To investigate further the functional mechanisms underlying the so-called xxxloss of psychic self-activationxxx following paramedian bithalamic lesions, we used transcranial magnetic stimulation (TMS) in a patient who presented with this clinical picture after paramedian bithalamic infarction due to arterial occlusion. The patient showed higher motor thresholds than the controls; the cortical silent period and intracortical inhibition to paired-pulse stimulation, two different forms of inhibition that are believed to reflect GABAergic mechanisms, were significantly increased; short latency afferent inhibition (SAI), a technique that may give direct information about the function of some cholinergic circuits in the human brain, was significantly reduced. This study first demonstrates that there are changes in the intracortical excitatory and inhibitory circuits in this neurobehavioral syndrome, that lead to cortical hypoexcitability. The modulation in GABAergic activity may result in excitability changes in those cholinergic cortical networks that are involved in SAI. TMS may provide important information on connections between the thalamus and cortex and may help in better understanding the role of the thalamo-cortical relationship in behavioural changes associated with thalamic stroke.
Useful keywords (using NLM MeSH Indexing)
Evoked Potentials, Motor/physiology
Transcranial Magnetic Stimulation/methods
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