Lentiform Nucleus Damage in Motivational Deficits in Dyskinetic Cerebral Palsy: A Work in Progress

Abstract

This report presents preliminary findings on the impact of lentiform nucleus damage on motivational deficits in individuals with dyskinetic cerebral palsy (DCP). It explores how disruptions in GABAergic signaling within the basal ganglia contribute to reduced motivation, emotional dysregulation, and heightened stress responses. The study suggests that these neurological impairments, rather than environmental or psychosocial factors alone, play a critical role in motivational deficits. It also highlights potential connections between DCP and conditions like Parkinson’s disease and PTSD. These findings are preliminary and may not reflect the final conclusions, requiring further research to confirm their implications.

Full text

Lentiform Nucleus Damage in Motivational Deficits in Dyskinetic Cerebral Palsy:
A Wo rk in Pro gre ss
Athena Stevens
Harvard Extension School
15 December 2024
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Lentiform Nucleus Damage in Motivational Deficits in Dyskinetic Cerebral Palsy
Dyskinetic cerebral palsy (DCP), a neuromuscular disorder acquired at birth and widely
recognized for abnormal muscle tone fluctuations, is linked to hypoxic lesions in the basal ganglia
(Monbaliu et al., 2017). The basal ganglia, which include the lentiform nucleus—a structure
comprising the putamen and globus pallidus—affect motor, associative, and limbic circuits
throughout the brain (Pierce & Péron, 2020). Damage to the lentiform nucleus disrupts emotional
and motivational regulation, as observed in conditions such as stroke, Parkinson’s disease, and
Huntington’s disease, where affected individuals experience motivational deficits such as avolition
—a reduction in motivation—or abulia—a complete loss of will (Barrios & Bauer, 2013; Le Heron
et al., 2018). Among all individuals with DCP examined by Ballester Plané (2019), damage to the
lentiform nucleus is consistently observable, suggesting that emotional and motivational challenges
in these individuals stem from neurological impairment rather than physical limitations alone.
However, clinical practice frequently overlooks these dimensions in favor of motor deficits. This
paper posits that damage to the lentiform nucleus in individuals with dyskinetic cerebral palsy
directly causes physiological changes in motivation due to the dysregulation of GABA production.
Understanding the emotional complexity of DCP
Individuals with dyskinetic cerebral palsy face a significantly higher risk of mental health
issues like anxiety, depression, and stress-related disorders compared to their nondisabled peers
(Smith et al., 2019). However, much of the research in this area has predominantly framed these
mental health comorbidities as reactions to social and environmental stressors associated with living
with a physical disability. Focusing mainly on psychosocial factors rather than the underlying
neurological influences, clinicians overlook the role of the neurological damage inherent in DCP.
Finding emotional dysregulation in cerebral palsy as a neurological outcome rather than just a
response to environmental factors underpinned research done by Honan and colleagues (2023).
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Neurological factors, including alterations in neurotransmitter production, play a pivotal role in
shaping the mental health outcomes associated with DCP, as highlighted in this study. As the core of
these neurological differences, anything affecting the lentiform nucleus modulates motivation,
emotion, and reward-related behaviors, further underscoring the structure’s critical role in
motivational outcomes. Consequently, damage to the lentiform nucleus will likely impact several
neurotransmitters, leading to physiological changes that hinder emotional and motivational
regulation alongside motor circuitry, as Pierce and Péron imply (2020). These disruptions highlight
the interconnected nature of the basal ganglia’s functions, where even minor impairments in one
area can cascade into widespread neurological and behavioral consequences. Such cascading effects
are particularly evident in the exaggerated fight-or-flight startle response frequently observed in
individuals with DCP.
One of the hallmarks of all forms of cerebral palsy is an extreme startle response (Ballester
Plané, 2019). Clinicians, including Ballester Plané, often dismiss this reaction to loud sounds or
unexpected events as a simple muscular reflex. However, the startle reflex is, by definition, an
uncontrolled movement in response to external stimuli. This suggests that the reaction is not merely
a motor misfire but instead involves a complex interplay between neural circuits responsible for
muscle contraction and relaxation. These circuits are regulated by the sympathetic and
parasympathetic nervous systems, indicating a broader neurophysiological imbalance.
The startle reflex involves disrupted communication between pathways for muscle contraction and
relaxation, according to Perpetuini et al. (2023). This disruption strongly implies that the startle
reflex engages both the motor circuit (muscle contraction) and the limbic circuit (relaxation),
linking physical and emotional systems. Such an interplay highlights that even the defining attribute
of dyskinetic cerebral palsy—the startle reflex—is far more than a physical response. A deeper
understanding of these disrupted neuromodulators in dyskinetic cerebral palsy could be achieved by
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drawing on research into stress-related disorders, which offers valuable insights into the effects of
GABA reduction in conditions such as post-traumatic stress disorder (PTSD).
Differences in GABA distribution within DCP and other disorders involving hypervigilance
The link between GABA production and changes in movement is visible in conditions
where the motor circuit is not directly affected. For example, people with PTSD often battle
hypervigilance, exaggerated fear responses, and a diminished ability to manage stress as well as
anxiety, all of which result from a reduction in GABA (Huang et al., 2023). This research
additionally highlights that an exaggerated startle response is a consistent characteristic of someone
with PTSD, amongst other heightened autonomic reactions. Within this hypervigilance are physical
muscle spasams creating a symptom of the psychopathology of post traumatic stress disorder.
These startle response visible in PTSD is created by the same unexpected stimuli as the start of
response visible in DCP, such as loud and unexpected noises (Ballester Plané, 2019). In both
conditions, the amygdala, often referred to as the brain's fear center, becomes either activated or
suppressed depending on the absence or presence of GABA as a modulator, as demonstrated by Jie
et al. (2018). While reductions in GABA increase the body's stress response during perceived
danger, understanding this neurotransmitter’s relationship to the basal ganglia and lentiform nucleus
is key to revealing its implications for DCP and its effects on motivation.
The basal ganglia is distinctive in that most of its neurons are inhibitory, relying heavily on
GABA as their primary neurotransmitter (Subramanian et al., 2017). GABA production and
signaling initiate in the lentiform nucleus, and a deficit in GABA transmission results in dyskinetic,
involuntary movements (Levy & Hallett, 2002). Damage to this area leads to reduced GABA
throughout the system and increased unwanted excitatory movement. This interplay between
movement, motivation, and regulation underscores the lentiform nucleus's central role in the
cortical-basal ganglia-thalamo-cortical loop, which governs sensory-motor processing as well as
associative and emotional systems (Aoki et al., 2019). This research highlights a fundamental
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neurological basis for DCP, demonstrating that its impact on mood and motivation extends beyond
purely social factors. Specific damage to the lentiform nucleus not only causes motor symptoms in
dyskinetic cerebral palsy but also directly affects motivation and emotional regulation, shaping an
individual’s psychological experience.
GABA Dysregulation resulting from altered patterns associated with dyskinetic cerebral palsy
Ambulatory individuals with DCP exhibit gait abnormalities. Similarly, constant
fluctuations in muscle tone mark the condition in individuals who cannot walk (Ballester-Plané et
al., 2017). This fluctuating muscular tension—between excitatory and inhibitory extremes—
impacts emotions and drive (Páscoa, Vohryzek, & Paul, 2023). In computational studies, Páscoa et
al. (2023) demonstrate that damage to motor networks can lead to a cascade of excitatory-inhibitory
neurophysiological imbalances. Their research also reveals that disruptions in physical balance
contribute to emotional disturbances, such as anxiety and mood fluctuations, often observed in
neurological conditions affecting motor function. Traditional examinations of dyskinetic cerebral
palsy attribute mood instability to fear of falling or frustration with the inability to participate in
everyday activities, as experienced by non-disabled individuals. However, this research suggests a
deeper cause. Specifically, the authors link their model's altered excitability patterns to biomarkers
associated with known side effects (Páscoa et al., 2023). The imbalance between excitatory and
inhibitory neurotransmission directly connects motor issues to emotional symptoms. Chronic
abnormal movement patterns alter levels of neurotransmitters like GABA and its excitatory
counterpart glutamate, creating long-term chemical downregulation of mood.
GABA and glutamate dysregulation can worsen mood disorders, including depression.
These neurotransmitters are crucial for the development of motor skills, muscle memory, and
neuroprotection, all of which support healthy aging (Bhattacharya, Chatterjee, & Roy, 2023). In
conditions like DCP and other neuromuscular disorders, disruptions in these pathways impair motor
acquisition and the ability to establish stable muscle-neuronal connections, further compounding the
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challenges associated with neurochemical imbalances. The ongoing muscular fluctuations seen in
DCP condition make automated movement different, if not impossible, for the subject with this
disability. Because GABA and glutamate levels are made within the area of the brain that is
damaged in DCP, motor function and neurochemical fluctuation from the norm directly impact the
central nervous system function as a whole and not simply involving movement. However, while
differences in movement might contribute to differences in a neurochemical balance within the
individual, an abundance of excited stimulation, as is typical with GABA dysregulation, will create
a chemical form of chronic stress.
Alongside the compromise of GABA's inhibitory function due to motor alterations,
excitatory neurotransmission by glutamate will conversely dominate, leading to increased agitation,
excitatory dysregulation, and cognitive fatigue. Chronic stress in the hippocampus triggers
increased glutamate release, weakens long-term potentiation, causes dendrite atrophy, and leads to
learning and memory deficits, as shown in Pal's (2021) findings. A constant fight-or-flight
excitatory state in the central nervous system disrupts the body's primary stress circuit, the
hypothalamic–pituitary–adrenal (HPA) axis, as the hippocampus directly regulates the HPA axis
response (Jones et al., 2022). Excess excitatory transmitters caused by imbalanced muscle
coordination directly impact the body's stress response system, acting through biological and
physiological mechanisms rather than social pressures on mood regulation. An ongoing increase in
glutamate impedes inhibitory responses, making it harder to adjust allostatic load and react to
shifting challenges. In DCP, motor control is inherently inconsistent and unpredictable,
complicating even routine movements (Monbaliu et al., 2017). Disruptions in GABAergic and
glutamate signaling, compounded by impaired dopamine production in the lentiform nucleus and
basal ganglia, intensify motor dysfunction and motivational deficits. This combination of
neurochemical imbalances highlights the profound challenges faced by individuals with DCP, as not
only physical but also emotional regulation and motivation become significantly impaired.
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The Role of Dopamine in Motivation within DCP
Because dopamine production occurs in the basal ganglia,! Rommelfanger (2010)
emphasizes the dopaminergic circuits within the globus pallidus and putamen, which comprise the
lentiform nucleus. This area's GABAergic projections aid in regulating and signaling dopamine
extending to regions such as the thalamus and brainstem (Rommelfanger, 2010). Therefore, the
disruption of GABAergic signaling causes dopamine production can be impaired, leading to motor
dysfunctions and reduced motivation. Rommelfanger directly connects this observation in
individuals with Parkinsonism, and other disorders with basal ganglia disruption such as ADHD.
Any lesion to the lentiform nucleus disrupts GABAergic and dopaminergic pathways, undermining
dopamine signaling and leading to deficits in movement, task engagement, and social interaction—
all of which are essential for motivation and emotional regulation.
Disruptions in GABA reduce dopamine levels, impairing both motor and motivational
functions. Altered dopamine signaling, as seen in Parkinson's disease, can lead to akinetic mutism, a
severe psychomotor disturbance where both movement and will are entirely absent (Bullock, 2016).
This introduces the corticostriatal–pallidal–thalamic loop where inclusion can extend the "pallidal"
element to the lentiform nucleus as illustrated by the author. Damage to this part of the circuit
disrupts dopamine modulation, reducing motivation and making it particularly difficult to initiate
actions from a resting state, similar to what Rommelfanger’s work implies. This loss of intention
affects both physical movement and the drive to act on a cognitive or emotional level. Thus these
disruptions help form a connection between dyskinetic cerebral palsy and conditions like avolition
or abulia.
Avolition and Abulia as Potential Side Effects of DCP
As supported above, abulia and, to a lesser extent, avolition marks a loss of motivation and
the inability to initiate purposeful actions, often linked to damage in the basal ganglia, particularly
the lentiform nucleus. Palmisano, Fasotti, and Bertens (2020) point out that up until this point,
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abulia and avolition have mostly been inferred conditions that are acquired later in life, such as
Parkinson's Disease, Huntington's Disease, stroke, and brain injury. At first glance, there is little
overlap between a birth injury such as dyskinetic cerebral palsy and pathology altering the will and
personality already established. However, they also discuss the cortico-basal ganglia loop as crucial
in driving motivation. Disruptions in this loop can lead to akinetic mutism, abulia, or apathy
(Palmisano et al., 2020). While this suggests that these so-called age-related illnesses are destroying
established brain structures and chemical pathways, a closer look into GABA's relationship to
dopamine suggests a more complicated reality.
A study specifically looking at the destruction of the same circuit in Parkinson's disease
notes that a decrease in dopaminergic receptors correlates to a decrease in GABA (Alharbi et al.,
2024). Alharbi and colleagues identify the critical role of GABAergic signaling in supporting
motivation and goal-directed behavior alongside dopamine in a bidirectional push-pull pathway.
This model contrasts the traditional "go-no-go" concept of how dopamine acts as an accelerator and
GABA the brakes within the brain's system. Disruption to GABA regulation and associated
neurochemical signaling in conditions such as late-life basal ganglia damage does not simply take
the breaks off and allow motivation to become boundless. Instead, the lack of counterbalance
contributes to an inability to initiate action. Given the complexity of the imbalance that occurs in a
bidirectional pathway established throughout a lifetime, damage to the circuit in early development
might also lead to a diminished capacity for initiating purposeful action and motivation.
Disruptions in cortico-basal ganglia circuitry are also visible in conditions like OCD and
ADHD, which typically emerge in childhood and thus reflect an alteration of the brain's
physiological systems and chemistry (Moustafa et al., 2014). These early disruptions suggest that
neurochemical imbalances in key circuits not only affect cognitive and motor regulation but also
hinder the development of stable behavioral patterns. Such impairments can set the stage for
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lifelong challenges with motivation, impulse control, and purposeful action. Conditions
characterized by cognitive and motor regulation impairments, driven by dopamine and GABA
imbalances, disrupt motivation, impulse control, and purposeful action (Leisman, Melillo, &
Carrick, 2013). This article points to numerous studies in which a decrease of inhibition, as found in
ADHD, correlates to a reduction in volume in frontostriatal regions as well as conversely increased
connection to the same area in people with OCD. These alterations in younger people are
independent of loss of mobility or other physical impairment but still affect cognitive, emotional,
and motivational processing. Conditions such as apathy and emotional regulation can be
independent of the late-life onset of a physical disability. More directly, Ballester Plané (2019)
observes that while individuals with cognitive disabilities show a decrease in this type of
connectivity, those with DCP without cognitive disabilities show an increase in both this and white
matter connectivity.
It is conceivable, therefore, that early damage may lead to differences within the brain's
chemical balance and connectivity within an individual born with DCP. These differences can either
lead to a decrease or an increase in motivation depending on the nature of the specific injury and
areas impacted by the hypoxia at birth. In the individual with a decrease between the basal ganglia
and the frontostriatal connectivity, a decrease in motivation and increased inhibition is very likely.
At the same time, if dysregulated dopamine and GABA activity in the basal ganglia can lead to
impaired motivation and impulse control, even in the absence of motor impairments as is evident in
conditions such as OCD and ADHD, then early childhood disruptions in normal brain and
neurochemical transmissions may lead to avolition and abulia as developmental consequences of
basal ganglia damage at birth. Recognizing these deficits as products of neurochemical imbalances
and physiological differences, rather than simply reactions and adjustments to physical disability,
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underscores the urgent need for treatment approaches that directly address the underlying
anatomical damage and disruptions resulting from dyskinetic cerebral palsy.
Integration of Overall Findings
Across studies, researchers consistently link lentiform nucleus damage and motivational
deficits to disruptions in GABAergic signaling, which critically impacts cognitive and motor
control. Kiemes et al. (2021) examined multimodal imaging studies, highlighting a significant link
between decreased GABA activity and impaired motivational states. Their findings suggest that
GABA dysregulation in the lentiform nucleus can lead to cognitive and emotional impairments as
well as physical disability. As GABA acts as the primary inhibitory neurotransmitter within the
basal ganglia, it is an inhibitory function crucial in stabilizing neural networks involved in
motivation. Damage to the GABAergic circuits within the basal ganglia disrupts dopaminergic
signaling, a critical factor in maintaining both motor function and motivational states, contributing
to symptoms such as apathy and motivational deficits commonly observed in Parkinson's disease
and other conditions with basal ganglia damage (Gu et al., 2022). This growing understanding of
the role of GABA in motivation and motor function underscores the importance of further research
into its specific mechanisms and pathways.
However, significant limitations persist in current research. Longitudinal studies on
dyskinetic cerebral palsy are limited, with most existing research concentrating primarily on the
motor aspects of the condition and neglecting its complex physiological and psychological
dimensions. GABA's role in motivation-related deficits is receiving increasing attention, but the
existing studies fail to provide sufficient insights. Villalobos and Magdaleno-Madrigal (2023)
highlight underexplored distinctions between specific GABA receptors and their effects on cortical
and thalamic circuits, suggesting that receptor-specific differences could provide insight into how
pathway damage impacts motivation and emotional regulation in basal ganglia-related disorders.
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Their findings imply that neurochemical imbalances may play a more significant role in motivation
and other mood disturbances than in movement or cognition. Depression and other mental health
challenges in individuals with DCP have historically been attributed to sociological factors, such as
reduced participation in enjoyable daily activities compared to non-disabled individuals, as
highlighted by Honan et al. (2023). In order to understand how lentiform nucleus damage alters
GABA production and inhibitory signaling underscores the need for deeper investigations into the
neurochemical pathways influencing mental health in DCP. Future research should address the
specific mechanisms by which GABA pathways contribute to motivational deficits and diminished
willpower in goal-directed activities.
Modulating GABA-A receptors shows potential for therapeutic benefits in neuropsychiatric
conditions, with enhanced GABA function potentially alleviating motivational and emotional
challenges associated with basal ganglia disorders (Thompson 2023). Targeting GABA-A receptors
therapeutically could benefit not only individuals with DCP but also those with Parkinson's disease,
Huntington's disease, dementia, and other conditions often classified as "age-related." Restoring
GABAergic balance has the potential to stabilize dopaminergic and glutamatergic signaling
networks, offering a promising avenue for improving emotional and motivational regulation across
multiple disorders. Additionally, recognizing psychiatric symptoms as secondary to neurological
damage in the lentiform nucleus—rather than attributing them solely to environmental factors or
loss of mobility—could transform both diagnostic and treatment paradigms. This shift would pave
the way for personalized medicine approaches that target condition-specific neurochemical
imbalances, moving beyond generalized treatments such as cognitive behavioral therapy. By
addressing the underlying neurochemical etiologies, interventions could become more precise and
effective, offering tailored solutions that directly tackle the root causes of psychiatric and
motivational challenges in individuals with basal ganglia-related disorders. Reforming current
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treatment approaches would also enable clinicians to better understand, empathize with, and more
accurately address the lived experiences of this population, ensuring that therapeutic strategies align
with appropriate treatment.
Conclusion
This paper explores the potential link between dyskinetic cerebral palsy and the
neuropsychiatric outcomes of avolition and abulia. Damage to the lentiform nucleus, a hallmark of
DCP, disrupts the regulation of neurotransmitters like GABA, glutamate, and dopamine, which are
critical for cognitive and emotional functions. Similar disruptions in disorders such as Parkinson’s
and Huntington’s have been linked to abulia, raising the question of whether DCP may cause
comparable effects. Understanding these outcomes as stemming from neurological dysfunction,
rather than physical limitations or generalized depression, has profound implications for mental
health interventions. Treatments may need to go beyond traditional psychotherapy to include
neurophysiologically targeted therapies, such as pharmacological support or neuromodulation.
Investigating these mechanisms could lead to more effective, individualized approaches for
managing mental health conditions in people with dyskinetic cerebral palsy and disabilities related
to lentiform nucleus abnormalities.
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