The external globus pallidus in patients with Parkinson's disease and progressive supranuclear palsy

Hardman, Craig D.; Halliday, Glenda M.

doi:10.1002/1531-8257(199907)14:4<626::aid-mds1012>3.0.co;2-u

Cited by 35 publications

(19 citation statements)

References 64 publications

(106 reference statements)

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“…In particular, pallidal atrophy has been previously reported, 23 and neurofibrillary tangles, neuropil threads, and neurodegeneration are consistently observed in the pallidosubthalamic complex and substantia nigra. 7,12,15,[25][26][27] Our results suggest that there is a reduction in the density of neurofibrillary tangles with ongoing atrophy subcortically. 28 This contrasts with increasing cortical tangle pathology that occurs with atrophic progression in PSP.…”

Section: Discussionmentioning

confidence: 56%

Regional brain atrophy in progressive supranuclear palsy and Lewy body disease

et al. 2000

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There have been no previous three‐dimensional volumetric studies of regional brain atrophy in patients with pathologically confirmed progressive supranuclear palsy (PSP). Postmortem cortical and subcortical volumes were compared with neuropathology in 9 patients with PSP, 15 patients with Parkinson's disease, 10 patients with dementia with Lewy bodies, and 23 controls. Cases with the neuritic pathology of Alzheimer's disease were excluded. The topography of brain atrophy differed according to clinicopathological phenotype. Patients with Parkinson's disease had atrophy confined to the amygdala. Atrophy of the frontal lobe was found in both PSP and dementia with Lewy bodies and correlated with increasing neurofibrillary tangle or Lewy body densities, respectively. Patients with PSP could be differentiated by their marked atrophy of the internal globus pallidus. Further analysis of variance revealed that trends for greater frontal lobe atrophy correlated with clinical dementia in PSP, whereas both greater frontal and hippocampal atrophy and higher densities of Lewy bodies and Lewy neurites correlated with clinical dementia in cases with Lewy bodies. The present study provides evidence for selective regional atrophy that correlates with the underlying pathology of PSP and Lewy body disease. Ann Neurol 2000;47:718–728

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Section: Discussionmentioning

confidence: 56%

Regional brain atrophy in progressive supranuclear palsy and Lewy body disease

et al. 2000

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“…28 Together with the ventrolateral and ventroanterior nuclei of the thalamus (motor thalamus), the globus pallidus participates in the motor circuit linking the basal ganglia to the motor cortex, premotor cortex, and SMA. [28][29][30][31] Our findings, of abnormally high ADC ave in the globus pallidus and lateral part of the thalamus, together with low FA in the primary motor cortex and SMA, are consistent with postmortem studies.…”

Section: Discussionmentioning

confidence: 99%

Diffusion Tensor Imaging Shows Different Topographic Involvement of the Thalamus in Progressive Supranuclear Palsy and Corticobasal Degeneration

Erbetta¹,

Mandelli²,

Savoiardo³

et al. 2009

AJNR Am J Neuroradiol

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BACKGROUND AND PURPOSE:In progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD), postmortem studies show different topographic involvement of the thalamus, basal ganglia, and their cortical connections. Diffusion tensor imaging (DTI) is an MR imaging technique sensitive to gray and white matter microstructure integrity. This study was performed to determine whether DTI may demonstrate microstructural differences between PSP and CBD, particularly within the thalamus and its cortical connections.

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“…Substance P (SP) is contained within striatal terminals of the direct pathway, whereas met-enkephalin (enk) is contained within terminals of the indirect pathway. The GP contains a high percentage of PVϩ neurons: Ϸ75% of GPi and 50% of GPe cells are positive for this calcium-binding protein (7). However, unlike those in the striatum, PVϩ cells in the GPi are projection neurons.…”

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confidence: 99%

Altered parvalbumin-positive neuron distribution in basal ganglia of individuals with Tourette syndrome

Kalanithi

Zheng

Kataoka

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

487

384

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Tourette syndrome (TS) is a childhood neuropsychiatric disorder characterized by motor and vocal tics. Imaging studies found alterations in caudate (Cd) and putamen volumes. To investigate possible alterations in cell populations, postmortem basal ganglia tissue from individuals with TS and normal controls was analyzed by using unbiased stereological techniques. A markedly higher total neuron number was found in the globus pallidus pars interna (GPi) of TS. In contrast, a lower neuron number and density was observed in the globus pallidus pars externa and in the Cd. An increased number and proportion of the GPi neurons were positive for the calcium-binding protein parvalbumin in tissue from TS subjects, whereas lower densities of parvalbumin-positive interneurons were observed in both the Cd and putamen of TS subjects. This change is consistent with a developmental defect in tangential migration of some GABAergic neurons. The imbalance in striatal and GPi inhibitory neuron distribution suggests that the functional dynamics of cortico-striato-thalamic circuitry are fundamentally altered in severe, persistent TS.T ourette syndrome (TS) is a childhood neuropsychiatric disorder characterized by persistent motor and vocal tics, which may or may not abate upon entering adulthood. Tics are sudden stereotyped motor sequences of varying intensity and complexity, often preceded by compulsions or sensory phenomena. Neither the etiology nor the pathophysiology of TS is well understood. Both genetic and environmental factors are thought to be important, but the exact role of each has not yet been identified (1). Epigenetic events that increase the risk of developing tic disorder or TS include perinatal hypoxic-ischemic events that damage the periventricular germinal matrix and adjacent deep regions of the brain (2). A considerable amount of data implicates the cortico-striato-thalamo-cortical circuit in TS pathophysiology, particularly basal ganglia (BG) abnormalities. The BG, a richly interconnected set of nuclei, is essential for the initiation and correct implementation of learned sequences of motor and cognitive segments that characterize purposive behavior. The two major inputs into the BG, from the cerebral cortex and the intralaminar nuclei of the thalamus, enter into the striatum, which consists of the caudate (Cd) and putamen (Pt). The firing of cortical inputs drives activity in both medium spiny neurons (MSNs) (3) and several types of interneurons, including parvalbumin (PV)-positive (PVϩ) GABAergic interneurons (4). Striatal PVϩ interneurons are connected by electrical junctions and form a web of inhibitory synapses throughout the striatum, coordinating the activities of MSNs, and likely increasing their threshold of firing in response to cortical inputs (5, 6). MSNs, which are the large majority of neurons in the striatum, project to the globus pallidus pars interna (GPi), either directly or indirectly via the subthalamic nucleus and the globus pallidus pars externa (GPe). These two pathways can be differentiate...

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The external globus pallidus in patients with Parkinson's disease and progressive supranuclear palsy

Cited by 35 publications

References 64 publications

Regional brain atrophy in progressive supranuclear palsy and Lewy body disease

Regional brain atrophy in progressive supranuclear palsy and Lewy body disease

Diffusion Tensor Imaging Shows Different Topographic Involvement of the Thalamus in Progressive Supranuclear Palsy and Corticobasal Degeneration

Altered parvalbumin-positive neuron distribution in basal ganglia of individuals with Tourette syndrome

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