Contralateral disappearance of parkinsonian signs after subthalamic hematoma

Sellal, François; Hirsch, Erwin F.; Lisovoski, F.; Mutschler, Véronique; Collard, M; Marescaux, C.

doi:10.1212/wnl.42.1.255

Cited by 94 publications

(29 citation statements)

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“…Unilateral lesions involving the STN and adjacent tissue are associated with dyskinesias characterized by hemiballism in the monkey (Whittier and Mettler, 1949;Carpenter et al, 1950;Hamada and DeLong, 1992). Furthermore, lesions of the STN ameliorate the symptoms of experimentally induced parkinsonism in monkeys (Bergman et al, 1990) as well as clinical parkinsonism in humans (Sellal et al, 1992). We recently have shown, however, that the relationship between SN and STN in the monkey (Dybdal et al, 1997) may be very different from the relationship in the rat (as shown here) or cat (Murer and Pazo, 1993); accordingly, there is a need for caution in the extrapolation from rodent models to humans.…”

Section: Discussionmentioning

confidence: 99%

Postural and Anticonvulsant Effects of Inhibition of the Rat Subthalamic Nucleus

2000

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The subthalamic nucleus (STN) plays a crucial role as a regulator of basal ganglia outflow by providing excitatory glutamatergic input into the two output nuclei of the basal ganglia, substantia nigra pars reticulata (SNpr), and entopeduncular nucleus. This study examined the effects of suppressing activity in the STN of the awake, behaving rat. Specifically, we evaluated the effects of unilateral and bilateral focal inhibition of STN on posture, locomotion, and susceptibility to limbic motor seizures.Unilateral microinjection of a GABA A receptor agonist (muscimol, 200 pmol) into STN produced a site-dependent contralaterally directed postural asymmetry without locomotor activation. This effect differed from responses produced by the same dose of muscimol placed into SNpr, which included locomotor activation in addition to contralaterally directed postural asymmetry. Locomotor activation and postural asymmetry were obtained also after blockade of glutamate transmission in SNpr by the unilateral application of kynurenate (100 nmol). Our observation that STN inhibition did not induce the locomotor activation characteristic of SNpr inhibition suggests that there are glutamatergic inputs to SNpr, other than those from STN, that are responsible for controlling locomotion.Bilateral, but not unilateral, injection of muscimol (200 pmol) into STN protected against limbic motor seizures evoked either by intravenous bicuculline or by focal application of bicuculline into anterior piriform cortex (area tempestas). These results demonstrate that focal inhibition of STN reproduces the postural asymmetry and anticonvulsant actions that are obtained with the inhibition of SNpr. This provides behavioral support for the concept that STN contributes a crucial tonic excitatory (glutamatergic) drive to the rat SNpr.

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Section: Discussionmentioning

confidence: 99%

Postural and Anticonvulsant Effects of Inhibition of the Rat Subthalamic Nucleus

2000

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“…To our knowledge, iron deposits in the subthalamic nuclei, revealed by cranial MRI, beside an iron-related pallidal diffuse T2-weighted hypointensity in HS has not been reported up to now. The subthalamic iron deposits in our subject may influence the clinical symptomatology of HS, because case reports describe disappearance of parkinsonian signs after subthalamic spontaneous hemorrhage or hemotoma [8, 9]. Iatrogenic lesioning of the subthalamic nucleus abolishes the excitatory drive from the subthalamic nucleus to the globus pallidus, followed by improvement of parkinsonian signs and appearance of severe and permanent dyskinesia [10].…”

Section: Discussionmentioning

confidence: 99%

Iron Deposits in the Subthalamic Nuclei in Hallervorden-Spatz Disease

et al. 1999

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“…Striatal dopamine loss is postulated to result in increased striatal inhibition of GPe, which in turn results in disinhibition of STN and increased basal ganglia output from GPi. This concept is supported by the fact that STN inactivation results in a substantial reduction of the severity of parkinsonian motor signs in monkeys (Bergman et al, 1990;Guridi et al, 1993;Baron et al, 2002) and human patients (Sellal et al, 1992;Gill and Heywood, 1997;Alvarez et al, 2001).…”

Section: Global Neuronal Activity Changes In Parkinsonismmentioning

confidence: 95%

Role of External Pallidal Segment in Primate Parkinsonism: Comparison of the Effects of 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Induced Parkinsonism and Lesions of the External Pallidal Segment

Soares¹,

Kliem²,

Betarbet³

et al. 2004

J. Neurosci.

179

185

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These experiments re-examined the notion that reduced activity in the external pallidal segment (GPe) results in the abnormalities of neuronal discharge in the subthalamic nucleus (STN) and the internal pallidal segment (GPi) and in the development of parkinsonian motor signs. Extracellular recording in two rhesus monkeys, which had been rendered parkinsonian by treatment with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), revealed that the average neuronal discharge rate decreased in GPe but increased in STN and GPi. After MPTP, neurons in all three nuclei tended to discharge in oscillatory bursts. In addition, GABA release in STN (measured with microdialysis) was reduced, indicative of reduced activity along the GPe-STN pathway. Finally, the concentration of glutamic acid dehydrogenase (GAD; measured with autoimmunoradiography) was increased in GPe and GPi, likely reflecting increased striatal input and increased activity of local axon collaterals, respectively. Surprisingly, GAD protein in STN remained unchanged, indicating that the usual assumption that GAD levels are determined primarily by the overall activity of GABAergic elements may be too simplistic. The results from the MPTP-treated animals were compared with results obtained in a second group of three animals with ibotenic acid lesions of GPe. GPe lesions resulted in increased discharge in STN and GPi, comparable with the changes seen after MPTP but did not induce oscillatory bursting and had no behavioral effects. The results indicate that a mere reduction of GPe activity does not produce parkinsonism. Other changes, such as altered discharge patterns in STN and GPi, may play an important role in the generation of parkinsonism.

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Contralateral disappearance of parkinsonian signs after subthalamic hematoma

Cited by 94 publications

References 0 publications

Postural and Anticonvulsant Effects of Inhibition of the Rat Subthalamic Nucleus

Postural and Anticonvulsant Effects of Inhibition of the Rat Subthalamic Nucleus

Iron Deposits in the Subthalamic Nuclei in Hallervorden-Spatz Disease

Role of External Pallidal Segment in Primate Parkinsonism: Comparison of the Effects of 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Induced Parkinsonism and Lesions of the External Pallidal Segment

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