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PubMed1995

High-resolution activation mapping of basal ganglia with functional magnetic resonance imaging.

We investigated the activation of the putamen and the external and internal division of the globus pallidus in 12 normal volunteers during rapid supination and pronation of their right or left hand, using functional MRI (fMRI). We observed an increase in signal intensity varying from 3.1 +/- 1.2% to 23.4 +/- 2.3% during activation. Activated areas were predominantly contralateral to the moving hand and smaller than 5 mm2. These findings indicate that fMRI allows study of the normal function of basal ganglia and may be of value in the investigation of basal ganglia disorders.

Adult↗
PubMedDate not supplied

[Calcification of the basal ganglia and cerebellum].

The basic clinical signs of calcifications of the basal ganglia and cerebellar dentate nuclei are discussed with separation of various forms of that disease. Particular attention was given to the factors which might predispose to the development of the so called idiopathic calcifications (Fahr syndrome), and secondary calcifications in various forms of parathyroid hypofunction.

Adolescent↗
PubMed2000

Deficit of striatal parvalbumin-reactive GABAergic interneurons and decreased basal ganglia output in a genetic rodent model of idiopathic paroxysmal dystonia.

The underlying mechanisms of various types of hereditary dystonia, a common movement disorder, are still unknown. Recent findings in a genetic model of a type of paroxysmal dystonia, the dt(sz) mutant hamster, pointed to striatal dysfunctions. In the present study, immunhistochemical experiments demonstrated a marked decrease in the number and density of parvalbumin-immunoreactive GABAergic interneurons in all striatal subregions of mutant hamsters. To examine the functional relevance of the reduction of these inhibitory interneurons, the effects of the GABA(A) receptor agonist muscimol on severity of dystonia were examined after microinjections into the striatum and after systemic administrations. Muscimol improved the dystonic syndrome after striatal injections to a similar extent as after systemic treatment, supporting the importance of the deficiency of striatal GABAergic interneurons for the occurrence of the motor disturbances. The disinhibition of striatal GABAergic projection neurons, as suggested by recent extracellular single-unit recordings in dt(sz) hamsters, should lead to an abnormal neuronal activity in the basal ganglia output nuclei. Indeed, a significantly decreased basal discharge rate of entopeduncular neurons was found in dt(sz) hamsters. We conclude that a deficit of striatal GABAergic interneurons leads by disinhibition of striatal GABAergic projection neurons to a reduced activity in the entopeduncular nucleus, i.e., to a decreased basal ganglia output. This finding is in line with the current hypothesis about the pathophysiology of hyperkinesias. The results indicate that striatal interneurons deserve attention in basic and clinical research of those movement disorders.

Action Potentials↗
PubMed1986

Autoradiographic analysis of D-[3H]aspartate binding in human basal ganglia.

The binding of D-[3H]aspartate to sections of human basal ganglia was measured autoradiographically. Highest binding was observed in the cerebral cortex, nucleus accumbens, caudate nucleus and putamen. The level of binding in the globus pallidus was low. D-[3H]Aspartate binding had a similar distribution to the high-affinity [3H]glutamate uptake sites and may be a useful marker for glutamate-aspartate terminals in human brain.

Aged↗
PubMed1996

Functional and pathophysiological models of the basal ganglia.

Because of new data, anatomical and functional models of the basal ganglia in normal and pathological conditions (e.g. Parkinson's and Huntington's diseases) have recently come under greater scrutiny. An update of these models is clearly timely, taking into consideration not only changes in neuronal discharge rates, but also changes in the patterning and synchronization of neuronal discharge, the role of extrastriatal dopamine, and expanded intrinsic and input/output connections of these nuclei.

Animals↗
PubMed2000

Parkinsonism after correction of hyponatremia with radiological central pontine myelinolysis and changes in the basal ganglia.

Parkinsonism has been rarely described following central pontine and extrapontine myelinolysis. We report a case of parkinsonism developing following rapid correction of hyponatremia with radiological evidence of central pontine myelinolysis and changes in the basal ganglia. A 56-year-old man developed drooling and bilateral hand tremors 3 weeks after correction of hyponatremia from 103 to 125 mmol/L over 14 h. He had a prominent 6 Hz resting tremor which worsened with action and mild cogwheel rigidity. Magnetic resonance imaging (MRI) showed changes consistent with central pontine myelinolysis and increased signal on T1-weighted images in the putamen bilaterally. His tremor responded well to L-dopa therapy. There have been several other cases of parkinsonism developing after central pontine/extrapontine myelinolysis. Increased signal in the basal ganglia on T1-weighted images has been described in another case of central pontine myelinolysis imaged about the same time after sodium correction as our case.

Antiparkinson Agents↗
PubMed1996

Proton MR spectroscopy of the basal ganglia in healthy children and children with AIDS.

PURPOSE: To evaluate proton magnetic resonance (MR) spectroscopy in children with the acquired immunodeficiency syndrome (AIDS) and to establish an age-dependent spectroscopic database of the normal basal ganglia in children. MATERIALS AND METHODS: Eighteen healthy children and 45 children with AIDS underwent both brain MR imaging and single-voxel MR spectroscopy with a long-echo-time point-resolved technique. A large part of the region of interest studied at MR spectroscopy included the basal ganglia. RESULTS: Seven patients with progressive encephalopathy and eight with static encephalopathy had significantly lower mean N-acetyl aspartate (NAA)/creatine (Cr) ratios than age-matched control subjects (P<.02). In determining the presence of progressive encephalopathy in children with AIDS, MR spectroscopy appears to be more sensitive and specific than MR imaging and immunologic testing. Thirty patients without encephalopathy had normal NAA/Cr ratios but significantly lower choline/Cr ratios than age-matched control subjects (P<.02). CONCLUSION: Proton MR spectroscopy may be a more sensitive diagnostic technique than MR imaging in childhood AIDS encephalopathy.

AIDS Dementia Complex↗
PubMed1983

[Germ cell tumor in the basal ganglia with elevated serum and CSF alpha-fetoprotein levels].

Intracranial germ cell tumors usually locate either in the pineal region or in the suprasellar region or both. Primary occurrence of germ cell tumor in the basal ganglia is rare. To our knowledge, only 17 cases have been reported in the literatures, and all the patients were Japanese. None of these patients presented elevated serum and CSF AFP levels in the literatures. We are reporting a patient with a germ cell tumor which developed in the left basal ganglia and showed high serum and CSF alpha-fetoprotein (AFP) levels. The patient was a 12-year-old boy who had been completely well until five months prior to the first admission when he developed weakness of right extremities. On admission he showed a right hemiparesis of mild degree and right hypesthesia. CT-scans demonstrated a homogeneous high density area over the caudate head and the putamen on the left side. The anterior limb of the left internal capsule and a part of the posterior limb were also involved. The lesion was moderately enhanced by the contrast medium. Stereotaxic biopsy of the lesion was uncontributory and he was discharged for follow up. Five months later, CT-scans demonstrated the enlargement of the high density area with perifocal edema. Then we performed a craniotomy, and the tumor which was soft and dark red in colour was biopsied at the wall of the anterior horn of the left lateral ventricle. Histopathology of the specimen showed germinoma of two-cell pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

Basal Ganglia↗
PubMed2003

Serotonergic regulation of the GABAergic transmission in the rat basal ganglia.

The GABAergic neurons represent a major neuronal population in the basal ganglia. Although alterations in serotonin (5-HT) transmission are associated with neurodegenerative diseases involving these regions, the influence exerted by 5-HT afferents on GABAergic populations remains poorly understood. Here, we examined the consequences of 5,7-dihydroxytryptamine-induced lesion of 5-HT neurons on glutamic acid decarboxylase (GAD) activity, mRNA expression of the two isoforms of the enzyme, GAD65 and GAD67, GABA uptake, and extracellular GABA levels in the striatum. The 5-HT depletion produced an increase in GAD activity without modifying GAD65 and GAD67 mRNA levels, suggesting that 5-HT acts at the posttranscriptional level to regulate striatal GABA synthesis. No change in GAD activity was measured in the main striatal target structures, the globus pallidus and substantia nigra. Striatal GABA uptake and extracellular levels of GABA measured under basal conditions in freely moving rats were maintained in a normal range following 5-HT deprivation. By contrast, depolarization-induced increases in extracellular levels of GABA were larger in the striatum of 5-HT-deprived rats than in controls, which may be accounted for by an increase in a releasable pool of GABA due to increased synthesis rate. Together, these results suggest that 5-HT afferents may exert a phasic inhibitory control on striatal GABA transmission. Therefore, a decrease in striatal 5-HT transmission in disease states, such as Parkinson's disease, may contribute to pathological changes in striatal GABA neuron activity by increasing their reactivity to depolarizing stimuli.

5,7-Dihydroxytryptamine↗
PubMed2000

Cellular distribution of ferric iron, ferritin, transferrin and divalent metal transporter 1 (DMT1) in substantia nigra and basal ganglia of normal and beta2-microglobulin deficient mouse brain.

We examined whether high levels of circulatory iron may cause iron accumulation in the brain. In particular, we focussed on the substantia nigra and basal ganglia as several papers have indicated that iron may accumulate here and cause death of dopaminergic neurons. Normal mice and a mouse model of hereditary haemochromatosis, the beta2-microglobulin (beta2m) knock out [beta2m (-/-)] mouse, which has high levels of circulating iron due to increased iron absorption, were examined. The iron concentration in livers were: 170+/-15 microg/g (mean +/- SD) in controls and 1010+/-50 microg/g in beta2m (-/-) mice (p<0.001), whereas in the brain the respective values were 47 +/-1 microg/g and 53+/-2 microg/g (p<0.02). Hence, the difference between cerebral iron levels of normal and beta2m (-/-) mice was small. Histological examination of the brains revealed an unequivocal distribution of ferric iron, ferritin, transferrin and divalent metal transporter 1 (DMT1), which were indistinguishable when normal and beta2m (-/-) mice were compared. In the substantia nigra and basal ganglia, ferric iron and the iron-binding proteins were present in identical cell types, which mainly comprised oligodendrocytes and microglia. Neurons were lightly labelled with transferrin and DMT1. The virtual lack of an increase in cerebral iron in beta2m (-/-) mice clearly shows that the blood-brain barrier (BBB) is capable of restricting the transport of excess plasma iron into the brain.

Animals↗
PubMed1983

Hemorrhagic infarction of the basal ganglia. An unusual complication of acute leukemia.

Hemorrhagic infarction of the basal ganglia was observed in 2 young adult patients with acute leukemia who presented with progressive hemiparesis combined with severe mental alterations. In case 1 (AML) lethal infarction due to thrombosis of both internal cerebral veins occurred during induction therapy for relapsed leukemia; in case 2 (cALL) a devastating stroke probably due to deep cerebral venous thrombosis happened during the third remission. Neither of them had hyperleukocytosis, signs of infection, disseminated intravascular coagulation or CNS leukemia. We discuss long-term glucocorticoid therapy (case 1) and combined prophylactic CNS treatment (case 2) as possible risk factors for cerebrovascular thrombosis in acute leukemia.

Acute Disease↗
PubMed1998

The basal ganglia and portal-systemic encephalopathy.

Despite decades of research, the pathogenesis of portal-systemic encephalopathy (PSE) remains puzzling. Current hypotheses on the pathophysiology of PSE usually deal with metabolic toxins like ammonia or disturbances in neurotransmitter systems, especially glutamatergic or GABA-ergic neurotransmission. With respect to clinical, neuropathological, MRI and PET findings this review advances the hypothesis that the known alterations of neurotransmission and astrocytic function in PSE might impair basal ganglia function in cirrhotics. The symptoms of PSE - whether cognitive, emotional or motor - are proposed to be a consequence of basal ganglia dysfunction.

Basal Ganglia↗
PubMedDate not supplied

Computed tomography of basal ganglia calcifications in pseudo- and idiopathic hypoparathyroidism.

It is well known that patients with pseudo (PHP)- and idiopathic (IHP) hypoparathyroidism are frequently associated with intracranial calcifications. The relative sensitivity of computed tomography (CT) and conventional skull radiography in detecting basal ganglia calcifications was studied in two patients with PHP and six with IHP. CT was more sensitive: the detection rate was 71% (5/7) for CT and 14% (1/7) for skull radiography. Furthermore, patients with more prolonged hypocalcemia showed a higher incidence of calcifications. Thus, CT was useful as a diagnostic technique in the early detection of calcified basal ganglia.

Adolescent↗
PubMed1984

The effect of manganese inhalation on basal ganglia dopamine concentrations in rhesus monkey.

Manganese (Mn) may produce neurotoxicity in man through inhalation of Mn dust. Animals exposed to excessive Mn develop neurological abnormalities, and neuropathological lesions in the brain mainly in the globus pallidus with decreased concentrations of the neurotransmitter, dopamine (DA), in the brain. Monkeys exposed to Mn by inhalation did not produce any abnormal movements. After two years, the animals were sacrificed and certain brain areas were compared to controls. There were significant decreases in DA concentration in caudate and globus pallidus, and there was a 60-80% increase in Mn concentration in the basal ganglia of the brain. The DA system in the basal ganglia is vulnerable to the effects of Mn, but the amount of Mn inhaled and the period of exposure would appear to determine whether abnormal neurological signs develop.

Animals↗
PubMed1994

Symmetrical lesions in the basal ganglia.

Bilateral and symmetrical non-space occupying lesions in the basal ganglia of 27 cases were studied. Nine cases had low attenuation lesions while the remaining 18 had high attenuation lesions due to bleeding or calcifications. The clinical presentations and final diagnosis were collated and related to these changes. In the low-attentuation cases, definite hypoxic-ischaemic insults were the aetiological basis for low attenuation lesions in 3 cases; and hypothesised to be the basis in the remaining six. Amongst the high attenuation group, bleeding was noted in 4 cases with trauma or cardiac arrest. The remainder had calcifications. It is suggested that a hypoxic-ischaemic pathophysiological phenomenon might have also accounted for some of these calcifications. The co-existence of both low and high attenuation lesions in the same patients in some of our cases tends to lend credence to this hypothesis.

Adult↗
PubMed2000

Metabolic effects of nigrostriatal denervation in basal ganglia.

In the past, functional changes in the circuitry of the basal ganglia that occur in Parkinson's disease were primarily analyzed with electrophysiological and 2-deoxyglucose measurements. The increased activity of the subthalamic nucleus (STN) observed has been attributed to a reduction in inhibition mediated by the external segment of the globus pallidus (GPe), secondary to the loss of dopaminergic-neuron influence on D2-receptor-bearing striato-pallidal neurons. More recently, in situ hybridization studies of cytochrome oxidase subunit I have confirmed the overactivity of the STN in the parkinsonian state. In addition, this technique has provided evidence that the change in STN activity is owing not only to decreased inhibition from the GPe but to hyperactivity of excitatory inputs from the parafascicular nucleus of the thalamus and the pedunculopontine nucleus in the brainstem.

Basal Ganglia↗
PubMed1981

Reduction in basal ganglia and substantia nigra substance P levels in Huntington's disease.

Substance P (SP) levels were determined by radioimmunoassay (RIA) in several regions of post-mortem brain of controls and Huntington's disease (HD) patients. In controls, highest SP levels were found in basal ganglia, substantia nigra and hypothalamus. Nigral pars reticulata contained 3--4-fold higher levels than pars compacta. In HD, SP levels were reduced in all basal ganglia and substantia nigra. The reductions ranged from 48% in caudate nucleus to over 90% in nigral pars reticulata. There were no changes in SP levels in HD frontal cortex, thalamus or hypothalamus.

Aged↗
PubMed1995

[The role of the basal ganglia in movement control].

It is now widely accepted that the basal ganglia (BG) are functionally organized with several segregated loops which start at a certain area in the cortex and project back to the same area in the cortex through the thalamus. The detailed functional organization of the BG motor loop has been described and used successfully to explain the mechanism of hypo- and hyper-kinetic disorders caused by BG disorders. Recent physiological and anatomical studies have provided new information concerning the function of these nuclei. The indirect pathway from the striatum to the external globus pallidus and then to the internal globus pallidus may be much more important than previous thought. The subthalamic nucleus may transmit excitatory input from the cortex as well as acting as a driving force on the globus pallidus. The role of BG output on the thalamus may not be to transfer information to the cortex via thalamocortical neurons, but rather to modulate the activity of cortico-thalamocortical loops. By varying it's discharge rate, the BG can change the membrane potentials of thalamocortical neurons which may result in focusing the activity of a specific cortico-thalamo-cortical loop and/or switching it to another.

Basal Ganglia↗