Projections of the lentiform nucleus in the monkey

Nauta, Walle J. H.; Mehler, William R.

doi:10.1016/0006-8993(66)90103-x

Cited by 734 publications

(92 citation statements)

References 45 publications

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“…With respect to the loss of neurons in the NPP reported here, the connections and location of the NPP suggested that a correlation might be made with the motor symptoms of the disease. The NPP lies in the region of the mesencephalic motor area (27,28), and work with experimental animals has suggested that the NPP region is interconnected with the basal ganglia and superior colliculus (8,(14)(15)(16)(17)(18)(29)(30)(31). It is unclear, however, to what degree the cholinergic neurons of the region participate in these connections (16,18).…”

Section: Discussionmentioning

confidence: 99%

“…Given the close association of the NPP with the extrapyramidal motor system (8,(14)(15)(16)(17)(18), we undertook a study of the NPP in autopsy material from the brains of persons who died with a diagnosis of idiopathic PD. We also determined the status of the nucleus in progressive supranuclear palsy (PSP), a parkinsonian syndrome associated with severe intellectual impairment (19 (9,20,21).…”

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confidence: 99%

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Neuronal loss in the pedunculopontine tegmental nucleus in Parkinson disease and in progressive supranuclear palsy.

Hirsch¹,

Graybiel²,

Duyckaerts³

et al. 1987

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

488

312

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In the brains of humans and other mammals, there are two principal groups of cholinergic nuclei aside from those forming the cranial motor nuclei. One group lies in the forebrain and includes the nucleus basalis of Meynert. The second group lies in the hindbrain and includes the nucleus tegmenti pedunculopontinus (NPP) group Ch5. The basal forebrain cholinergic cell groups, which innervate widespread areas of the neocortex, undergo degeneration in Alzheimer disease and also in parkinsonism associated with dementia. We here report that the hindbrain NPP Ch5 cell group, thought to innervate many nuclei of the extrapyramidal motor system, the superior colliculus, and the substantia innominata, undergoes degeneration in idiopathic Parkinson disease and in the parkinsonian syndrome of progressive supranuclear palsy. These findings strongly suggest that degeneration in the brainstem in Parkinson disease is not confined to catecholamine-containing neurons, but that cholinergic neurons of the NPP are also vulnerable. The findings further raise the possibility that certain symptoms of Parkinson disease and progressive supranuclear palsy have their genesis in pathology of these cholinergic neurons.,The cardinal neuropathologic characteristics of Parkinson disease (PD) are massive cell loss in the dopamine-containing substantia nigra pars compacta (1, 2), with variable degeneration in other aminergic nuclei of the brainstem, and the appearance of intracellular Lewy bodies in neurons of both the hindbrain and forebrain (3). It is now recognized that in some if not most parkinsonian brains there is further a cholinergic defect and loss of neurons in the nucleus basalis of Meynert, the principal cholinergic nucleus of the forebrain (4-6). A matter of particularly active study in the past 5 years has been the possibility that cell loss in the nucleus basalis could underlie the dementia exhibited by some parkinsonian patients (5, 6).A second major set of cholinergic nuclei exists in the hindbrain (7-11), and one of these nuclei, the Ch5 group of Mesulam et al. (7), corresponds in location to one of the principal nuclei associated with the basal ganglia: the nucleus tegmenti pedunculopontinus (NPP) (11-13). Given the close association of the NPP with the extrapyramidal motor system (8, 14-18), we undertook a study of the NPP in autopsy material from the brains of persons who died with a diagnosis of idiopathic PD. We also determined the status of the nucleus in progressive supranuclear palsy (PSP), a parkinsonian syndrome associated with severe intellectual impairment (19 METHODSHistochemistry. Observations were made on postmortem specimens from the brains of four control individuals who died without known neurologic or psychiatric deficit, six patients who had suffered from PD, and three patients who had suffered from PSP. The diagnoses were confirmed postmortem on the basis of neuropathological examination and retrospective examination of clinical records. The mean ages were 85 ± 3 years (range 83-90 years) for the co...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Neuronal loss in the pedunculopontine tegmental nucleus in Parkinson disease and in progressive supranuclear palsy.

Hirsch¹,

Graybiel²,

Duyckaerts³

et al. 1987

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

488

312

View full text Add to dashboard Cite

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“…But this medial segment of GP sends also efferents toward intralaminar thalamic nuclei and then to diffuse areas of neocortex, toward the brain stem and toward the habenular nuclei. [49][50][51][52] It has been suggested from investigations in the rat53 that fibres destined for the habenula arise primarily from the rostral half of the entopedoncular nucleus-the rat's equivalent of medial globus pallidus and that this part of the nucleus might be termed the ' limbic pallidum". The pallidal organisation in its output elements seems more complex in primates.54 55 A central zone can be described where most neurons send axonal branches to both the thalamus and the mid-brain, and a peripheral limbic zone which encroaches upon lateral hypothalamus and whose cells project only to the habenula.…”

Section: Role Of Pallidal Lesionmentioning

confidence: 99%

Pure psychic akinesia with bilateral lesions of basal ganglia.

Laplane¹,

Baulac²,

Widlöcher³

et al. 1984

Journal of Neurology, Neurosurgery & Psychiatry

171

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SUMMARY Three patients showed dramatic psychic akinesia after recovery from toxic encephalopathy. They had no or only mild motor disorders. The spontaneous psychic akinesia was reversible when the patient was stimulated, as if there was a loss of self psychic activation. Intellectual capacities were normal. Two patients had stereotyped behaviours resembling compulsions. In all patients CT cans showed bilateral lesions in the basal ganglia, mainly within the globus pallidus.Mental disorders occur very frequently in basal ganglia diseases, such as Wilson's, Parkinson's, Hallervorden-Spatz diseases, Huntington chorea, and progressive supranuclear palsy ... The clinical picture of these mental disorders however, are extremely varied; they consist of psychiatric disorders, personality changes and often various degrees of intellectual deterioration, but this last feature can be absent. In spite of this diversity a peculiar clinical picture characterisation by slowing down of thought processes, inertia and memory disorders has been identified in several degenerative diseases, and has been described under the term of 'subcortical dementia".' 2 Degenerative lesions are generally not limited to the basal ganglia, so eventual role in mental processes cannot be established. Contrarily, in the motor control field, there is much anatomical, physiological and clinical evidence (the two latter largely from the study of Parkinson's disease), leading to the conclusion that basal ganglia should be regarded as organs of motor control, as recently emphazised by Marsden.3 We have recently drawn attention to a psychic picture,4 5 possibly the consequence of bilateral subcortical lesions in the basal ganglia, which was characterised by pure psychic akinesia without permanent dementia, and by pseudo-obsessional activities. We now report three similiar cases, which, in combination with some clinical and anatomical data in the literature, may furnish some support to Address for reprint requests: Dr D Laplane, H6pital de la Salpetriere, 47 (table).Two years after the encephalopathy, he began to show stereotyped activities. The most frequent consisted in mental counting, for example, up to twelve or a multiple of twelve, but sometimes it was a more complex calculation. Such mental activities sometimes were accompanied by gestures, such as a finger pacing of the counts.

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“…[3][4][5][6] Recently, the PPN has attracted interest as a potential deep brain stimulation (DBS) target to improve freezing of gait (FOG). Low-frequency PPN DBS (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) in parkinsonian nonhuman primates (NHPs) helps to alleviate akinesia in conjunction with levodopa treatment. 7 Small, open-label, nonblinded clinical studies have demonstrated that PPN DBS can improve akinesia and FOG in patients with advanced Parkinson disease (PD) [8][9][10] or with progressive supranuclear palsy.…”

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confidence: 99%

Physiological identification of the human pedunculopontine nucleus

Shimamoto

Larson

Ostrem

et al. 2009

Journal of Neurology, Neurosurgery & Psychiatry

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Background The pedunculopontine nucleus (PPN) is a brainstem structure with widespread connections to the basal ganglia. Despite the recent introduction of PPN deep brain stimulation (DBS) for the treatment of gait disorders, little is known about its physiology in humans. Methods We analyzed the discharge characteristics of single neurons in the PPN region in four patients and PPN local field potentials (LFP) in one patient, recorded during the course of DBS implantation. Two patients had Parkinson’s disease and two had non-sinemet responsive parkinsonism. Cell locations were plotted in the coordinate system of a human brainstem atlas. Results Fifty-six units in the PPN region were studied, of which 32 mapped to within PPN boundaries. The mean (+/− SD) discharge rate of neurons in the PPN was 23.2 (+/− 15.6) Hz. Spontaneous neuronal firing rate and burst discharge rate were significantly different between neurons in the region dorsal to PPN and those in the PPN. Responses to passive movement of contralateral and ipsilateral limbs were found. Theta and beta band oscillations were present in the PPN LFP. Conclusion PPN discharge characteristics may prove useful in the electrophysiologic identification of PPN during DBS implantation surgery.

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Projections of the lentiform nucleus in the monkey

Cited by 734 publications

References 45 publications

Neuronal loss in the pedunculopontine tegmental nucleus in Parkinson disease and in progressive supranuclear palsy.

Neuronal loss in the pedunculopontine tegmental nucleus in Parkinson disease and in progressive supranuclear palsy.

Pure psychic akinesia with bilateral lesions of basal ganglia.

Physiological identification of the human pedunculopontine nucleus

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