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At least 19 recordsLinked to original sources

PubMed1979

Basal ganglia calcification in Down's syndrome.

Basal ganglia calcification has been observed in autopsy material of 7% of children suffering from Down's Syndrome. The incidence of this finding in the general neurological population is approx. 0.3%. The present report is the first case of Down's Syndrome with basal ganglia calcification diagnosed in life by computed axial tomography. This case illustrates that dense basal ganglia calcification can exist with no signs or symptoms of a movement disorder.

Adolescent↗

PubMed2025

Genetic background of neurological disorders with basal ganglia calcification.

BACKGROUND: Bilateral basal ganglia calcifications (BGCs), if severe, are known hallmarks for idiopathic BGC disease (IBGC), but if milder, are often considered radiological findings of unknown significance. In previous studies, only a minority of patients with BGC had monogenic forms of IBGC. METHODS: We studied consecutive patients from a tertiary neurology clinic with bilateral BGCs of variable severity, and their families. We analyzed known IBGC genes, and an extended panel of genes linked to monogenic stroke and metabolic conditions. Clinical, radiological, and genetic data were collected, including vascular risk factors, cerebrovascular events, imaging findings (total calcification score, white matter hyperintensities, ischemic/hemorrhagic lesions), and relevant family history. RESULTS: Twenty-four families with BGCs and neurological symptoms were analyzed. Disease-causing variants were identified in 14 families (58.3%). Eight patients had IBGC (variants in SLC20A2, PDGFB, MYORG), 4 had mitochondrial disease (MT-TL1), and 2 had monogenic vascular conditions (GAL, MAP3K6). Three variants were novel. BGC severity was highest in IBGC cases, while vascular and mitochondrial cases had milder calcifications. White matter hyperintensities were seen in 94.7% of cases and correlated highly with the total calcification score. Clinical vascular events had occurred in 41.7% cases. No monogenic cause was found in 10 patients, although many of these showed clinical or radiological features suggestive of monogenic disease. CONCLUSIONS: Bilateral BGCs can occur in many neurogenetic disorders apart from IBGCs, and a broader genetic search increases the diagnostic yield. Patients with BGCs frequently had clinical cerebrovascular events, which emphasizes the role of cerebrovascular pathology in BGCs.

Humans↗

PubMed1975

Basal ganglia calcification as a late radiation effect.

Basal ganglia calcification following radiation therapy has rarely been documented in the literature. A case of diffuse bilateral basal ganglia calcification developing 6 years after irridiation of a hypothalamic glioma is presented. Review of previous reports and other causes of basal ganglia calcification are discussed.

Astrocytoma↗

PubMed1979

Calcification of the basal ganglia: computerized tomography and clinical correlation.

During a 1-year period, 4219 consecutive computerized tomograms (CT) were reviewed for basal ganglia calcification; 14 patients with such calcification were identified. Calcifications on CT scan were bilateral in 12 of these cases and unilateral in 2. All bilateral calcifications were symmetric. The globus pallidus was the site of calcification in 13 of the 14 patients. Bilateral dentate nucleus calcification was seen in one patient. Skull radiograms were normal in all but one. Patients had diverse symptoms that were often explained by other findings, suggesting that calcifications may be coincidental and that basal ganglia calcification may not be a nosologic entity. Disturbances of calcium metabolism were not found in these patients, minimizing the pathophysiologic significance of altered calcium metabolism and the need for extensive endocrinologic evaluation. The finding of basal ganglia calcification alone does not justify invasive diagnostic procedures. Extrapyramidal signs may be associated with basal ganglia calcification; parkinsonism associated with basal ganglia calcification differs from idiopathic parkinsonism in being resistant to levodopa therapy.

Adult↗

PubMed1992

Parkinson's disease and basal ganglia calcifications: prevalence and clinico-radiological correlations.

We reviewed computerized tomograms (CT) for basal ganglia and dentate nucleus calcifications in 79 patients with Parkinson's disease (PD), 54 patients with Alzheimer's disease (AD) and 109 controls aged 50 or more. When it was determined, no patient had disturbances in calcium metabolism. We found: (1) 30 subjects out of 242 (12.3%) with calcification located within the lenticular nucleus in 28. (2) Calcifications were unilateral in 11 and asymmetric in 11. (3) The prevalence of calcifications was 21.5% in PD, 9.2% in AD and 7.3% in controls and were significantly more severe in PD than in C and AD (P less than 0.02). (4) PD patients with calcifications were clinically indistinguishable from those without calcification. (5) Calcifications within the basal ganglia were not associated with a levodopa-resistance. We suggest the basal ganglia calcifications are more frequent in PD, but we cannot explain why, since post-synaptic lesions have never been showed in PD.

Aged↗

PubMed1979

Clinical correlations of CT scan-detected calcifications of the basal ganglia.

A review of CT scans of 7,081 patients demonstrated calcifications of the basal ganglia in 53. The calcifications were evident in the skull roentgenograms of only 4 patients out of 40 in whom both CT scans and plain roentgenograms were available, demonstrating the superior resolution of this new method. Seventy-five percent of the patients were older than 50 years of age. Of the younger patients, 5 had had prior cranial irradiation; 1 had received cranial irradiation and intrathecal methotrexate therapy for meningeal leukemia; and 2 others had deep-seated arteriovenous malformations. Serum concentrations of calcium and phosphorus were normal in all 46 patients in whom they were measured. We conclude that the detection of small calcifications of the basal ganglia in persons above 50 years of age is infrequently associated with either clinical signs of basal ganglia dysfunction or calcium and phosphorus abnormalities. Calcium deposition in these patients may be related to vascular changes associated with aging. In younger patients a specific pathogenetic factor or underlying process is infrequently found.

Adolescent↗

PubMed1992

Excitatory amino acid binding sites in the basal ganglia of the rat: a quantitative autoradiographic study.

Quantitative receptor autoradiography was used to determine the distribution of excitatory amino acid binding sites in the basal ganglia of rat brain. alpha-Amino-3-hydroxy-5-methylisoxazole-4-propionic acid, N-methyl-D-aspartate, kainate, quisqualate-sensitive metabotropic and non-N-methyl-D-aspartate, non-kainate, non-quisqualate glutamate binding sites had their highest density in striatum, nucleus accumbens, and olfactory tubercle. Kainate binding was higher in the lateral striatum but there was no medial-lateral striatal gradient for other binding sites. N-Methyl-D-aspartate and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid binding sites were most dense in the nucleus accumbens and olfactory tubercle. There was no dorsal-ventral gradient within the striatal complex for the other binding sites. Other regions of the basal ganglia had lower densities of ligand binding. To compare binding site density within non-striatal regions, binding for each ligand was normalized to the striatal binding density. When compared to the striatal complex, alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid and metabotropic binding sites had higher relative density in the globus pallidus, ventral pallidum, and subthalamic nucleus than other binding sites. Metabotropic binding also had a high relative density in the substantia nigra. Non-N-methyl-D-aspartate, non-kainate, non-quisqualate glutamate binding sites had a high relative density in globus pallidus, ventral pallidum, and substantia nigra. N-Methyl-D-aspartate binding sites had a low relative density in pallidum, subthalamic nucleus, substantia nigra and ventral tegmental area. Our data indicate heterogeneous distribution of excitatory amino acid binding sites within rat basal ganglia and suggest that the character of excitatory amino acid-mediated neurotransmission within the basal ganglia is also heterogeneous.

Animals↗

PubMed1976

Alteration of basal ganglia evoked responses by reserpine and L-dopa.

The effects of reserpine and L-Dopa on basal ganglia evoked potentials were investigated in cats. The caudate response resulting from substantia nigra stimulation and the substantia nigra response elicited by globus pallidus stimulation were increased at several hours after the systemic administration of reserpine. L-Dopa in the presence of dopa decarboxylase inhibition (MK-486) depressed these responses and reversed the effect of reserpine at 0.5 h after administration. Reserpine did not reverse the L-Dopa effect. Reserpine and L-Dopa caused no significant change in responses between other basal ganglia structures. These data give evidence that the basal ganglia are major sites for reserpine and L-Dopa action.

Animals↗

PubMed1992

Radiotherapy of germinomas involving the basal ganglia and thalamus.

Nine patients with histologically confirmed germinomas of the basal ganglia and thalamus (GBT) were treated by radiotherapy. The average dose of 52.5 Gy was delivered to the tumor bed, 37 Gy to the whole brain and 24.8 Gy to the CNS axis. The local control, which was verified by CT scan, was achieved in all patients. All patients are alive 11 to 96 months after radiotherapy. As with other intracranial germinomas, geminomas of the basal ganglia and thalamus respond well to radiotherapy and the prognosis is good after treatment.

Adolescent↗

PubMed1992

Familial calcification of the basal ganglia: a case report and review of the literature.

Although calcification of the basal ganglia is a relatively common and asymptomatic finding on cranial computed tomography, familial idiopathic calcification of the basal ganglia (ICBG) is a rare disorder with neurological and behavioral manifestations. Attention has recently been drawn to the frequency with which cases are diagnosed as schizophrenic (Cummings et al. 1983; Lowenthal, 1986; Davison, 1987). We report a family in which a mother and son have ICBG, but while the son has a paranoid schizophrenia and intellectual deterioration, the mother shows no psychiatric illness. A review of the relevant literature suggests that psychosis is not as common as usually supposed, and may only be coincidentally associated with familial ICBG. Moreover, we find little convincing evidence that familial ICBG is an independent entity; instead, and in agreement with earlier authorities (Bruyn et al. 1964), we argue that published accounts and our own cases provide evidence that the condition is related to pseudo-hypoparathyroidism (PHP) and, therefore, may be due to a defect in a guanine nucleotide binding protein.

Adult↗

PubMed1992

Patterns of termination of cerebellar and basal ganglia efferents in the rat thalamus. Strictly segregated and partly overlapping projections.

There is a widely held view that the cerebellum and basal ganglia act via separate subcortical channels. In rodent, however, electrophysiological evidence suggests that the output of these two systems is partly sent to a common set of thalamic neurons. In this study, the pattern of thalamic innervations provided by the deep cerebellar nuclei, the entopeduncular nucleus, and the substantia nigra pars reticulata was reinvestigated in the rat using the anterograde tracers Phaseolus vulgaris leucoagglutinin and wheat germ agglutinin. Although the results confirm the existence of some overlap in the cerebellar and basal ganglia projection fields, they also show that in such convergent areas the cerebellar innervation is modest and consists of sparsely distributed fibers of thin diameter that provide a few scattered terminal boutons. These observations are consistent with the view that, in rodent as in higher mammalian species, the cerebellum and the basal ganglia act mainly via distinct thalamo-cortical channels.

Animals↗

PubMed1977

The biochemistry of the basal ganglia and Parkinson's disease.

The metabolic pathways for five transmitters in the basal ganglia are briefly described; the results of determinations of their concentrations, of their rate-limiting enzymes and of their degradation products are summarized. The changes found in Parkinson's disease are described. While dopamine synthesis in the basal ganglia is defective in this condition, abnormalities of other transmitters occur, and their possible significance is discussed.

Acetylcholine↗

PubMed1979

[Electron microscopic and histochemical study of the localization of adenylate cylase and acetylcholinesterase in the synapses of the rat cerebral cortex and basal ganglia].

Synapses of the brain cortex and basal ganglia of the rat were studied by means of electron histochemical reactions to adenylate cyclase and acetylcholinesterase. Three types of synapses, viz. cholinergic, adrenergic and mixed, were identified. Typification was carried out on the basis of presynaptic terminal vesicle characteristics and localization of the mentioned enzymes of the synapse receptor area.

Acetylcholinesterase↗

PubMed1992

Rolling mouse Nagoya as a mutant animal model of basal ganglia dysfunction: determination of absolute rates of local cerebral glucose utilization.

In order to elucidate the neuronal mechanism of the motor disturbances of the Rolling mouse Nagoya (rolling), a neurological mutant mouse (genotype rol/rol) showing frequent lurching and falling over on walking, we determined absolute rates of local cerebral glucose utilization (LCGU) with the [14C]deoxyglucose method. The rates were compared with those of heterozygote (+/rol) with normal behavior, and of normal mice (+/+) of the same strain (C3Hf/Nga). Rolling showed marked and significant increases in LCGU in the structures of the basal ganglia such as the globus pallidus, entopeduncular nucleus, substantia nigra pars compacta and pars reticulata, and subthalamic nucleus, confirming our previous finding with semiquantitative LCGU determination. Additional significant but much less marked increases in LCGU of rolling were found in some structures of the brainstem and limbic system, such as the pedunculopontine nucleus, red nucleus, ventral tegmental area, lateral habenula, and CA1 and CA3 of the hippocampus. Although rolling has been regarded as an animal model of cerebellar ataxia, rolling showed no alterations of LCGU in the cerebellum. The heterozygote showed intermediate increases in LCGU between rolling and normal mice in the basal ganglia structures such as the globus pallidus, substantia nigra pars reticulata and subthalamic nucleus. Our findings indicate that rolling has a definite, genetically determined dysfunction of the basal ganglia. The primary site of the basal ganglia dysfunction might probably be in the striatum, involving both the neostriatum and limbic striatum, and resulting in secondary dysfunction in their target structures.

Animals↗

PubMedDate not supplied

Selective release of glutamine and glutamic acid produced by perfusion of GLP-1 (7-36) amide in the basal ganglia of the conscious rat.

Glucagon-like peptide 1 (GLP-1)(7-36) amide, a member of the family of glucagon and related peptides, synthesized by intestinal L cells, has a well-defined distribution in rat brain. In addition, specific GLP-1(7-36) amide receptors have also been localized in some regions of the brain, which suggests that this novel gut-brain peptide has a role in brain function. Accordingly, we investigated the effects of this peptide on the release of amino acid neurotransmitters in the basal ganglia of conscious rats after its perfusion through a concentric "push-pull" cannula system with an artificial cerebrospinal fluid. To obtain stable basal levels of amino acids, the basal ganglia were perfused with an artificial cerebrospinal fluid for 2 h at a flow rate of 20 microliters/min and then with GLP-1(7-36) amide for 10 min, followed by 40 min poststimulation perfusion. GLP-1(7-36) amide produced an immediate increase (p less than 0.01) of the extracellular levels of glutamine and glutamic acid in the basal ganglia. By contrast, this peptide has no effect on the levels of aspartic acid, glycine, and serine. Because glutamine is a metabolic precursor of glutamic acid and is synthesized almost exclusively in astrocytes, these findings suggest a stimulatory effect of GLP-1(7-36) amide on astrocytes and/or neurons of the rat basal ganglia.

Animals↗

PubMed1975

Morphology of the basal ganglia in Parkinson's disease.

This work consists in part of volume measurements for the caudate nucleus, putamen and pallidum; and in part of a determination of cell-distribution and cell density in the corpus striatum from 9 paralysis agitans patients and 15 control persons from the Institute of Forensic Medicine. All 24 brains were sectioned on a specially constructed apparatus. For each of the individual sections, the size of the basal ganglia was determined by measurements of the section thickness with a capillary tube and area measurements were made by microscopic projection method combined with planimetric methods. For the first six control brains, the area measurements were also taken using point-counting method. The values thus obtained were used in the basic formula for a truncated cone and the volume of the basal ganglia for the individual hemispheres was calculated. The only exception was a single hemisphere where the volume of the basal ganglia was determined after dissecting out and weighing these structures. The results showed that the volume measurements of the corpus striatum and the pallidum in these two groups of brains were quite similar, when differences due to body height, age, and brain weight were taken into account. The volume of the basal ganglia decreased with age in both groups of brains and increased with brain weight. The shrinkage of the tissue as a consequence of the histological procedures was also determined. The shrinkage from fresh to formalin-fixed condition was determined by comparing the distance between the same two marked points in the fresh and formalin-fixed tissue. The shrinkage from the formalin-fixed condition to the completed histological preparation was determined by comparing the distance between known structural characteristics, as measured on photographs showing the formalin-fixed sections, lying beside a millimeter scale, with the same distance on the histologically treated preparations. The accumulated shrinkage in volume was 47.3%.

Adult↗

PubMed1978

[Radiological diagnosis and differential diagnosis of calcifications of the basal ganglia (author's transl)].

The radiological appearance and main features of calcifications of the basal ganglia in metabolic, toxic and hypoxemic disorders, degenerative and systemic diseases, tumors as well as infectious and parasitic lesions are described and demonstrated by typical radiographs. The roentgenological differential diagnosis and etiological classification are debated on occurence, incidence, localization, and topography with regard to individual structures of the basal ganglia, distribution pattern and according to the dimension, shape, margin and density pattern of these calcifications.

Basal Ganglia↗

PubMed1992

Effects of reversible blockade of basal ganglia on a voluntary arm movement.

1. The effects of a reversible blockade of basal ganglia were examined in two monkeys trained to perform a visually guided, step-tracking arm movement around the elbow joint. To block glutamatergic excitation, kynurenate (a glutamate antagonist) was locally injected into the putamen and the external segment (GPe) and the internal segment (GPi) of the globus pallidus contralateral to the arm tested. Muscimol [a gamma-aminobutyric acid (GABA) agonist] was also used to suppress neuronal activity in these structures. The drugs were injected in the arm area of the putamen, which was identified by microstimulation or by recording neural activity. For the GPe and GPi, injections were made into the area medioventral to the arm area of the putamen. 2. The blockade of the putamen caused abnormal braking of the arm movements. The first step of the movement became hypometric, and multiple steps were necessary to reach the target. The electromyographic (EMG) analysis revealed an increase of burst activity in the antagonist muscles and a decrease of that in the agonist muscles at the fast movements. The tonic activity increased in the extensor muscles during a holding period. 3. The blockade of the GPi caused dysmetric movements. Amplitude and peak velocity of the first step of movement largely fluctuated among trials. It became difficult for the animal to brake and adjust its arm onto the target. 4. The blockade of the GPe caused a flexion posture at the elbow joint of the contralateral arm. The tonic activity of the flexor muscles increased. Cocontraction of the agonist and antagonist muscles was also observed. 5. These results suggest that the putaminopallidal system of the basal ganglia contributes to both of two motor functions: 1) static control to maintain the posture with tonic muscle activity, and 2) dynamic control to enable fast movements.

Animals↗