assessed so far in unipolar depression. We conclude that several methodological shortcomings in volumetric MRI research on the basal ganglia in affective disorders make it necessary to imply more research in this area. We suggest (a) better MRI methods (we do not have a single volumetric 3 Tesla study in this patient group); (b) studies of medication-naïve patients (thus ruling out the medication effect); (c) Studies that directly compare unipolar depressed and bipolar patients are needed to determine whether these apparent differences in morphometric abnormalities, as observed through the mediating comparison with healthy subjects, are real.

Basal Ganglia↗
PubMed1996

Calcium-binding proteins in primate basal ganglia.

This paper describes the distribution of the calcium-binding proteins calbindin-D28k. Parvalbumin and calretinin in primate basal ganglia. The data derive from immunocytochemical studies undertaken in squirrel monkeys (Saimiri sciureus) and in normal human individuals. In the striatum, calbindin labels medium-sized spiny projection neurons whereas parvalbumin and calretinin mark two separate classes of aspiny interneurons. The striatal matrix compartment is markedly enriched with calbindin while striatal patches (striosomes) display a calretinin-rich neuropil. In the pallidum, virtually all neurons contain parvalbumin but none express calbindin. Calretinin occurs only in a small subpopulation of both large and small pallidal neurons. In the subthalamic nucleus, there exists a multitude of parvalbumun-positive cells and fibers but the number of calretinin and calbindin-positive neuronal elements is small. In the substantia nigra/ventral tegmental area complex, calbindin and calretinin occur principally in dopaminergic neurons of the dorsal tier of the pars compacta and in those of the ventral tegmental area. Parvalbumin is strictly confined to the GABAergic neurons of the pars reticulata and lateralis. Calbindin-rich fibers abound in the pars reticulata and lateralis, while calretinin-positive axons are confined to the pars compacta. These results indicate that calbindin and parvalbumin are distributed according to a strikingly complementary pattern in primate basal ganglia. Calretinin is less ubiquitous but occurs in all basal ganglia components where it labels distinct subsets of neurons. Such highly specific patterns of distribution indicate that calbindin, parvalbumin and calretinin may work in synergy within primate basal ganglia.

Animals↗