Identifying Subtle Clinical Indicators to Diagnose Spasticity

Join Cameron Miller-Patterson, MD, assistant professor of neurology at Virginia Commonwealth University in the movement disorders division, as he unravels mysteries and nuances of spasticity management. Dr Miller-Patterson discusses the subtle clinical indicators, the importance of patient history, and the challenges faced by clinicians. Discover how a meticulous diagnosis influences treatment choices and management plans, and explore the world of spasticity management.

Answers have been lightly edited for clarity. 

Evi Arthur, Neurology Learning Network: What are the key clinical indicators that clinicians should look for when assessing a patient for spasticity, and how do these signs aid in the diagnosis of spasticity-related disorders?

Dr Cameron Miller-Patterson: Spasticity is defined as an increase in muscle tone or a muscle’s stretch reflex, so that there is greater resistance to passive movement than would normally be expected. It is usually described as “velocity-dependent,” meaning that the more a spastic muscle is stretched, the more resistance to passive movement it provides. This is something that can be tested at the bedside to determine whether spasticity is present. Other signs on exam that point towards spasticity are joint contractures due to increased muscle tone, increased deep tendon reflexes, and clonus. Since spasticity develops due to damage to upper motor neuron pathways in the brain or spinal cord, the distribution of spasticity in a given individual can aid in the diagnosis. For example, if one arm and leg are spastic it might suggest damage to one hemisphere of the brain. Alternatively, if both legs are affected, it might suggest damage to the thoracic spinal cord.

Arthur, NLN: What are the various diagnostic tests and imaging techniques used to confirm spasticity? How do these tests help differentiate spasticity from other movement disorders or neurological conditions with similar symptoms?

Dr Miller-Patterson: Spasticity is mostly diagnosed by the exam findings I described. Determining whether or not the increase in muscle tone is “velocity-dependent” is important because rigidity is also defined as an increase in muscle tone that is not velocity-dependent and is often due to different diagnoses such as Parkinson disease. Once you determine that someone has spasticity based on the exam, further workup such as an MRI of the brain or spinal cord may be indicated to further determine the underlying cause of the spasticity, such as stroke, multiple sclerosis, and myelopathy. If there has been a steady progression of weakness and spasticity, an electromyography and nerve conduction study may be indicated to evaluate for diagnoses such as amyotrophic lateral sclerosis.

Arthur, NLN: In your experience, how crucial is a detailed patient history in the assessment of spasticity? Are there specific questions you recommend clinicians ask to get the full picture?

Dr Miller-Patterson: The history is very important in determining the cause of spasticity. Key questions may include when it developed (such as early childhood or adulthood), whether there were other symptoms prior to the development of spasticity, such as dysphagia, weakness, numbness, or changes in bowel or bladder function, whether there was any trauma preceding the development of spasticity such as a head injury or fall, and whether there is any family history of spasticity that might point towards a genetic etiology.

Arthur, NLN: What are the common challenges or complexities faced by clinicians when diagnosing spasticity, especially in cases where symptoms are subtle or overlap with other neurological conditions? How do you approach these challenges in your clinical practice?

Dr Miller-Patterson: Oftentimes the cause of spasticity is clear from the history and from further workup. For example, diagnoses that lead to spasticity such as stroke, multiple sclerosis, and myelopathy can usually be determined from an MRI. One challenge may be distinguishing spasticity from rigidity as I discussed previously, since they are both defined as an increase in muscle tone but the diagnoses associated with each are usually different.

Arthur, NLN: In the context of spasticity management, how important is it to establish an accurate diagnosis, and how does the diagnosis influence the choice of treatment options? How do you approach personalized treatment plans for patients?

Dr Miller-Patterson: Determining the underlying cause of spasticity can be important for management of that specific diagnosis. For example, determining that spasticity is due to underlying multiple sclerosis may be important for the initiation of disease-modifying therapies, or for determining appropriate secondary stroke prevention if due to a prior stroke. It is also important as prognostic information for the patient and family. For example, if spasticity is due to cerebral palsy, we would not expect to see a dramatic progression in functional limitations over time, whereas we would in someone who has spasticity due to amyotrophic lateral sclerosis. Regardless of the underlying etiology, there are therapies that can be utilized to alleviate the symptoms of spasticity such as pain and stiffness. These include oral muscle relaxants like baclofen or tizanidine, as well as botulinum toxin injections into the affected muscles. 

Cameron Miller-Patterson, MD, is an assistant professor of neurology at Virginia Commonwealth University in the Movement Disorders Division. His clinical interests include Parkinson disease and other movement disorders, deep brain stimulation programming, and implementation of botulinum toxin injections for the treatment of a variety of movement disorders.