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What Happens To The Basal Ganglia In Parkinson’s

When People Talk About Parkinsons They May Mention The Effects It Has On The Substantia Nigra But Did You Know That There Are Other Areas Of The Brain That Are Affected By The Condition

What brain areas are affected by Parkinson’s?

Jun 4, 2018

Parkinson’s is a condition that causes the gradual loss of the dopamine-producing brain cells of the substantia nigra — an area of the brain located just above where the spinal cord meets the midbrain. It is these cells that produce and release the neurotransmitter dopamine, which has a key role in turning thought about movement into action.

While this definition of the condition is useful to briefly explain Parkinson’s, the whole story is somewhat more complex. Over the last 30 years, it has become accepted that Parkinson’s also causes a number of non-motor symptoms, such as changes in sleep, smell and even the way we think, which likely involve other areas of the brain.

Now scientists are looking at the broader effects of the condition on the brain in an attempt to better understand why people experience different symptoms. The finding could lead us to new treatments that tackle more than just the motor symptoms of the condition.

Computational Basal Ganglia Modelling Can Predict The Behavioural Results Of Dbs Induced Dynamic Circuit Alterations In Patients With Parkinsons Disease Open in new tab

The computational basal ganglia model can predict task effects. The model architecture comprises a simplified version of the cortex–basal ganglia–thalamic loop . The model’s SMA comprises four distinct neurons, each encoding a combination of stimulus type with spatial location . The subsequent structures integrate the condition-specific activity in two cells , encoding the two spatial locations to which motor responses can be directed. The respective model computations result in different levels of motor cortex output that is directly translated into cursor movement. Lesions of the hyperdirect pathway best predicted the reaction times during DBS , while lesions of the indirect pathway best predicted movement times . Overall, relevant original behavioural results could be replicated by our models for both reaction times and movement times . All predictions were robust after leave-one-out cross validation, through which performance time of left out participants could be significantly predicted from the model of the remaining participants for patients off and on subthalamic DBS and healthy controls. D1 = striatal dopamine receptor 1 positive medium spiny neuron; D2 = striatal dopamine receptor 2 positive medium spiny neuron; GPi = internal pallidum.

Reaction Time Modulation Is Correlated With The Amount Of Corticosubthalamic Fibres Affected By Subthalamic Stimulation Open in new tab

Fibre tracking from active deep brain stimulation contacts. All subthalamic deep brain stimulation electrodes were localized and transferred to MNI space Top: All active contact locations; middle: average location of active contacts ; and bottom: an example of the volume accounted for fibre tracking surrounding active contacts . All fibres traversing the STN and the active contact were identified and selected from a whole-brain group connectome resulting in a structural pathway . A significant correlation of relative amount of sensorimotor cortex projecting fibres to all fibres traversing the active contact and absolute amount of sensorimotor cortex projecting fibres was found with the DBS induced % change in reaction time. Volumetric correlation analysis revealed a significant cluster in the medial frontal cortex overlapping with the supplementary motor area .

Modelling The Effect Of Losing Dopamine Neurons On The Concentration Of Dopamine And On D1 And D2 Signalling

While the above models seek the consequences of dopamine depletion on the dynamics of the striatum and wider basal ganglia network, others have pursued the equally profound question of how the loss of midbrain dopamine cells creates a complex landscape of adaptations to that loss and subsequent changes in dopamine dynamics during the development of Parkinson’s disease. They suggest that a more nuanced approach is needed to understand the effects of dopamine loss on striatum and thus on basal ganglia function.

Passive stabilisation seemingly provides a simple hypothesis24 27 for why the cardinal signs of Parkinson’s disease develop after substantial loss of midbrain dopamine neurons. The motor features of Parkinson’s disease are often thought to be a consequence of a gradual loss of dopamine tone; from this perspective, the delayed appearance of the motor signs of Parkinson’s disease could be explained as a consequence of this passive stabilisation of dopamine tone.

Relationship Between The Different Pattern Abnormalities And The Behavioral Manifestations Of Parkinsonism


There is little question that neuronal activities in the basal ganglia-thalamo-cortical circuits are altered in PD, but it is less clear to what extent these alterations account for the motor symptoms of the disease.

One experimental approach to this problem has been to examine the effects of inactivation of the dysfunctional brain region. Experimental and clinical evidence indicate that lesions or inactivation of the “overactive” STN or GPi ameliorate parkinsonian symptoms in parkinsonian animals and in PD patients . The knowledge gained from such lesioning experiments is limited, however. One problem is that lesions disrupt all activity in the lesioned nucleus, thus providing little insight into the role of specific activity changes. A more general consideration is that improvement of a behavioral abnormality after a lesion does not necessarily confirm that activity in the lesioned brain region was a primary cause for the abnormal behavioral patterns. For instance, the lesion could have induced plastic changes in other brain regions that could be responsible for the behavioral improvement.

Contributions Of Research Using The Mptp Monkey Model To Understanding The Pathophysiology Of Pd

Using the MPTP monkey model of PD electrophysiological recordings in the STN, globus pallidus internus and globus pallidus externus were performed by several groups . Compared to the naive state these studies reported changes in mean discharge rate with increased rates in the STN and GPi and decreased rates in GPe as well as a loss of specificity and increased number of cells responsive to passive manipulation . Based on these findings a “rate model” of PD was proposed in which the direct pathway, projections from the putamen to GPi, was underactive and the indirect pathway, projections from putamen to GPe, was overactive . This model hypothesized that mean discharge rates in the STN would therefore be increased in PD, leading to excessive activation of the GPi and suppression of thalamocortical activity leading in turn to the manifestation of Parkinson’s motor signs . A seminal test of this hypothesis was published in Science in 1990 .

During this time the number of pallidotomies grew and given PD is a progressive disorder bilateral pallidotomies were required for patients with disease affecting both sides of the body. Complications with bilateral pallidotomy, however, were too frequent, with some reporting cognitive changes, gait disorders, worsening PD, and/or hypophonia . An alternative approach was needed, and deep brain stimulation for PD, developed by Alim Louis Benabid, was brought to the operating room .

Parkinsons Disease A Fatal Cycle Of Falling And Rising Activity In The Basal Ganglia

As the disease progresses, Parkinson’s patients find it increasingly difficult to voluntarily control body movements. The disease is associated with oscillations of electrical activity in specific brain areas known as basal ganglia. Dr. Arvind Kumar and his colleagues at the Bernstein Center Freiburg have used neuronal network simulations to develop a model to explain these rhythmic oscillations. Do other brain areas also contribute to Parkinson’s disease symptoms? Can the new model be used to optimise the treatment of Parkinson’s disease; how can deep brain simulation counteract Parkinson’s symptoms and how can the method be improved? Can movements in Parkinson’s patients be voluntarily controlled by willpower? Kumar and his colleagues are focusing specifically on the interaction between different brain areas.

Use Of The Insights From Pathophysiology Studies To Improve Surgical Pd Therapies

While a causal link between the electrophysiologic abnormalities and parkinsonian motor signs remains elusive, our knowledge of the electrophysiological activities in the basal ganglia and related structures in PD can, nevertheless, be used to improve surgical therapies, such as DBS or lesioning approaches. For example, it may be possible to use the power distribution in LFP signals as a substitute for the currently used time-consuming microelectrode recording methods to guide the placement of DBS electrodes. In studies of intra-operatively recorded LFPs from DBS electrodes that were advanced towards the STN , the beta band power in LFP signals was found to be maximal at the surgical target in the dorsal STN . However, this technique is at present clearly limited by the low spatial resolution of LFP signal recordings . A related use of recordings from DBS electrodes is to choose the best stimulation contact of already implanted electrodes based on the amount of beta-band power that can be recorded from them .

Action Sequencing Impairment As Deficit In Timing: Corticalsubcortical Substrates


PD patients have a difficulty in performing action sequences, including completing sequences of heterogeneous movements in correct order.84,85 Here we discuss a cortical–subcortical circuit that may underlie this symptom. The circuit, shown on Figure 5, is mainly based on data supporting the contribution of pre-SMA, SMA, Cer and BG in managing action sequences.17,33,36,37 Different types of neurons in pre-SMA and SMA help to encode not only where in a sequence the action is but also the conditional links between the previous response and the upcoming response, often in a highly specific manner.38 In this respect, it has been shown that pre-SMA and SMA neurons respond before some sequences but not others ,34 that some neurons of pre-SMA and SMA respond only to the rank order of a movement in the sequence ,86 and that pre-SMA and SMA cells also encode the number of movements that remain to be made to complete a sequence to obtain a reward.87

Role Of Dopamine In Development Of Electrophysiological Changes In Parkinsonism

Although it is often mentioned that the changes in electrophysiologic activity that were discussed above are consequent to the loss of dopamine in the striatum, the link between the disrupted striatal dopaminergic transmission and altered activity patterns in basal ganglia, thalamus and cortex is not entirely clear. Several studies have attempted to investigate this issues using locally or systemically administered dopamine receptor agonists or antagonists.

In PD patients, systemic infusions of therapeutic effective doses of the non-selective dopamine agonist apomorphine was shown to decrease the firing rates of GPi cells, and of STN cells with activity related to limb tremor; it also decreased the proportion of STN and GPi cells with responses to passive movements . However, in other studies, dopamine receptor agonist treatment did not fully reduce burst firing in basal ganglia neurons of parkinsonian animals or patients , and was shown to even promote neuronal bursting when locally applied in the STN or in GPi or SNr . Furthermore, acute blockade of dopaminergic transmission failed to increase beta band activity in subthalamic LFPs of rats, despite the presence of motor symptoms .

From Theory To Computational Models Of The Bgctxcer System Imparements In Pd

The brain system proposed in Figure 2 as the cortical–subcortical network producing PD symptoms has a clear, distinct feature: it involves highly recurrent circuits. In this article, we aimed to link PD symptoms to specific impairments of the network, but this exercise has an inherently limited scope: it can only partially disentangle the circular causations involved by the above-discussed circuits, and on this basis offer quantitative predictions. For example, we proposed specific hypotheses to explain tremor and freezing, but it is not possible to establish if such hypotheses are self-consistent and sound only on a verbal basis. Computational models have the power to prove the self-consistency of hypothesis as those proposed here.4,51,69,94,109,114 This is a necessary condition to establish the validity of theories . For this reason, we consider here possible approaches to follow to translate the verbal theories presented here into operational computational models able to offer sound explanations and quantitative predictions on PD symptoms.

Analytical Approaches To Extracellular Recordings And Definition Of Terms

Most electrophysiologic in vivo recordings utilize extracellular recording methods, thus reflecting electrical potentials at the sites of electrodes that are positioned in the extracellular space, at some distance from the sources of the electrical activity, i.e., neuronal cell bodies or axons. The principal contributors to the recorded potentials are neuronal events in which ions are moving, i.e., action potentials and synaptic currents. The former can be detected as spikes in extracellular recordings, while the latter are recordable as low-frequency fluctuations of recorded potentials.

Freezing As Response Conflict Impairment: Corticalsubcortical Substrates

What is Your Basal Ganglia? How it Works for You

Freezing is the inability to begin or continue a voluntary discrete or rhythmic movement. It can affect walking, writing, speech, and is also associated with deficits in a number of executive functions including attention and conflict resolution.6366 The vast range of conditions provoking or relieving freezing supports the involvement of a complex brain network including both cortical and subcortical areas.65,67

Pivoting on the anatomical connections between BG and Ctx8,10 and between BG and Cer,13,14, and on recent data about the involvement of pre-SMA30,31,63,68 and Cer31,32,63 in freezing, we propose here some system-level hypotheses on the possible alterations of cortical–subcortical circuits that might underlie freezing . Striatum modulates the output nuclei of BG through two pathways. The first is the direct pathway that involves a Str GABAergic connection directly inhibiting GPi and substantia nigra pars reticulata . The second is the indirect pathway involving two sub-routes: the short indirect pathway, linking the external globus pallidus to GPi/SNr via GABAergic connections; and the long indirect pathway linking GPe to STN which in turn projects to GPi/SNr.69

Balance Of The Direct And Indirect Pathways During Evidence Accumulation

Previous work suggests that the corticostriatal pathway can effectively adjust the decision threshold during perceptual decision making . The mechanism involved works best in the presence of a strong nonlinearity, i.e., an abrupt suppression of SNr activity immediately before the onset of a saccadic response , which was observed in physiological recording of monkeys performing saccade tasks . With a gradual intensification of CD activity during evidence accumulation in the random-dot task , however, the direct pathway projection would cause the SNr activity to ramp down in a graded way, rather than exhibiting a sudden drop of activity just before a saccade.

Functional Anatomy Of The Bgtc Circuit And The Mptp Monkey Model Of Pd

From the time of early surgical therapies reported in the 1930s, where little was understood regarding anatomical organization and functional connectivity of BGTC circuitry, by the 1990s a mass of research on the BGTC network led to models describing the functional anatomy of the basal ganglia. Drawing upon years of anatomy and electrophysiology studies in monkeys beginning with a seminal study by Mahlon DeLong in 1971 regarding the role of the pallidum in movement, in 1986 Alexander et al. described the basal ganglia in terms of several functionally segregated BGTC circuits. These consisted of motor, oculomotor, associative, and limbic circuits each originating from separate cortical regions projecting to different regions of the striatum, pallidum, and thalamus while returning to the cortical areas from which they took origin. From there models of the intrinsic circuitry of the basal ganglia were developed and the concept of direct and indirect pathways with excitatory and inhibitory connections was established . Subsequent tracer studies further defined motor subcircuits and the hyperdirect pathway, a direct projection from the cortex to the subthalamic nucleus .

F The Role Of Abnormal Bg Discharge In The Expression Of Parkinsonism

The link between specific changes in the discharge patterns of BG neurons and the behavioral manifestations of PD remain tenuous. One approach to investigating this issue is to examine the temporal relationship between the development of parkinsonism and the occurrence of abnormal discharge patterns in the BG. Such studies have confirmed that the neuronal activity in STN and GPi is increased prior to the onset of motor symptoms . Furthermore, BG interventions such as lesions or DBS of GPi or STN dramatically and immediately improve parkinsonian signs, supporting a role of BG discharge abnormalities in the development of parkinsonism .

Evidence for a direct role of abnormal BG activities in parkinsonism also comes from studies involving electrical stimulation of the STN in monkeys. These experiments have shown that motoric impairments can be induced with stimulation patterns fashioned after those recorded in parkinsonian animals , that movement is slowed by stimulation at beta-band frequencies , and that parkinsonism can be improved with oscillatory trains of stimuli timed to eliminate the beta-band activities in the BG .

Mechanisms Of Deep Brain Stimulation Therapy For Parkinsons Disease

Hypoxic Ischemic Encephalopathy: Long

The now routine use of deep brain stimulation for treating the cardinal motor signs of Parkinson’s disease has proved remarkably effective. But this effectiveness has raised a host of questions over its mechanisms of action and effects on the brain, questions that have inspired many computational modelling efforts. The majority of these models have studied high frequency stimulation of the STN, as this has emerged as the primary clinical target for deep brain stimulation therapy.

One class of models have sought to separate the hypotheses of deep brain stimulation exciting or inhibiting the neurons in the target region.S66 To do so, these models have studied the effects of simulated deep brain stimulation current pulses on a detailed model of a single neuron and its axon cable . The models have primarily revealed axonal effects,S67 whereby the stimulation pulses entrain action potentials directly in the axons immediately surrounding the electrode. Such models predict that deep brain stimulation thus regularises the output of the STN.

How Does Parkinson Disease Affect The Basal Ganglia Motor Circuit

The basal ganglia motor circuit modulates the cortical output necessary for normal movement .

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Signals from the cerebral cortex are processed through the basal ganglia-thalamocortical motor circuit and return to the same area via a feedback pathway. Output from the motor circuit is directed through the internal segment of the globus pallidus and the substantia nigra pars reticulata . This inhibitory output is directed to the thalamocortical pathway and suppresses movement.

Two pathways exist within the basal ganglia circuit, the direct and indirect pathways, as follows:

  • In the direct pathway, outflow from the striatum directly inhibits the GPi and SNr; striatal neurons containing D1 receptors constitute the direct pathway and project to the GPi/SNr

  • The indirect pathway contains inhibitory connections between the striatum and the external segment of the globus pallidus and between the GPe and the subthalamic nucleus ; striatal neurons with D2 receptors are part of the indirect pathway and project to the GPe

The STN exerts an excitatory influence on the GPi and SNr. The GPi/SNr sends inhibitory output to the ventral lateral nucleus of the thalamus. Dopamine is released from nigrostriatal neurons to activate the direct pathway and inhibit the indirect pathway. In Parkinson disease, decreased striatal dopamine causes increased inhibitory output from the GPi/SNr via both the direct and indirect pathways .

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Reviewpathophysiology Of The Basal Ganglia In Parkinson’s Disease rights and content

Insight into the organization of the basal ganglia in the normal, parkinsonian and l-dopa-induced dyskinesia states is critical for the development of newer and more effective therapies for Parkinson’s disease. We believe that the basal ganglia can no longer be thought of as a unidirectional linear system that transfers information based solely on a firing-rate code. Rather, we propose that the basal ganglia is a highly organized network, with operational characteristics that simulate a non-linear dynamic system.

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Loss Of Dopamine And Plastic Changes In The Basal Ganglia In Pd

In PD, the dopaminergic nigrostriatal pathway progressively degenerates. The dopaminergic projections to the sensorimotor striatum are affected more strongly than those to the associative and limbic striatal regions, contributing to the preponderance of movement problems in PD . The loss of striatal dopamine is associated with morphological changes throughout the basal ganglia, including a reduction in the density of dendritic spines of MSNs in the striatum and alterations in intrastriatal and pallido-subthalamic connectivity, as we discuss below.

Although the loss of dopaminergic SNc cells remains the best known pathological feature of PD, it is clear that other types of neurons also degenerate, including neurons in the serotonergic raphe nuclei, the noradrenergic locus coeruleus, the olfactory tubercle, the intralaminar nuclei of the thalamus, and regions of the cerebral cortex and the peripheral nervous system . It is still not well understood how these changes in the brain stem, which occur relatively early in the disease, contribute to the motor and non-motor manifestations of parkinsonism.

Damaged Basal Ganglia Cause Parkinsons And Huntingtons Diseases

Disorders & Diseases of the Basal Ganglia (incl. Stroke ...

Justine and I read alot about health, wellness, aging, Yoga and especially senior health. We often are sending each other articles and links about some interesting news or tidbits and asking each other what we think.  It could be anything from some medical research study, an anatomy concept or some new healing approach to an ailment.  Here is a “Food for Thought” article that is worth reading and pondering.

And because we Yoga Teachers all love and appreciate Anatomy… here’s a tidbit that came across my desk this week.

What is Basal Ganglia and what is its purpose in our body? 

It is a network of circuits deep inside the hemispheres of your brain. The basal ganglia coordinate movement, behavior, and emotions. They make things that happen in sequence possible, like walking and dancing, learning patterns, forming habits, and stopping activities then starting new ones. Damaged basal ganglia cause Parkinson’s and Huntington’s diseases.

Hmmm.. so this got me thinking about all the different movement patterns we do in our Gentle and Chair Yoga classes and how beneficial they are to our brain health…. especially as we age.  And I loved that they included “dancing” in the mix of movements for brain health because Chair Yoga Dancing has become the number one hit in my classes over the past year or so! We are rocking our Basal Ganglia!

Keep reading, learning and sharing!


Whats The Outlook For People Whove Had A Basal Ganglia Stroke

Your short-term and long-term outlook after a basal ganglia stroke depends on how quickly you were treated and how many neurons were lost. The brain can sometimes recover from injury, but it will take time. Be patient and work closely with your healthcare team to take steps toward recovery.

A basal ganglia stroke could have lasting effects that may interfere with your quality of life. Having any type of stroke increases your risk of having another stroke. Having a basal ganglia stroke or other damage to that part of the brain may also increase your risk of developing Parkinson’s disease.

If you stick with your rehabilitation program and take advantage of services in your community, you may be able to improve your chances for recovery.

What Is Your Basal Ganglia: Other Areas Of The Basal Ganglia

The globus pallidus is located right inside the putamen and it receives inputs from the caudate and putamen and provides outputs to the substantia nigra.

The nucleus accumbens lies just below the putamen, and it receives signals from the prefrontal cortex and sends other signals back to the globus pallidus. Dopamine is used to carry messages to the nucleus accumbens, so for patients who have motor disability diseases, this is the area that is targeted by drugs for the further release of dopamine, which is supposed to help stimulate or “kick on” physical activity.

The substantia nigra is found in the upper portions of the midbrain, underneath the thalamus, and it uses dopamine neurons to send signals to the striatum. Although its exact function is not yet known, this structure is involved in our physical comprehension of rewards for specific activities. GABA neurons are also secreted here, which function to control eye movements.

Parkinson’s Disease Caused By Stroke: Vascular Parkinsonism

A stroke involving the substantia nigra or basal ganglia is called vascular Parkinsonism. Similar to other strokes, damage is caused primarily by a lack of blood supply to these regions of the brain. Generally, the strokes associated with Parkinsonism are termed small vessel strokes as they aren’t normally catastrophic. Diagnosis of small vessel strokes can be confirmed with diagnostic tests such as CT or MRI of the brain.

It typically takes several small strokes to produce the symptoms of vascular Parkinsonism. In some cases, small vessel strokes can also produce a type of dementia called vascular dementia. As such, it is not unusual for people who have vascular Parkinsonism to also have vascular dementia.

Whats Involved In The Recovery From Basal Ganglia Stroke

Basal ganglia dysfunction in PD. Diagram representing the ...

If you’ve had a stroke, you should participate in stroke rehabilitation. If your balance was affected by the stroke, rehab specialists can help you learn to walk again. Speech therapists can help you if your ability to speak was affected. Through rehab, you’ll also learn exercises and drills you can do at home to further your recovery.

In the case of basal ganglia stroke, recovery can be especially complicated. A right-sided stroke can make it difficult to perceive sensations on your left side even after the stroke is over. You may have difficulty knowing where your left hand or foot is in space. Making simple movements may become more difficult.

In addition to visual difficulties and other physical problems, you may also have emotional challenges. You could become more emotional than you were before the basal ganglia stroke. You may also become depressed or anxious. A mental health professional can help you treat these conditions through a combination of therapy and medication.

Analysis Of Electrical Activity Of Neuronal Populations

Field potential recordings , electrocorticograms , and electroencephalograms ) offer a rich source of information. It is generally accepted that LFPs are generated by transmembrane flow of current, and thus reflect synaptic activity within a population of neurons in an area several hundred micrometers in diameter around the electrode . While relatively easy to record, the interpretation of these data is not straightforward. Field potential recordings are most often analyzed using frequency domain analysis methods, comparing the spectral content of the signals in different behavioral states. Another use of these signals is to analyze the presence of stimulation- or event related potentials, i.e., synaptic potentials related to electrical stimulation of the tissue, or potentials that precede or follow a behavioral event. Individual evoked potentials are often not visible, so that averaging techniques have to be used to extract stereotypically recurring waveforms.

Field potential signals recorded simultaneously at different locations within the brain can also be used for cross-spectral or coherence analyses which can provide information on the coupling of activity of brain regions. Phase shifts in such studies have been used to identify causality relationships, or to determine the direction of information flow within the network under study.

What Happens When There Is Damage To The Basal Ganglia 5/5Damage to the basal gangliabasal ganglia

Though motor disorders are the most common associated with the basal ganglia, recent research shows that basal ganglia disorders can lead to other dysfunctions such as obsessive–compulsive disorder and Tourette syndrome.

Subsequently, question is, what is the basal ganglia responsible for? Basal ganglia are strongly interconnected with the cerebral cortex, thalamus, and brainstem, as well as several other brain areas. The basal ganglia are associated with a variety of functions, including control of voluntary motor movements, procedural learning, habit learning, eye movements, cognition, and emotion.

Also question is, can you recover from a basal ganglia stroke?

Your short-term and long-term outlook after a basal ganglia stroke depends on how quickly you were treated and how many neurons were lost. The brain can sometimes recover from injury, but it will take time. Be patient and work closely with your healthcare team to take steps toward recovery.

Where is the basal ganglia located and what does it do?

The basal ganglia are a set of brain structures located beneath the cerebral cortex that receive information from the cortex, transmit it to the motor centers, and return it to the part of the cerebral cortex that is in charge of motion planning.

Engaging Neuroplasticity To Treat Basal Ganglia Damage

Neuroplasticity refers to your brain’s ability to repair itself and create new neural pathways. These new pathways are formed through repetitive, therapeutic exercise.

This means one of the best ways to treat the many effects of basal ganglia damage is to exercise your affected muscles.

Of course, this can be hard to do, especially when the basal ganglia causes abnormal movements. That’s why your best option is to work with both a P.T. and a neurologist. They can collaborate and help you find the ideal approach.

For example, you might need medication to get dystonia under control first. Once the dystonia goes down, you can work on exercising the affected muscle to engage neuroplasticity.

Basal Ganglia Nigrostriatal Pathway And Parkinsons

Procedural Memory – Serious Games Analytics

“Hope arouses, as nothing else can arouse, a passion for the possible.” William Sloane Coffin

“Walk on, walk on with hope in your heart, and you’ll never walk alone, you’ll never walk alone.” Oscar Hammerstein II

Introduction: I have been trying to learn more about brain physiology and the inner workings as it relates to Parkinson’s. To do this, the region of the brain known as the basal ganglia has been a learning point for me. One of the big issues motor-wise with Parkinson’s is that we have slow movement, well, the functioning of the basal ganglia explains it. Or should I say, the absence of dopamine in the basal ganglia provides us with the answer.

Remember, if you have Parkinson’s, we have all learned that our symptoms are caused by the loss/reduction of dopamine from the pars compacta region of the substantia nigra in our mid-brain. Okay, then what happens? Before venturing into the description of how the basal ganglia works, let me start by comparing the human body to an automobile. See if this analogy makes any sense to you.

“In a time of destruction, create something.” Maxine Hbowong Kingston

“In a time of destruction, create something.” Maxine Hbowong Kingston

The therapeutic goal for a person-with-Parkinson’s is to try to maintain what is left of these dopaminergic neurons by attempting to achieve neuroprotection of this critical part of the brain. Here is what is important regarding physiological function of the motor function of the basal ganglia.


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