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PubMed1992

Calbindin-D28k in the basal ganglia of patients with parkinsonism.

An immunohistochemical study was carried out to investigate the topographic distribution of calbindin-D28k in the human basal ganglia and substantia nigra and its alterations in patients with idiopathic Parkinson's disease (PD), parkinsonism-dementia complex on Guam, progressive supranuclear palsy, and striatonigral degeneration. In normal control subjects, calbindin-D28k immunoreactivity was identified in the medium-sized neurons and neuropil of the matrix compartment of the striatum, the woolly fiber arrangements of the globus pallidus, and the fiber structures of the pars reticulata of the substantia nigra. Calbindin-D28k expression in the basal ganglia of patients with PD and parkinsonism-dementia on Guam was not different from that of control subjects, suggesting that the matrical output pathway is spared in these disorders. In contrast, its disruption is inferred from the observed disorganization of woolly fibers in the globus pallidus of patients with progressive supranuclear palsy and the reduced calbindin-D28k reactivity in the putaminal matrix and the pars reticulata of the substantia nigra of subjects with striatal degeneration. Thus, our results indicate that calbindin-D28k is a useful marker for the projection system from the matrix compartment and that its expression is modified in patients with progressive supranuclear palsy and striatal degeneration.

Aged↗
PubMed1998

Bilateral functional MRI activation of the basal ganglia and middle temporal/medial superior temporal motion-sensitive areas: optokinetic stimulation in homonymous hemianopia.

OBJECTIVE: To determine to what extent sensorimotor control is achieved for each hemisphere separately or interactively during small-field optokinetic stimulation in patients with complete homonymous hemianopia. DESIGN: Functional and structural neuroimaging using high-resolution magnetic resonance imaging. SETTING: University medical center research facility. PATIENTS: Three patients with complete homonymous hemianopia after acute infarction of the right posterior cerebral artery. MAIN OUTCOME MEASURES: Anatomical location of activated structures during horizontal optokinetic stimulation and T2-weighted anatomical magnetic resonance imaging. RESULTS: Occipitotemporal cortical areas (Brodmann areas 39 and 40) were the only activated cortical structures that showed statistically significant (P<.01) activation on the affected hemisphere. Of the subcortical areas, activation of thalamic nuclei appeared to be missing on the affected side, whereas the basal ganglia (putamen, globus pallidus, and caudate nucleus) were bilaterally activated. CONCLUSIONS: Bilateral activation of the basal ganglia confirms the concept of the basal ganglia-thalamocortical motor loop and of the efference copy of oculomotor pathways from each hemisphere. Our findings suggest 2 possible explanations for the activation of occipitotemporal areas (the human homolog of middle temporal/medial superior temporal areas) on the infarcted hemisphere: involvement of direct extrastriatal visual pathways or interhemispheric callosal connections between right and left middle temporal/medial superior temporal areas.

Aged↗
PubMed1997

[31P magnetic resonance spectroscopy(MRS) study in basal ganglia of patients with Parkinson's disease].

We report 31P magnetic resonance spectroscopy(MRS) to study regional high energy phosphate and phospholipid metabolism in basal ganglia of patients with Parkinson's disease(PD) in comparison with normal controls. The ratio of phosphomonoester(PME)/phosphocreatine(PCr), phosphodiester(PDE)/PCr and total Adenosine triphosphate(ATP) tend to decrease and the ratio of PDE/PME tend to elevate compared with controls. Moreover these findings are correlated with the duration of illness. Our results suggest that neural elements in basal ganglia may be damaged in PD. In conclusion, 31P-MRS appears to be useful for the study of neural damage and degeneration in vivo.

Adenosine Triphosphate↗
PubMed1982

Basal ganglia calcifications on CT: relation to hypoparathyroidism.

Eleven of 12 patients with primary hypoparathyroidism had CT evidence of bilateral intracerebral calcifications, mostly within the basal ganglia, but also in other sites. None of the 12 patients with secondary hypoparathyroidism had intracerebral calcifications. Among 20 patients with calcifications discovered incidentally, idiopathic hypoparathyroidism was diagnosed in 2 patients. Four patients had calcifications associated with antiepileptic treatment, parkinsonism, or Kearns-Sayre syndrome. The cause of the calcifications was unknown in 14 patients. No specific neurologic sign was related to the localization of the intracerebral calcifications. Incidentally discovered basal ganglia calcifications should lead to endocrinologic evaluation of parathyroid function. CT examination of the skull may be used to ascertain the diagnosis of idiopathic hypoparathyroidism.

Basal Ganglia Diseases↗
PubMed1978

Intracerebral displacement of basal ganglia following septal cannulation.

The effects of septal cannulation on the displacement of basal ganglia form the basis of the present communication. In experimental rats, in which a cannula is chronically implanted for 30 days between the medial and lateral septal nuclei by stereotaxic procedures, considerable shift of the basal ganglion is always observed on the operated side. The displacement takes place along the long axis of the ganglion either rostrally or caudally. Besides gross asymmetry in their relative sizes, no histological differences are observed between the ganglia of the two sides. Control animals, in which the cannula is withdrawn immediately after the septal lesion, manifest similar, but less pronounced movements of the basal ganglia. The probable underlying mechanisms for such intracerebral shifts are discussed and the role of indirect mechanical forces is outlined. The extraordinary degree of plasticity of the subcortical nuclear masses in terms of mobility is also emphasized.

Animals↗
PubMed1991

The temporal structure of spike trains in the primate basal ganglia: afferent regulation of bursting demonstrated with precentral cerebral cortical ablation.

We studied the temporal pattern of discharge of single units in the basal ganglia of awake primates sitting quietly. Bursting was studied with a procedure that identified individual bursts in a spike train, quantifying burst intensity (surprise), bursts per 1000 spikes, spikes per burst and burst length. Autocorrelation techniques were used to assess the dependencies of spike trains on the temporal order of intervals. Striatal units had a greater tendency to burst (79% of units) than pallidal units (50%). The caudate nucleus and putamen had nearly identical burst properties on all measures. In the pallidum, bursting was more prevalent in the external segment and bursts were more intense and more frequent than in the internal segment. The autocorrelation analysis revealed that the temporal structure of the spike train was more dependent on the order of intervals in the striatum than in the pallidum. Bursting units had an increased probability of discharge after each spike and the relative refractory period was shorter in bursting units than units without bursts. Very few units exhibited cyclic discharge properties. Ablations of areas 4 and 6 in the precentral cortex demonstrated that striatal bursting was under afferent control. The putamen, which receives more cortical afferents from areas 4 and 6 than the caudate nucleus, had fewer and less intense bursts after the afferents were lesioned. Burst intensity did not change in the pallidum after the lesion. The findings indicate that bursting properties contribute to discharge variability in the basal ganglia and suggest that information transfer in the striatum may utilize bursts. In contrast, rate coding may be a more important mechanism for units in the pallidum.

Action Potentials↗
PubMed1987

Postasphyxial encephalopathy in term infants. Sonographic demonstration of increased echogenicity of the thalamus and basal ganglia.

Sonographic abnormalities secondary to postasphyxial encephalopathy in neonates are reviewed. This report emphasizes an additional finding, increased echogenicity of the thalamus and basal ganglia, demonstrated in four term infants. This abnormal finding is generally noted in the second week following asphyxia. In some cases, the increased thalamic echogenicity may be a temporary finding. A representative case is described and possible pathologic correlates are discussed.

Asphyxia Neonatorum↗
PubMed2001

Induction of Fos-like immunoreactivity in the basal ganglia by ether anaesthesia: effects of injections of muscimol in rostral versus caudal substantia nigra pars reticulata.

Exposing rats to ether anaesthesia for 20 min induced a massive expression of c- fos like (FL) immunoreactivity in specific regions of the brain, including the basal ganglia. This expression of FL immunoreactivity in the basal ganglia was successfully blocked by local injections of muscimol (GABA(A) agonist) in the substantia nigra (SN). This model was used to investigate our recent finding that inhibition of caudal SN pars reticulata (SNpr) with muscimol is more potent in suppressing the motor component of tonic seizures than comparable inhibition of the rostral part. Two experiments were carried out. In experiment I, the effects of ether anaesthesia on c- fos expression in the brain were investigated. Brain sections taken from untreated control rats and stained immunocytochemically with c- fos antibodies. The results showed no FL immunoreactivity in the SNpr, subthalamic nucleus (STN), entopeduncular nucleus (EPN) and globus pallidus (GP). However, a few scattered FL immunoreactive nuclei were observed in the caudate-putamen (CPu). In rats exposed to ether, numerous FL immunoreactive nuclei were detected in the SNpr, STN, EPN and GP. In the CPu, a slight increase in number of labelled nuclei was noted. In experiment II, rats were prepared with intracranial chronic cannulae through which the effects of muscimol (60 ng) injected unilaterally in either the rostral or caudal SNpr on c- fosexpression induced by ether were investigated. Injections in both sites caused remarkable suppression of the ether-induced c- fos throughout the ipsilateral SNpr; however, the rostral injection also inhibited the expression of c- fos in the STN, EPN and GP. The implications of these results for microinjection mapping studies of the SN are discussed.

Anesthetics, Inhalation↗
PubMed1993

Ischemic lesions in basal ganglia in children after minor head injury.

Twenty-three children under the age of 6 1/2 years developed immediate unilateral weakness after an apparently minor head injury. Computed tomography disclosed a hypodense lesion in the basal ganglia. The lesion appeared to be caused by an infarct in the basal ganglia. All but one of the children recovered completely within 4 months.

Basal Ganglia↗
PubMed1978

Cortex, basal ganglia and cerebellum in motor control.

For voluntary movement, function generators are necessary that are located in the brain-stem, cerebellum and basal ganglia. Following lesions of these generators, voluntary movements are impaired while stimulus-dependent movements are still possible. This discussion also applies to speech production. The motor function generators cooperate with the whole cerebral cortex since both tactical adaptation to the environment and strategic guidance by the motivation system contribute to voluntary action. The motor cortex plays an epicritical role, adding advanced tactile and proprioceptive guidance for those movements that need this kind of regulation, especially the fine finger movements which depend entirely on the motor cortex. The complexity of the cerebral potentials preceding voluntary movement corresponds to the activity of several motor subsystems acting in concert.

Animals↗
PubMed1984

Role of thalamic motor nuclei in bilateral regulation of serotoninergic transmission in cat basal ganglia.

The effects of unilateral application of GABA (10(-5) M) into thalamic motor nuclei (ventralis medialis-ventralis lateralis, VM-VL) on 5-HT transmission in basal ganglia were investigated in halothane-anaesthetized cats implanted with several push-pull cannulae. The release of [3H]5-HT continuously synthesized from [3H]tryptophan was estimated in both caudate nuclei (CN), both substantia nigrae (SN) and in the dorsal raphe nucleus (DRN). [3H]5-HT release was decreased in the two CN and in the two SN but was enhanced in the DRN when GABA was applied into the VM-VL. These results indicate that thalamic motor nuclei are involved in a bilateral regulation of serotoninergic transmission in the basal ganglia.

Animals↗
PubMed1996

Choline-containing compounds detected by proton magnetic resonance spectroscopy in the basal ganglia in bipolar disorder.

Choline-containing compounds (Cho) were examined by proton magnetic resonance spectroscopy (1H-MRS) in the left subcortical region, including basal ganglia, in 19 euthymic patients with bipolar disorder and 19 age-matched normal controls. Ten of the patients were treated with lithium; the remaining 9 were not treated with lithium for at least 30 d. The Cho to creatine + phosphocreatine (Cr) peak ratio in the bipolar patients (0.75 +/- 0.38 [mean +/- SD]) was higher than that in the normal controls (0.52 +/- 0.26, P < 0.05). There was no significant difference in the Cho:Cr peak ratio between patients treated with lithium (0.63 +/- 0.36) and without lithium (0.89 +/- 0.35). These results do not support the hypothesis that lithium increases the brain choline-containing compounds, but rather imply that membrane breakdown may occur in the basal ganglia of patients with bipolar disorder.

Adult↗
PubMed2000

Proton magnetic resonance spectroscopy of human basal ganglia: response to cocaine administration.

BACKGROUND: Proton magnetic resonance spectroscopy was used to determine the effects of intravenous cocaine or placebo administration on human basal ganglia water and metabolite resonances. METHODS: Long echo time, proton magnetic resonance spectra of water and intracellular metabolites were continuously acquired from an 8-cm(3) voxel centered on the left caudate and putamen nuclei before, during, and after the intravenous administration of cocaine or a placebo in a double-blind manner. RESULTS: Cocaine, at both 0.2 and 0.4 mg/kg, did not alter the peak area for water. Cocaine at 0.2 mg/kg induced small and reversible increases in choline-containing compounds and N-acetylaspartate peak areas. Cocaine at 0.4 mg/kg induced larger and more sustained increases in choline-containing compounds and N-acetylaspartate peak areas. No changes in either water or metabolite resonances were noted following placebo administration. CONCLUSIONS: These increases in choline-containing compounds and N-acetylaspartate peak areas may reflect increases in metabolite T2 relaxation times secondary to osmotic stress and/or increased phospholipid signaling within the basal ganglia following cocaine administration. This is the first report of acute, drug-induced changes in the intensity of human brain proton magnetic resonance spectroscopy resonance areas.

Adult↗
PubMedDate not supplied

Neonatal asphyxia: vulnerability of basal ganglia, thalamus, and brainstem.

Two infants who suffered acute intrapartum asphyxia resulting in severe neonatal encephalopathy are described. Although computed tomography revealed no abnormalities, magnetic resonance imaging documented unequivocal lesions in the thalamus, basal ganglia, parasagittal cortex, brainstem tectum, and midline cerebellum in one patient and in the basal ganglia and parasagittal cortex in the other. Thus, magnetic resonance imaging was more sensitive than computed tomography in detecting acute brain damage after neonatal asphyxia and may become an important tool in improving our understanding of the relationship between adverse perinatal events, neonatal encephalopathy, and neurologic morbidity.

Asphyxia Neonatorum↗
PubMed2000

Possible mechanisms in infants for selective basal ganglia damage from asphyxia, kernicterus, or mitochondrial encephalopathies.

Magnetic resonance imaging and neuropathologic studies have demonstrated remarkably selective patterns of injury to subregions of the basal ganglia in children. Examples are kernicterus and certain mitochondrial encephalopathies, which cause selective injury to the globus pallidus, and near-total perinatal asphyxia, which causes lesions in the putamen and thalamus. To explain the differential vulnerability of nuclei within millimeters of each other, we hypothesize that their locations within the neurotransmitter-specific circuitry of the basal ganglia motor loop are important. In severe hypoxic-ischemic encephalopathy, excitatory glutamatergic pathways into the putamen and thalamus are overactive, but the globus pallidus might be protected because its activity is silenced by inhibitory neuronal activity. In contrast, the relatively high resting neuronal activity in the globus pallidus might make it more vulnerable to less intense, subacute oxidative stresses from mitochondrial toxins such as bilirubin or from genetic mitochondrial disorders. This hypothesis has implications for designing neuroprotective therapies and for treating associated chronic movement disorders.

Asphyxia Neonatorum↗
PubMed1991

[Two cases of familial idiopathic basal ganglia calcifications (BCG) with non-symptomatic family members].

We reported two families each propositus of which exhibited extrapyramidal signs and dementia with bilateral basal ganglia calcifications (BGC), while some of the other non-symptomatic family members showed BCG on brain CT by further examinations. Family 1) A 49-year-old woman was normal until her mid 40s when her memory began to fail. At age 40, dementia, finger-tremor and rigidity were observed and with brain CT and Magnetic Resonance Imaging, BCG and dentate calcifications were found. Her two daughters (20 years old and 26 years old) were free of any neuropsychiatric symptoms, but with CT examinations disclosed BCG. Family 2) A 40-year-old man. His symptoms started at 33 years old. He noticed gradually increasing finger-tremor, rigidity and dysarthria. At 40 years he showed mild dementia and BCG on Brain CT. His mother (64 years old) was non-symptomatic but CT showed that she had BCG. In the two families the calcium, phosphorous and parathyroid hormone levels, and Ellsworth-Howard test were normal. Other specific etiology including infections and somatic abnormalities was not discovered. Familial idiopathic basal ganglia calcification was considered to be rare. But the main purpose of this report is to point out that we must pay attention to the possibility of BCG of non-symptomatic family members if one showed dementia and extrapyramidal signs, and BCG on Brain CT in middle age.

Adult↗
PubMedDate not supplied

Primary hypothyroidism with pituitary hyperplasia and basal ganglia calcifications.

Pituitary enlargement as a result of hypothyroidism is a well recognized entity with several reports over the last decade. Hypothyroidism is only rarely recognized as a cause of basal ganglia calcifications, despite several large computer tomography (CT) studies. We present a case of primary hypothyroidism in which both pituitary hyperplasia and basal ganglia calcifications were observed in a young female who presented with hyperprolactinemia. Hypothyroidism should always be considered in the evaluation of hyperprolactinemia.

Adult↗
PubMed2004

Regulation of dopamine receptor and neuropeptide expression in the basal ganglia of monkeys treated with MPTP.

In Parkinson's disease (PD), striatal dopamine deficiency has been associated with complex changes in the functional and neurochemical anatomy of the basal ganglia. In this study, we simultaneously analyzed the regulation of D1 and D2 dopamine receptors and levels of the neuropeptides, substance P, and enkephalin (ENK) in various basal ganglia nuclei following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced dopaminergic denervation of striatum in nonhuman primates. Both unilateral and bilateral lesioned animals were used for this study. Striatal dopamine deficiency resulted in distinct alterations in D1, D2, substance P, and enkephalin levels and distribution: (1) Both D1 and D2 protein levels were significantly up-regulated in striatum. (2) There was an overall up-regulation of striatal substance P expression following dopamine denervation. (3) Substance P distribution was 'reversed' in dopamine depleted striatum: striosomes, which normally express higher levels of substance P, showed decreased expression, whereas substance P expression was up-regulated in the matrix. (4) Substance P expression was up-regulated in the internal segment of the globus pallidus (GPi), but remained unchanged in substantia nigra (SN). (5) Enkephalin levels were increased in striatum and the external segment of the globus pallidus (GPe), but not in substantia nigra. All the changes were more pronounced in the bilateral lesioned monkeys, though the data represent a pooled statistical evaluation of unilateral and bilateral lesioned monkeys. Our studies indicate that D1 and D2 dopamine receptors and substance P and enkephalin undergo regulatory changes in response to nigrostriatal dopamine denervation. Simultaneous study of the alterations in these various components of the 'direct' and 'indirect' pathways in the same animals will enable better understanding of the pathophysiology of PD and its therapeutic targets.

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