Cortical dysfunction underlies disability in multiple sclerosis

• Published in: Multiple sclerosis 2012-04, Vol.18 (4), p.425-432
• Main Authors: Vucic, Steve, Burke, Therese, Lenton, Kerry, Ramanathan, Sudarshini, Gomes, Lavier, Yannikas, Con, Kiernan, Matthew C
• Format: Article
• Language: English
• Subjects: Adult; Aged; Atrophy; Atrophy - physiopathology; Biological and medical sciences; Conduction; Cortex; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Evoked Potentials, Motor; Excitability; Female; Humans; Male; Medical sciences; Middle Aged; Motor Cortex - pathology; Motor Cortex - physiopathology; Motor evoked potentials; Multiple sclerosis; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis; Multiple Sclerosis, Chronic Progressive - pathology; Multiple Sclerosis, Chronic Progressive - physiopathology; Multiple Sclerosis, Relapsing-Remitting - pathology; Multiple Sclerosis, Relapsing-Remitting - physiopathology; Neural Conduction; Neural Inhibition - physiology; Neurology; Substantia grisea; Transcranial Magnetic Stimulation
• ISSN: 1352-4585; 1477-0970
• DOI: 10.1177/1352458511424308

Background: Gray matter atrophy has been implicated in the development of secondary progressive multiple sclerosis (SPMS). Cortical function may be assessed by transcranial magnetic stimulation (TMS). Determining whether cortical dysfunction was a feature of SPMS could be of pathophysiological significance. Objectives: Consequently, novel paired-pulse threshold tracking TMS techniques were used to assess whether cortical dysfunction was a feature of SPMS. Methods: Cortical excitability studies were undertaken in 15 SPMS, 25 relapsing–remitting MS patients (RRMS) and 66 controls. Results: Short interval intracortical inhibition (SPMS 3.0 ± 2.1%; RRMS 12.8 ± 1.7%, p < 0.01; controls 10.5 ± 0.7%, p < 0.01) and motor evoked potential (MEP) amplitude (SPMS 11.5 ± 2.2%; RRMS 26.3 ± 3.6%, p