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PubMed1980

[Clinical, endocrinological, and computerized tomography scans for symmetrical calcification of the basal ganglia (author's transl)].

Symmetrical calcification of the basal ganglia was found in 2% of 8000 computerized tomography (CT) scans. Of 19 cases, only 2 were detectable on conventional skull films. The less prominent calcifications were most often found in the region of the pallidum, the knee of the internal capsule. Also, the lesions were generally symmetrical. Thus these factors must be considered basic morphological characteristics of the pathophysiological process. Additional neurological disorders were present in 6 patients. Neurological symptoms in the remaining 13, when present, depended on the extent of the lesion. The most common finding was tremor, although disturbances of fine motor control, transient lateralizing signs, and seizures were also noted. No particular constellation of symptoms or signs permitted accurate clinical localization of the lesions. The patients could be divided into three groups on the basis of clinical findings: (1) young people with marked cerebral calcinosis ('idiopathic' calcification of basal ganglia), (2) patients with hypoparathyroidism, and (3) older patients with relatively little calcification. Most patients with calcific lesions will be included in the third group. Any calcification of basal ganglia detected by CT scans demands careful evaluation of calcium metabolism.

Adult↗
PubMedDate not supplied

Glutamatergic influences on the basal ganglia.

Glutamate is the predominant excitatory neurotransmitter of the basal ganglia, where it acts on ionotropic and metabotropic receptors. In the best studied of the basal ganglia disorders, Parkinson's disease, there is compelling evidence that the activities of glutamatergic pathways are altered. Of particular importance, the glutamatergic subthalamic nucleus becomes overactive. Pharmacologic blockade of subthalamic neurotransmission has antiparkinsonian symptomatic effects and may also help to protect the remaining dopamine neurons of the substantia nigra from excitotoxic neurodegeneration. Development of drugs to manipulate the glutamatergic system with appropriate pharmacologic and anatomic selectivity is likely to dramatically improve our ability to treat disorders of the basal ganglia.

Animals↗
PubMed1994

Parvalbumin-containing GABAergic neurons in the basal ganglia output system of the rat.

The output of the basal ganglia is directed through the entopeduncular nucleus (EPN) and the substantia nigra pars reticulata (SNR) and pars lateralis (SNL), which provide a gamma-aminobutyric acidergic (GABAergic) projection to various nuclei of the thalamus and brainstem. Although many neurons within the SNR and EPN have been described as modality specific, the morphological and neurochemical similarities preclude their precise identification. In the present study, the immunocytochemical localization of parvalbumin, a calcium-binding protein, is used in combination with axonal tracing to verify neuronal heterogeneity within the SNR, SNL, and EPN. The results reveal that the majority of neurons in all three centers contain parvalbumin. The parvalbumin-containing neurons are distributed in the caudal two-thirds of the EPN, the rostral part of the SNL, and the lateral two-thirds of the entire rostrocaudal extent of the SNR, the areas involved in sensorimotor function of the basal ganglia. Moreover, the nigrothalamic, nigrocollicular, and EPN-thalamic neurons possess parvalbumin immunoreactivity, whereas the EPN-habenular neurons are devoid of parvalbumin immunoreactivity. The results indicate a neurochemical heterogeneity within the GABAergic output neurons of the basal ganglia and suggest that the parvalbumin-containing neurons of the SNR, SNL, and EPN are the tonically active output neurons that form a major link in the disinhibitory neuronal circuit of the basal ganglia, especially that concerned with sensorimotor function.

Animals↗
PubMed2003

Conditional ablation of striatal neuronal types containing dopamine D2 receptor disturbs coordination of basal ganglia function.

Dopamine (DA) exerts synaptic organization of basal ganglia circuitry through a variety of neuronal populations in the striatum. We performed conditional ablation of striatal neuronal types containing DA D2 receptor (D2R) by using immunotoxin-mediated cell targeting. Mutant mice were generated that express the human interleukin-2 receptor alpha-subunit under the control of the D2R gene. Intrastriatal immunotoxin treatment of the mutants eliminated the majority of the striatopallidal medium spiny neurons and cholinergic interneurons. The elimination of these neurons caused hyperactivity of spontaneous movement and reduced motor activation in response to DA stimulation. The elimination also induced upregulation of GAD gene expression in the globus pallidus (GP) and downregulation of cytochrome oxidase activity in the subthalamic nucleus (STN), whereas it attenuated DA-induced expression of the immediate-early genes (IEGs) in the striatonigral neurons. In addition, chemical lesion of cholinergic interneurons did not alter spontaneous movement but caused a moderate enhancement in DA-induced motor activation. This enhancement of the behavior was accompanied by an increase in the IEG expression in the striatonigral neurons. These data suggest that ablation of the striatopallidal neurons causes spontaneous hyperactivity through modulation of the GP and STN activity and that the ablation leads to the reduction in DA-induced behavior at least partly through attenuation of the striatonigral activity as opposed to the influence of cholinergic cell lesion. We propose a possible model in which the striatopallidal neurons dually regulate motor behavior dependent on the state of DA transmission through coordination of the basal ganglia circuitry.

Animals↗
PubMed2003

Does asymmetric basal ganglia or thalamic activation aid in seizure foci lateralization on ictal SPECT studies?

UNLABELLED: Basal ganglia or thalamic activation has been reported in ictal SPECT studies of patients with intractable epilepsy. We hypothesized that lateralization of activation of these subcortical structures may aid in the lateralization of seizure foci in patients in whom the cortical focus is subtle or equivocal. METHODS: This was a retrospective analysis of 72 ictal (99m)Tc-ethylcysteinate dimer SPECT studies in 43 patients with intractable epilepsy in whom seizure laterality could be eventually determined. All patients underwent video-electroencephalography (EEG) monitoring, MRI, and one or more ictal SPECT scans as well as an interictal SPECT scan. Intracranial electrode EEG monitoring and surgery were performed as clinically indicated. Ictal and interictal studies were coregistered with patients' MRI scans using automated software, and ictal minus interictal subtraction images were obtained. The presence of asymmetric basal ganglia or thalamic activation was determined by 2 experienced observers who were unaware of clinical information. The final seizure focus was determined by surgical cure in 37 patients. In patients in whom surgery was not indicated or initial surgery was performed at another institution (n = 6), a consistent focus detected by intracranial electrode monitoring or repeated stereotypical seizures all originating from the same site on video-surface EEG monitoring was considered to indicate the final seizure focus. RESULTS: Thirty-five patients had neocortical seizures and 8 had mesial temporal lobe seizures. Asymmetric basal ganglia activation was seen in 22 (30.6%) studies. This activation was ipsilateral to the final determined seizure focus in 17 of 22 of these studies (77.3%) and contralateral in 5 of 22 (21.7%). Asymmetric thalamic activation was seen in 15 studies (20.8%), of which 12 of 15 (80%) were ipsilateral to the final seizure focus, whereas 3 of 15 (20%) were contralateral. In 3 of 5 studies with contralateral basal ganglia activation and 1 of 3 studies with contralateral thalamic activation, the SPECT study as a whole was found to be falsely localizing. In another 2 cases of contralateral subcortical activation, the SPECT study as a whole was considered nonlocalizing. Worse outcome was not observed in patients with false ictal SPECT subcortical lateralization; however, the presence of asymmetric subcortical uptake, regardless of relationship to seizure focus, was associated with decreased incidence of seizures at 1 y after surgery. CONCLUSION: Although asymmetric basal ganglia or thalamic activation is common, it is rarely the sole indicator of seizure localization. However, it may be a useful confirmatory sign in subtle cases of cortical localization. In cases of false ictal SPECT subcortical lateralization, the basal ganglia appear to follow cortical activation pattern. Furthermore, there appears to be a correlation between lateralizing uptake in subcortical structures on ictal SPECT and postsurgical outcome in intractable epilepsy patients.

Adult↗
PubMed1994

The functions of the basal ganglia and the paradox of stereotaxic surgery in Parkinson's disease.

The basal ganglia play a role in controlling movement. The motor circuits within the striato-pallidal complex are thought to facilitate desired movement and inhibit unwanted movement through their influence via thalamus, mainly on precentral motor cortical regions. Lesions in the motor thalamus, or in the globus pallidus, therefore might be expected to impair voluntary movement. But stereotaxic lesions in patients with Parkinson's disease directed at the motor thalamus verified at autopsy, and lesions in the globus pallidus, which improve rigidity and tremor, apparently do not worsen parkinsonian hypokinesia and bradykinesia; nor do they regularly cause dyskinesias. Reasons for this discrepancy are reviewed. It is concluded that the motor circuits of the basal ganglia are part of a distributed motor system which can operate, albeit imperfectly, in the absence of striato-pallido-thalamo-cortical feedback. There may, however, be subtle defects in motor performance after thalamic and pallidal lesions which have escaped attention. Further consideration leads to two hypotheses concerning normal basal ganglia motor function. First, it seems most likely that it is a pause in firing of medial pallidal and substantia nigra reticulata neurons that, by disinhibition of thalamic targets, permits movements generated by cortical motor areas. An increase in firing of medial pallidal neurons, which so far has been the major focus of attention, may be more concerned with inhibition of unwanted movement. Secondly, we suggest that the basal ganglia play a particular role in motor control. A change in firing of medial pallidal neurons appears to occur too late to initiate a new movement. However, the motor circuit within the striato-pallidal system routinely receives a continuous delayed read-out of cortical motor activity and issues an output directed via thalamus mainly to premotor cortical regions. This may permit the routine automatic execution of sequences of movements generated in cortical motor areas. There is evidence that other regions of the striatum respond to significant external or internal cues as dictated by their cortical inputs, the significance being determined by memory, novelty, emotional and other contexts. We suggest that such events capture the attention of the non-motor striatum, which then interrupts the routine operation of the motor circuit, perhaps at the level of the medial pallidum and substantia nigra pars reticulata, to permit new cortical motor action.

Animals↗
PubMed1993

Physiology of basal ganglia disorders: an overview.

The pathophysiology of the movement disorders arising from basal ganglia disorders has been uncertain, in part because of a lack of a good theory of how the basal ganglia contribute to normal voluntary movement. An hypothesis for basal ganglia function is proposed here based on recent advances in anatomy and physiology. Briefly, the model proposes that the purpose of the basal ganglia circuits is to select and inhibit specific motor synergies to carry out a desired action. The direct pathway is to select and the indirect pathway is to inhibit these synergies. The clinical and physiological features of Parkinson's disease, L-DOPA dyskinesias. Huntington's disease, dystonia and tic are reviewed. An explanation of these features is put forward based upon the model.

Basal Ganglia Diseases↗
PubMed2004

Neural responses in multiple basal ganglia regions during spontaneous and treadmill locomotion tasks in rats.

To investigate the role of basal ganglia in locomotion, a multiple-channel, single-unit recording technique was used to record neural activity simultaneously in the dorsal lateral striatum (STR), globus pallidus (GP), subthalamic nucleus (STN) and substantia nigra pars reticulata (SNr) during spontaneous and treadmill locomotion tasks in freely moving rats. Active and quiescent phases appeared alternately in a spontaneous movement session that lasted 60 min. Principal component analysis of the ensemble neural activity from each region revealed a close correlation with spontaneous motor activity. Most of the neurons in these four basal ganglia areas increased their firing rates during the active phase. In the treadmill locomotion task, the firing rates of neurons in all recording areas, especially in the STN, increased significantly during locomotion. In addition, neural responses related to tone cue, initiation and termination of treadmill were observed in a subset of neurons in each basal ganglia region. Detailed video analysis revealed a limb movement related neural firing, predominantly in the STR and the GP, during treadmill walking. However, the proportion of neurons exhibiting limb movement related firing was significantly greater only in the STR. A few neurons in the STR (4.8%) and the GP (3.4%) discharged in an oscillatory pattern during treadmill walking, and the oscillatory frequency was similar to the frequency of the step cycle. This study demonstrates a variety of neural responses in the major basal ganglia regions during spontaneous and forced locomotion. General activation of all major basal ganglia regions during locomotion is more likely to provide a dynamic background for cortical signal processing rather than to directly control precise movements. Implications of these findings in the model of basal ganglia organization are discussed.

Action Potentials↗
PubMed2006

Anatomy and physiology of the basal ganglia: implications for deep brain stimulation for Parkinson's disease.

Central to surgical management of movement disorders is an understanding of the anatomy and physiology of the basal ganglia. The basal ganglia have been a target for neuromodulation surgery since Russell Meyers' pioneering works in the late 1930s. With the development of deep brain stimulation as the gold standard of surgical intervention for movement disorders, there has been a concomitant evolution in the understanding of the role the basal ganglia plays in the genesis of normal and abnormal motor behaviors. The fundamental concept of the cortico-striato-pallido-thalamocortical loop will be explored in the context of deep brain stimulation. The current targets for deep brain stimulation for Parkinson's disease, the subthalamic nucleus, the globus pallidus internus, and the ventral intermediate nucleus, will be discussed in the framework of the current physiological and anatomical models of Parkinson's disease (PD). Finally, the current understandings of the mechanisms underpinning the beneficial effects of deep brain stimulation for PD will be discussed.

Basal Ganglia↗
PubMed2006

Basal ganglia lesions following carbon monoxide poisoning.

PRIMARY OBJECTIVES: Carbon monoxide (CO) is the most common cause of poisoning and may result in basal ganglia lesions. This study reviewed the literature of carbon monoxide poisoning and basal ganglia lesions and prospectively assessed the prevalence of basal ganglia lesions in a cohort of patients with CO poisoning. RESEARCH DESIGN: Literature review and prospective cohort study. METHODS: This study conducted a comprehensive review of the literature and assessed 73 CO-poisoned patients for basal ganglia lesions on sequential MR scans. Magnetic resonance scans were obtained on day 1, 2 weeks and 6 months post-CO poisoning. RESULTS: The literature review found basal ganglia lesions occur in 4-88% of subjects. Only one patient was found with globus pallidus lesions at 2 weeks and 6 months following CO poisoning, that were not present on the initial day 1 MR scan. CONCLUSIONS: Basal ganglia lesions, including lesions of the globus pallidus, may be less common than previously reported.

Adolescent↗
PubMedDate not supplied

Stuttering and the basal ganglia circuits: a critical review of possible relations.

UNLABELLED: The possible relation between stuttering and the basal ganglia is discussed. Important clues to the pathophysiology of stuttering are given by conditions known to alleviate dysfluency, like the rhythm effect, chorus speech, and singing. Information regarding pharmacologic trials, lesion studies, brain imaging, genetics, and developmental changes of the nervous system is reviewed. The symptoms of stuttering are compared with basal ganglia motor disorders like Parkinson's disease and dystonia. It is proposed that the basal ganglia-thalamocortical motor circuits through the putamen are likely to play a key role in stuttering. The core dysfunction in stuttering is suggested to be impaired ability of the basal ganglia to produce timing cues for the initiation of the next motor segment in speech. Similarities between stuttering and dystonia are indicated, and possible relations to the dopamine system are discussed, as well as the interaction between the cerebral cortex and the basal ganglia. Behavioral and pharmacologic information suggests the existence of subtypes of stuttering. LEARNING OUTCOMES: As a result of this activity, the reader will (1) become familiar with the research regarding the basal ganglia system relating to speech motor control; (2) become familiar with the research on stuttering with indications of basal ganglia involvement; and (3) be able to discuss basal ganglia mechanisms with relevance for theory of stuttering.

Basal Ganglia↗
PubMed1997

A Quantitative MRI Study of the Basal Ganglia in Depression in HIV Seropositive Men.

UNLABELLED: HIV (Human Immunodeficiency Virus) infection is associated with high rates of depressive symptomatology. There is evidence that such infection is associated with damage to the basal ganglia. It has also been suggested that the basal ganglia are implicated in the aetiology of affective disorders. OBJECTIVE: This study examined the association between basal ganglia atrophy and depression in HIV seropositive men. We hypothesized that depressed HIV seropositive patients would have smaller basal ganglia compared with nondepressed HIV positive comparison subjects. METHOD: Using quantitative magnetic resonance imaging (MRI) techniques we compared for the basal ganglia volumes of sixteen depressed, and sixteen group-matched nondepressed HIV seropositive homosexual men. RESULTS: We found no significant difference in basal ganglia volumes between the two groups. CONCLUSIONS: We suggest that depression, at least in the early stages of HIV infection, is not associated with basal ganglia atrophy.

Basal Ganglia↗
PubMed2003

Mineralization of the basal ganglia: implications for neuropsychiatry, pathology and neuroimaging.

This article examines the evidence for and against the existence of basal ganglia mineralization as a defined clinico-pathological entity. In reviewing the literature on basal ganglia mineralization, this article emphasizes evidence derived from different neuroimaging modalities, genetics, metabolic studies, postmortem series and their possible neuropsychiatric correlates. Relevant articles were collected through Medline and Index Medicus searches. Researchers have encountered multiple difficulties in accepting basal ganglia mineralization as a distinct entity. This syndrome lacks set clinical criteria or a unique etiology; not surprisingly, numerous articles have applied varied definitions. Because many of the reported cases have not been examined postmortem, both the extent and nature of their mineralization remains uncertain. Furthermore, researchers have considered small foci of basal ganglia mineralization a normal phenomenon of aging. However, when brain deposits are extensive, they are associated with a set of age-dependent, progressive clinical symptoms. They include cognitive impairment, extrapyramidal symptoms and psychosis. Most cases are related to abnormalities of calcium metabolism, but rare familial cases of idiopathic origin have been reported. Overabundant mineralization of the brain is judged pathological based on its amount, distribution and accompanying clinical symptoms. Although its relation with calcium dysregulation is well known, modern studies have emphasized abnormalities of iron and dopamine metabolism. The authors suggest that these metabolic abnormalities may link basal ganglia mineralization to psychotic symptomatology.

Basal Ganglia↗
PubMed1984

Physiology of the basal ganglia: an overview.

The major anatomical connections of the basal ganglia are reviewed, emphasizing the inputs to the striatum and efferent projections from the major output nuclei, the internal segment of globus pallidus and the pars reticulata of substantia nigra. The results from lesioning experiments, electrical stimulation, and chronic recording of single neuron activity have provided a wealth of data concerning the physiology of the basal ganglia. Although the deficits resulting from disease of the basal ganglia are well recognized, the specific role which these structures play in the control of normal movements remains speculative.

Basal Ganglia↗
PubMed1996

[New findings on the morphology and motor function of basal ganglia].

This paper presents results of new investigations on morphology and motor function of basal ganglia, which point to the fact that their dimensions are individual and not correlated with the dimension of the corresponding hemisphere. Basal ganglia motor function is studied on the basis of disturbances which occur if they are damaged, both in sick people and experimental animals. Analysis of recorded single-neuron activity, in animals and in patients undergoing special surgical procedures, is especially instructive for understanding this function. According to new insights there are at least five multiple neuronal regions: motor, oculomotor, limbic, dorsolateral prefrontal and lateral orbitofrontal region. Morphologic and functional studies partly disagree in interpreting connections among these regions. On the basis of functional studies it is considered that parallelism and functional separation exist, while on the basis of morphologic studies it is considered that at the level of basal ganglia output convergence occurs. New insights speak about parallelism and convergence at the same time. It is thought that inside basal ganglia motor region there are two divided systems, direct and indirect, which direct the output impulses towards talamus. The direct leads to facilitation of cortically started movements, and the indirect to suppression of unwanted motor behavior. On the basis of literature data we can conclude that basal ganglia support cortically generated movements, participate in sequential movements, suppress unwanted motor activity and in altered circumstances stop the course of started motor sequences allowing new, adequate motor activity.

Animals↗
PubMed1998

Cognitive deficits following stroke in the basal ganglia.

OBJECTIVE: To examine the effect of a stroke in the basal ganglia on cognitive functioning. DESIGN: As part of a larger prospective study on the neuropsychological and psychosocial consequences of stroke, 12 patients with a stroke confined to the basal ganglia were examined. SETTING: The patients were assessed in one of the three participating hospitals. SUBJECTS: The results of 12 patients with a stroke in the basal ganglia (mean age 55 years), were compared to 24 controls (mean age 54.3 years). MAIN OUTCOME MEASURES: Different aspects of memory, attention and concentration, visuospatial and visuoconstructive functions, language and arithmetic were assessed using neuropsychological tests. RESULTS: The data show a significant abnormality in cognitive functioning on all cognitive domains. CONCLUSIONS: The results stress the notion that subcortical damage may lead to substantial neuropsychological disorders and have clear implications for neurological rehabilitation.

Basal Ganglia↗
PubMed1998

Differential activation of dorsal basal ganglia during externally and self paced sequences of arm movements.

The basal ganglia are thought to be critically involved in motor control. However, the relative contributions of the various sub-components are not known. Although, in principle, functional magnetic resonance imaging (fMRI) provides adequate resolution to image the basal ganglia at the spatial scale of the individual nuclei, activating these nuclei with fMRI has proven to be difficult. Here we report two tasks, involving externally and self paced sequences of arm movements, which resulted in significant activation of contralateral posterior (post-commissural) putamen and globus pallidus. This activation did not significantly differ between the tasks. In contrast, significant activation of the contralateral and ipsilateral anterior caudate and anterior putamen was observed only during externally paced arm movements. These results suggest a dissociation in the roles of the anterior and posterior dorsal basal ganglia: the anterior caudate and putamen may be involved in sensory to motor mapping and the posterior putamen and globus pallidus may be involved in the motor response itself. The findings support the hypothesis that the basal ganglia may be involved in gating sensory influences onto motor areas.

Adult↗
PubMed1998

1H MR spectroscopy of the basal ganglia in childhood: a semiquantitative analysis.

Proton MR spectra of the basal ganglia were obtained from 28 patients, 24 male and 14 female, median age 16.3 months (5 weeks to 31 years). They included 17 patients with normal MRI of the basal ganglia without metabolic disturbance (control group) and 11 patients with various metabolic diseases: one case each of high serum sodium and high serum osmolarity, cobalamin C deficiency, Leigh disease, Galloway-Mowat syndrome, Pelizaeus-Merzbacher disease, hemolytic-uremic syndrome and Wilson disease and two cases of Alagille syndrome and methylmalonic acidemia with abnormal MRI of the basal ganglia or blood or urine analysis (abnormal group). The MR spectrum was measured by using STEAM. The MR-visible water content of the region of interest was obtained. Levels of myoinositol, choline, creatine and N-acetylaspartate were measured using a semiquantitative approach, with absolute reference calibration. In the control group, there was a gradual drop of water content over the first year of life; N-acetylaspartate, creatine and myoinositol levels showed no significant change with age, in contrast to the occipital, parietal and cerebellar regions. Choline showed a gradual decrease for the first 2 years of life and then remained fairly constant. In the abnormal group the water content was not significantly different. N-Acetylaspartate was decreased in patients with high serum sodium and high serum osmolarity, cobalamin C deficiency, Leigh disease and one case of methylmalonic acidemia. Decreased creatine was also found in Leigh disease, and decreased choline in Galloway-Mowat syndrome and Wilson disease. Myoinositol was elevated in the patient with abnormally high serum sodium, and decreased in the hemolytic-uremic syndrome.

Adolescent↗