Basal ganglia and post-stroke rehabilitation outcomes

The basal ganglia (BG) are involved in multiple circuits in the brain including : a motor loop, cognitive loop, limbic loop, and an oculomotor loop. These ganglia are actively receiving and sending signals to and from the cerebral cortex, thalamus, brain stem and cerebellum, hence the clinical presentations such as: Rigidity, bradykinesia, tremors, ataxia, difficulty swallowing and speaking (pseudobulbar palsy), impaired facial expressions and spontaneous movements,  impaired decision making, memory and attention, personality changes, lack of motivation,  mood disorders, pseudobulbar affect or emotional palsy ( uncontrolled laughter and crying) . All these clinical presentations make the basal ganglia an important area of the brain to study and understand in order to design effective treatment plans (Weng et al., 2017) . Although several disorders and syndromes may be present with BG dysfunction, such as Parkinson’s, Huntington’s, Wilson’s disease, and even obsessive compulsive disorder, but this post focuses on the post-stroke aspect of such disorders and  its relationship to the post-stroke rehabilitation outcomes.

Anatomy of Basal Ganglia

The basal ganglia area lies deep in the basal forebrain and midbrain regions and includes :

1- The Striatum: caudate nucleus, putamen and nucleus accumbens.

2- The Pallidum :  medial and lateral globus pallidus.

3- The subthalamic nucleus.

4- The substantia nigra.

Its GABA, glutamate and dopaminergic pathways (McGeer, Staines, & McGeer, 1984) combined with  all these parts that interact with the neighbouring areas from the anterior to posterior and even the brain stem, make these ganglia a true conductor of goal directed actions in the brain (Lanciego, Luquin, & Obeso, 2012). (for a comprehensive neuroanatomy of BG read ” functional neuroanatomy of the basal ganglia” by Lanciego et al, 2012. )

 

BG area is supplied by multiple arteries, but the anterior circulation (carotids) which originates from the aortic arch plays a important role in feeding these ganglia. The carotids cephalically branch out as the internal carotid to the middle cerebral artery (MCA) and then deeper into smaller arteries such as the anterior choroidal artery where BG gets its blood supply. any embolic, thrombotic or lacunar events can impede the blood flow to these areas. The location of the impediment is considered in order to clinically classify different types of strokes . e.g. large MCA strokes or small vessel multi infarct disease which affects the micro vasculature of the deeper structures (lacunar).

Figure : The circle of Willis and the blood supply to the deep structures such as basal ganglia and thalamus.

 

The main question that is frequently asked is, why the Basal ganglia is involved in majority of stroke cases? and the answer lies in the epidemiological studies of the prevalence of the anterior circulation and the middle cerebral artery infarcts. if we add up the prevalence of MCA, >1 territory  and small vessel infarcts we would have a hypothetical number of about 73% which corresponds to the potential cases that involve BG.

As mentioned above, BG circuits are constantly involved in a feedback loop mechanisms and any structural, and network damage to the cortex, or other connectivity issues can promote imbalances in BG functions(Kalaria, Akinyemi, & Ihara, 2016).  This lack of harmony in the neural network has also been studied in thalamic atrophy after stroke, where the ipsilateral thalamus have shown signs of inactivity, imbalance and shrinkage (Tamura, et al, 1991).

 

How does it translate into rehabilitation outcomes?

Although BG dysfunctions do not always present the same way and strokes in general are similar to finger prints, but knowing that BG is an important component of motor learning and procedural memory, and has a role in mood, motivation and impulsivity,  can equip clinicians with valuable information to predict outcomes to a certain degree, design better treatment plans, and prevent adverse outcomes (Tian et al., 2017). for example, these patients are often impulsive which makes them susceptible to falls. Also, having an impaired procedural memory negatively affects the carry over and durability of therapies, though they might re-learn movements by sensory substitution such as visual or auditory cues. Motivational is another area that clinicians need to pay attention to, these patients often have difficulties engaging in goal directed behaviour and require strategies to motivate them to increase interest and participation.

Having said that in the modern integrated stroke care system and its multidisciplinary approach to treat and rehab stroke patients, information such as neuroimaging  and the exact location of the infarct/s, have not found its place and value. In community hospitals or outpatient stroke rehab facilities, a rehab specialist, physiatrist or a physio/OT rarely pay attention to such important details and rehabilitation plans are mainly designed based on generic plans and approaches such as ADL, upper extremity or lower extremity, balance, ambulation, using  Bobath (NDT) or constraint induced movement therapy techniques, and etc. The time has come to use these valuable information to move away from the cookbook medicine and generic rehab paradigms and engage in a more personalized approach.

 

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References:

  • Herrero, M.-T., Barcia, C., & Navarro, J. M. (2002). Functional anatomy of thalamus and basal  ganglia.  Child’s Nervous System: ChNS: Official Journal of the International Society for Pediatric Neurosurgery, 18(8),    386–404. https://doi.org/10.1007/s00381-002-0604-1
  • Kalaria, R. N., Akinyemi, R., & Ihara, M. (2016).Stroke injury, cognitive impairment and vascular            dementia. Biochimica et Biophysica Acta, 1862(5), 915–925. https://doi.org/10.1016/j.bbadis.2016.01.015
  • Lanciego, J. L., Luquin, N., & Obeso, J. A. (2012). Functional Neuroanatomy of the Basal Ganglia. Cold    Spring Harbor Perspectives in Medicine, 2(12). https://doi.org/10.1101/cshperspect.a009621
  • McGeer, E. G., Staines, W. A., & McGeer, P. L. (1984). Neurotransmitters in the basal ganglia. The  Canadian Journal of Neurological Sciences. Le Journal Canadien Des Sciences Neurologiques, 11(1 Suppl),  89–99.
  • Tamura, A., Tahira, Y., Nagashima, H., Kirino, T., Gotoh, O., Hojo, S., & Sano, K. (1991). Thalamic atrophy following cerebral infarction in the territory of the middle cerebral artery. Stroke, 22(5), 615–618.
  • Tian, Q., Chastan, N., Bair, W.-N., Resnick, S. M., Ferrucci, L., & Studenski, S. A. (2017). The brain map of    gait variability in aging, cognitive impairment and dementia-A systematic review. Neuroscience and  Biobehavioral Reviews, 74(Pt A), 149–162. https://doi.org/10.1016/j.neubiorev.2017.01.020
  • Weng, L., Xie, Q., Zhao, L., Zhang, R., Ma, Q., Wang, J., … Huang, R. (2017). Abnormal structural  connectivity between the basal ganglia, thalamus, and frontal cortex in patients with disorders of  consciousness. Cortex; a Journal Devoted to the Study of the Nervous System and Behavior, 90, 71–87.  https://doi.org/10.1016/j.cortex.2017.02.011

 

 

 

 

 

 

 

 

 

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