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== Introduction to the Basal Ganglia ==
<div class="editorbox"> '''Original Editor '''- [[User:Lucinda hampton|Lucinda hampton]] '''Top Contributors''' - {{Special:Contributors/{{FULLPAGENAME}}}}</div>
[[File:Overview of the basal ganglia - Kenhub.png|alt=Overview of the basal ganglia (corpus striatum) - lateral view|300x300px|right]]
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The '''basal ganglia''' is not a single structure in the brain but rather are a group of subcortical nuclei and other associated structures, located at the base of the forebrain.<ref>Yanagisawa N. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6117491/ Functions and dysfunctions of the basal ganglia in humans.] Proc Jpn Acad Ser B Phys Biol Sci. 2018;94(7):275-304. </ref>
'''Original Editor '''- Your name will be added here if you created the original content for this page.  
 
They are primarily involved in motor control and motor initiation<ref name=":1" />, as well as motor learning, executive functions and emotional behaviours. The basal ganglia also play an important role in reward and reinforcement, addictive behaviours and habit formation.<ref name=":0">Lanciego JL, Luquin N, Obeso JA. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3543080/ Functional neuroanatomy of the basal ganglia.] Cold Spring Harbor perspectives in medicine. 2012 Dec 1;2(12):a009621.</ref> 
 
Basal ganglia network dysfunction can lead to various movement disorders,<ref name=":0" /> such as [[Parkinson's]] and [[Huntington Disease|Huntington disease.]]
== Structure of the Basal Ganglia ==
The basal ganglia is made up of multiple separate structures that link together in several different ways.  The interconnected pathways are what define the function of the basal ganglia.  Below is a photo gallery which shows different views of the basal ganglia to include its various structures and neural networks.<gallery>
File:Basal ganglia anatomy.jpg|Basal ganglia nuclei
File:Striatum.png|Corpus striatum of the basal ganglia
File:PD Basal Ganglia etc.png|Basal ganglia structures
File:Basal ganglia nuclei.jpeg|Basal ganglia nuclei in relation to other subcortical structures.
</gallery>


'''Top Contributors''' - {{Special:Contributors/{{FULLPAGENAME}}}}  &nbsp; 
=== Corpus Striatum ===
</div>  
'''Corpus Striatum''' is the largest component of the basal ganglia, it is a heterogeneous structure with a volume of around 10 cm<sup>3</sup>. It receives afferent inputs from various cortical and subcortical structures and sends outputs to different basal ganglia nuclei.<ref name=":0" />  
== Introduction ==
[[File:PD Basal Ganglia etc.png|right|frameless|290x290px]]
The “basal ganglia” refers to a group of subcortical nuclei responsible primarily for motor control, as well as other roles such as motor learning, executive functions, emotional behaviors, and play an important role in reward and reinforcement, addictive behaviours and habit formation. Proposed more than two decades ago, the classical basal ganglia model shows how information flows through the basal ganglia back to the cortex through two pathways with opposing effects for the proper execution of movement<ref name=":0">Lanciego JL, Luquin N, Obeso JA. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3543080/ Functional neuroanatomy of the basal ganglia.] Cold Spring Harbor perspectives in medicine. 2012 Dec 1;2(12):a009621.Available from:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3543080/ (last accessed 12.1.2020)</ref>.


Much of the model has remains today however the model has been modified and amplified with the emergence of new data. The basal ganglia network is now viewed as multiple parallel loops and re-entering circuits whereby motor, associative, and limbic territories are engaged mainly in the control of movement, behavior, and emotions. These parallel circuits subserve the other functions of the basal ganglia engaging associative and limbic territories.<ref name=":0" />
There are two main divisions in the corpus striatum:  


Disruption of the basal ganglia network forms the basis for several movement disorders.
# '''Dorsal Striatum''' (DS): mostly involved in the control of conscious motor movements and executive functions.   
#* '''Caudate nucleus''': is a paired subcortical structure and is involved in many "higher" neurological functions such as (1) movement execution, (2) learning, (3) memory, (4) reward and motivation, (5) emotion, and (6) "romantic interactions"<ref name=":8">Driscoll; M, Bollu P, Tadi P. Neuroanatomy, Nucleus Caudate [Internet]. 24 July 2024 [cited 01 July 2024]. Available from:[https://www.ncbi.nlm.nih.gov/books/NBK557407/#:~:text=The%20caudate%20nucleus%20functions%20not,mostly%20the%20ipsilateral%20frontal%20lobe. https://www.ncbi.nlm.nih.gov/books/NBK557407/]</ref>
# '''Ventral Striatum''': involved in the limbic functions of reward and aversion. It is made up of the nucleus accumbens and the olfactory tubercle.<ref name=":1">Young CB, Sonne J. [https://www.ncbi.nlm.nih.gov/books/NBK537141/ Neuroanatomy, basal ganglia.] InStatPearls [Internet] 2018 Dec 28. StatPearls Publishing.</ref> 
## '''Nucleus accumbens''' in the neural interface between "motivation and action" or the "limbic-motor interface"  It is involved in a wide range of  goal-directed behaviors including (1) feeding, (2) sexual, (3) reward, (4) stress-related, and (5) drug self-administration<ref>Fernández-Espejo E. How does the nucleus accumbens function? [Internet]. 2000 May;30(9):845-9.[cited 01 July 2024]. Available from: [https://pubmed.ncbi.nlm.nih.gov/10870199/#:~:text=Introduction%3A%20The%20nucleus%20accumbens%20is,self%2Dadministration%20behaviors%2C%20etc. https://pubmed.ncbi.nlm.nih.gov/10870199/]</ref>
## '''Olfactory tubercle''' is thought to be involved in odor-guided motivated and eating behaviours.<ref>Murata K. Hypothetical Roles of the Olfactory Tubercle in Odor-Guided Eating Behavior [Internet]. Front Neural Circuits. 2020; 14: 577880..[cited 01 July 2024]. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7686465/</ref>  It likely works in tandem with the nucleus accumbens.


== Structure ==
=== Lenticular Nuclei ===
The basal ganglia are a cluster of subcortical nuclei deep to cerebral hemispheres. The largest component of the basal ganglia is the corpus striatum which contains the caudate and lenticular nuclei (the putamen, globus pallidus externus, and internus), the subthalamic nucleus (STN), and the substantia nigra (SN). These structures intricately synapse onto one another to promote or antagonize movement.<ref name=":1">Young CB, Sonne J. [https://www.ncbi.nlm.nih.gov/books/NBK537141/ Neuroanatomy, basal ganglia.] InStatPearls [Internet] 2018 Dec 28. StatPearls Publishing.Available from:https://www.ncbi.nlm.nih.gov/books/NBK537141/ (last accessed 12.1.2020)</ref>


Divisions of the Basal Ganglia ie  subcortical nuclei.
# '''Putamen''': communicates with many different regions of the cerebral cortex and forms multiple connections within the basal ganglia. It is involved in (1) learning and motor control, (2) speech articulation, (3) language functions, (4) reward, (5) cognitive functioning, and (6) addiction.  The putamen also plays a role in modulating sensory and motor aspects of pain.<ref>Ghandili M, Munakomi S. Neuroanatomy, Putamen [Internet]. 30 January 2023 [cited 01 July 2024]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542170/</ref>
[[File:Striatum.png|right|frameless|400x400px]]
# '''Globus Pallidus''' which can be further divided into two parts: globus pallidus externus, and internus. <ref>Javed N, Cascella M. [https://www.ncbi.nlm.nih.gov/books/NBK557755/ Neuroanatomy, Globus Pallidus.] [Updated 2023 Feb 20]. In: StatPearls [Internet].</ref>  The primary role of the globus pallius is controlling conscious and proprioceptive movements.<ref>Javed N, Cascella M. Neuroanatomy, Globus Pallidus [Internet]. 20 February 2023 [cited 01 July 2024]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557755/</ref>
# '''Corpus Striatum'''- (The largest subcortical brain structure of the basal ganglia is the striatum with a volume of approximately 10 cm). It is a heterogeneous structure that receives afferents from several cortical and subcortical structures and projects to various basal ganglia nuclei.<ref name=":0" /> Within the striatum, there are two main divisions  
* dorsal striatum (DS) see image, shown in red. Primarily involved in control over conscious motor movements and executive functions.  The dorsal striatum consists of the caudate nucleus and the putamen. A white matter, nerve tract (the internal capsule) in the dorsal striatum separates the caudate nucleus and the putamen.   
* ventral striatum, responsible for limbic functions of reward and aversion. Consists of nucleus accumbens and the olfactory tubercle.<ref name=":1" />. 
3. Internal and External segments of '''Globus Pallidus (NB''' until the first half of the 19th century the globus pallidus and putamen were considered one structure, collectively referred to as the ''lentiform'' or ''lenticular'' nucleus<ref>Neuroscientificallychallenged Know your brain [[Globus Pallidus]] 9.1.2019 Available from: https://www.neuroscientificallychallenged.com/blog/know-your-brain-globus-pallidus (last accessed 14.1.2020)</ref>)[[File:PD Basal ganglia .jpg|right|frameless]]
3. '''Subthalamic Nucleus''' (STN) -  a lens-shaped cell group that makes up the largest part of the subthalamus 


4. '''Substantia Nigra''' (SN) - (“black substance” in Latin) is a long nucleus located in the midbrain but considered functionally a part of the basal ganglia because of its reciprocal connections with other brainstem nuclei. It consists of two components, the pars compacta and the pars reticulata, which have different connections and use different neurotransmitters.<ref>Jacobs LK, Sapers BL. [https://www.sciencedirect.com/science/article/pii/B9780443068980000335 Neurological Disease.] InPerioperative Medicine 2011 (pp. 343-359). Springer, London.Available from:https://www.sciencedirect.com/science/article/pii/B9780443068980000335 (last accessed 13.1.2020)</ref>
=== Subthalamic Nucleus ===
The 2 minute video below outlines BG concepts
'''Subthalamic Nucleus''' (STN): a lens-shaped cell group that makes up a large part of the subthalamus.<ref>Basinger H, Joseph J. Neuroanatomy, Subthalamic Nucleus. [Updated 2022 Oct 31]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK559002/</ref>  It has neural projections into the globus pallidus and assists with movement regulation. Specifically, the subthalmic nucleus plays a critical role in the prevention of unwanted movements. For example, a lesion of the subthalamic nucleus can result in hemiballismus (please see below for more details on this disorder).<ref>Basinger H, Joseph J. Neuroanatomy, Subthalamic Nucleus [Internet]. 31 October 2022 [cited 01 July 2024]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK559002/</ref>
{{#ev:youtube|https://www.youtube.com/watch?v=OD2KPSGZ1No|width}}<ref>Neuroscientifically Challenged Basal ganglia available from: https://www.youtube.com/watch?v=OD2KPSGZ1No (last accessed 14.1.2020)</ref>  
== Basal Ganglia - Current Concepts  ==
The original functional organization of the basal ganglia was conceived as a loop, in which cortical afferent activity is dispatched to and modulated by the basal ganglia, which subsequently sends back a signal to the cortex to facilitate (or inhibit) motor activity. The basal ganglia were featured as a “go through” station within the motor loop. Current thinking now is that the basal ganglia has several loops, where cortical and subcortical projections interact with internal reentry loops forming a complex network, ideally designed for selecting and inhibiting simultaneously occurring events and signals<ref name=":0" />.


Main circuits of the basal ganglia are shown below. (Very complicated and involved circuits exist)
=== Substantia Nigra ===
'''Substantia Nigra''', means "black substance" in Latin. The substantia nigra is located in the midbrain but is considered part of the basal ganglia.<ref name=":9">Jacobs LK, Sapers BL. [https://www.sciencedirect.com/science/article/pii/B9780443068980000335 Neurological Disease.] InPerioperative Medicine 2011 (pp. 343-359). Springer, London.</ref>  The substania nigra is critical in modulating motor movement and reward functions as part of the greater basal ganglia circuitry.  Of great clinical significance are connections between the substantia nigra and the putamen.  Damage to this connection has been linked to the motor deficits seen in persons with Parkinson's. <ref>Sonne J, Reddy V, Beato MR. Neuroanatomy, Substantia Nigra [Internet]. 24 October 2022 [cited 01 July 2024]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK536995/</ref><br />


Coronal slices that have been superimposed to include the involved basal ganglia structures. + and - signs at the point of the arrows indicate respectively whether the pathway is excitatory or inhibitory in effect. Green arrows refer to excitatory glutamatergic pathways, red arrows refer to inhibitory GABAergic pathways and turquoise arrows refer to dopaminergic pathways that are excitatory on the direct pathway and inhibitory on the indirect pathway. Note that dis-inhibitory pathways in effect are excitatory on the feedback to the cortex, while dis-dis-inhibitory pathways in effect are inhibitory.
The two optional videos below provide further information on the structure and function of the basal ganglia:<div class="row">
[[File:Basal ganglia circuits.png|center|frameless|834x834px]]
  <div class="col-md-6"> {{#ev:youtube|OD2KPSGZ1No|250}} <div class="text-right"><ref>Neuroscientifically Challenged Basal ganglia . Available from:  https://www.youtube.com/watch?v=OD2KPSGZ1No [last accessed 14/01/2020]</ref></div></div>
  <div class="col-md-6"> {{#ev:youtube|mNc-6q6YAAw|250}} <div class="text-right"><ref>Armando Hasudungan. The Basal Ganglia Clinical Anatomy. Available from: https://www.youtube.com/watch?v=mNc-6q6YAAw [last accessed 05/01/2024]</ref></div></div>
</div>


== Pathophysiology  ==
The basal ganglia are particularly associated with movement disorders. Associated with damage to the BG are: tremors; involuntary muscle movements; abnormal increase in tone; difficulty initiating movements; abnormal posture.


Movement disorders comprise a variety of motor problems, not all of which are associated with dysfunction of the basal ganglia. Those that have a clearly established pathological basis and are caused by pathophysiological mechanisms directly involving the basal ganglia include<ref name=":1" />
== Function of the Basal Ganglia  ==
 The classical basal ganglia model suggested that "information flows through the basal ganglia back to the cortex through two pathways with opposing effects for the proper execution of movement."<ref name=":02">Lanciego JL, Luquin N, Obeso JA. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3543080/ Functional neuroanatomy of the basal ganglia.] Cold Spring Harbor perspectives in medicine. 2012 Dec 1;2(12):a009621.</ref> In this "loop", cortical input is sent to the basal ganglia, where it is modified and then sent back to the cortex. As a result of this feedback, motor activity is either facilitated or inhibited.<ref name=":02" />  


'''[[Parkinson's|Parkinson Disease]]'''
This model has been reviewed and updated. It is now believed that the basal ganglia have "multiple parallel loops and re-entering circuits whereby motor, associative, and limbic territories are engaged mainly in the control of movement, behaviour, and emotions."<ref name=":02" />


The most notorious disease of the basal ganglia. Classic clinical symptoms include bradykinesia, resting tremor, postural instability, and shuffling gait. This disease is a result of neurodegeneration of the SNpc dopaminergic neurons. Often found in the Parkinsonian striatum, alpha-synuclein protein aggregates form toxic “Lewy bodies,” which are inclusions within neurons. The substantia nigra, due to degeneration, loses its grossly visible dark pigmentation, a concomitant sign of dopamine biosynthesis dysfunction. This loss of dopamine depresses the nigrostriatal pathway. With decreased dopaminergic input the striatum exerts less positive motor activity and more negative motor inhibition. This gives the characteristic hypokinetic dysfunction found in these patients.<ref name=":1" /> 
The following image illustrates various excitatory and inhibitory pathways from the basal ganglia to the cortex.<ref name=":0" />
[[File:Basal ganglia circuits.png|center|alt=This is a diagram of the flow of excitatory and inhibitory pathways through the basal ganglia.|frame|Basal ganglia circuits]]


'''[[Huntington Disease]]'''
== Associated Conditions  ==
Dysfunction of the basal ganglia is associated with specific movement disorders, and can cause issues such as (1) tremor, (2) involuntary muscle movements, (3) abnormal increase in tone, (4) difficulty initiating movements, and (5) abnormal posture. The following sections discuss movement disorders associated with basal ganglia dysfunction.<ref name=":1" />


Huntington disease is a hyperkinetic movement disorder. Its cause is a genetic defect manifesting as a CAG repeat on chromosome 4p on the HTT gene. This creates an abnormally long Huntington gene which leads to neuronal death in the caudate and the putamen. The indirect pathway is interrupted and leads to a hyperkinetic presentation. Symptoms include involuntary movements such as chorea, cognitive degeneration, and psychiatric dysfunction.<ref name=":1" />  
=== Parkinson's ===
[[Parkinson's]] is the second most common neurodegenerative disorder. Its aetiology is multifactorial, with both genetic and environmental risk factors identified.<ref>Ben-Shlomo Y, Darweesh S, Llibre-Guerra J, Marras C, San Luciano M, Tanner C. The epidemiology of Parkinson's disease. The Lancet. 2024;403(10423):283-92.</ref> Parkinson's is characterised "by the progressive loss of dopaminergic neurons and the formation of Lewy bodies in the affected brain areas".<ref name=":3">Zhou, ZD, Yi LX, Wang DQ, Lim TM, Tan EK. [https://translationalneurodegeneration.biomedcentral.com/articles/10.1186/s40035-023-00378-6 Role of dopamine in the pathophysiology of Parkinson’s disease]. Transl Neurodegener. 2023;12(44). </ref> Because of the degeneration of dopaminergic neurons, there is less dopamine available in the substantia nigra and striatum, which causes various clinical signs of Parkinson's, such as:<ref name=":3" />


'''Hemiballism'''
* tremor
* postural instability
* [[bradykinesia]] or slow movement
* rigidity or stiffness
* decreased coordination
* shuffling gait


Hemiballism (from the Greek “to throw”) is used to describe hyperkinetic, involuntary, forceful movements of the ipsilateral arm and leg. Commonly, a lesion in the contralateral subthalamic nuclei causes hemiballism. Given that the subthalamus is part of the indirect pathway this lesion reduces or eliminates indirect pathway signaling, leading to a relative over-abundance of activity in the direct pathway. Such causes include [[stroke]], [[Overview of Traumatic Brain Injury|traumatic brain injury]], [[Motor Neurone Disease MND|amyotrophic lateral sclerosis]], nonketotic hyperglycemia, neoplasm, vascular malformation, and other causes.<ref name=":1" />  
=== Huntington's Disease ===
[[Huntington Disease|Huntington's disease]]<ref name=":4">Matz OC, Spocter M. The Effect of Huntington's Disease on the Basal Nuclei: A Review. Cureus. 2022;14(4):e24473.</ref> is a progressive, inherited neurodegenerative disease. It is associated with neuropsychiatric symptoms, movement disorders (usually chorea) and cognitive impairment / dementia.<ref name=":5">Stoker TB, Mason SL, Greenland JC, Holden ST, Santini H, Barker RA. [https://pn.bmj.com/content/practneurol/22/1/32.full.pdf Huntington's disease: diagnosis and management]. Pract Neurol. 2022 Feb;22(1):32-41. </ref><ref>Medina A, Mahjoub Y, Shaver L, Pringsheim T. [https://movementdisorders.onlinelibrary.wiley.com/doi/full/10.1002/mds.29228 Prevalence and incidence of Huntington's disease: an updated systematic review and meta-analysis]. Mov Disord. 2022 Dec;37(12):2327-35. </ref> Huntington's disease occurs in individuals with a CAG expansion in the huntingtin gene.<ref name=":5" />  There is neurodegeneration in many parts of the brain, the striatum<ref name=":5" /> and cortex are particularly affected.<ref name=":6">Kim A, Lalonde K, Truesdell A, Gomes Welter P, Brocardo PS, Rosenstock TR, Gil-Mohapel J. [https://www.mdpi.com/1422-0067/22/16/8363 New avenues for the treatment of Huntington's disease]. Int J Mol Sci. 2021 Aug 4;22(16):8363. </ref>  Symptoms usually start in individuals aged between 30-50 years. A key motor symptom is chorea (i.e. "brief, involuntary movements that generally affect the trunk, face, and arms"<ref name=":6" />). Chorea affects voluntary movements, ultimately affecting walking, speaking and swallowing.<ref name=":6" />


'''Tourette Syndrome'''
Cognitive impairments include:<ref name=":6" />


Tourette syndrome has been shown to have a significant neurological basal ganglia component which manifests as sudden, repetitive uncontrolled movements and vocalizations, called “tics.” These tics have been associated with dysfunction of the GABAergic projections from the striatum, leading to a relative increase in dopaminergic activity much like in hemiballism and Huntington’s disease
* decreased executive function (difficulty with attention, concentration, multi-tasking, decision making)
* depression
* loss of memory
* decreased insight


Additionally parts of the basal ganglia play a key role in reward and reinforcement, addictive behaviors and habit formation. Pathophysiological processes underlying psychiatric disorders such as [[depression]] and obsessive compulsive disorder involve the basal ganglia and their connections with many other structures (particularly to the prefrontal cortex and the limbic system).<ref>Stathis P, Panourias IG, Themistocleous MS, Sakas DE. [https://www.ncbi.nlm.nih.gov/pubmed/17691350/ Connections of the basal ganglia with the limbic system: implications for neuromodulation therapies of anxiety and affective disorders]. InOperative Neuromodulation 2007 (pp. 575-586). Springer, Vienna. Available from: https://www.ncbi.nlm.nih.gov/pubmed/17691350/ (last accessed 13.1.2020)</ref> In terms of cognitive disorders, basal ganglia abnormalities have been found in individuals with [[schizophrenia]]<ref>Kéri S. [https://www.ncbi.nlm.nih.gov/m/pubmed/17854895/ Interactive memory systems and category learning in schizophrenia]. Neuroscience & Biobehavioral Reviews. 2008 Jan 1;32(2):206-18. Available from: https://www.ncbi.nlm.nih.gov/m/pubmed/17854895/ (last accessed 13.1.2020)</ref> and may explain have a learning deficits associated with the disorder.
The most common psychiatric conditions are:<ref name=":6" />


[[Lacuna Infarcts ( Small Vessel Disease)|Silent Cerebral Infarcts]] - of interest a 2008 study found that approx. 5% of healthy middle aged adults have microlesions in their BG. <ref>Das RR, Seshadri S, Beiser AS, Kelly-Hayes M, Au R, Himali JJ, Kase CS, Benjamin EJ, Polak JF, O'Donnell CJ, Yoshita M. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712254/ Prevalence and correlates of silent cerebral infarcts in the Framingham offspring study.] Stroke. 2008 Nov 1;39(11):2929-35.Available from:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712254/ (last accessed 13.1.2020)</ref>
* depression
* irritability
* increased impulsivity


=== Physiotherapy - implications from recent studies ===
=== Hemiballism ===
The importance and value of [[Exercise Physiology|exercise]] is being coming more and more apparent for a whole raft of health conditions. Here is a few of the latest findings re exercise and BG function.[[File:Exercise older person.jpg|right|frameless]]
Hemiballism (from the verb “to throw” in Greek) is a rare movement disorder that causes "high amplitude movement of an entire limb or limbs on one side of the body."<ref name=":7">Hawley JS, Weiner WJ. Hemiballismus: current concepts and review. Parkinsonism Relat Disord. 2012 Feb;18(2):125-9.</ref> Hemiballism can be caused by several conditions, but acute cases are often associated with focal lesions in the contralateral basal ganglia and subthalamic nucleus lesion.<ref name=":7" /> Individuals with hemiballism tend to have a good prognosis.<ref name=":7" />
# A 2016 study by Becker et al<ref>Becker L, Kutz DF, Voelcker-Rehage C. [https://www.jneurology.com/articles/exerciseinduced-changes-in-basal-ganglia-volume-and-their-relation-to-cognitive-performance.html Exercise-induced changes in basal ganglia volume and their relation to cognitive performance.] Available https://www.jneurology.com/articles/exerciseinduced-changes-in-basal-ganglia-volume-and-their-relation-to-cognitive-performance.html (last accessed 13.1.2020)</ref>. into cognitive performance and BG changes concluded that physical activity, especially motor fitness level training, might be a promising tool that leads to structural changes in the basal ganglia. This might have the potential to diminish the cognitive decline in older adults and to support the academic success in children and young adults.
# Exercise is beneficial and should be routinely prescribed in the management of PD (may aid in BG function)<ref name=":2" />.
# Exercise effects on basal ganglia damage<ref name=":2">Petzinger GM, Fisher BE, Akopian G, Holschneider DP, Wood R, Walsh JP, Lund B, Meshul C, Vuckovic M, Jakowec MW. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691073/ The role of exercise in facilitating basal ganglia function in Parkinson’s disease]. Neurodegenerative disease management. 2011 Apr;1(2):157-70. Available from:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691073/ (last accessed 13.1.2020)</ref>
* The adult brain possesses a tremendous capacity for experience-dependent [[neuroplasticity]], even in the context of aging and neurodegenerative disorders including PD, where the activation of neurotrophic factors may play a key role.
* Animal models of [[Drugs for the Treatment of Parkinson's|dopamine]] depletion are beginning to reveal the underlying mechanisms by which exercise can remodel the brain through alteration in neuronal synaptic connections, especially dopaminergic and glutamatergic neurotransmission within the basal ganglia.
4.Epidemiological studies, clinical observations, and animal research indicate that appropriately dosed physical activity and exercise may not only reduce the risk of developing PD in vulnerable populations but also benefit PD patients by potentially protecting the residual nigrostriatal dopamine neurons or directly restoring the dysfunctional cortico-basal ganglia motor control circuit, and these benefits may be mediated by exercise-triggered production of endogenous neuroprotective molecules such as neurotrophic factors<ref>Hou L, Chen W, Liu X, Qiao D, Zhou FM. [https://www.frontiersin.org/articles/10.3389/fnagi.2017.00358/full Exercise-induced neuroprotection of the nigrostriatal dopamine system in Parkinson's disease]. Frontiers in aging neuroscience. 2017 Nov 3;9:358. Available from: https://www.frontiersin.org/articles/10.3389/fnagi.2017.00358/full (last accessed 14.1.2020)</ref>.


5. Animal studies have been instrumental in providing evidence for exercise-induced neuroplasticity of corticostriatal circuits that are profoundly affected in Parkinson’s disease. Exercise has been implicated in modulating dopamine and glutamate neurotransmission, altering synaptogenesis, and increasing cerebral blood flow. In addition, recent evidence supports that the type of exercise may have regional effects on brain circuitry, with skilled exercise differentially affecting frontal-striatal related circuits to a greater degree than pure aerobic exercise (with skilled exercise differentially affecting frontal related circuits more so than pure aerobic exercise). These effects are not mutually exclusive eg peddling on a recumbent bicycle may be considered predominantly aerobic with minimal skill or cognitive engagement whilst at the other end of the spectrum juggling may represent a highly skilled task with minimal aerobic involvement. However, many exercises such as swimming and running involve a combination of both skilled and aerobic exercise<ref>Petzinger GM, Holschneider DP, Fisher BE, McEwen S, Kintz N, Halliday M, Toy W, Walsh JW, Beeler J, Jakowec MW. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4621077/ The effects of exercise on dopamine neurotransmission in Parkinson’s disease: targeting neuroplasticity to modulate basal ganglia circuitry.] Brain plasticity. 2015 Jan 1;1(1):29-39.Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4621077/ (last accessed 14.1.2020)</ref>. These results indicate that the community Parkinson Dance classes that exist are a great option, as are many other structured classes.
=== Tourette Syndrome ===
Tourette syndrome is a persistent neurodevelopmental condition associated with motor and phonic tics.<ref name=":2">Johnson KA, Worbe Y, Foote KD, Butson CR, Gunduz A, Okun MS. Tourette syndrome: clinical features, pathophysiology, and treatment. Lancet Neurol. 2023 Feb;22(2):147-58. </ref> While its pathophysiology is not fully understood, tics may be due to "inhibitory dysfunction within the sensorimotor cortico-basal ganglia network".<ref name=":2" /> Tourette syndrome can significantly impact quality of life, and treatment options are expanding.<ref name=":2" />


== References ==
== References ==
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Latest revision as of 03:28, 2 July 2024

Original Editor - Lucinda Hampton Top Contributors - Lucinda hampton, Jess Bell, Lauren Heydenrych, Stacy Schiurring, Kim Jackson, Tony Lowe, Joao Costa, Rucha Gadgil and Aminat Abolade

Introduction to the Basal Ganglia[edit | edit source]

Overview of the basal ganglia (corpus striatum) - lateral view

The basal ganglia is not a single structure in the brain but rather are a group of subcortical nuclei and other associated structures, located at the base of the forebrain.[1]

They are primarily involved in motor control and motor initiation[2], as well as motor learning, executive functions and emotional behaviours. The basal ganglia also play an important role in reward and reinforcement, addictive behaviours and habit formation.[3]

Basal ganglia network dysfunction can lead to various movement disorders,[3] such as Parkinson's and Huntington disease.

Structure of the Basal Ganglia[edit | edit source]

The basal ganglia is made up of multiple separate structures that link together in several different ways. The interconnected pathways are what define the function of the basal ganglia. Below is a photo gallery which shows different views of the basal ganglia to include its various structures and neural networks.

  • Basal ganglia nuclei

    Basal ganglia nuclei

  • Corpus striatum of the basal ganglia

    Corpus striatum of the basal ganglia

  • Basal ganglia structures

    Basal ganglia structures

  • Basal ganglia nuclei in relation to other subcortical structures.

    Basal ganglia nuclei in relation to other subcortical structures.

Corpus Striatum[edit | edit source]

Corpus Striatum is the largest component of the basal ganglia, it is a heterogeneous structure with a volume of around 10 cm3. It receives afferent inputs from various cortical and subcortical structures and sends outputs to different basal ganglia nuclei.[3]

There are two main divisions in the corpus striatum:  

  1. Dorsal Striatum (DS): mostly involved in the control of conscious motor movements and executive functions.
    • Caudate nucleus: is a paired subcortical structure and is involved in many "higher" neurological functions such as (1) movement execution, (2) learning, (3) memory, (4) reward and motivation, (5) emotion, and (6) "romantic interactions"[4]
  2. Ventral Striatum: involved in the limbic functions of reward and aversion. It is made up of the nucleus accumbens and the olfactory tubercle.[2] 
    1. Nucleus accumbens in the neural interface between "motivation and action" or the "limbic-motor interface" It is involved in a wide range of goal-directed behaviors including (1) feeding, (2) sexual, (3) reward, (4) stress-related, and (5) drug self-administration[5]
    2. Olfactory tubercle is thought to be involved in odor-guided motivated and eating behaviours.[6] It likely works in tandem with the nucleus accumbens.

Lenticular Nuclei[edit | edit source]

  1. Putamen: communicates with many different regions of the cerebral cortex and forms multiple connections within the basal ganglia. It is involved in (1) learning and motor control, (2) speech articulation, (3) language functions, (4) reward, (5) cognitive functioning, and (6) addiction. The putamen also plays a role in modulating sensory and motor aspects of pain.[7]
  2. Globus Pallidus which can be further divided into two parts: globus pallidus externus, and internus. [8] The primary role of the globus pallius is controlling conscious and proprioceptive movements.[9]

Subthalamic Nucleus[edit | edit source]

Subthalamic Nucleus (STN): a lens-shaped cell group that makes up a large part of the subthalamus.[10]  It has neural projections into the globus pallidus and assists with movement regulation. Specifically, the subthalmic nucleus plays a critical role in the prevention of unwanted movements. For example, a lesion of the subthalamic nucleus can result in hemiballismus (please see below for more details on this disorder).[11]

Substantia Nigra[edit | edit source]

Substantia Nigra, means "black substance" in Latin. The substantia nigra is located in the midbrain but is considered part of the basal ganglia.[12] The substania nigra is critical in modulating motor movement and reward functions as part of the greater basal ganglia circuitry. Of great clinical significance are connections between the substantia nigra and the putamen. Damage to this connection has been linked to the motor deficits seen in persons with Parkinson's. [13]

The two optional videos below provide further information on the structure and function of the basal ganglia:

[14]
[15]


Function of the Basal Ganglia[edit | edit source]

 The classical basal ganglia model suggested that "information flows through the basal ganglia back to the cortex through two pathways with opposing effects for the proper execution of movement."[16] In this "loop", cortical input is sent to the basal ganglia, where it is modified and then sent back to the cortex. As a result of this feedback, motor activity is either facilitated or inhibited.[16]

This model has been reviewed and updated. It is now believed that the basal ganglia have "multiple parallel loops and re-entering circuits whereby motor, associative, and limbic territories are engaged mainly in the control of movement, behaviour, and emotions."[16]

The following image illustrates various excitatory and inhibitory pathways from the basal ganglia to the cortex.[3]

This is a diagram of the flow of excitatory and inhibitory pathways through the basal ganglia.
Basal ganglia circuits

Associated Conditions[edit | edit source]

Dysfunction of the basal ganglia is associated with specific movement disorders, and can cause issues such as (1) tremor, (2) involuntary muscle movements, (3) abnormal increase in tone, (4) difficulty initiating movements, and (5) abnormal posture. The following sections discuss movement disorders associated with basal ganglia dysfunction.[2]

Parkinson's[edit | edit source]

Parkinson's is the second most common neurodegenerative disorder. Its aetiology is multifactorial, with both genetic and environmental risk factors identified.[17] Parkinson's is characterised "by the progressive loss of dopaminergic neurons and the formation of Lewy bodies in the affected brain areas".[18] Because of the degeneration of dopaminergic neurons, there is less dopamine available in the substantia nigra and striatum, which causes various clinical signs of Parkinson's, such as:[18]

  • tremor
  • postural instability
  • bradykinesia or slow movement
  • rigidity or stiffness
  • decreased coordination
  • shuffling gait

Huntington's Disease[edit | edit source]

Huntington's disease[19] is a progressive, inherited neurodegenerative disease. It is associated with neuropsychiatric symptoms, movement disorders (usually chorea) and cognitive impairment / dementia.[20][21] Huntington's disease occurs in individuals with a CAG expansion in the huntingtin gene.[20] There is neurodegeneration in many parts of the brain, the striatum[20] and cortex are particularly affected.[22] Symptoms usually start in individuals aged between 30-50 years. A key motor symptom is chorea (i.e. "brief, involuntary movements that generally affect the trunk, face, and arms"[22]). Chorea affects voluntary movements, ultimately affecting walking, speaking and swallowing.[22]

Cognitive impairments include:[22]

  • decreased executive function (difficulty with attention, concentration, multi-tasking, decision making)
  • depression
  • loss of memory
  • decreased insight

The most common psychiatric conditions are:[22]

  • depression
  • irritability
  • increased impulsivity

Hemiballism[edit | edit source]

Hemiballism (from the verb “to throw” in Greek) is a rare movement disorder that causes "high amplitude movement of an entire limb or limbs on one side of the body."[23] Hemiballism can be caused by several conditions, but acute cases are often associated with focal lesions in the contralateral basal ganglia and subthalamic nucleus lesion.[23] Individuals with hemiballism tend to have a good prognosis.[23]

Tourette Syndrome[edit | edit source]

Tourette syndrome is a persistent neurodevelopmental condition associated with motor and phonic tics.[24] While its pathophysiology is not fully understood, tics may be due to "inhibitory dysfunction within the sensorimotor cortico-basal ganglia network".[24] Tourette syndrome can significantly impact quality of life, and treatment options are expanding.[24]

References[edit | edit source]

  1. ↑ Yanagisawa N. Functions and dysfunctions of the basal ganglia in humans. Proc Jpn Acad Ser B Phys Biol Sci. 2018;94(7):275-304.
  2. ↑ 2.0 2.1 2.2 Young CB, Sonne J. Neuroanatomy, basal ganglia. InStatPearls [Internet] 2018 Dec 28. StatPearls Publishing.
  3. ↑ 3.0 3.1 3.2 3.3 Lanciego JL, Luquin N, Obeso JA. Functional neuroanatomy of the basal ganglia. Cold Spring Harbor perspectives in medicine. 2012 Dec 1;2(12):a009621.
  4. ↑ Driscoll; M, Bollu P, Tadi P. Neuroanatomy, Nucleus Caudate [Internet]. 24 July 2024 [cited 01 July 2024]. Available from:https://www.ncbi.nlm.nih.gov/books/NBK557407/
  5. ↑ Fernández-Espejo E. How does the nucleus accumbens function? [Internet]. 2000 May;30(9):845-9.[cited 01 July 2024]. Available from: https://pubmed.ncbi.nlm.nih.gov/10870199/
  6. ↑ Murata K. Hypothetical Roles of the Olfactory Tubercle in Odor-Guided Eating Behavior [Internet]. Front Neural Circuits. 2020; 14: 577880..[cited 01 July 2024]. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7686465/
  7. ↑ Ghandili M, Munakomi S. Neuroanatomy, Putamen [Internet]. 30 January 2023 [cited 01 July 2024]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542170/
  8. ↑ Javed N, Cascella M. Neuroanatomy, Globus Pallidus. [Updated 2023 Feb 20]. In: StatPearls [Internet].
  9. ↑ Javed N, Cascella M. Neuroanatomy, Globus Pallidus [Internet]. 20 February 2023 [cited 01 July 2024]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557755/
  10. ↑ Basinger H, Joseph J. Neuroanatomy, Subthalamic Nucleus. [Updated 2022 Oct 31]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK559002/
  11. ↑ Basinger H, Joseph J. Neuroanatomy, Subthalamic Nucleus [Internet]. 31 October 2022 [cited 01 July 2024]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK559002/
  12. ↑ Jacobs LK, Sapers BL. Neurological Disease. InPerioperative Medicine 2011 (pp. 343-359). Springer, London.
  13. ↑ Sonne J, Reddy V, Beato MR. Neuroanatomy, Substantia Nigra [Internet]. 24 October 2022 [cited 01 July 2024]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK536995/
  14. ↑ Neuroscientifically Challenged Basal ganglia . Available from: https://www.youtube.com/watch?v=OD2KPSGZ1No [last accessed 14/01/2020]
  15. ↑ Armando Hasudungan. The Basal Ganglia Clinical Anatomy. Available from: https://www.youtube.com/watch?v=mNc-6q6YAAw [last accessed 05/01/2024]
  16. ↑ 16.0 16.1 16.2 Lanciego JL, Luquin N, Obeso JA. Functional neuroanatomy of the basal ganglia. Cold Spring Harbor perspectives in medicine. 2012 Dec 1;2(12):a009621.
  17. ↑ Ben-Shlomo Y, Darweesh S, Llibre-Guerra J, Marras C, San Luciano M, Tanner C. The epidemiology of Parkinson's disease. The Lancet. 2024;403(10423):283-92.
  18. ↑ 18.0 18.1 Zhou, ZD, Yi LX, Wang DQ, Lim TM, Tan EK. Role of dopamine in the pathophysiology of Parkinson’s disease. Transl Neurodegener. 2023;12(44).
  19. ↑ Matz OC, Spocter M. The Effect of Huntington's Disease on the Basal Nuclei: A Review. Cureus. 2022;14(4):e24473.
  20. ↑ 20.0 20.1 20.2 Stoker TB, Mason SL, Greenland JC, Holden ST, Santini H, Barker RA. Huntington's disease: diagnosis and management. Pract Neurol. 2022 Feb;22(1):32-41.
  21. ↑ Medina A, Mahjoub Y, Shaver L, Pringsheim T. Prevalence and incidence of Huntington's disease: an updated systematic review and meta-analysis. Mov Disord. 2022 Dec;37(12):2327-35.
  22. ↑ 22.0 22.1 22.2 22.3 22.4 Kim A, Lalonde K, Truesdell A, Gomes Welter P, Brocardo PS, Rosenstock TR, Gil-Mohapel J. New avenues for the treatment of Huntington's disease. Int J Mol Sci. 2021 Aug 4;22(16):8363.
  23. ↑ 23.0 23.1 23.2 Hawley JS, Weiner WJ. Hemiballismus: current concepts and review. Parkinsonism Relat Disord. 2012 Feb;18(2):125-9.
  24. ↑ 24.0 24.1 24.2 Johnson KA, Worbe Y, Foote KD, Butson CR, Gunduz A, Okun MS. Tourette syndrome: clinical features, pathophysiology, and treatment. Lancet Neurol. 2023 Feb;22(2):147-58.
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