SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
This article deals with the neuroanatomic aspects of the basal ganglia with regard to different neurotransmitter systems and to different diseases. A general scheme of these circuits with the overall distinction between limbic-associative and motor components and circuits is presented.
We tested the hypothesis that basal ganglia dysfunction may be related to procedural learning impairment in schizophrenia. We determined the N-acetylaspartate/choline (NAA/Cho) ratio in the left striatal area in 11 young first-episode antipsychotic-naive patients and matched controls. Procedural learning was assessed by the four-disk version of the Tower of Hanoi. Analysis of variance showed that the number of moves and the execution time had a significant group effect (P=0.02, P<0.0001, respectively). Correlation analysis between procedural learning and the NAA/Cho ratio showed a negative significant correlation only in patients, measured by both time (P=0.006) and by moves (P=0.001). In summary, we found that schizophrenic patients have impaired procedural learning, and that this impairment is related to basal ganglia metabolism.
Performance on the Wisconsin Card Sort Test (WCST) of patients with schizophrenia, Parkinson's disease (PD), and Huntington's disease (HD) was simulated by a neural network model constructed on principles derived from neuroanatomic loops from the frontal cortex through the basal ganglia and thalamus. The model provided a computational rationale for the empirical pattern of perseverative errors associated with frontal cortex dysfunction and random errors associated with striatal dysfunction. The model displayed perseverative errors in performance when the gain parameter of the activation function in units representing frontal cortex neurons was reduced as an analog of reduced dopamine release. Random errors occurred when the gain parameter of the activation function in units representing striatal neurons was reduced, or when the activation level was itself reduced as an analog of a striatal lesion. The model demonstrated that the perseveration of schizophrenic, Huntington's, and demented Parkinsonian patients may be principally due to ineffective inhibition of previously learned contextual rules in the frontal cortex, while the random errors of Parkinson's and Huntington's patients are more likely to be due to unsystematic errors of matching in the striatum. The model also made specific, empirically falsifiable predictions that can be used to explore the utility of these putative mechanisms of information processing in the frontal cortex and basal ganglia.
OBJECTIVES: The authors report the results of gamma knife (GK) radiosurgery on a clinical series of selected patients with basal ganglia arteriovenous malformations (BGAVMs) in the brain. Clinical, epidemiological, anatomical and functional characteristics of BGAVMs and of supratentorial cortical AVMs are comparatively analyzed, and their influence on radiosurgical outcome is discussed. METHODS: At our Department, 33 BGAVMs (21 with FU > 2 years) and 209 cortical AVMs (110 with FU > 2 years) with a radiosurgical volume </= 10 cc were treated with GK between February 1993 and July 2001. Mean age, male/female ratio (M/F), and incidence of haemorrhagic onset in the two subgroups of patients were as follows: 25.5 years (5 - 62 years), 16 M/17 F, and 30/33 (91%) in BGAVMs; 34.4 years (8 - 74 years), 124 M/85 F, and 107/209 (51%) in cortical AVMs. Statistical analysis performed using the contingency table method and deviance analysis according to generalized linear models showed that the differences in age and incidence of haemorrhagic onset were highly significant. RESULTS: The rates of complete obliteration, permanent morbidity, bleeding/rebleeding during the latency period, and unsuccessful embolisation attempts in the two subgroups of patients were as follows: 81%, 4%, 8%, and 41.7%, respectively, in BGAVMs; 85.5%, 2%, 2%, and 2% in cortical AVMs. Statistical analysis did not show any significant difference between the two subgroups of patients in the rates of complete obliteration, permanent morbidity, or latency period bleeding/rebleeding, while difference in failed embolization rates resulted to be highly significant (P = 0.00003). CONCLUSIONS: In our experience, the different clinical, epidemiological and anatomico-functional characteristics of BGAVMs and cortical AVMs do not seem to influence the radiosurgical outcome, since complete obliteration and permanent neurological sequelae rates were very similar in these two subgroups of patients. GK may be considered the first choice treatment modality for BGAVMs with < 10 cc volume, since it offers a very high cure rate, very low permanent morbidity, and zero mortality. Although haemorrhagic onset is much more frequent in BGAVMs than in cortical AVMs, the difference between the bleeding/rebleeding rates in the two subgroups of patients during the latency period is not statistically significant, and seems to be limited to the first year after GK.
In a group of 3,800 computed tomography examinations, 14 patients (0.4%) were found to have high attenuating lesions suggesting calcifications within the basal ganglia. The lesions were bilateral in all patients. A majority of the patients had psychic symptoms and convulsions. Electroencephalographic changes were frequent and extrapyramidal symptoms occurred. Until now only three patients have been endocrinologically examined. One of them had hypoparathyroidism. Since parathyroid dysfunction frequently is associated with calcifications of the basal ganglia, these patients should be referred for endocrinological evaluation.
To define the site of pathology in Tourette's syndrome (TS), we performed a volumetric MRI study of basal ganglia structures and lateral ventricles on 37 children with this disorder and 18 controls. There were no statistically significant differences in the size of the right or left caudate, putamen, globus pallidus, or ventricles in these populations. In contrast, there were significant differences for measures of symmetry in the putamen and the lenticular region. Virtually all controls (17 right- and one left-handed) had a left-sided predominance of the putamen, whereas in 13 of 37 TS subjects, a right predominance exceeded that of any control. Statistical comparisons among TS patients, with (n = 18) or without (n = 19) attention-deficit hyperactivity disorder (ADHD), and controls showed significant differences for the volume of the left globus pallidus and for lenticular asymmetry. Post hoc evaluations showed that in the TS + ADHD group, the volume of the left globus pallidus was significantly smaller than the volume of the right and that lenticular asymmetry was due to a greater right-sided predominance in the TS+ADHD group. This study lends further support to proposals that claim the basal ganglia is involved in the pathogenesis of TS and also suggests that the comorbid problem of ADHD is related to regional changes that differ from those primarily associated with tics.
This study compares the basal ganglia of rats, marmosets, macaques, baboons, and humans. It uses established protocols to estimate the volume and number of neurons within the output nuclei (internal globus pallidus, IGP; and nondopaminergic substantia nigra, SNND), two internal relay and modulating nuclei (subthalamic nucleus, STh; and external globus pallidus, EGP), and a modulator of the striatum (dopaminergic substantia nigra, SND). Nuclear boundaries were defined by using immunohistochemistry for striatal afferents. Total numbers of Nissl-stained and parvalbumin-immunoreactive neurons were calculated by using the fractionator technique. Comparisons between species were standardized relative to brain mass (rats < marmosets < macaques < baboons < humans). The EGP consistently had more neurons relative to the IGP, STh, and SND, which had similar neuronal numbers within each species. The SNND had proportionally more neurons in rats than in primates (especially humans). The distribution of SND neurons varied substantially between rats and primates (very few ventrally located neurons in rats) with humans containing fewer SND neurons than other primates. The reduction in SND neurons in humans suggests less dopaminergic regulation of the basal ganglia system compared with other species. The consistency in the number of IGP neurons across all species, combined with the reduction in SNND neurons in humans, suggests a greater emphasis on output pathways through the IGP and that there are proportionally more STh and EGP neurons in humans.
A 59-year-old female patient suddenly developed vomiting and gait disturbances followed by decreasing consciousness. CT scans revealed a hemorrhage within the left basal ganglia region with rupture into the ventricles and consecutive hydrocephalus. On angiography an aneurysm in the region of the caput nuclei caudati was shown to be the source of the bleeding. On repeat-angiography 4 months later the aneurysm was no longer visualized, probably due to thrombosis. This is an extraordinary case of a basal ganglia aneurysm comparable with the aneurysms of Willis' circle, but located in a region where generally microaneurysms--mostly combined with hypertension or moyamoya disease--can be found.
Despite recent advances in the understanding of the pathophysiology of movement disorders, little is known about the precise function the basal ganglia play in the control of movement. We review an approach to studying the function of neural systems that is based on the use of a class of computer models known as parallel distributed processors (PDPs) and indicate its potential range of applications to the study of movement disorders. PDPs can be used to construct computational devices that take into account the anatomical and pharmacological properties of real neural systems. They can also provide computational-level insights that can lead to novel hypotheses concerning brain function. We discuss both these approaches and outline a scheme of the functional organization of the basal ganglia, which predicts some of the pathophysiological mechanisms that mediate movement disorders and which can be formally modeled on a computer.
Explore the source record for details and available documents.
Positron emission tomography imaging has revealed basal ganglia and thalamic abnormalities in cerebral blood flow, metabolism and neurotransmission in patients with partial epilepsy. Although these changes remain of uncertain significance, this involvement could be associated with the initiation, propagation or control of seizures. This paper will review the imaging data obtained using positron emission tomography in patients with partial and generalized epilepsy.
We report three Japanese children with chronic active Epstein-Barr virus (EBV) infection and neurologic findings that included symmetric calcifications in the bilateral basal ganglia. This finding, common in pediatric acquired immunodeficiency syndrome (AIDS), suggests that EBV could be responsible for calcification in the basal ganglia seen in children with AIDS and in other idiopathic diseases.
Previous studies using radioimmunoassay procedures have failed to show age-related changes in the concentration of Met- and Leu-enkephalin or neurotensin in rat basal ganglia. In contrast, using a combined high-pressure liquid chromatography (HPLC)-radioimmunoassay (RIA) technique we now report considerable decreases in the levels of these neuropeptides in areas of basal ganglia of 22 months old-compared to 3 months-old male Wistar rats. The concentration of Met-enkephalin was greatly reduced in the striatum and nucleus accumbens, but not in substantia nigra, of old compared to young animals. There was a similarly large decrease in Leu-enkephalin content in striatum of old rats with less marked decreases occurring in both the nucleus accumbens and substantia nigra. Neurotensin levels in the striatum and substantia nigra were greatly reduced in old rats, with a less marked decrease in the nucleus accumbens.
The current study examines in an animal model the relation of excessive iron accumulation in the basal ganglia to the pathology of Parkinsonism and Hallervoden-Spatz disease. Following a unilateral microinjection of excitatory amino acids, kainate, or quinolinate to the anterior olfactory nucleus/ventral striatal region, an increase in histochemical iron concentration was observed in the ipsilateral ventral pallidum, the islands of calleja, the globus pallidus, the entopeduncular nucleus, the ventral thalamus, and the substantia nigra pars reticulata. The iron was observed both in glia and as intensification of patches in the neuropil. In a second group of rats, after microinjection of ibotenate or quisqualate to the nucleus basalis of Meynert, iron accumulated in the ipsilateral entopeduncular nucleus and pars reticulata of substantia nigra. Increased iron accumulation, compared to that in the contralateral side, was stable for months after a single microinjection. In the basal ganglia distal from the site of EAA injection, no gross morphological changes were associated with the increased iron accumulation. The implications of these findings to the pathology of Parkinson's and Hallervorden-Spatz diseases are discussed.
Neurosarcoidosis may spread from the basal leptomeninges via the Virchow-Robin spaces to form intraparenchymal masses. We present a case of sarcoidosis whose first presentation was that of secondary amenorrhoea without other neurological symptoms. Discovery of a mass invading the basal ganglia, hypothalamus, pituitary stalk and midbrain led to a search for systemic involvement. After the diagnosis was proven by mediastinal biopsy, steroids were used effectively to shrink the tumour. Sequential magnetic resonance imaging (MRI) studies demonstrate dramatic reduction in the mass over a six month period. A high index of suspicion for sarcoidosis in intracranial masses, particularly in young adults, is advocated.
Echogenic stripes in the basal ganglia were identified sonographically in a 4-month-old infant with human immunodeficiency virus (HIV) infection. This lenticulostriate arteriopathy correlated well with histologically identified early alterations of HIV encephalopathy in children. At 3 years and 5 months, CT examination performed after three seizures showed calcification in the area of the sonographically affected arteries but no signs of progressive encephalopathy. The child's mental and motor development have remained normal until now. Cerebral sonography performed in early infancy may allow identification of HIV encephalopathy even before its clinical manifestation.
In the present study we have investigated the efferent projections of both the dorsal and the ventral pallidum of the pigeon basal ganglia, using the sensitive anterograde tracer biotinylated dextran amine [Veenman C. L. et al. (1992) J. Neurosci. Meth. 41, 239-254]. Injections of biotinylated dextran amine in the pigeon dorsal pallidum produced numerous fibers and terminals in specific nuclei of the thalamus, hypothalamus, pretectum and midbrain tegmentum. In the thalamus, labeled fibers and terminals were observed in the avian thalamic reticular nucleus, the proposed motor part of the avian ventral tier (ventrointermediate area), the avian parafascicular nucleus (nucleus dorsointermedius posterior), as well as in the avian nucleus subrotundus (which may be comparable to the posterior intralaminar nuclei of mammals). Labeled fibers and terminals were also observed in the avian subthalamic nucleus (anterior nucleus of the ansa lenticularis), in the pretectum (nucleus spiriformis lateralis) and in the avian substantia nigra pars reticulata. Injections of biotinylated dextran amine in the pigeon ventral pallidum produced fibers and terminals in specific centers of the telencephalon, hypothalamus, thalamus, epithalamus, and midbrain and isthmic tegmentum. Labeled fibers and terminals were also observed in the avian subthalamic nucleus and the inmediately adjacent lateral hypothalamus, the avian thalamic reticular nucleus, the avian medidorsal nucleusaand posterior intralaminar nuclei, and the lateral habenula. Finally, labeled fibers and terminals were found in the ventral tegmental area, the avian substantia nigra pars compacta and the midbrain/isthmic tegmentum, which includes the pedunculopontine tegmental nucleus. Our results indicate that both the dorsal and ventral pallida of birds have unique and specific projection patterns, which are very similar to those of their counterparts in mammals. Our study suggests that these avian basal ganglia regions may be related mainly to somatomotor and limbic functions, respectively.
Action is controlled by both motivation and cognition. The basal ganglia may be the site where these kinds of information meet. Using a memory-guided saccade task with an asymmetric reward schedule, we show that visual and memory responses of caudate neurons are modulated by expectation of reward so profoundly that a neuron's preferred direction often changed with the change in the rewarded direction. The subsequent saccade to the target was earlier and faster for the rewarded direction. Our results indicate that the caudate contributes to the determination of oculomotor outputs by connecting motivational values (for example, expectation of reward) to visual information.