PMID- 14706225
OWN - NLM
STAT- MEDLINE
DCOM- 20040428
LR  - 20190724
IS  - 0022-510X (Print)
IS  - 0022-510X (Linking)
VI  - 217
IP  - 2
DP  - 2004 Feb 15
TI  - Enhanced intracortical inhibition in cerebellar patients.
PG  - 205-10
AB  - OBJECTIVE: The aim of the study was to examine intracortical excitability in 
      cerebellar patients. METHODS: Short-latency intracortical inhibition (SICI), 
      long-latency intracortical inhibition (LICI) and intracortical facilitation (ICF) 
      to paired transcranial magnetic stimulation (TMS) were investigated in 8 patients 
      with 'pure' cerebellar syndromes and in 14 age-matched normal controls. The 
      conditioning stimulus for short-latency intracortical inhibition and 
      intracortical facilitation was set at 70% of the resting motor threshold (RMT) 
      and preceded the test stimulus (110-120% of the resting motor threshold) by 
      interstimulus intervals (ISIs) of 1-30 ms. For the long-latency intracortical 
      inhibition determinations, the conditioning stimulus was set at 120% of the 
      resting motor threshold and preceded the test stimulus (also 120% of the resting 
      motor threshold) by interstimulus intervals of 30-500 ms. RESULTS: No 
      statistically significant differences were found between patients and controls as 
      regards either short-latency intracortical inhibition or intracortical 
      facilitation. A significant prevalence of long-latency intracortical inhibition 
      was present in cerebellar patients at interstimulus intervals of 200-500 ms 
      (conditioned MEP amplitude=29-41% of test MEP) as compared to controls (71-96% of 
      test MEP). The amplitude of conditioned MEPs was persistently less than 45% of 
      the test MEP in six patients, who were studied at interstimulus intervals up to 
      1000 ms. CONCLUSIONS: Long-latency intracortical inhibition was prevalent and 
      abnormally longer-lasting in patients. Tonic hyperactivation of a subpopulation 
      of GABAergic interneurons in the motor cortex of patients may be the mechanism 
      responsible for this abnormality. Our findings seem to be specific to cerebellar 
      diseases and are the opposite of those found in movement disorders such as 
      dystonia and Parkinson's disease. These data suggest that the cerebellum and the 
      basal ganglia may have opposite influences in tuning the excitability of the 
      motor cortex.
FAU - Tamburin, Stefano
AU  - Tamburin S
AD  - Section of Neurological Rehabilitation, Department of Neurological Sciences and 
      Vision, University of Verona, Italy. s.tamburin@yahoo.com
FAU - Fiaschi, Antonio
AU  - Fiaschi A
FAU - Marani, Silvia
AU  - Marani S
FAU - Andreoli, Annalisa
AU  - Andreoli A
FAU - Manganotti, Paolo
AU  - Manganotti P
FAU - Zanette, Giampietro
AU  - Zanette G
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - J Neurol Sci
JT  - Journal of the neurological sciences
JID - 0375403
RN  - 56-12-2 (gamma-Aminobutyric Acid)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Cerebellar Diseases/*physiopathology
MH  - Cerebellum/physiopathology
MH  - Electric Stimulation
MH  - Evoked Potentials, Motor/physiology
MH  - Female
MH  - Humans
MH  - Interneurons/physiology
MH  - Magnetics
MH  - Male
MH  - Middle Aged
MH  - Motor Cortex/*physiopathology
MH  - Neural Inhibition/*physiology
MH  - Neural Pathways/*physiopathology
MH  - Reaction Time/physiology
MH  - gamma-Aminobutyric Acid/metabolism
EDAT- 2004/01/07 05:00
MHDA- 2004/04/29 05:00
CRDT- 2004/01/07 05:00
PHST- 2004/01/07 05:00 [pubmed]
PHST- 2004/04/29 05:00 [medline]
PHST- 2004/01/07 05:00 [entrez]
AID - S0022510X03003289 [pii]
AID - 10.1016/j.jns.2003.10.011 [doi]
PST - ppublish
SO  - J Neurol Sci. 2004 Feb 15;217(2):205-10. doi: 10.1016/j.jns.2003.10.011.