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PubMed2005

The cerebellum communicates with the basal ganglia.

The cerebral cortex is interconnected with two major subcortical structures: the basal ganglia and the cerebellum. How and where cerebellar circuits interact with basal ganglia circuits has been a longstanding question. Using transneuronal transport of rabies virus in macaques, we found that a disynaptic pathway links an output stage of cerebellar processing, the dentate nucleus, with an input stage of basal ganglia processing, the striatum.

Animals↗
PubMed1983

Reaction of the substantia nigra to massive basal ganglia infarction.

The human substantia nigra can react to destruction of the basal ganglia in several ways. In ten brains with massive unilateral infarction of the basal ganglia slight to moderate nerve cell loss was present in the ipsilateral substantia nigra. The severe nerve cell loss reported in mostly young experimental animals was not observed. One case also displayed a fine network of myelinated and unmyelinated fibers surrounding pigmented nerve cells and dendrites in the ispilateral substantia nigra. Electron microscopy of the substantia nigra from this case showed neurofilamentous hyperplasia, paired helical filaments and rare straight filaments, but only on the side ipsilateral to the striatal infarct. The nerve cell loss in the ten cases was interpreted as a mainly retrograde degeneration, the perineuronal sprouts in case 10 as a reaction to partial deafferentation, and the paired helical filaments as either a retrograde or a transsynaptic reaction in the substantia nigra ipsilateral to the basal ganglia destruction.

Aged↗
PubMed1994

Pedunculopontine nucleus in the squirrel monkey: projections to the basal ganglia as revealed by anterograde tract-tracing methods.

The efferent projections of the pedunculopontine nucleus (PPN) to the basal ganglia have been studied in the squirrel monkey (Saimiri sciureus) with [3H]leucine and Phaseolus vulgaris-leucoagglutinin (PHA-L) as anterograde tracers. Following unilateral injections of [3H]leucine or PHA-L in the central portion of the PPN, numerous autoradiographic linear profiles or PHA-L-labeled fibers ascend to the forebrain, both ipsilaterally and contralaterally. These fibers form a compact bundle that courses in the central portion of the mesopontine tegmentum. At rostral mesencephalic levels, this bundle splits into ventromedial and dorsolateral fascicles that arborize in basal ganglia and thalamic nuclei, respectively. The substantia nigra and the subthalamic nucleus are by far the most densely innervated structures of the basal ganglia. In these two nuclei, labeled fibers arborize profusely ipsilaterally and less abundantly contralaterally. The labeled fibers in the substantia nigra are thin and varicose and arborize almost exclusively in the pars compacta, where they closely surround the soma and proximal dendrites of dopaminergic neurons. In the subthalamic nucleus, labeled fibers are also thin and appear to contact more than one neuron along their course. Numerous labeled fibers also occur in the pallidal complex, where they arborize most profusely in the internal segment. Several thick, labeled fibers oriented dorsolaterally in the pallidal complex give rise to thinner fibers that closely surround the soma and proximal dendrites of pallidal neurons. Some labeled fibers are also scattered in the striatum. These fibers abound in the peripallidal and ventral portions of the putamen, are more sparsely distributed in the remaining portion of the putamen as well as in the caudate nucleus, and are virtually absent in the ventral striatum. These results reveal that the PPN gives rise to a massive and highly ordered innervation of the basal ganglia in the squirrel monkey. This nucleus may thus act as an important relay in the basal ganglia circuitry in primates.

Animals↗
PubMed2002

Mid-gestation right basal ganglia lesion: clinical observations in two children.

OBJECTIVE: To describe the neurobehavioral syndrome in two children with destruction of the right basal ganglia ostensibly from amniocentesis needle penetration at 17 weeks of gestation. BACKGROUND: Early-life unilateral lesions of the basal ganglia are rare and the resulting syndrome not described. METHODS: Both children had repeated clinical assessments, MRI and (18)F-fluorodeoxyglucose PET scans, and psychometric and achievement testing over 10 years. RESULTS: Right basal ganglia destruction was similar and virtually coextensive in both children; optic nerve and oculomotor dysfunction were disparate. One had a right temporal pole porencephalic cyst with anomalous overlying cortex. The clinical syndrome included left hemiparesis with distal spasticity and without hypotrophy; extraocular movement disorders; severe episodic disinhibition, impulsiveness, hitting reflexively, and extreme emotional lability. Outbursts of screaming and cursing resembled "sham rage." Both had mild intellectual retardation with competent language but poor nonverbal and visual-spatial abilities, visual memory, and daily living and socialization skills. CONCLUSIONS: The shared behavioral and cognitive syndrome is most reasonably attributed to the right basal ganglia lesions, which were complete and coextensive in both, whereas other lesions were partial, milder, and disparate. Early destruction of the right basal ganglia may preclude normal development of right hemisphere functions without evidence of plasticity and appears associated with intense disinhibition and impulsiveness of aggressive attack activities and with general lability and dyscontrol of emotion.

Adolescent↗
PubMed2006

Basal ganglia germinoma in children with associated ipsilateral cerebral and brain stem hemiatrophy.

BACKGROUND: Germinoma is the most common and least-malignant intracranial germ cell tumor, usually found in the midline. Germinoma that arises in the basal ganglia, called ectopic germinoma, is a rare and well-documented entity representing 5% to 10% of all intracranial germinomas. The association of cerebral and/or brain stem atrophy with basal ganglia germinoma on CT and MRI is found in 33% of the cases. OBJECTIVE: To review the literature and describe the CT and MRI findings of basal ganglia germinoma in children, known as ectopic germinoma, with associated ipsilateral cerebral and brain stem hemiatrophy. MATERIALS AND METHODS: Three brain CT and six brain MRI studies performed in four children at two institutions were retrospectively reviewed. All patients were male (case 1, 14 years; case 2, 13 years; case 3, 9 years; case 4, 13 years), with pathologically proved germinoma arising in the basal ganglia, and associated ipsilateral cerebral and/or brain stem hemiatrophy on the first imaging study. It is important to note that three of these children presented with cognitive decline, psychosis and slowly progressive hemiparesis as their indication for imaging. RESULTS: Imaging results on initial scans were varied. In all patients, the initial study showed ipsilateral cerebral and/or brain stem hemiatrophy, representing Wallerian degeneration. All patients who underwent CT imaging presented with a hyperdense or calcified lesion in the basal ganglia on unenhanced scans. Only one of these lesions had a mass effect on the surrounding structures. In one of these patients a large, complex, heterogeneous mass appeared 15 months later. Initial MR showed focal or diffusely increased T2 signal in two cases and heterogeneous signal in the other two. CONCLUSION: The association of a focal lesion in the basal ganglia of children with progressive hemiparesis, neuropsychiatric symptoms and ipsilateral cerebral and/or brain stem hemiatrophy should prompt the diagnosis of ectopic germinoma, avoiding delay in the diagnosis and further irreversible clinical deterioration, in a malignancy with an otherwise favorable prognosis. In these patients, hemiatrophy preceding or accompanying the imaging depiction of a basal ganglia mass lesion is thought to be caused by a paraneoplastic process.

Adolescent↗
PubMed2000

Lesch-Nyhan disease and the basal ganglia.

The purpose of this review is to summarize emerging evidence that the neurobehavioral features of Lesch-Nyhan disease (LND), a developmental disorder caused by congenital deficiency of the purine salvage enzyme hypoxanthine-guanine phosphoribosyltransferase (HPRT), may be attributable to dysfunction of the basal ganglia. Affected individuals have severe motor disability described by prominent extrapyramidal features that are characteristic of dysfunction of the motor circuits of the basal ganglia. They also display disturbances of ocular motility, cognition, and behavioral control that may reflect disruption of other circuits of the basal ganglia. Though neuropathologic studies of autopsy specimens have revealed no obvious neuroanatomical abnormalities in LND, neurochemical studies have demonstrated 60-90% reductions in the dopamine content of the basal ganglia. In addition, recent PET studies have documented significant reductions in dopamine transporters and [18F]fluorodopa uptake in the basal ganglia. These findings support the proposal that many of the neurobehavioral features of LND might be related to dysfunction of the basal ganglia.

Animals↗
PubMed2005

Bilateral basal ganglia and cerebellar lesions in an alcoholic hyperosmolar patient.

Bilateral symmetrical basal ganglia lesions may be caused by hypoxic/ischemic injury. However, similar lesions have not been described in the cerebellar cortex. To report a case of bilateral basal ganglia and cerebellar lesions in an alcoholic patient with hyperglycemia and hypotension. A 47-year-old alcoholic man with hypotension of unknown duration and hyperosmolarity had mild weakness of the left upper extremity. Neuroimaging revealed abnormality of bilateral symmetric globus pallidus and inferior cerebellum. Prolonged hypotension with hyperosmolarity may give rise to bilateral basal ganglia and cerebellar lesions.

Alcoholism↗
PubMed2003

Dissociating hippocampal versus basal ganglia contributions to learning and transfer.

Based on prior animal and computational models, we propose a double dissociation between the associative learning deficits observed in patients with medial temporal (hippocampal) damage versus patients with Parkinson's disease (basal ganglia dysfunction). Specifically, we expect that basal ganglia dysfunction may result in slowed learning, while individuals with hippocampal damage may learn at normal speed. However, when challenged with a transfer task where previously learned information is presented in novel recombinations, we expect that hippocampal damage will impair generalization but basal ganglia dysfunction will not. We tested this prediction in a group of healthy elderly with mild-to-moderate hippocampal atrophy, a group of patients with mild Parkinson's disease, and healthy controls, using an "acquired equivalence" associative learning task. As predicted, Parkinson's patients were slower on the initial learning but then transferred well, while the hippocampal atrophy group showed the opposite pattern: good initial learning with impaired transfer. To our knowledge, this is the first time that a single task has been used to demonstrate a double dissociation between the associative learning impairments caused by hippocampal versus basal ganglia damage/dysfunction. This finding has implications for understanding the distinct contributions of the medial temporal lobe and basal ganglia to learning and memory.

Aged↗
PubMed2000

[Asymptomatic familial basal ganglia calcification with autosomal dominant inheritance: a family report].

We report here a pedigree of basal ganglia calcification with autosomal dominant inheritance. Following a traffic accident, the proband, a seven-year-old boy, was incidentally noted by cranial computed tomography to have calcification of the bilateral basal ganglia. Six affected members spanning three generations, aged from 5 to 57 years, also had calcification in various degree. None of them had clinical symptoms. There were neither abnormal data nor any characteristic physical symptoms associated with parathyroid disorders. There was no consanguinity. Both sexes were affected and the sex ratio was 0.5. Male-to-male transmission was documented. These findings suggested an autosomal dominant trait. The clinico-radiological findings in our pedigree were different from those of the previously reported cases of familial basal ganglia calcification, that infants were affected and that clinical symptoms were absent in elderly patients. These facts suggest our pedigree is a new type of familial basal ganglia calcification with autosomal dominant inheritance.

Basal Ganglia Diseases↗
PubMed1997

Subthalamic ablation reverses changes in basal ganglia oxidative metabolism and motor response to apomorphine induced by nigrostriatal lesion in rats.

In Parkinson's disease, the functional architecture of the basal ganglia nuclei undergoes profound alterations, one of the most important of which is overactivity of the basal ganglia output nuclei. This phenomenon seems to be intimately related to pathological overactivity of the subthalamic nucleus, which directly modulates the basal ganglia output through its glutamatergic projections. In this study, we investigated the effects of unilateral subthalamic nucleus lesions on the activities of succinate dehydrogenase and cytochrome oxidase, two markers of neuronal activity, in rats with prior unilateral lesions of the nigrostriatal tract. We also explored the effect of subthalamic nucleus lesions on the rotational response to systemic apomorphine. Rats with unilateral lesions of the nigrostriatal tract showed ipsilateral increases in enzyme activity in the basal ganglia output nuclei, entopeduncular nucleus and substantia nigra pars reticulata. Selective subthalamic nucleus destruction completely reversed this phenomenon. In addition, subthalamic nucleus lesions abolished the rotational response to apomorphine. These results confirm that overactivity of the subthalamic nucleus plays a pivotal role in the functional alterations of basal ganglia associated with Parkinson's disease. They also shed further light on the neural mechanisms through which manipulations of subthalamic activity can ameliorate Parkinson's disease symptoms.

Animals↗
PubMed2000

Role of the basal ganglia in the control of purposive saccadic eye movements.

In addition to their well-known role in skeletal movements, the basal ganglia control saccadic eye movements (saccades) by means of their connection to the superior colliculus (SC). The SC receives convergent inputs from cerebral cortical areas and the basal ganglia. To make a saccade to an object purposefully, appropriate signals must be selected out of the cortical inputs, in which the basal ganglia play a crucial role. This is done by the sustained inhibitory input from the substantia nigra pars reticulata (SNr) to the SC. This inhibition can be removed by another inhibition from the caudate nucleus (CD) to the SNr, which results in a disinhibition of the SC. The basal ganglia have another mechanism, involving the external segment of the globus pallidus and the subthalamic nucleus, with which the SNr-SC inhibition can further be enhanced. The sensorimotor signals carried by the basal ganglia neurons are strongly modulated depending on the behavioral context, which reflects working memory, expectation, and attention. Expectation of reward is a critical determinant in that the saccade that has been rewarded is facilitated subsequently. The interaction between cortical and dopaminergic inputs to CD neurons may underlie the behavioral adaptation toward purposeful saccades.

Animals↗
PubMed2000

Chronological changes in nonhaemorrhagic brain infarcts with short T1 in the cerebellum and basal ganglia.

Our purpose was to investigate nonhaemorrhagic infarcts with a short T1 in the cerebellum and basal ganglia. We carried out repeat MRI on 12 patients with infarcts in the cerebellum or basal ganglia with a short T1. Cerebellar cortical lesions showed high signal on T1-weighted spin-echo images beginning at 2 weeks, which became prominent from 3 weeks to 2 months, and persisted for as long as 14 months after the ictus. The basal ganglia lesions demonstrated slightly high signal from a week after the ictus, which became more intense thereafter. Signal intensity began to fade gradually after 2 months. High signal could be seen at the periphery until 5 months, and then disappeared, while low or isointense signal, seen in the central portion from day 20, persisted thereafter.

Adult↗
PubMed2000

Pathophysiology of the basal ganglia in Parkinson's disease.

Insight into the organization of the basal ganglia in the normal, parkinsonian and L-dopa-induced dyskinesia states is critical for the development of newer and more effective therapies for Parkinson's disease. We believe that the basal ganglia can no longer be thought of as a unidirectional linear system that transfers information based solely on a firing-rate code. Rather, we propose that the basal ganglia is a highly organized network, with operational characteristics that simulate a non-linear dynamic system.

Animals↗
PubMed1982

[Germinoma originating in the basal ganglia--report of 2 cases].

We reported two cases of germinoma originating in the basal ganglia among the 50 cases of intracranial germinoma which were experienced at the Department of Neurosurgery, Hokkaido University Hospital. (Case 1) A 8-year-old boy was admitted to our hospital in October 1977, because of precocious puberty and left hemiparesis. Plain CT showed an irregularly-defined high density lesion in the right basal ganglia, which had several low density spots and was moderately enhanced on contrast CT. Endocrinological examination by radioimmunoassay revealed abnormally high level of serum luteinizing hormone and scanty level of serum follicle stimulating hormone. Beta-subunit of human chorionic gonadotropin (HCG) showed 46.4 ng/ml. Following radiation, the lesion on CT disappeared and beta-subunit turned to be in the normal range. It was concluded that the precocious puberty was due to hypersecretion of HCG by the tumor. About 2 years after the first admission, the tumors were disseminated to the spinal cord, followed several months later by the intracranial recurrence. The neurosurgical exploration was performed to both intracranial and spinal tumor lesions, which were proved to be germinoma by histological examination. Postoperative course was uneventful without recurrent signs. (Case 2) A 10-year-old boy was admitted to our hospital with 6-month history of right hemiparesis in February, 1979. CT at the first admission disclosed a slight high density lesion in the left basal ganglia, which had low density area suggesting cyst formation and was moderately enhanced on contrast CT. CT after one year showed multiple cysts in the tumor and displacement of neighboring structures. In February, 1980, a piece of the tumor was removed under bifrontal craniotomy and histologically diagnosed to be germinoma. Following radiation, the tumor disappeared on CT and his clinical features improved. In August, 1981, no recurrent signs were noted. From our 2 cases and review of the literature, it can be concluded that germinoma originating in the basal ganglia is rare and have high radiosensitivity as well as germinoma arising in the other sites, and common symptoms and signs are hemiparesis in all cases, not accompanied by intracranial hypertension in the early stage.

Basal Ganglia↗
PubMed1996

Proton magnetic resonance spectroscopy of the basal ganglia in patients with schizophrenia: a preliminary report.

To examine metabolic changes in the left basal ganglia in chronic schizophrenia, we performed proton magnetic resonance spectroscopy (1H-MRS) in 21 medicated schizophrenic patients and 21 gender and age-matched normal controls. Compared to the normal subjects, the schizophrenic patients showed a significantly increased level of choline containing compounds (Cho) (t = 2.60, p < 0.05) and ratio of Cho to N-acetylaspartate (NAA) (t = 2.46, p < 0.05) in the left basal ganglia. No significant correlation was observed between the 1H-MRS measurements in the left basal ganglia and clinical symptom scores as evaluated using the Brief Psychiatric Rating Scale (BPRS). The chlorpromazine equivalent neuroleptic dosage was positively correlated with the level of NAA (r = 0.38, p < 0.05) and negatively correlated with the Cho/NAA ratio (r = -0.34, p < 0.05). These findings suggest that these changes in metabolites in the left basal ganglia may reflect some of the functional and morphological abnormalities reported previously for the brain in schizophrenia.

Adolescent↗
PubMed1982

Basal ganglia pathways to the tectum: the afferent and efferent connections of the lateral spiriform nucleus of pigeon.

Previous studies have demonstrated that the lateral spiriform nucleus (SpL) of the avian pretectum receives a major input from the ipsilateral basal ganglia (Karten and Dubbeldam, '73) and projects to the ipsilateral optic tectum (Brecha et al., '76). The present study has further detailed the anatomical organization of the afferent and efferent connections of SpL, with particular reference to (1) the sources of afferent inputs to SpL, (2) the projection targets of SpL, and (3) the laminar termination pattern of the SpL projection to the tectum. The SpL was found to receive clear-cut major inputs from only three nuclei: (1) the ipsilateral paleostriatum primitivum (PP) of the basal ganglia (the avian homologue of the mammalian globus pallidus), (2) the ipsilateral anterior nucleus of the ansa lenticularis (ALa) of the diencephalon, and (3) the ipsilateral nucleus tegmentipedunculopontinus (TPc) of the mesencephalon. Both TPc and ALa have previously been noted themselves to receive major inputs from the ipsilateral PP (Karten and Dubbeldam, '73). Two other cell groups may give rise to a slight projection to the ipsilateral SpL: (1) the posterior nucleus of the ansa lenticularis (ALp) of the diencephalon and (2) the nucleus semilunaris (SLu) of the isthmic brainstem. The ALp also receives a major input from PP (Karten and Dubbeldam, '73). Two other cell groups may give rise to a slight projection to the ipsilateral SpL: (1) the posterior nucleus of the ansa lenticularis (ALp) of the diencephalon and (2) the nucleus semilunaris (SLu) of the isthmic brainstem. The ALp also receives a major input from PP (Karten and Dubbeldam, '73), while SLu receives a major tectal projection (Hunt and Kunzle, '76a). The ipsilateral tectum was found to be the only projection target of SpL. The present data suggest that the SpL projection to the tectum is restricted to layers 8-13, with layers 11-13 receiving the heaviest projection from SpL. Among layers 8-10, layer 9 receives the lightest projection from SpL. The present results indicate that SpL receives only a limited number of inputs, which in all likelihood relay largely basal ganglia input to SpL. Since SpL projects only to the tectum, the sole function of SpL apparently is the transmission of ipsilateral basal ganglia influences to the avian optic tectum. Tectal layers 8-15 have been previously found to represent the layers of origin of the descending pathways of the avian tectum to hindbrain motor and "premotor" cell groups (Reiner and Karten, '82). In view of the purported involvement of the basal ganglia in motor functions, the basal ganglia pathway to the ipsilateral tectum via SpL may represent a major route by which the avian basal ganglia exert influences over motor functions.

Afferent Pathways↗
PubMedDate not supplied

[Acute encephalitis: bilateral lesions of the basal ganglia].

OBJECTIVE: To refer two children with acute encephalitis and bilateral basal ganglia lesion and its neurological outcome. CLINICAL CASES: Two girls, one of 9 years and the other of 15 months of age were affected by acute encephalitis, bilateral basal ganglia lesion was found on MRI in both children. Abnormal movements (tremor, choreoatetosis) and dystonia were the main symptomatology. In the first girl a mild dystonic posture on her hand and minor bradykinesia was the only found after a 4 year follow up. The other child, after 17 months of the beginning of her disease, still has generalized dystonia and choreoatetosis movements. Control MRI studies, in both patients remain without changes. CONCLUSION: In acute encephalitis, basal ganglia lesion in two children, produced different neurological sequelae, probably related to the age of the presentation of the disease.

Acute Disease↗
PubMed2000

GluR1 glutamate receptor subunit is regulated differentially in the primate basal ganglia following nigrostriatal dopamine denervation.

Nigrostriatal dopaminergic denervation is associated with complex changes in the functional and neurochemical anatomy of the basal ganglia. The excitatory neurotransmitter glutamate mediates neural signaling at crucial points of this circuitry, and glutamate receptors are differentially distributed in the basal ganglia. Available evidence suggests that the glutamatergic corticostriatal and subthalamofugal pathways become overactive after nigrostriatal dopamine depletion. In this study, we have analyzed the regulation of the GluR1 subunit of the a-amino-3-hydroxy-5-methyl-4-isoxazole propionate glutamate receptor in the basal ganglia of primates following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced dopamine denervation. The dopamine denervation resulted in distinct alterations in GluR1 distribution: (1) GluR1 protein expression was markedly increased in caudate and putamen, and this was most pronounced in the striosomes; (2) GluR1 protein was altered minimally in subthalamic nucleus; (3) expression of GluR1 was down-regulated in the globus pallidus by 63% and in the substantia nigra by 57%. The down-regulation of GluR1 expression in the output nuclei of the basal ganglia, the internal segment of the globus pallidus and the substantia nigra pars reticulata, may be a compensation for the overactive glutamatergic input from subthalamic nucleus, which arises after striatal dopamine denervation. Our results indicate that the glutamatergic system undergoes regulatory changes in response to altered basal ganglia activity in a primate model of Parkinson's disease. Targeted manipulation of the glutamatergic system may be a viable approach to the symptomatic treatment of Parkinson's disease.

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