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Unlocking the Secrets of Brain-Body Connection in Ankle Injuries 🧠🦶
Sports Med U | Educating Minds, Elevating Potential
Brain Neuroplasticity Related to Lateral Ankle Ligamentous Injuries: A Systematic Review
In today’s letter
Overview of Brain Neuroplasticity Related to Lateral Ankle Ligamentous Injuries: A Systematic Review
Analogy for muscle growth
Rapid Results = This systematic review indicates the presence of neurological adaptation in patients with chronic ankle instability or who experienced a lateral ankle sprain.
Clinical take away = Introduce proprioceptive, dual tasking, neuromuscular control & explosives as early as possible
Bite-size study - Infographic style!
Deeper look
Definitions:
There are a lot of words in this article that make the head spin – let’s get some definitions out of the way – If you fall asleep, I don’t blame you
Corticomotor Excitability: Corticomotor excitability refers to the ability of the motor cortex (the part of the brain responsible for controlling voluntary muscle movements) to generate neural impulses and subsequently induce muscle contractions.
Corticospinal Inhibition: Corticospinal inhibition is the process by which the motor cortex reduces or inhibits the activity of the corticospinal tract, which is responsible for transmitting motor signals from the brain to the spinal cord and muscles. Inhibition can occur to modulate muscle activity and prevent unwanted movements.
Corticomotor Output Mapping: Corticomotor output mapping involves the study and representation of the areas of the motor cortex that control specific muscles or movements. It helps in understanding the organization of motor control in the brain.
Postcentral Gyrus: The postcentral gyrus is a region of the cerebral cortex located in the parietal lobe of the brain. It is primarily responsible for processing somatosensory information, including touch, temperature, and proprioception (sense of body position).
Afferent Information: Afferent information refers to sensory signals or information that travels from the periphery (e.g., skin, muscles, organs) towards the central nervous system (the brain and spinal cord).
Afferent neurons transmit sensory data for processing.
Somatosensory Cortex: The somatosensory cortex is a part of the brain, typically found in the parietal lobe, responsible for processing sensory information related to touch, pressure, temperature, and pain. It plays a crucial role in somatosensation.
Somato-Sensation: Somato-sensation is the collective term for sensory perceptions related to the body's surface, including touch, temperature, pain, and proprioception.
Afferent Information Decoupling: Afferent information decoupling refers to the process of separating or altering the transmission of sensory signals within the nervous system. This may be done experimentally or clinically to study or manipulate sensory perception.
Transcranial Magnetic Stimulation (TMS): Transcranial magnetic stimulation is a non-invasive neurostimulation technique that uses magnetic fields to stimulate specific regions of the brain. It is used for research and therapeutic purposes to modulate brain activity.
Cortical Silent Period: The cortical silent period is a brief interruption in the electrical activity of the motor cortex that occurs after a voluntary muscle contraction. It is a neurophysiological phenomenon often studied in the context of motor control and neurology
Aim of study
To determine if ankle sprains and chronic ankle instability cause changes in brains signalling, cortical mapping, or neuroplasticity
Background info
Athletic populations experience a high rate of 11.3 ankle sprains per 1000 athlete exposures.
Ankle sprains cause pain by damaging ligaments, muscles, and nerves, leading to issues like swelling, joint laxity, and neuromuscular deficits.
Chronic Ankle Instability (CAI) patients often suffer persistent symptoms a year after initial injury, including self-reported disability, instability, and reduced physical activity.
Central nervous system changes partially account for the high re-injury rate following initial ankle sprains.
CAI patients show structural and functional brain alterations in response to various stimuli, such as repetitive ankle sprains.
These alterations involve different neural circuit activation and changes in brain connectivity, particularly in motor-related regions
Methods
Systematic review | 20 articles | 356 patients with chronic ankle instability |10 with lateral ankle sprain | 46 copers
The focus is on brain structure and function, excluding studies on other injuries, animals, cadavers, treatment interventions, or those not related to brain function and structure.
Studies with copers were included. Copers were defined as individuals having a history of at least one ankle sprain but without persistent dysfunctions or feelings of giving way
Results
3 studies observed reduced corticomotor excitability in both peroneus longus and tibialis anterior muscles in CAI patients compared to healthy controls.
Corticospinal inhibition was assessed in five transcranial magnetic stimulation studies, revealing a prolonged cortical silent period in CAI patients for tibialis anterior and gastrocnemius muscles compared to copers and controls.
Corticomotor output mapping can explore supraspinal motor control within the corticospinal pathway, showing that the cortical representation of the peroneus longus muscle is notably smaller in CAI patients compared to healthy controls in terms of map area and volume
Discussion key points
Functional Brain adaptation
Corticomotor excitability reflects neuron firing ease in the motor cortex.
Studies show reduced corticomotor excitability in regions of the primary motor cortex involved in controlling leg muscles (peroneus longus, tibialis anterior, soleus, gastrocnemius medialis).
This reduced communication efficiency in the pyramidal tracts may contribute to neuromuscular deficits in postural control. Smaller map areas and volumes suggest more focused neuron clusters communicating with the peroneus longus muscle in CAI patients.
As a result, motor cells on the peroneus longus border are less dedicated to its function, with other brain areas compensating. This altered muscle excitability may explain modified movement strategies leading to ankle re-injury.
Decreased corticomotor map area and volume in CAI may limit motor cortex self-organization
Brains understanding of sensory information
This section might be a bit harder to follow – The simplified version is that proprioceptive feedback from foot to brain is altered.
Initial findings indicate alterations in the postcentral gyrus due to reduced afferent information coupling.
The degree of decoupling increases with stimulus intensity.
This might result in impaired preparatory or reactive responses to specific stimuli, given the significance of the somatosensory cortex in proprioception.
Changes in sensory receptors and the somatosensory cortex could impact injury risk by distorting proprioception perception.
Altered somatosensation may influence a patient's joint perception and positioning
Fear
Fear of injury also contributes to the disability experienced by LAS patients.
One study examined neural activity during injury-related appraisal and identified significant deactivation in the dorsal anterior cingulate cortex, a part of the limbic system.
This deactivation correlated with increased fear levels, indicating that LAS patients experience more fear when encountering sprain-related stimuli than healthy individuals.
Over time, the initial passive appraisal and avoidance coping strategy become maladaptive, causing patients to avoid sports due to their fear of (re)injury
Structural brain adaptation
We've discussed functional adaptations in CAI patients, such as difficulty activating ankle muscles. Now, structural evidence in the corticospinal tract supports the idea that electrophysiological changes occur in CAI.
LAS injuries with these characteristics could potentially cause harmful alterations in white matter microstructure controlling postural control and raise the risk of future musculoskeletal injuries
Clinical use
Deficits in corticomotor pathways can lead to compensatory movements and changes in joint function in CAI patients, often failing to prevent recurrent LAS and causing ongoing pain, instability, and activity limitations.
Brain adaptations following injury contribute to patient-reported disability in CAI cases, unlike copers who show no significant functional or structural changes compared to healthy individuals.
Rehabilitation should address central adaptations and guide LAS and CAI patients toward non-dysfunctional outcomes, with active strategies like resistance, proprioceptive, balance training, and motor learning potentially mitigating sensorimotor issues and reducing LAS recurrence.
Consideration of injury-related fear is vital in CAI rehabilitation, as patients with effective coping skills are more likely to return to sport than those with avoidance tendencies. Utilizing tools like the Injury-Psychological Readiness to Return to Sport Scale can aid clinicians in making informed decisions regarding return to sport.
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