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PubMed2003

Neuropathological evaluation of the diencephalon, basal ganglia and upper brainstem in alobar holoprosencephaly.

Holoprosencephaly (HPE) is caused by the impaired cleavage of the embryonic prosencephalon, and in the severest type, alobar HPE, the normally bilateral diencephalon and basal ganglia are fused and tend to incorporate into the upper brainstem. The detailed neuropathological features of HPE remain to be elucidated, although disturbed regulation in body temperature and electrolyte balance are frequently observed. We immunohistologically examined the expression of hypothalamic hormones, neurotransmitters, calcium-binding proteins and neuropeptides in six female autopsy cases of alobar HPE. Eight age-matched controls formed the comparative basis for the immunoreactivity of these markers during the fetal period. Neurons immunoreactive for either vasopressin or orexin-A were noted in the fused diencephalon in five HPE cases, and colocalization of vasopressin and tyrosine hydroxylase occurred in HPE cases surviving more than 6 months. Tyrosine hydroxylase-immunoreactive fibers and neurons were observed in the fused diencephalon and basal ganglia in all the six cases. Parvalbumin-immunoreactive structures were identified in the fused diencephalon and basal ganglia in five cases, and the apparent red nucleus was identified by anti-parvalbumin immunostaining in two cases aged more than 1 year. Five cases demonstrated substance P-immunoreactive structures in the diencephalon, and a substantia nigra-like structure in the midbrain was visualized by immunostainings for both tyrosine hydroxylase and substance P in four cases. Only two cases aged more than 1 year had immunoreactivity for methionine-enkephalin in the basal ganglia and substantia nigra. These data suggest that the fused diencephalon and basal ganglia exhibited functional developments in alobar HPE, and the disturbed expression of the markers may be involved in hypothalamic and/or motor abnormalities in patients.

Basal Ganglia↗
PubMed2006

Bilateral basal ganglia activation associated with sensorimotor adaptation.

Sensorimotor adaptation tasks can be classified into two types. When subjects adapt movements to visual feedback perturbations such as in prism lens adaptation, they perform kinematic adaptations. When subjects adapt movements to force field perturbations such as with robotic manipulanda, they perform kinetic adaptations. Neuroimaging studies have shown basal ganglia involvement in kinetic adaptations, but have found little evidence of basal ganglia involvement in kinematic adaptations, despite reports of deficits in patients with diseases of the basal ganglia, such as Parkinson's and Huntington's disease, in these. In an effort to resolve such apparent discrepancy, we used FMRI to focus on the first few minutes of practice during kinematic adaptation. Human subjects adapted to visuomotor rotations in the context of a joystick aiming task while lying supine in a 3.0 T MRI scanner. As demonstrated previously, early adaptive processes were associated with BOLD activation in the cerebellum and the sensory and motor cortical regions. A novel finding of this study was bilateral basal ganglia activation. This suggests that, at least for early learning, the neural correlates of kinematic adaptation parallel those of other types of skill learning. We observed activation in the right globus pallidus and putamen, along with the right prefrontal, premotor and parietal cortex, which may support spatial cognitive processes of adaptation. We also observed activation in the left globus pallidus and caudate nucleus, along with the left premotor and supplementary motor cortex, which may support the sensorimotor processes of adaptation. These results are the first to demonstrate a clear involvement of basal ganglia activation in this type of kinematic motor adaptation.

Adaptation, Physiological↗
PubMed2003

Motor performance and anatomic magnetic resonance imaging (MRI) of the basal ganglia in autism.

This study was conducted to examine the volume of the basal ganglia in individuals with autism and to evaluate whether performance on specific motor tasks correlated with the volume of these structures. Volumetric measurements of the caudate nucleus and putamen were obtained from magnetic resonance images (MRI) of 40 non-mentally retarded individuals with autism and 41 healthy controls. Motor performance was assessed in these subjects by using the Finger Tapping Test, the Grooved Pegboard Test, and the measurement of Grip Strength. No volumetric differences of the basal ganglia were found between the two groups after adjusting for brain volume. The autistic subjects' performance was slower on the Grooved Pegboard Test and weaker on Grip Strength. Our findings suggest that the motor deficits observed in autism may not be related to structural abnormalities of the basal ganglia, and other brain regions, such as the cerebellum and the frontal lobe, may be involved in the pathophysiology of motor disturbances in autism.

Adolescent↗
PubMed1997

Perivascular spaces in the basal ganglia of the human brain: their relationship to lacunes.

There is evidence for lymphatic drainage of interstitial fluid from the brain along perivascular spaces in a number of mammalian species. Ultrastructural studies suggest that there are similar drainage pathways in the human cerebral cortex. Perivascular spaces in the basal ganglia, however, differ from those in the cortex in that they dilate to form lacunes and rarely accumulate beta-amyloid (amyloid angiopathy) in Alzheimer's disease; in the cortex, lacunes are rare but amyloid angiopathy is common. The aim of the present study is to compare the structure of perivascular spaces in the basal ganglia and at the anterior perforated substance with perivascular spaces in the cerebral cortex. Eight postmortem brains from patients aged 23-80 years (mean 68 y) were examined by light microscopy, by scanning and transmission electron microscopy and by direct visualisation of etched paraffin blocks. The results show that arteries in the basal ganglia are surrounded by 2 distinct coats of leptomeninges separated by a perivascular space which is continuous with the perivascular space around arteries in the subarachnoid space. The inner layer of leptomeninges closely invests the adventitia of the vessel wall and the outer layer is continuous with the pia mater on the surface of the brain at the anterior perforated substance. Veins in the basal ganglia have no outer layer of leptomeninges and thus the perivascular space is continuous with the subpial space. The anatomy of the periarterial spaces in the basal ganglia differs significantly from that in the cerebral cortex where there is only a single periarterial layer of leptomeninges. Differences in structure of perivascular spaces around arteries may reflect relative efficiencies in the drainage of interstitial fluid from different sites in the brain. Furthermore, the structure of the perivascular spaces may contribute to the relatively high frequency of lacunes in the basal ganglia, and the low frequency of amyloid angiopathy at this site in Alzheimer's disease.

Adult↗
PubMed1992

Organic schizophrenic syndrome associated with symmetrical basal ganglia sclerosis and XO/XY-mosaic.

Psychopathological alterations associated with symmetrical basal ganglia sclerosis have been well characterized. A preponderance of a so-called organic affective syndrome has been reported (König 1989), but schizophrenic syndromes have also been described, in particular in young patients (Cummings et al 1983). Symmetrical basal ganglia sclerosis may be secondary to ischemia, hypoxia, trauma, intoxications, inflammations, or hyporesp. pseudohypoparathyroidism. Among idiopathic forms sporadic as well as familial ones with dominant and recessive inheritance have been observed (Billard et al 1989).

Adult↗
PubMed2002

Anti-basal ganglia antibodies in acute and persistent Sydenham's chorea.

OBJECTIVE: To determine the sensitivity and specificity of methods to detect anti-basal ganglia antibodies (ABGA) in Sydenham's chorea (SC). BACKGROUND: SC is a delayed manifestation of group Abeta hemolytic streptococcal infection typically associated with rheumatic fever (RHF). SC is characterized by chorea and motor and neuropsychiatric symptoms. Patients with SC produce antibodies that cross-react with streptococcal, caudate, and subthalamic nuclei antigens detected using an immunofluorescent (IF) method with inconsistent reports of positivity. METHODS: The authors developed ELISA and Western immunoblotting (WB) methods to detect ABGA and compared these assays to IF. They investigated samples from patients with acute SC (n = 20), persistent SC (n = 16), control samples from RHF (n = 16), and healthy pediatric volunteers (n = 11). RESULTS: ABGA ELISA had a sensitivity of 95% and specificity of 93% in acute SC. Both WB and IF had a sensitivity of 100% and specificity of 93%. In the persistent SC group, ABGA sensitivity dropped to 69% using WB and to 63% using IF. Three common basal ganglia antigens were identified by WB in both acute and persistent SC (40 kDa [n = 15], 45 kDa [n = 15], and 60 kDa [n = 13]). There was no antibody reactivity to cerebellum, cerebral cortex, or myelin antigen preparations in any group. CONCLUSIONS: These results support the hypothesis that Syndenham's chorea is an autoantibody-mediated disorder. Western immunoblotting and immunofluorescence are the best methods for detecting anti-basal ganglia antibodies, and reactivity to basal ganglia antigens of 40, 45, and 60 kDa were commonly seen in both acute and persistent cases of SC.

Acute Disease↗
PubMed1992

Neurological disorders in 166 patients with basal ganglia calcification: a statistical evaluation.

Patients investigated at our institute during the last decade included 166 (1.2%) who showed uni- or bilateral basal ganglia calcification on computed tomography. We tested the significance of this neuroradiological observation by statistical comparison of these patients' clinical disorders with the findings in a random sample of 622 patients without basal ganglia calcification. The odds for the most common neurological disturbances were similar in patients with and without basal ganglia calcification. After adjustment for differences in age and brain atrophy there was no evidence of a significantly increased risk of dementia (odds ratio 1.1), cerebral infarction (1.4), epilepsy (0.9), vertigo (1.6), headache (1.8), or alcoholism (0.9), which represented the most common diagnoses. We conclude that basal ganglia calcification cannot be considered as a clinically relevant neuroradiological finding in the majority of cases and that it should not be used as an explanation for frequently observed neurological disturbances.

Basal Ganglia Diseases↗
PubMed1998

Immunohistochemical localization of metabotropic glutamate receptors mGluR1a and mGluR2/3 in the rat basal ganglia.

Metabotropic glutamate receptors (mGluRs), which couple glutamate to second messengers, have important roles in the regulation of movement by the basal ganglia. We used two polyclonal antisera to mGluR1a and mGluR2/3 and confocal laser microscopy to investigate the localization of these receptors in the basal ganglia of the rat. The mGluRs were visualized in combination with an antibody to tyrosine hydroxylase (TH), an antibody to microtubule-associated protein 2 (MAP2, a dendritic marker), or SV2 (an antibody to a protein associated with presynaptic terminals). In the neostriatum, punctate mGluR1a immunoreactivity (ir) was present in the neuropil. This staining did not colocalize with MAP2-ir or SV2-ir and was not altered by decortication or unilateral 6-hydroxydopamine (6-OHDA) lesions. In the globus pallidus and substantia nigra pars reticulata, however, mGluR1a-ir was tightly clustered along large MAP2-ir dendrites. In contrast to the variations in mGluR1a-ir staining, similar punctate neuropil mGluR2/3-ir staining was observed within all basal ganglia structures. In the neostriatum, these puncta were abundant; unlike mGluR1a, many mGluR2/3-ir puncta colocalized with SV2-ir, and striatal mGluR2/3-ir puncta were markedly reduced in number after decortication. Neither mGluR1a-ir nor mGluR2/3-ir could be detected in TH-ir soma within substantia nigra pars compacta, or in TH-ir striatal terminals. Overall, our observations suggest that mGluR1a and mGluR2/3 receptors have distinct cellular localizations in different components of the basal ganglia circuitry and are likely to subserve distinct functions. Our data support the presence of mGluR2/3 on the terminals of corticostriatal afferents, where they may regulate glutamate release. In contrast, mGluR1a appears to be a postsynaptic receptor of neurons in the neostriatum, globus pallidus, and substantia nigra pars reticulata.

Animals↗
PubMed2003

Dysfunction of the basal ganglia, but not the cerebellum, impairs kinaesthesia.

Precise knowledge about limb position and orientation is essential for the ability of the nervous system to plan and control voluntary movement. While it is well established that proprioceptive signals from peripheral receptors are necessary for sensing limb position and motion, it is less clear which supraspinal structures mediate the signals that ultimately lead to the conscious awareness of limb position (kinaesthesia). Recent functional imaging studies have revealed that the cerebellum, but not the basal ganglia, are involved in sensory processing of proprioceptive information induced by passive and active movements. Yet psychophysical studies have suggested a prominent role of the basal ganglia in kinaesthesia. This study addresses this apparent dichotomy by investigating the contributions of the cerebellum and the basal ganglia to the perception of limb position. Using a passive movement task, we examined the elbow position sense in patients with a dysfunction of the basal ganglia (Parkinson's disease, n = 9), patients with cerebellar degeneration [spinocerebellar ataxia (SCA) types 6 and 8, n = 6] and age-matched healthy control subjects (n = 11). In comparison with healthy control subjects, Parkinson's disease patients, but not SCA patients, were significantly impaired in the ability to detect displacements correctly. A 1 degrees forearm displacement was correctly recognized in >75% of trials by control subjects and SCA patients, but only in 55% of Parkinson's disease patients. Only at 6 degrees displacement did Parkinson's disease patients exhibit a response rate similar to those of the two other groups. Thresholds for 75% correct responses were 1.03 degrees for controls, 1.15 degrees for cerebellar patients and 2.10 degrees for Parkinson's disease patients. This kinaesthetic impairment significantly correlated with the severity of disease in Parkinson's disease patients, as determined by the Unified Parkinson's Disease Rating Scale (r = -0.7, P = 0.03) and duration of disease (r = -0.7, P = 0.05). In contrast, there was no significant correlation between performance and the daily levodopa equivalent dose. These results imply that an intact cerebro-basal ganglia loop is essential for awareness of limb position and suggest a selective role of the basal ganglia but not the cerebellum in kinaesthesia.

Adult↗
PubMed1988

Differential mood changes following basal ganglia vs thalamic lesions.

Patients with computed tomographic scan-verified unilateral lesions in the basal ganglia or thalamus were examined for the presence of poststroke mood disorders. Patients with left-sided basal ganglia lesions (mainly in the head of the caudate nucleus) showed a significantly higher frequency and severity of depression, as compared with patients with right-sided basal ganglia or thalamic (left- or right-sided) lesions. Results suggest that damage to biogenic amine pathways and/or frontocaudate projections may play an important role in the modulation of mood.

Aphasia↗
PubMed2003

Encephalitis lethargica syndrome: 20 new cases and evidence of basal ganglia autoimmunity.

In 1916, von Economo first described encephalitis lethargica (EL), a CNS disorder presenting with pharyngitis followed by sleep disorder, basal ganglia signs (particularly parkinsonism) and neuropsychiatric sequelae. Since the 1916-1927 epidemic, only sporadic cases have been described. Pathological studies revealed an encephalitis of the midbrain and basal ganglia, with lymphocyte (predominantly plasma cell) infiltration. The EL epidemic occurred during the same time period as the 1918 influenza pandemic, and the two outbreaks have been linked in the medical literature. However, von Economo and other contemporary scientists thought that the 1918 influenza virus was not the cause of EL. Recent examination of archived EL brain material has failed to demonstrate influenza RNA, adding to the evidence that EL was not an invasive influenza encephalitis. By contrast, the findings of intrathecal oligoclonal bands (OCB) and beneficial effects of steroid treatments have provoked the hypothesis that EL may be immune-mediated. We have recently seen 20 patients with a similar EL phenotype, 55% of whom had a preceding pharyngitis. The patients had remarkable similarity to the historical descriptions of EL: sleep disorder (somnolence, sleep inversion or insomnia), lethargy, parkinsonism, dyskinesias and neuropsychiatric symptoms. CSF examination commonly showed elevated protein and OCB (75 and 69% respectively). Investigation found no evidence of viral encephalitis or other recognized causes of rapid-onset parkinsonism. MRI of the brain was normal in 60% but showed inflammatory changes localized to the deep grey matter in 40% of patients. We investigated the possibility that this phenotype could be a postinfectious autoimmune CNS disorder, and therefore similar to Sydenham's chorea. Anti-streptolysin-O titres were elevated in 65% of patients. Furthermore, western immunoblotting showed that 95% of EL patients had autoantibodies reactive against human basal ganglia antigens. These antibodies were also present in the CSF in four patients tested. By contrast, antibodies reactive against the basal ganglia were found in only 2-4% of child and adult controls (n = 173, P < 0.0001). Rather than showing polyspecific binding, these antibodies bound to common neural autoantigens of molecular weight 40, 45, 60 and 98 kDa. Regional tissue comparisons showed that the majority of these autoantigens were specific to or enriched in CNS tissue. Immunohistochemistry with secondary staining localized antibody binding to neurons rather than glial populations. Further investigation is required to determine whether these antibodies affect neuronal function (i.e. whether they are pathogenic anti-neuronal antibodies). Histopathology in one case demonstrated striatal encephalitis with perivenous B- and T-lymphocytic infiltration. We believe an EL-like syndrome is still prevalent, and propose that this syndrome may be secondary to autoimmunity against deep grey matter neurons.

Adolescent↗
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↗
PubMed1994

Nitric oxide synthase mRNA expression in human subthalamic nucleus, striatum and globus pallidus: implications for basal ganglia function.

The distribution of NOS mRNA within human basal ganglia was investigated using in situ hybridisation histochemistry (ISHH). Greater than 95% of subthalamic nucleus neurons were NOS mRNA-positive, between 1.5% and 2% of striatal neurons were positive and scattered NOS mRNA-positive neurons were detected in the medial, but not lateral globus pallidus. Levels of NOS mRNA expression per neuron were considerably higher in the striatum than in the pallidum or subthalamus. These findings have implications for basal ganglia function and disease states.

Amino Acid Oxidoreductases↗
PubMed1992

Basal ganglia teratomas: report of three cases.

Three cases of intracranial teratomas occurring at the basal ganglia of three young male patients were reported. Their radiologic appearances closely resembled each other with multicystic tumor masses located deep in the basal ganglia. Histology showed teratocarcinoma, combined immature teratoma and germinoma, and teratoma with malignant transformation. These tumours represent a distinct clinico-radiologic group of lesions and serve as an addition to the dearth of information reported about the histological subtypes of intracranial teratomas.

Adult↗
PubMed2003

Proton magnetic resonance spectroscopy of basal ganglia in chronic fatigue syndrome.

Fatigue is a common symptom of neurological diseases that affect basal ganglia function. We used proton magnetic resonance spectroscopy ((1)H MRS) to study the metabolic functions of the basal ganglia in chronic fatigue syndrome (CFS) to test the hypothesis that fatigue in CFS may have a neurogenic component. (1)H MRS of left basal ganglia was carried out in eight non-psychiatric patients with CFS and their results were compared to age- and sex-matched healthy asymptomatic healthy controls. A highly significant increase in the spectra from choline-containing compounds was seen in the CFS patient group (p < 0.001). In the absence of regional structural or inflammatory pathology, increased choline resonance in CFS may be an indicator of higher cell membrane turnover due to gliosis or altered intramembrane signalling.

Adult↗
PubMed2003

Task-set switching deficits in early-stage Huntington's disease: implications for basal ganglia function.

Executive functions are likely mediated by interconnected circuits including frontal lobe and basal ganglia structures. We assessed the executive function of task switching in patients with early-stage Huntington's disease (HD), a neurodegenerative disease affecting the basal ganglia. In two experiments, the HD patients had greater difficulty when switching than when repeating a task than matched controls, and this was true even when scaling for the overall slowing of the patients. In the first experiment, HD patients had a switching deficit even in a "pure" condition where they had to switch, predictably, and with substantial preparation time, between stimuli having only one possible response, indicating a switching deficit different from that for patients with Parkinson's disease or frontal lobe trauma, and possibly relating to inadequate activation of stimulus-response links or "response set." In the more elaborate second experiment, we could not account for the switching deficit of the patients in terms of inadequate preparation in advance of a switch, deficient suppression of task-set processing from the preswitch trial, or impaired suppression of interference due to the presence of a competing task set. Instead, we found that part of the switching deficit was due to elevated reaction time and errors on switch trials for a repeated response (same button press as on preswitch trial) relative to an alternated response (different button press from preswitch trial). We argue that this elevated "repetition effect" for the HD patients is due to excessive inhibition of the just-performed response in advance of a switch. Alterations in the "response-setting" process alone (Experiment 1) and both the response-setting and "response inhibition" process (Experiment 2) probably arise from striatal pathology in HD, thus accounting for the task-switching deficits and showing how basal ganglia implemented response processes may underpin executive function.

Adult↗
PubMed2004

Exercise-induced behavioral recovery and neuroplasticity in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mouse basal ganglia.

Physical activity has been shown to be neuroprotective in lesions affecting the basal ganglia. Using a treadmill exercise paradigm, we investigated the effect of exercise on neurorestoration. The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mouse model provides a means to investigate the effect of exercise on neurorestoration because 30-40% of nigrostriatal dopaminergic neurons survive MPTP lesioning and may provide a template for neurorestoration to occur. MPTP-lesioned C57 BL/6J mice were administered MPTP (four injections of 20 mg/kg free-base, 2 hr apart) or saline and divided into the following groups: (1). saline; (2). saline + exercise; (3). MPTP; and (4) MPTP + exercise. Mice in exercise groups were run on a motorized treadmill for 30 days starting 4 days after MPTP lesioning (a period after which MPTP-induced cell death is complete). Initially, MPTP-lesioned + exercise mice ran at slower speeds for a shorter amount of time compared to saline + exercise mice. Both velocity and endurance improved in the MPTP + exercise group to near normal levels over the 30-day exercise period. The expression of proteins and genes involved in basal ganglia function including the dopamine transporter (DAT), tyrosine hydroxylase (TH), and the dopamine D1 and D2 receptors, as well as alterations on glutamate immunolabeling were determined. Exercise resulted in a significant downregulation of striatal DAT in the MPTP + exercise compared to MPTP nonexercised mice and to a lesser extent in the saline + exercised mice compared to their no-exercise counterparts. There was no significant difference in TH protein levels between MPTP and MPTP + exercise groups at the end of the study. The expression of striatal dopamine D1 and D2 receptor mRNA transcript was suppressed in the saline + exercise group; however, dopamine D2 transcript expression was increased in the MPTP + exercise mice. Immunoelectron microscopy indicated that treadmill exercise reversed the lesioned-induced increase in nerve terminal glutamate immunolabeling seen after MPTP administration. Our data demonstrates that exercise promotes behavioral recovery in the injured brain by modulating genes and proteins important to basal ganglia function.

Animals↗