Changes in motor cortex inhibition over time in patients with amyotrophic lateral sclerosis
Autor: | Stefano Tamburin, Paolo Manganotti, Nicola Refatti, Antonio Forgione, Nicolo' Rizzuto, Giampietro Zanette |
---|---|
Přispěvatelé: | Zanette, G., Tamburin, S., Manganotti, Paolo, Refatti, N., Forgione, A., Rizzuto, N. |
Jazyk: | angličtina |
Rok vydání: | 2002 |
Předmět: |
Adult
Male medicine.medical_specialty Neurology Time Factors amyotrophic lateral sclerosis (ALS) Patients medicine.medical_treatment Central nervous system transcranial magnetic stimulation (TMS) intracortical inhibition (ICI) motor cortex hyperexcitability Statistics Nonparametric Central nervous system disease Degenerative disease medicine Humans Amyotrophic lateral sclerosis Aged Amyotrophic Lateral Sclerosis Motor Cortex Neural Inhibition Middle Aged medicine.disease Evoked Potentials Motor Transcranial magnetic stimulation medicine.anatomical_structure Silent period Female Neurology (clinical) Psychology Neuroscience Motor cortex |
Popis: | Abnormal balance between intracortical inhibitory and excitatory mechanisms has been found to contribute to the genesis of motor cortex hyperexcitability in amyotrophic lateral sclerosis (ALS), but data are lacking on the role of these abnormalities in the pathophysiology of the disease. We evaluated the resting motor threshold (RMT), the cortical silent period (CSP) to single-pulse transcranial magnetic stimulation (TMS), early intracortical inhibition (ICI), early intracortical facilitation (ICF) and late ICI to paired-pulse TMS in 40 patients with ALS. These parameters were correlated with disease duration and clinical features. They were also monitored over time in selected patients. The main abnormal TMS findings were: (a). reduced or even absent early and late ICI; six out of 9 patients, with normal early ICI at the first recording, developed abnormal ICI after several months; (b). reduced cortical silent period duration with increasing TMS intensity. ICF and RMT were not affected. Impairment of early and late ICI correlated significantly with disease duration, the diagnostic categories and the clinical evidence of upper motor neuron involvement. The alteration of different cortical inhibitory functions seems to take place with disease progression, rather than being the primary event in the pathogenesis of ALS. The impaired inhibition is considered as being due to both depletion of specific subpopulations of intracortical GABAergic neurons and mechanisms involved in motor cortex reorganization following progressive neuronal loss. Clarification of the importance of these factors in the pathogenesis of the disease may have diagnostic and therapeutic implications. |
Databáze: | OpenAIRE |
Externí odkaz: |