Motor cortex disinhibition in normal-pressure hydrocephalus: Clinical article

Andrei V. Chistyakov, Hava Hafner, Alon Sinai, Boris Kaplan, Menashe Zaaroor

Research output: Contribution to journalArticle

Abstract

Object. Previous studies have shown a close association between frontal lobe dysfunction and gait disturbance in idiopathic normal-pressure hydrocephalus (iNPH). A possible mechanism linking these impairments could be a modulation of corticospinal excitability. The aim of this study was 2-fold: 1) to determine whether iNPH affects corticospinal excitability; and 2) to evaluate changes in corticospinal excitability following ventricular shunt placement in relation to clinical outcome. Methods. Twenty-three patients with iNPH were examined using single- and paired-pulse transcranial magnetic stimulation of the leg motor area before and 1 month after ventricular shunt surgery. The parameters of corticospinal excitability assessed were the resting motor threshold (rMT), motor evoked potential/M-wave area ratio, central motor conduction time, intracortical facilitation, and short intracortical inhibition (SICI). The results were compared with those obtained in 8 age-matched, healthy volunteers, 19 younger healthy volunteers, and 9 age-matched patients with peripheral neuropathy. Results. Significant reduction of the SICI associated with a decrease of the rMT was observed in patients with iNPH at baseline evaluation. Ventricular shunt placement resulted in significant enhancement of the SICI and increase of the rMT in patients who markedly improved, but not in those who failed to improve. Conclusions. This study demonstrates that iNPH affects corticospinal excitability, causing disinhibition of the motor cortex. Recovery of corticospinal excitability following ventricular shunt placement is correlated with clinical improvement. These findings support the view that reduced control of motor output, rather than impairment of central motor conduction, is responsible for gait disturbances in patients with iNPH.

Original languageEnglish (US)
Pages (from-to)453-459
Number of pages7
JournalJournal of Neurosurgery
Volume116
Issue number2
DOIs
StatePublished - Feb 2012
Externally publishedYes

Fingerprint

Normal Pressure Hydrocephalus
Motor Cortex
Transcranial Magnetic Stimulation
Healthy Volunteers
Neurologic Gait Disorders
Motor Evoked Potentials
Frontal Lobe
Peripheral Nervous System Diseases
Gait
Leg

Keywords

  • Corticospinal excitability
  • Disinhibition
  • Normal-pressure hydrocephalus
  • Transcranial magnetic stimulation

ASJC Scopus subject areas

  • Clinical Neurology
  • Surgery

Cite this

Chistyakov, A. V., Hafner, H., Sinai, A., Kaplan, B., & Zaaroor, M. (2012). Motor cortex disinhibition in normal-pressure hydrocephalus: Clinical article. Journal of Neurosurgery, 116(2), 453-459. https://doi.org/10.3171/2011.9.JNS11678

Motor cortex disinhibition in normal-pressure hydrocephalus : Clinical article. / Chistyakov, Andrei V.; Hafner, Hava; Sinai, Alon; Kaplan, Boris; Zaaroor, Menashe.

In: Journal of Neurosurgery, Vol. 116, No. 2, 02.2012, p. 453-459.

Research output: Contribution to journalArticle

Chistyakov, AV, Hafner, H, Sinai, A, Kaplan, B & Zaaroor, M 2012, 'Motor cortex disinhibition in normal-pressure hydrocephalus: Clinical article', Journal of Neurosurgery, vol. 116, no. 2, pp. 453-459. https://doi.org/10.3171/2011.9.JNS11678
Chistyakov, Andrei V. ; Hafner, Hava ; Sinai, Alon ; Kaplan, Boris ; Zaaroor, Menashe. / Motor cortex disinhibition in normal-pressure hydrocephalus : Clinical article. In: Journal of Neurosurgery. 2012 ; Vol. 116, No. 2. pp. 453-459.
@article{46aed75b36e0486d822d46cd0abd1bd5,
title = "Motor cortex disinhibition in normal-pressure hydrocephalus: Clinical article",
abstract = "Object. Previous studies have shown a close association between frontal lobe dysfunction and gait disturbance in idiopathic normal-pressure hydrocephalus (iNPH). A possible mechanism linking these impairments could be a modulation of corticospinal excitability. The aim of this study was 2-fold: 1) to determine whether iNPH affects corticospinal excitability; and 2) to evaluate changes in corticospinal excitability following ventricular shunt placement in relation to clinical outcome. Methods. Twenty-three patients with iNPH were examined using single- and paired-pulse transcranial magnetic stimulation of the leg motor area before and 1 month after ventricular shunt surgery. The parameters of corticospinal excitability assessed were the resting motor threshold (rMT), motor evoked potential/M-wave area ratio, central motor conduction time, intracortical facilitation, and short intracortical inhibition (SICI). The results were compared with those obtained in 8 age-matched, healthy volunteers, 19 younger healthy volunteers, and 9 age-matched patients with peripheral neuropathy. Results. Significant reduction of the SICI associated with a decrease of the rMT was observed in patients with iNPH at baseline evaluation. Ventricular shunt placement resulted in significant enhancement of the SICI and increase of the rMT in patients who markedly improved, but not in those who failed to improve. Conclusions. This study demonstrates that iNPH affects corticospinal excitability, causing disinhibition of the motor cortex. Recovery of corticospinal excitability following ventricular shunt placement is correlated with clinical improvement. These findings support the view that reduced control of motor output, rather than impairment of central motor conduction, is responsible for gait disturbances in patients with iNPH.",
keywords = "Corticospinal excitability, Disinhibition, Normal-pressure hydrocephalus, Transcranial magnetic stimulation",
author = "Chistyakov, {Andrei V.} and Hava Hafner and Alon Sinai and Boris Kaplan and Menashe Zaaroor",
year = "2012",
month = "2",
doi = "10.3171/2011.9.JNS11678",
language = "English (US)",
volume = "116",
pages = "453--459",
journal = "Journal of Neurosurgery",
issn = "0022-3085",
publisher = "American Association of Neurological Surgeons",
number = "2",

}

TY - JOUR

T1 - Motor cortex disinhibition in normal-pressure hydrocephalus

T2 - Clinical article

AU - Chistyakov, Andrei V.

AU - Hafner, Hava

AU - Sinai, Alon

AU - Kaplan, Boris

AU - Zaaroor, Menashe

PY - 2012/2

Y1 - 2012/2

N2 - Object. Previous studies have shown a close association between frontal lobe dysfunction and gait disturbance in idiopathic normal-pressure hydrocephalus (iNPH). A possible mechanism linking these impairments could be a modulation of corticospinal excitability. The aim of this study was 2-fold: 1) to determine whether iNPH affects corticospinal excitability; and 2) to evaluate changes in corticospinal excitability following ventricular shunt placement in relation to clinical outcome. Methods. Twenty-three patients with iNPH were examined using single- and paired-pulse transcranial magnetic stimulation of the leg motor area before and 1 month after ventricular shunt surgery. The parameters of corticospinal excitability assessed were the resting motor threshold (rMT), motor evoked potential/M-wave area ratio, central motor conduction time, intracortical facilitation, and short intracortical inhibition (SICI). The results were compared with those obtained in 8 age-matched, healthy volunteers, 19 younger healthy volunteers, and 9 age-matched patients with peripheral neuropathy. Results. Significant reduction of the SICI associated with a decrease of the rMT was observed in patients with iNPH at baseline evaluation. Ventricular shunt placement resulted in significant enhancement of the SICI and increase of the rMT in patients who markedly improved, but not in those who failed to improve. Conclusions. This study demonstrates that iNPH affects corticospinal excitability, causing disinhibition of the motor cortex. Recovery of corticospinal excitability following ventricular shunt placement is correlated with clinical improvement. These findings support the view that reduced control of motor output, rather than impairment of central motor conduction, is responsible for gait disturbances in patients with iNPH.

AB - Object. Previous studies have shown a close association between frontal lobe dysfunction and gait disturbance in idiopathic normal-pressure hydrocephalus (iNPH). A possible mechanism linking these impairments could be a modulation of corticospinal excitability. The aim of this study was 2-fold: 1) to determine whether iNPH affects corticospinal excitability; and 2) to evaluate changes in corticospinal excitability following ventricular shunt placement in relation to clinical outcome. Methods. Twenty-three patients with iNPH were examined using single- and paired-pulse transcranial magnetic stimulation of the leg motor area before and 1 month after ventricular shunt surgery. The parameters of corticospinal excitability assessed were the resting motor threshold (rMT), motor evoked potential/M-wave area ratio, central motor conduction time, intracortical facilitation, and short intracortical inhibition (SICI). The results were compared with those obtained in 8 age-matched, healthy volunteers, 19 younger healthy volunteers, and 9 age-matched patients with peripheral neuropathy. Results. Significant reduction of the SICI associated with a decrease of the rMT was observed in patients with iNPH at baseline evaluation. Ventricular shunt placement resulted in significant enhancement of the SICI and increase of the rMT in patients who markedly improved, but not in those who failed to improve. Conclusions. This study demonstrates that iNPH affects corticospinal excitability, causing disinhibition of the motor cortex. Recovery of corticospinal excitability following ventricular shunt placement is correlated with clinical improvement. These findings support the view that reduced control of motor output, rather than impairment of central motor conduction, is responsible for gait disturbances in patients with iNPH.

KW - Corticospinal excitability

KW - Disinhibition

KW - Normal-pressure hydrocephalus

KW - Transcranial magnetic stimulation

UR - http://www.scopus.com/inward/record.url?scp=84856773970&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84856773970&partnerID=8YFLogxK

U2 - 10.3171/2011.9.JNS11678

DO - 10.3171/2011.9.JNS11678

M3 - Article

C2 - 21999318

AN - SCOPUS:84856773970

VL - 116

SP - 453

EP - 459

JO - Journal of Neurosurgery

JF - Journal of Neurosurgery

SN - 0022-3085

IS - 2

ER -