Spasticity is a common word that comes up while discussing neurological syndromes, especially those which are dubbed as UMNS or UPPER MOTOR NEURON SYNDROMES.
Our body is a fascinating machine, our brain has ways to oversee every function of all otherwise independently capable organs and organ systems. It just has to fine-tune the functions that are happening, sort of like a spell checker on an already-spelled essay. More often than not this regulation is inhibitory in nature, especially when we talk of the musculoskeletal system, it is controlled by corticospinal pathways (brain-spine tracts) which inhibit the activity in a few ways that ultimately a fine-tuned and calculated movement (output) is produced.
But, what about when the tuner breaks!? When an Upper Motor Neuron Lesion strikes?
An upper motor neuron syndrome for those unaware of the term can be essentially understood by the analogy that when you are a silly kid (muscles, organs); your parent or guardian or caretaker (the brain) has certain ways like rewards, advice, long lectures and that cold gaze of doom (the upper motor neuron inhibition) that keeps you in check while you are under their supervision, but as soon as they are out of the house (i.e. UMN inhibitions are lifted off) you go absolutely randy and mischievous and unleash all your hyperactivity (spasticity). (Upper motor neurons thus can simply refer to the means with which the brain controls activity)
This is essentially what goes on inside someone who has a UMNS.
Stroke and Cerebral Palsy being the two well-known UMNS have almost the same disabling feature; that being said, what’s truly a disabling factor in both of these conditions is the presence of ‘Spasticity’.
It is the inability to voluntarily move a joint due to already flexing muscles; just to say it very crudely.
“Imagine not being able to use half of your body or both your legs or arms or all of it, just because your brain has lost its control on them, it’s like being betrayed by your own body”
Just by the looks of things so far many of you may have guessed that this is going to be a very technical topic, so if you aren’t looking for the ‘HOWs’ and all the technicalities you can just go for the simplified explanations in summaries of the subtopics below.
And for those who want to learn a bit more just keep reading.
Defining Spasticity
Spasticity for those more familiar with the concept is defined as a ‘stretch reflex disorder’ or ‘the velocity dependant increase in the muscle tone due to exaggeration of stretch reflexes’ this to the most extent explains what happens when there is spasticity and what ‘is’ spasticity, but it fails to take in account the entirety of it.
It is indeed a phenomenon that exists due to the imbalances between supraspinal inhibition and excitation, directed toward the spinal cord, disturbing the stretch reflex, but it’s also necessary to observe that there exists a delay between the occurrence of the trauma and manifestation of the spastic features*.
Summary:
Like an awesome machine our body has some inbuilt safety features, let’s call them ‘reflexes’. One very common example of such reflexes would be when you jerk your hand away when it touches a hot object, or when you freakingly jump around having felt ‘something spidery’ on your neck, these are all means to protect you from burning your hand or when there actually is a spider.
Similarly, there exists a reflex that protects muscles from an injury known as a ‘stretch reflex’, with this; any muscle or a group of muscles when pulled too fast or too much beyond a point will contract to counter any possible injuries that may occur.
Conventionally; it is believed that when our brain (our guardian) can’t oversee this behavior (reflex) and stop (inhibit) it, it leads to a state where the muscle becomes perpetually stiff (or spastic).
But scientists have since wondered why this doesn’t happen right away.
What about the delay then?
The delay between the neurological trauma and the occurrence of spasticity shows that it is not just a release phenomenon.
What this implies is that there must be some other factors responsible for the hypertonicity and development of spasticity.
We now attribute hypertonicity to reflex-mediated (spinal cord and central) factors and ‘soft tissue changes in the muscles involved, later being called ‘non-reflex or Intrinsic hypertonicity’
Summary:
When a person experiences a neurological trauma or stroke, the phenomenon of ‘spasticity’ takes some time to develop, this led to scientists questioning whether it is simply a disorder where the brain (guardian) stopped overlooking(inhibiting) the activity(reflexes) and the craziness (spasticity) just happened? or is it more complex?
They eventually concluded that there must be some other factors responsible alongside the conventionally believed stuff, and they proposed the idea that something occurs in the muscles and spinal cord (brain’s relay center, more like a highway for all the information) that plays a role in the disease process as well.
Let’s talk a bit more about UMNS
Before we move further let’s explore a bit more about the features of UMNS, in Stroke or neurological trauma that leads to UMN lesions.
Features: There are a few features like loss of dexterity, weakness, diminished DTRs & hypotonia which are known as the negative features (apparent immediately), and features like spasticity, exaggerated DTRs, clonus, positive support reactions, co-contraction, spastic dystonia, associated reactions, and positive Babinski’s sign are known as the positive features (Babinsky’s sign is seen with the negative signs initially).
Central Control: It is often believed that spasticity is related to the pyramidal system. Instead, it’s the imbalance between DRST(Dorsal Reticulospinal Tracts) and MRST(Medial Reticulospinal Tracts) + VST(Vestibulospinal Tracts) that leads to hypertonicity.
From the diagram above we can see that cortical stimulation of DRST results in the inhibition of the stretch reflex in the spinal cord, whereas MRST which is devoid of any cortical connection reinforces the stretch reflexes.
Thus, it’s easy to assume that the reduction of cortical inputs via DRST and stimulatory outpost via MRST (and VST to some extent) is responsible for the reflex spasticity.
[Note- all these tracts inhibit the flexor withdrawal, thus flexor spasms are predominantly seen in Stroke]
Summary:
At this point it is important to know how our brain controls these functions, as we already have mentioned the spinal cord previously, is like a highway for all the information that goes into the brain from the body and comes from the brain towards the body, and within this highway, there are these lanes/roads known as ‘Tracts’ and much like actual roads, these are very specific in where they go and also in what information they carry. So, if there are any disruptions in these pathways, the brain loses control over what it’s supposed to overlook.
What do Immobilization, Plastic changes, and soft tissue changes have in common?
The fact that all natures of inhibitions, be it presynaptic or postsynaptic are reduced in spasticity, makes it a truly disabling feature.
Let’s talk about immobilization and its impact-
What’s most concerning to know about this is that there is a linear decrease in Post Activation Depression with Immobilization due to negative features. PAD(Post Activation Depression) is a phenomenon wherein passive dorsiflexion or some active movements of the ankle lead to depression/inhibition of the soleus H-reflex, this inhibitory reflex is not cortically mediated and is related to the development and severity of hypertonicity, as it is seen that early mobilization and physical activity leads to partial normalization of PAD and even reduced hypertonicity in some patients.
Co-Contraction- the inability to relax the antagonist muscle to produce a movement, is one of the most functionally disabling and limiting factors present.
Hypersensitivity or ‘Denervation Supersensitivity’ of the stretch reflex and Alpha motor neuron deprived of cortical inhibitions could be because of the formation of new receptors or change in morphology of already present receptors, regardless all of this leads to alpha motor neuron releasing certain growth factors that cause local sprouting from surrounding interneurons and formation of abnormal synapses and reflex pathways, that can sometimes lead to excitatory connections and overactivity, contributing more to spasticity
Immobilization at shorter lengths decreases sarcomeres in series and increases the connective tissue amount instead, producing more resistance to passive movement, more sensitivity to stretch, and increased resting discharges of spindles as these fibrosed units transmit any pulling force to the spindles more readily. These muscle contractures and fibrosis become very difficult to differentiate clinically when they occur without shortening, truly complicating the process.
All the plastic changes and soft tissue changes have but one thing in common paired with immobilization they make spasticity absolutely worse.
Summary:
Co-Contraction- just imagine the frustration you’ll feel when you try to move your hand forward but something just holds you back and doesn’t let you move no matter what, in this case, it’s the body that holds the movements back by not letting some muscles relax.
Immobilization- our muscles are quite stretchy and elastic because of their usual composition, but in a UMNS we initially have to immobilize the person or make them absolutely static due to extreme weakness and for protection. But when it is not done properly or done for longer than needed, the body starts to replace muscle with other kinds of tissues naturally; as the muscle which is meant to move is not being used to move, and that creates all sorts of trouble for the patient and increases their disability.
What about Pain!?
It is observed that Eccentric Contractions are more disruptive to the muscle fibers and can lead to the release of nociceptive substances (more commonly known as DOMS)
Similarly, this is what happens in a spastic muscle when we try to lengthen it, and not to forget that any UMNS tilts the whole body weight distribution system producing more joint stresses and sensory disturbances, leading to a vicious cycle of increasing pain, spasticity, and disability.
Summary:
Imagine the first-day post-workout after a long time, the pain and soreness, that pain is perpetually experienced by people having UMNS, even when they are on a road to recovery. So, if you know someone who is going through a similar condition, it is preferable to be acquainted with and mindful of what they might be going through.
Conclusion:
“Understanding it all is not as important as understanding the point of it”
To simplify everything above: ‘Identify the least amount of time you have to immobilize your patient, maintain passive mobility, and get them up and moving as soon as they must’, because not only will you be improving their functionality and independence you’d be limiting the extent of their disability even if it’s a smaller fraction of it.
And for those who may not be involved in the rehabilitation process, a little compassion and awareness can only help make someone’s life worth living a day more.
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