Abnormal projection of corticospinal tracts in a patient with congenital mirror movements

Cincotta, Massimo; Ragazzoni, Roberto; Scisciolo, G. de; Pinto, Fausto J.; Maurri, S.; Barontini, F

doi:10.1016/s0987-7053(05)80075-9

Cited by 32 publications

(20 citation statements)

References 14 publications

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“…Our TMS findings are consistent with those of previous TMS studies of two DCC -CMM patients 20–22 . In all six of the DCC -CMM patients studied here, stimulation of the motor cortex hand representation elicited ipsilateral MEPs, whereas in healthy volunteers the MEPs are strictly contralateral to the stimulated hemisphere 18, 35–37 .…”

Section: Discussionsupporting

confidence: 92%

“…Two CMM patients with initially unknown genetic status were eventually found to carry a DCC mutation, years after publication of their neurophysiological data. In these two patients, unilateral transcranial magnetic stimulation (TMS) of the primary motor cortex elicited bilateral motor responses, suggesting the existence of bilateral CST projections to the spinal cord 20–22 . However, further neurophysiological and neuroimaging data are needed to validate these results and to clarify to what extent the pyramidal decussation is morphologically and functionally abnormal in DCC -CMM patients.…”

Section: Introductionmentioning

confidence: 94%

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Non cell-autonomous role of DCC in the guidance of the corticospinal tract at the midline

Welniarz

Morel

Pourchet

et al. 2017

Sci Rep

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DCC, a NETRIN-1 receptor, is considered as a cell-autonomous regulator for midline guidance of many commissural populations in the central nervous system. The corticospinal tract (CST), the principal motor pathway for voluntary movements, crosses the anatomic midline at the pyramidal decussation. CST fails to cross the midline in Kanga mice expressing a truncated DCC protein. Humans with heterozygous DCC mutations have congenital mirror movements (CMM). As CMM has been associated, in some cases, with malformations of the pyramidal decussation, DCC might also be involved in this process in human. Here, we investigated the role of DCC in CST midline crossing both in human and mice. First, we demonstrate by multimodal approaches, that patients with CMM due to DCC mutations have an increased proportion of ipsilateral CST projections. Second, we show that in contrast to Kanga mice, the anatomy of the CST is not altered in mice with a deletion of DCC in the CST. Altogether, these results indicate that DCC controls CST midline crossing in both humans and mice, and that this process is non cell-autonomous in mice. Our data unravel a new level of complexity in the role of DCC in CST guidance at the midline.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 94%

Non cell-autonomous role of DCC in the guidance of the corticospinal tract at the midline

Welniarz

Morel

Pourchet

et al. 2017

Sci Rep

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show abstract

“…10 Using single-and paired-pulse transcranial magnetic stimulation in the above-mentioned DCC-MM patient, we have previously demonstrated that each M1 cortex was abnormally connected to both sides of the spinal cord via separate crossed and uncrossed fastconducting corticospinal projections. 8,9 Together, these findings provide experimental evidence that DCC deficiency results in altered corticospinal tract decussation in humans, as in the rodent model, and confirm the crucial role of the DCC/Netrin-1 system in axonal pathfinding during corticospinal tract development. …”

Section: Resultssupporting

confidence: 67%

“…8,9 DCC Kanga mice that have constitutive DCC insufficiency have a hopping gait, moving their hind legs in concert. 10 This reflects disrupted decussation of corticospinal tract axons.…”

Section: Resultsmentioning

confidence: 99%

A novel DCC mutation and genetic heterogeneity in congenital mirror movements

Depienne

Cincotta²,

Billot³

et al. 2011

Neurology

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“…Ipsilateral responses have also been found in other neurological conditions, such as cerebral gliomas, 6 congenital mirror movements, 14,15 X-linked Kallmann's syndrome, 16 or Klippel-Feil syndrome. 17 In the case of patients with congenital mirror movements, evidence has been obtained for bilateral branching of corticomotoneuronal axons.…”

mentioning

confidence: 93%

Ipsilateral Motor Responses to Focal Transcranial Magnetic Stimulation in Healthy Subjects and Acute-Stroke Patients

Alagona

Delvaux

Gérard

et al. 2001

Stroke

138

102

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Background and Purpose-Prevalence and characteristics of ipsilateral upper limb motor-evoked potentials (MEPs) elicited by focal transcranial magnetic stimulation (TMS) were compared in healthy subjects and patients with acute stroke. Methods-Sixteen healthy subjects and 25 patients with acute stroke underwent focal TMS at maximum stimulator output over motor and premotor cortices. If present, MEPs evoked in muscles ipsilateral to TMS were analyzed for latency, amplitude, shape, and center of gravity (ie, preferential coil location to elicit them). In stroke patients, possible relationships between early ipsilateral responses and functional outcome at 6 months were sought. Results-With relaxed or slightly contracting target muscle, maximal TMS over the motor cortex failed to elicit ipsilateral MEPs in the first dorsal interosseous (FDI) or biceps of any of 16 normal subjects. In 5 of 8 healthy subjects tested, ipsilateral MEPs with latencies longer than contralateral MEPs were evoked in FDI muscle (in biceps, 6 of 8 subjects) during strong (Ͼ50% maximum) contraction of the target muscle. In 15 of 25 stroke patients, ipsilateral MEPs in the unaffected relaxed FDI (in biceps, 6 of 25 stroke patients) were evoked by stimulation of premotor areas of the affected hemisphere. Their latencies were shorter than those that MEPs evoked in the same muscle by stimulation of the motor cortex of the contralateral unaffected hemisphere. Such responses were never obtained in normal subjects and were mostly observed in patients with subcortical infarcts. Patients harboring these responses had slightly better bimanual dexterity after 6 months. Conclusions-Ipsilateral

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Abnormal projection of corticospinal tracts in a patient with congenital mirror movements

Cited by 32 publications

References 14 publications

Non cell-autonomous role of DCC in the guidance of the corticospinal tract at the midline

Non cell-autonomous role of DCC in the guidance of the corticospinal tract at the midline

A novel DCC mutation and genetic heterogeneity in congenital mirror movements

Ipsilateral Motor Responses to Focal Transcranial Magnetic Stimulation in Healthy Subjects and Acute-Stroke Patients

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