By: Catherine Joachin
What is the basal ganglia?
The basal ganglia are a group of structures lodged between the cerebral cortex and the brainstem that control voluntary movement. It is comprised of the caudate nucleus, globus pallidus, nucleus accumbent, putamen, substantia nigra, and subthalamic nucleus (Cleveland Clinic, n.d.).
Functions of the basal ganglia
The basal ganglia mainly acts as a filter for information going to the motor cortex. Through different circuits, the basal ganglia can promote certain motor signals and suppress involuntary movements by sending only relevant, coveted projections to the cerebral cortex and other areas of the brain via the thalamus (Cleveland Clinic, n.d.). In other words, the basal ganglia plays an incremental role in processing and propagating brain activity.
The basal ganglia also performs non-motor functions related to procedural learning, habit formation, attention, reward-related behavior, and emotion (Lanciego et al., 2012).
Complications of the basal ganglia
Damage to basal ganglia nerve cells will result in the progressive degeneration of motor functions. This can translate into uncontrollable limb movements, a loss of balance, tremors, spasms, gait problems, poor coordination, trouble walking, and other movement disorder symptoms (Cleveland Clinic, n.d.; Yanagisawa, 2018).
Non-motor capabilities can also be affected by injury to this area. Notable examples include vision difficulties and speech impairment (Cleveland Clinic, n.d.).
Basal ganglia dysfunction is associated with several medical conditions including Wilson disease, multiple system atrophy, Parkinson’s disease, progressive supranuclear palsy, Huntington’s disease, and multiple sclerosis to name a few (Cleveland Clinic, n.d.).
Epilepsy-related complications
Involuntary movements caused by damage to basal ganglia structures might resemble and be mistaken for epileptic seizures. Unpredictability is a common feature of both seizures and movement disorder contractions; however, basal ganglia-related movement disorders are not generally accompanied by a loss of consciousness or awareness (Atrium Health Wake Forest Baptist, n.d.)
There is a body of literature that postulates that the caudate, putamen, nucleus accumbens, and pallidum are involved in temporal lobe epilepsy. Rektor and colleagues (2012) suggest that while that may be the case, it is unlikely that the basal ganglia contributes to the production of clinical seizures considering that no epileptiform activity has been recorded in this brain region. Instead, evidence suggests that the basal ganglia plays an inhibitory role during temporal lobe seizures. The extent of this involvement, however, is still poorly delineated. Research speculates that the basal ganglia plays a role in influencing and spreading electrical brain activity via feedback pathways (Vuong et Devergnas, 2017; Brier, 2020).
Imaging studies have suggested an association between the basal ganglia and epilepsy through dystonia, a prevalent feature observed in mesiotemporal epilepsy characterized by involuntary muscle contractions (Feddersen et al., 2012). Dystonic posturing (DP) is suspected to result from irregular activation of putaminal and extratemporal cortical areas during temporal lobe seizures, inferring that the basal ganglia affects the propagation of seizures (Rusu et al., 2005).
Treatment options for epilepsy complications
Treatment options very much depend on the condition affected by basal ganglia damage. Despite the fact that the basal ganglia does not contribute to the production of epileptic seizures, its involvement in information relay could direct future research into new pharmacological avenues. In fact, researchers already have been looking into introducing antiepileptic drugs to treat hyperkinetic movement disorders, which are characterized by excessive, uncontrollable limb activity (Siniscalchi et al., 2010).
Conclusion
The basal ganglia is a network of subcortical nuclei that propagates motor information going to the cerebral cortex. An injury to this brain area will affect the execution and control of movements. Basal ganglia pathways might enter into the neural circuitry at play in epilepsy, but it does not contribute to the genesis of epileptic seizures.
References:
Atrium Health Wake Forest Baptist (n.d.). Episodes Mistaken for Seizures. Atrium Health Wake Forest Baptist. Retrieved from https://www.wakehealth.edu/stories/falseseizures#:~:text=Movement%20disorders%20such%20as%20Tourette’s,throats%20or%20even %20curse%20involuntarily
Broer, S. (2020). Not Part of the Temporal Lobe, but Still of Importance? Substantia Nigra and Subthalamic Nucleus in Epilepsy. Frontiers in Systems Neuroscience, 14, 581826. https://doi.org/10.3389/fnsys.2020.581826
Cleveland Clinic (n.d.). Basal Ganglia. Cleveland Clinic. Retrieved from https://my.clevelandclinic.org/health/body/23962-basal-ganglia#function
Feddersen, B., Remi, J., Kilian, M., Vercueil, L., Deransart, C., Depaulis, A., & Noachtar, S. (2012). Is ictal dystonia associated with an inhibitory effect on seizure propagation in focal epilepsies? Epilepsy Research, 99(3), 274–280. https://doi.org/10.1016/j.eplepsyres.2011.12.007
Lanciego, J. L., Luquin, N., & Obeso, J. A. (2012). Functional neuroanatomy of the basal ganglia. Cold Spring Harbor Perspectives in Medicine, 2(12), a009621–a009621. https://doi.org/10.1101/cshperspect.a009621
Mordekar, S. R., Rittey, C. D., Connolly, D. J., & Baxter, P. S. (2011). Reversible basal ganglia signal changes associated with vigabatrin treatment in infants with epilepsy. Journal of Pediatric Neurology, 9(4), 483–487. https://doi.org/10.3233/JPN-2012-0522
Rusu, V., Chassoux, F., Landre, E., Bouilleret, V., Nataf, F., Devaux, B. C., Turak, B., & Semah, F. (2005). Dystonic posturing in seizures of mesial temporal origin : Electroclinical and metabolic patterns. Neurology, 65(10), 1612–1619. https://doi.org/10.1212/01.wnl.0000184510.44808.50
Siniscalchi, A., Gallelli, L., & De Sarro, G. (2010). Use of Antiepileptic Drugs for Hyperkinetic Movement Disorders. Current Neuropharmacology, 8(4), 359–366. https://doi.org/ 10.2174/157015910793358187
Vuong, J., & Devergnas, A. (2018). The role of the basal ganglia in the control of seizure. Journal of Neural Transmission, 125(3), 531–545. https://doi.org/10.1007/s00702-017-1768-x
Yanagisawa, N. (2018). Functions and dysfunctions of the basal ganglia in humans. Proceedings of the Japan Academy, 94(7), 275–304. https://doi.org/10.2183/pjab.94.019
