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PubMedDate not supplied

Basal ganglia volumes following CO poisoning: A prospective longitudinal study.

Carbon monoxide (CO) poisoning may result in focal and diffuse neuropathological changes, including basal ganglia lesions. The effect of CO poisoning on basal ganglia volumes over time is unclear. We assessed basal ganglia volumes longitudinally following CO poisoning. We prospectively enrolled 73 CO poisoned patients who underwent brain MR imaging on day 1 (baseline), 2 weeks, and 6 months post-CO poisoning. Basal ganglia volumes were obtained. One patient had bilateral globus pallidus lesions at two weeks and 6 months. Of the CO-poisoned patients 28% had volume reduction in at least one basal ganglia structure by 6 months, of which 21% had putamen, 15% had caudate, 15% had globus pallidus, and 16% had total basal ganglia volume reduction. Putamen volumes were significantly smaller from baseline to six months (p = 0.02). Verbal memory and mental processing speed correlated with smaller putamen and globus pallidus volumes. Carbon monoxide poisoning results in basal ganglia volume reduction 6 months post CO poisoning. Slow mental processing speed and impaired memory correlated with smaller putamen and globus pallidus volumes. Clinicians need to be aware of basal ganglia neuropathologic changes in the absence of observable lesions following CO poisoning.

Adolescent↗
PubMed2001

An MRI study of basal ganglia volumes in first-episode schizophrenia patients treated with risperidone.

OBJECTIVE: The basal ganglia may contribute to extrapyramidal movement disorders, affective disturbances, and cognitive deficits in schizophrenia. Basal ganglia volumes are putatively affected by antipsychotic medications. The purpose of this study was to determine the long-term effects of risperidone treatment in a cohort of first-episode patients with schizophrenia. METHOD: The subjects were 30 patients with first-episode schizophrenia, 12 patients chronically treated with typical antipsychotics, and 23 healthy comparison subjects. They were scanned by magnetic resonance imaging at baseline. The first-episode patients received 1 year of continuous risperidone treatment, after which they and the comparison subjects were rescanned. Caudate, putamen, and globus pallidus volumes were determined from coronal images. RESULTS: The baseline caudate, putamen, and globus pallidus volumes were significantly larger in the chronically treated patients than in the untreated first-episode subjects and comparison subjects. These volumes did not differ between the first-episode patients and healthy comparison subjects. Basal ganglia volumes were unchanged after 1 year of exposure to risperidone in the first-episode subjects. Extrapyramidal movement disorders were present in the majority of chronically treated patients and more than one-third of the never-medicated first-episode patients at baseline. CONCLUSIONS: This group of first-episode patients did not exhibit abnormalities of basal ganglia volumes, nor were basal ganglia volumes affected by exposure to risperidone. Movement disorders were observed in both first-episode and chronically treated patients, suggesting effects of both illness and medications.

Adult↗
PubMed1984

Afferent and efferent relationships of the basal ganglia.

A survey of the known circuitry of the basal ganglia leads to the following conclusions. (1) No complete account can yet be given of the neural pathways by which the basal ganglia affect the bulbospinal motor apparatus. Channels of exit from the basal ganglia originate from the internal pallidal segment, the pars reticulata of the substantia nigra, and the subthalamic nucleus, and each of these is directed in part rostrally to the cerebral cortex by way of the thalamus, in part caudally to the midbrain. The postsynaptic extension of the mesencephalic channels to bulbar and spinal motor neurons is largely unknown. Since the ascending channels are collectively of greatest volume, the notion remains plausible that the basal ganglia act in considerable part by modulating motor mechanisms of the cortex. (2) Recent findings in the rat suggest that the striatum is subdivided into a ventromedial, limbic system-afferented region and a dorsolateral, 'non-limbic' region largely corresponding to the main distribution of corticostriatal fibres from the motor cortex. These two subdivisions appear to give rise to different striatofugal lines, the outflow from the limbic-afferented sector partly re-entering the circuitry of the limbic system. (3) The limbic-afferented striatal sector suggests itself as an interface between the motivational and the more strictly motor aspects of movement. This suggestion is strengthened by evidence that the 'limbic striatum' seems enabled by its striatonigral efferents to modulate not only the source of its own dopamine innervation but also that of a large additional striatal region.

Animals↗
PubMed1996

Proton magnetic resonance spectroscopy of basal ganglia in chronic schizophrenia.

Proton spectra in the regions of the right and left basal ganglia were studied in 14 medicated patients with chronic schizophrenia using proton magnetic resonance spectroscopy (1H MRS). Ratios of N-acetyl-aspartate (NAA) to choline-containing compounds (Cho) were significantly reduced in the bilateral basal ganglia regions compared to normal subjects. The relative level of Cho was increased in the left basal ganglia region in comparison to normal subjects. This finding suggests the presence of disturbances in phospholipid metabolism in the basal ganglia. The level of NAA was decreased in the bilateral basal ganglia regions, which may indicate neuronal dysfunction. The 1H MRS study demonstrated dysfunctions in the basal ganglia regions in medicated patients with chronic schizophrenia.

Adult↗
PubMed2005

The basal ganglia: learning new tricks and loving it.

The field of basal ganglia research is exploding on every level - from discoveries at the molecular level to those based on human brain imaging. A remarkable series of new findings support the view that the basal ganglia are essential for some forms of learning-related plasticity. Other new findings are challenging some of the basic tenets of the field as it now stands. Combined with the new evidence on learning-related functions of the basal ganglia, these studies suggest that the basal ganglia are parts of a brain-wide set of adaptive neural systems promoting optimal motor and cognitive control.

Animals↗
PubMed1993

Multiple output channels in the basal ganglia.

The neural circuits that link the basal ganglia with the cerebral cortex are critically involved in the generation and control of voluntary movement. Retrograde transneuronal transport of herpes simplex virus type 1 was used to examine the organization of connections in the cebus monkey between an output nucleus of the basal ganglia, the internal segment of the globus pallidus (GPi), and three cortical areas: the primary motor cortex, the supplementary motor ara, and the ventral premotor area. Spatially separate regions of the GPi were labeled after virus injections into each cortical area. The GPi projects to multiple cortical motor areas, and this pallidal output is organized into discrete channels. This information provides a new anatomical framework for examining the function of the basal ganglia in skeletomotor control.

Animals↗
PubMed1997

Major depression and the basal ganglia.

In the last decade, major changes in our understanding of basal ganglia functions have occurred. Traditionally the basal ganglia were considered to be involved only in the modulation of movement. Recent research has suggested that the basal ganglia also take part in complex fronto-subcortical networks that have an important role in cognition reward, and mood regulation. The authors review recent findings that implicate basal ganglia abnormalities in the pathophysiology of mood disorders and discuss their potential implications for future developments in the pharmacotherapy of depressive disorder.

Antidepressive Agents↗
PubMed1982

Basal ganglia infarction demonstrated by radionuclide brain imaging.

Four cases of basal ganglia infarction demonstrated by radionuclide brain imaging are presented. Bilateral basal ganglia infarctions in two patients were probably related to methanol intoxication and meningoencephalitis, and unilateral basal ganglia infarctions in two other patients were presumably due to cerebral atherosclerosis and/or hypertension. Various causes and mechanisms of basal ganglia infarction as well as positive findings of radionuclide brain imaging are briefly reviewed.

Basal Ganglia↗
PubMed1999

Variation in echogenicity of the basal ganglia: anisotropic effect.

We observed that the fetal brain demonstrates relatively increased echogenicity of the basal ganglia compared with the thalami and cortical brain parenchyma, which we did not observe on neonatal sonograms. We hypothesized that the difference in relative echogenicity was due to differences in imaging techniques and anisotropic effects for prenatal and postnatal brain images. In 18 consecutive neonates, we obtained coronal images of the basal ganglia and thalami through the anterior fontanelle and axial images through the anterolateral fontanelle with both 5 and 7.5 MHz transducers. Two observers determined whether increased echogenicity or conspicuity of the basal ganglia was present, comparing the axial and coronal planes. We observed relatively increased echogenicity of the basal ganglia in the axial plane in 11 of the 16 examinations in this series. Of these 11, the increased echogenicity effect was manifest only in the axial plane in seven neonates. In the four instances in which the increased basal ganglia echogenicity was seen in both the coronal and axial planes, the effect was better shown in axial plane in all four. We did not observe any cases of increased echogenicity of the basal ganglia only in the coronal plane. The increased echogenicity was more conspicuous with the lower frequency transducer in 10 of the 11 examinations. We believe that the change in echogenicity of the basal ganglia is predominantly an anisotropic effect. Observing that increased echogenicity of the basal ganglia can disappear or decrease when comparing images in the axial to the coronal plane or be better demonstrated with lower frequency transducers might be a means by which to distinguish this phenomenon from true pathologic processes of the neonatal brain.

Anisotropy↗
PubMed2000

Functional changes of the basal ganglia circuitry in Parkinson's disease.

The basal ganglia circuitry processes the signals that flow from the cortex, allowing the correct execution of voluntary movements. In Parkinson's disease, the degeneration of dopaminergic neurons of the substantia nigra pars compacta triggers a cascade of functional changes affecting the whole basal ganglia network. The most relevant alterations affect the output nuclei of the circuit, the medial globus pallidus and substantia nigra pars reticulata, which become hyperactive. Such hyperactivity is sustained by the enhanced glutamatergic inputs that the output nuclei receive from the subthalamic nucleus. The mechanisms leading to the subthalamic disinhibition are still poorly understood. According to the current model of basal ganglia organization, the phenomenon is due to a decrease in the inhibitory control exerted over the subthalamic nucleus by the lateral globus pallidus. Recent data, however, suggest that additional if not alternative mechanisms may underlie subthalamic hyperactivity. In particular, given the reciprocal innervation of the substantia nigra pars compacta and the subthalamic nucleus, the dopaminergic deficit might influence the subthalamic activity, directly. In addition, the increased excitatory drive to the dopaminergic nigral neurons originating from the hyperactive subthalamic nucleus might sustain the progression of the degenerative process. The identification of the role of the subthalamic nucleus and, more in general, of the glutamatergic mechanisms in the pathophysiology of Parkinson's disease might lead to a new approach in the pharmacological treatment of the disease. Current therapeutic strategies rely on the use of L-DOPA and/or dopamine agonists to correct the dopaminergic deficit. Drugs capable of antagonizing the effects of glutamate might represent, in the next future, a valuable tool for the development of new symptomatic and neuroprotective strategies for therapy of Parkinson's disease.

Animals↗
PubMed1997

Basal ganglia volume in adults with Down syndrome.

This study was designed to determine the effects of aging on the volume of the basal ganglia in individuals with Down syndrome (DS) and to examine the relationship between basal ganglia volumes, neuropsychological test performance, and dementia status in this population. Subjects were 32 adults with DS. Basal ganglia volumes from 22 of these subjects were compared with those of 22 cognitively-normal individuals, who were individually matched on age, sex, and race. Performance on neuropsychological tests was correlated with basal ganglia volumes for 32 individuals with DS, and basal ganglia volumes of five demented DS subjects were compared with those of 14 non-demented DS subjects. Results indicated larger putamen volumes in the DS subjects, despite significantly smaller total brain volumes. Volumes of caudate and globus pallidus did not differ between DS and control subjects. Although there were some significant correlations between basal ganglia volumes and age, neuropsychological test performance, and dementia status in the DS subjects, these associations appeared to be a reflection of neurodevelopmental or atrophic reductions in overall brain volume rather than a reflection of specific basal ganglia abnormality. Correlations between age and volumes of basal ganglia and total brain were not significantly greater in non-demented DS subjects than in control subjects. Results suggest that volume reductions of the basal ganglia are not a salient feature of aging or of the dementia associated with DS.

Adult↗
PubMed1984

Motor disorders in basal ganglia disease.

The clinical motor symptoms of basal ganglia disease are explored in relation to possible functions of this region of the human brain. It is concluded that Parkinsonian akinesia, and the dyskinesias of chorea, hemiballism and torsion dystonia are likely to represent the critical abnormalities of motor action in human basal ganglia lesions. These motor disorders involve most muscles, all classes of movement, and the individual sequential components of movement, but spare the overall motor plan. It is suggested that Parkinsonian akinesia is due to putaminal dysfunction disrupting the normal automatic execution of learned motor plans. The dyskinesias of chorea, hemiballism and torsion dystonia are conceived as being due to dysfunction of other strio-pallidal regions superimposed upon the normal function of the motor strio-pallidal system.

Basal Ganglia↗
PubMed2001

Basal ganglia motor function in relation to Hallervorden-Spatz syndrome.

Hallervorden-Spatz syndrome (HSS) is a degenerative neurologic disorder associated with progressive rigidity, dystonia, impaired voluntary movement, dysarthria, and mental deterioration. Pathologically, there is iron deposition in the basal ganglia, with destruction of basal ganglia output neurons. Recent advances in the understanding of basal ganglia functional anatomy and physiology make it possible to hypothesize how specific neural mechanisms relate to specific clinical manifestations of HSS. Experimental lesions of the basal ganglia output nucleic cause involuntary muscle contractions, similar to contractions observed in dystonia. A model of selection and suppression of competing motor patterns by the basal ganglia is presented in relation to the manifestations of damage to basal ganglia output neurons. It is hypothesized that the dystonia and other motor abnormalities seen in HSS can be attributed to degeneration of basal ganglia output neurons.

Basal Ganglia↗
PubMed2005

Birdbrains could teach basal ganglia research a new song.

Recent advances in anatomical, physiological and histochemical characterization of avian basal ganglia neurons and circuitry have revealed remarkable similarities to mammalian basal ganglia. A modern revision of the avian anatomical nomenclature has now provided a common language for studying the function of the cortical-basal-ganglia-cortical loop, enabling neuroscientists to take advantage of the specialization of basal ganglia areas in various avian species. For instance, songbirds, which learn their vocal motor behavior using sensory feedback, have specialized a portion of their cortical-basal ganglia circuitry for song learning and production. This discrete circuit dedicated to a specific sensorimotor task could be especially tractable for elucidating the interwoven sensory, motor and reward signals carried by basal ganglia, and the function of these signals in task learning and execution.

Animals↗
PubMedDate not supplied

[Informational analysis of the basal ganglia related system].

This paper describes a major cerebral system whose contours are only emerging: the "basal ganglia related system". This is made up of the "system of the basal ganglia" itself plus its inputs and outputs. The system of the basal ganglia may be divided into the "basal ganglia core" comprising the striatum and its pallidal and nigral targets and the "regulators of the core". Distinguishable include regulators of the striatum (the dopaminergic pars compacta and the central complex of the thalamus or centre median-parafascicularis), regulators of the pallidonigrum (the subthalamic nucleus and the pedunculopontine complex) and internal regulators (at first the lateral nucleus of the pallidum). The main input to this system comes from the cerebral cortex. The main output is the thalamus and from it to the cortex. The whole "basal ganglia related system" may thus be seen as a cortico-cortical circuit passing through the basal ganglia. Information processing in the system is very complex. New data presented here emphasize two connections: cortico-striate and striato-pallidonigral connections. It is stressed that the first uses complex combinations of confluence or difluence on small matricial islands. This step could be a selection and reorganisation of cortical information. The second process is a strong "dynamically focused convergence" combining information from different upstream sources in order to derive an adequate informational product for the production of harmonious and adapted motricity.

Basal Ganglia↗
PubMed1999

Motor actions of cannabinoids in the basal ganglia output nuclei.

The levels of CB1 cannabinoid receptors in the basal ganglia are the highest in the brain, comparable to the levels of dopamine receptors, a major transmitter in the basal ganglia. This localization of receptors is consistent with the profound effects on motor function exerted by cannabinoids. The output nuclei of the basal ganglia, the globus pallidus (GP) and substantia nigra reticulata (SNr), apparently lack intrinsic cannabinoid receptors. Rather, the receptors are located on afferent terminals, the striatum being the major source. Cannabinoids blocked the inhibitory action of the striatal input in the SNr. Furthermore, cannabinoids blocked the excitatory effect of stimulation of the subthalamic input to the SNr revealing, along with data from in situ hybridization studies, that this input is another likely source of cannabinoid receptors to the SNr. Similar actions of cannabinoids were observed in the GP. Behavioral studies further revealed that the action of cannabinoids differs depending upon which input to the output nuclei of the basal ganglia is active. The inhibitory striatal input is quiescent and the cannabinoid action is observable only upon stimulation of the striatum, while the noticeable effect of cannabinoids under basal conditions would be on the tonically active subthalamic input. These data suggest that the recently discovered endogenous cannabinergic system exerts a major modulatory action in the basal ganglia by its ability to block both the major excitatory and inhibitory inputs to the SNr and GP.

Animals↗
PubMed1986

Effects of estrogen on the basal ganglia.

Recent research suggests that estrogen regulates the activity of dopamine-containing fibers originating in the midbrain and terminating in the basal ganglia, and/or dopamine-sensitive cells in the basal ganglia. The mechanism by which estrogen acts is not clear, since cells in neither of these regions concentrate estrogens. Nevertheless, estrogens clearly affect behaviors mediated by the basal ganglia, as illustrated in human patients suffering from extrapyramidal disorders. Both biochemical and behavioral research in animals has confirmed that estrogen modulates basal ganglia function, but there has not been agreement concerning either the locus, the direction, or the mechanism of its action. These topics are the focus of this review. The effects of estrogen on behaviors mediated by DA in the basal ganglia depend on the dose of estrogen administered, the time interval between estrogen treatment and testing, the behavior measured, and the part of the basal ganglia from which the behavior is elicited. A high dose of estrogen results in an initial suppression and later enhancement of DA-related behaviors elicited from the striatum. However, no later enhancement of these behaviors occurs if a low dose of estrogen is given. Even after low doses of estrogen, the latency to behavioral suppression varies depending upon the behavior measured. These varying latencies suggest that more than one mechanism is involved in the effects of estrogen on basal ganglia output. In addition, estrogen may also act on some regions in the mesolimbic DA system. While estrogen may act indirectly via the catechol estrogens and prolactin, it has been demonstrated that estrogen can act directly on the striatum. These findings are related to the effects of estrogen on human extrapyramidal disorders.

Acetylcholine↗
PubMed2001

A re-evaluation of the current model of the basal ganglia.

The current model of basal ganglia organization has been developed progressively over the last two decades in the light of key observations made at both experimental and clinical levels. This model has been highly successful in that it has stimulated a large amount of research in the field. However, several experimental and clinical findings that are at odds with the model have accumulated during the last decade. This paper reviews some of our own single-axon tracing studies in primates, which call for a re-evaluation of the current basal ganglia model.

Journal Article↗