Tuesday, September 25, 2018

Deep Dive into TIGHTNESS - Cleaning up our terminology

15-20 min read (Grab a cup of coffee :) ) 

The concept of tightness is one that has long baffled me as a clinician. It’s a word that gets tossed around loosely and that doesn’t always accurately describe the clinical situation at hand.  The intention of this blogpost is to hopefully get a little clearer on terminology surrounding what is meant by “tightness”.


I give credit to the stellar group of clinicians from a recent Movement Links seminar teaching experience over the summer.  The level of clinical reasoning was top notch and I felt inspired to further my understanding of muscle tone and terminology such as tightness.  Thus, down the rabbit hole I went and this is the result as of this moment in time.  As usual and as the saying goes, the more you know, the more you discover there’s so much more to learn. 

My first step when I feel the word “tight” coming into my vocabulary, whether it be within a patient interaction or in a casual chat with a colleague, or even in a teaching/classroom environment is to differentiate:

Is this patient perception or clinician perception?

When the words, “tight”, “stiff”, “concrete”, “cement” come out of a patient or client’s mouth, she (I’m going with feminine pronouns this post J) at this point is describing her perception of her problem.  The words are simply descriptors. 

I can’t tell you how many times I’ve missed the boat on this one because I’ve made an erroneous assumption as to what I think the patient’s problem is without truly listening to the person sitting in front of me.  Example: when I use the word “pain” over and over and over again when the patient’s descriptor is “tightness” and finally the patient yells at me: “It’s not pain, it’s tightness!!!”.  Eeeek.  As a result, I make every attempt to as much as possible capture the words from the patient’s mouth and use those words when describing the clinical presentation.

“How’s the tightness?” or “What’s going on with the concrete feeling in your low back area?”

If the word “tightness” is truly coming from my own perception of an aspect of the clinical presentation, I know I need to dig deeper and ask myself: “What do I mean by what I’m thinking/seeing/feeling/thinking again/interpreting?”  To answer this question, it’s helpful to do a review of concepts. 


The definition of muscle tone is: the force with which a muscle resists being lengthened.  (Shumway-Cook A, Woollacott MH, 2012; Basmajian, 1985) Muscle stiffness is defined as the change in tension per unit change in length. (Weppler, 2010) From my research into this topic, the terms tone, tightness, and stiffness are often used interchangeably as there is ambiguity in the current literature. 

A muscle with excess tone, or excess resistance to passive stretch, is said to be hypertonic. A muscle with insufficient tone or resistance to being lengthened is termed, hypotonic.  However, the use of the terms, “hypertonia” and “hypotonia” do not provide details of the underlying mechanism.

We do know that there are structural central nervous system (CNS) lesions that produce changes in muscle tone.  Examples of CNS structural lesions are indicated in Table 1:

CNS Lesions à Hypertonicity
Nervous system lesions à Hypotonicity
Upper Motor Neuron pathologies
CVA (later stages)
Cerebellar disorders
Joubert Syndrome

Table 1: Examples of structural CNS lesions as they related to potential hyper or hypo-tonicity (Shumway-Cook A, Wollacott MH, 2012)
 Our subjective and objective exams, to include a full neurological exam, should help us hypothesize or rule in a potential CNS lesion as an underlying cause of muscle tone change in partnership with a physician.

We also know that there are structural connective tissue conditions that will create changes in passive joint mobility and that these are typically also accompanied by changes in muscle tone.  Examples are listed in Table 2:

Ehlers-Danlos syndrome
Marfan syndrome
Osteogenesis imperfecta
Generalized joint hypermobility syndrome
Congenital talipes equinovarus
Idiopathic toe walking
Symptomatic generalized hypomobility
Acquired hypomobility

Table 2: Examples of connective tissue conditions and relationship to hyper or hypo mobility (Schleip R, et al, 2012)

Each of the above conditions carry their own unique features that can assist in differential diagnoses of each of these conditions in partnership with other members of the healthcare team.

Passive joint mobility can lead to predictions about muscle tone.  In general, we may expect that hypermobile individuals may also exhibit lower tone, and conversely, hypomobile individuals may exhibit higher tone.

In addition, aside from a pathoanatomical diagnosis, there is a wide spectrum of hypo -> hypermobility and hypo -> hypertonia.  Reasons for this are varied. One classification is offered by Robert Schleip in his book, Fascial Fitness.  This book is written for both clinicians and lay-people alike and this classification is one that the general population can easily understand.  Here is the question:

Are you a Viking type or are you a Flexible Dancer type?  See distinguishing features in the tables below: (Table 3)

Viking Type
Flexible Dancer Type
Firm connective tissue
Strong, compact
High stability
Lack of flexibility
Men (not always)
Loose soft tissue
More delicate

More flexible
Women (not always)

Table 3: Distinguishing features between Viking and Flexible Dancer Types (Schleip R, 2017)

At this point, we’ve now discussed the spectrum of hypo- hyper-tonia in the context of differentiating out CNS structural lesions, specific pathoanatomical connective tissue conditions, as well as identifying human variation in connective tissue make-up. 

Let’s next dig into the components of muscle tone and how this may relate to your assessment/management process. 

At this point, I’m going to replace the word, “muscle” with “MYOFASCIA” as it relates to discussions of tone.  Current evidence demonstrates that muscle and connective tissue are intimately connected and thus it becomes difficult to differentiate muscle from connective tissue in the assessment/management process.

Myofascial tone has an active component (CNS-mediated) and a passive component (non-CNS mediated). (Fig 1)

Figure 1: simplified chart to explain the components of muscle tone (Mense S, 2010)

 Let’s discuss the active component first.

The active component of muscle tone comes from nervous system mediation or involvement.  Historically, muscle tone was thought to be purely a neural phenomenon (Frankel and Collins, 1903). Essentially, the belief was that we as humans are able to stand on two feet with a certain amount of muscle tone that helps to hold us up, and that this tone was driven solely by a neurological mechanism. Passive components were not considered during that era. (Masi AT, et al, 2008)

The neural or CNS-mediated component of muscle tone is influenced by a host of factors, both peripheral and central. 

The figure below from Siegfried Mense’s Muscle Pain: Understanding the Mechanisms, (Mense S, 2010) conveys the complexity of inter--connections that influence the alpha motor neuron.  (Fig 2) As you can see from the schematic below, there are large influences from the periphery, such as skin, ligament, myofascia, joint capsule, as well as influences from the brain and all its complexity that all play into ultimately the excitation or not of the alpha motor neuron that leads to muscle contraction or lack thereof.

 Fig 2: Caption: Image taken from Menses S. Muscle Pain: Understanding the Mechanisms, 2010 Note the myriad of afferent input, processing, and efferent output that ultimately contribute to CNS-mediated muscle tone 
CNS-mediated muscle tone can occur for a variety of reasons. 
1.   The experience of pain, for whatever its underlying cause, can produce muscle tone changes. 
2.   Previous movement experiences may also mediate muscle tone via descending input from the brain.  A tissue that has not experienced a particular range of motion in years, for whatever the reason, may reflexively contract during muscle length assessment.  Part of this may be adaptive changes, but part of it may be the nervous system’s way of protecting the tissue/body part from an unfamiliar range. 

The second component of myofascial tone is the contribution from non-contractile or passive component.  It is now understood that a certain component of our ability to stand erect and maintain postural stability comes from passive myofascial tone.  There is both an elastic and viscoelastic compontent to myofascial stiffness.  Elastic stiffness is velocity-independent while viscoelastic stiffness is affected by the speed of movement. (Masi A, 2008)

There are a few theories as to the underlying mechanisms that create the passive component of myofascial tone: (Mense S, 2010)
1.    Small number of cross-bridges between myosin heads and actin filaments that cycle slowly and generate a tensile force = cross-bridge model
2.    Friction between layers of connective tissue and the ability of layers of myofascial tissue to glide past each other


Assessment of Muscle tone in the clinic involves:
1.   Observation
2.   Dynamic palpation
3.   Static palpation

What you observe:
 Look at the human being as a whole, from a global perspective.  How would you characterize your initial impression of the human in front of you on a spectrum of hypo – to normal – to hypertonia.  Refer to the top of this blog, particularly the difference between “Viking type” and “Flexible Dancer” type, to help you develop these quick first impressions.  

After a quick global glance, take a more detailed look at muscle contour, shape, symmetry, size, etc.  These observations may provide clues as to the status of your patient’s motor system.

Next, observe your patient’s movements and movement patterns.  What tissues or areas of the body are contracting? Which areas appear not to be contracting?

What you palpate:
Dynamic Palpation: muscle length assessment:
We are unable to separate out the CNS-mediated vs passive components of muscle tone via muscle length assessment.  Therefore, in order to hypothesize about the contribution of each component to what we’re feeling, we must develop keen palpatory skills.  This occurs with time and deliberate, thoughtful practice.  This art of palpation should be an ongoing skill we all need to hone in on. 

Pay attention to the build-up of resistance as you take the tissue through passive length assessment. 

Questions to ask yourself?
-       Is there an active “fight” to your applied force?
-       Does the limb and the tissue feel active/contracted/unable to relax? 
-       Does this active fight against your force prevent you from reaching what you feel should be the end point of the limb’s available range based on the functional tasks the patient aims to perform and what you know to be the pre-requisites for that particular task? 
-       What do you make of the end-feel? Is it bouncy?

If you are encountering these findings, you may be encountering CNS-mediated tone, for whatever its underlying reason. (pain experience, previous movement repertoire).  When you encounter this and you feel it to be a relevant finding contributing to your patient’s clinical presentation, you then realize you may need to impart an intervention or an input that communicates with the nervous system.  What kinds of interventions communicate with the nervous system? Many. Too many to cover here.

Now that we’ve gone over clues to CNS-mediated tone, what are the clues to passive tone?
Your palpatory findings will tell you. 
-       You would likely recognize an ability of the tissue to relax and let go. 
-       You’d encounter a slower build-up of resistance that ends with a firm end feel that may or may not meet the requirements for what you determine that patient to need for their desired functional task. 
-       Along the way, as you take the limb through its range and feel for the build-up of tension, you may encounter tension in certain areas of the connective tissue at various places in the range.  The interpretation of these findings may be lack of the ability of various layers of the myofascial tissue to appropriately glide past each other. 

Your interventions if you find these areas of tension to be of importance to your patient’s clinical presentation are varied.  Tools and interventions, again, are many.

Ultimately, as stated above, one of your endpoints as you assess muscle length or any sort of passive range testing is the following question:

Does this range meet the requirements necessary for the task my client wants to perform? 

Example: You’re assessing the myofascia of the wrist flexors, or in other words, assessing passive wrist extension range of motion because your client experiences a sensation of tightness in her anterior forearm.  This is just one component of your objective exam as you work to decipher the cause of her perception of tightness.

Scenario 1: You reach an end feel at 70 degrees wrist extension.  Your next step is to relate this finding to the tasks enjoyed and desired by your client.  If your client’s meaningful tasks or movements require more than 70 degrees wrist extension, (there are many, such as pushups, handstands, etc) the underlying cause of this restriction in range of motion needs to be addressed before your client can perform this task.

Scenario 2: You reach an end feel at 105 degrees of wrist extension.  This tells us that your client has enough myofascial tissue length to meet the requirements for many tasks that require wrist extension, in fact more than enough.  You’ll have dig deeper to uncover the root of the perceived tightness experienced by your client.  The tightness in Scenario 2 is not due to a lack of passive range.

Static palpation:

Perform in standing.
Light tapping on tissues may confirm your initial observations about muscle tone.  If what you palpate is firm and springy, the underlying tissue may have a higher degree of tone. A tissue that is softer or looser may be an area of hypotonicity.

Perform in a gravity-eliminated position:
Theoretically, in a gravity-eliminated position, the CNS should no longer be actively mediating muscle tone and tissues should be in a relaxed state.  However, due to a variety of influences, the CNS isn’t always able to “let go” of tissues even when in a supported position.  Your continued observation and palpatory skills will help you hone in on areas of hyper and hypotonicity as you systematically palpate tissues of interest. 
-       Is the entire muscle compartment contracted? Perhaps you’re encountering a muscle spasm. 
-       Are you encountering a hyper-irritable taut band within a muscle belly? Perhaps you’re encountering a trigger point, which may have a passive and an active component to it. 


Ultimately, we’re aiming to uncover our patients’ movement stories.  In the case of this topic, TIGHTNESS, we’re on the hunt to uncover the WHAT and the WHY.  The perception of tightness on the part of our patients may lead them to perform any number of sometimes helpful, and sometimes unhelpful strategies to alleviate it, to include the hypermobile individual with a constant sensation of needing to stretch or “self-crack” various joints, to the older adult who is slow to move initially in the morning due to various areas of the body feeling “tight” or “stiff”, to the discomfort associated with a nerve mobility deficit that produces a type of tightness/discomfort that leads to the instinct to “stretch it away”.

Our challenge as clinicians.

Clinically, each of us, at various points fall prey to quick conclusions or “autopilot” responses to our patients’ perceptions of tightness.  An area is tight? Rub it away. Stretch it.  Tape it.  Scrape it.  Cup it.  Manip it. Slide/glide it, etc.  We may at times, be correct in our assessment from the various clinical patterns we’ve accumulated throughout our careers that lead us to make quick decisions. 

However, it’s imperative for clinicians to recognize that “tightness” is just one of the many unpleasant sensations of the human experience that act as warning signals to indicate that the human feels threatened and needs protection.  We, as clinicians must take time to listen carefully to our patients, perform a thorough and precise examination, and to hypothesize as to the driving factors causing the “threat” and then, get about the business of creating safety, for whatever that entails.

Kelly is a physiotherapist living and practicing in New York City.  Her work and this blog have been influenced by many approaches and teachers, to include Clare Frank and Movement Links, Inc, Dynamic NeuromuscularStabilization, Maitland approach, Movement System Impairment (MSI) approach, The Janda Approach to Muscle Imbalance, Barcelona Scoliosis Physical TherapySchool (BSPTS) Schroth-based method, Functional Range Systems, “ExplainPain” by Lorimer Moseley and David Butler, as well as the greater pain science body of work, and most of all, her patients.


Basmajian JV, D Luca CJ. Muscles alive: their functional revealed by electromyography, 5th ed. Baltimore: Williams & Wilkins; 1985.

Masi AT, Hannon JC. Human resting muscle tone (HRMT): Narrative introduction and modern concepts. Journal of Bodywork and Movement Therapies. 2008;12:320-332.

Masi AT, Nair K, Evans, T, Ghandour Y. Clinical, biomechanical, and physiological translational interpretations of human resting myofascial tone or tension. International Journal of Therapeutic Massage and Bodywork. 2010;3(4):16-28.

Mense S, Gerwin RD. Muscle Pain: Understanding the Mechanisms. Springer Science & Business Media; 2010.

Schleip R, Bayer J. Fascial Fitness- How to be resilient, elegant and dynamic in everyday life and sport. Lotus Publishing; 2017. (English version)

Schleip R, Findley TW, Chaitow L, Huijing PA. Fascia- The Tensional Network of the Human Body. Edinburgh: Churchill Livingstone Elsevier; 2012.

Shumway-Cook A, Wollacott MH. Motor Control- Translating Research into Clinical Practice, 4th ed. Baltimore: Lippincott Williams & Wilkins; 2012.

Weppler CH, Magnusson SP. Increasing muscle extensibility: a matter or increasing length or modifying sensation? Phys Ther. 2010;90:438-449.