  The mechanisms underlying pathologically synchronized neural oscillations in
Parkinson's disease (PD) and generalized epilepsies are jointly explored via a
neural field model of the corticothalamic-basal ganglia (CTBG) system. The
basal ganglia (BG) are approximated as a single effective population and their
roles in modulating oscillatory corticothalamic (CT) dynamics and vice versa
are analyzed. Besides normal EEG rhythms, enhanced activity around 4 Hz and 20
Hz exists in the model, consistent with characteristic frequencies in PD. These
rhythms result from resonances in loops between the BG and CT populations,
analogous to those underlying epileptic oscillations in a previous CT model.
Dopamine depletion is argued to weaken the dampening of these resonances in PD,
and network connections explain the significant coherence between BG, thalamic,
and cortical activity around 4-8 Hz and 20 Hz. Parallels between the afferent
and efferent connection sites of the thalamic reticular nucleus (TRN) and BG
predict low dopamine to correspond to a reduced likelihood of tonic-clonic
(grand mal) seizures, agreeing with experimental findings. Further, the model
predicts an increased likelihood of absence (petit mal) seizure resulting from
low dopamine levels matching experimental findings. Suppression of absence
seizure activity is shown when afferent and efferent BG connections to the CT
system are strengthened, consistent with other CTBG modeling studies. The BG
are demonstrated to suppress activity of the CTBG system near tonic-clonic
seizure states, providing insight into the reported efficacy of current
treatments in BG circuits. Sleep states of the TRN are also found to suppress
pathological PD activity matching observations. Overall, the findings
demonstrate strong parallels between coherent oscillations in generalized
epilepsies and PD, and provide insights into possible comorbidities.
