Beyond the Diagnosis: Clinical Evaluation and Management of Spasticity

Oliver Hart

Curious guide/storyteller

Claire Brooks

Spasticity and rehabilitation expert

Oliver Hart

I've got a patient with a flexed elbow. Modified Ashworth two. Easy. Spastic elbow flexors. Inject the biceps.

Claire Brooks

Maybe.

Oliver Hart

Oh, here we go.

Claire Brooks

What's stopping the elbow from extending?

Oliver Hart

The spasticity.

Claire Brooks

You don't know that yet. Could be spasticity. Could be a contracture. Could be weak triceps. Could be abnormal cocontraction of flexors and extensors. Could be an associated reaction. Could be pain. Could be dystonia. Could be multiple things at once.

Oliver Hart

But the Ashworth score is two.

Claire Brooks

That tells you there is resistance to passive movement. It does not tell you that the resistance is the reason the patient cannot reach for a cup. And it definitely does not tell you what to treat.

Oliver Hart

So today's lesson is-HOST B: Stop treating numbers. Treat problems. SEGMENT 1 - FIRST, STOP CALLING EVERYTHING SPASTICITY

Oliver Hart

Let's clean up the vocabulary. Someone has an upper motor neuron lesion. Their limb feels tight. Is that spasticity?

Claire Brooks

Not automatically. Spasticity is only one component of the upper motor neuron syndrome. Other manifestations include weakness, exaggerated reflexes, clonus, impaired coordination, abnormal motor control, problems with motor planning, and over time contracture and mechanical muscle changes.

Oliver Hart

So "tightness" is a symptom. Not a diagnosis.

Claire Brooks

Exactly. SEGMENT 2 - THE CLASSIC DEFINITION: VELOCITY MATTERS

Oliver Hart

What's the physiologic hallmark that separates spasticity from just being stiff?

Claire Brooks

Velocity dependence. Classically, spasticity refers to an exaggerated stretch-reflex response in which resistance increases when the muscle is stretched more rapidly.

Oliver Hart

So if I move the elbow slowly and it moves fairly easily, but a fast stretch produces a catch-HOST B: That is much more suggestive of spasticity.

Oliver Hart

And if resistance is there equally at every speed?

Claire Brooks

Now you need to think beyond classic spasticity: fixed contracture, mechanical stiffness, rigidity, or other causes of hypertonia. Spastic muscle responses are also length- and position-dependent, which SEGMENT 3 - THE STRETCH REFLEX, WITHOUT MAKING IT MISERABLE

Claire Brooks

Fair. Think of the muscle spindle as a motion sensor embedded inside muscle. When the muscle is stretched, the spindle detects how much muscle length changed and how quickly. Group Ia afferents are especially sensitive to rate of change. That information enters the spinal cord and increases alpha motor neuron activity back to the same muscle, causing it to contract and resist the stretch.

Oliver Hart

Built-in length protection.

Claire Brooks

Exactly. At the same time, Ia inhibitory interneurons help relax the antagonist. That is reciprocal inhibition. Gamma motor neurons tune spindle sensitivity, spinal inhibitory circuits regulate the arc, and SEGMENT 4 - THE CORTICOSPINAL TRACT IS NOT THE WHOLE SPASTICITY STORY

Oliver Hart

Here is something I think surprises people. Damage the corticospinal tract-you get spasticity. Right?

Claire Brooks

Not necessarily. An isolated corticospinal tract lesion tends to cause weakness, loss of dexterity, hypotonia, and hyporeflexia rather than classic spasticity.

Oliver Hart

Wait. So what pathway are we blaming?

Claire Brooks

A major part of the model focuses on the reticulospinal system, especially imbalance between SEGMENT 5 - THE RETICULOSPINAL BRAKE AND GAS PEDAL

Oliver Hart

Make the reticulospinal tract memorable.

Claire Brooks

Imagine spinal reflex excitability controlled by a brake and an accelerator. The dorsal reticulospinal tract contributes strong inhibitory influence-think brake. The medial reticulospinal tract has more facilitatory influence-think accelerator. The vestibulospinal tract also adds facilitatory input. After certain UMN lesions, inhibitory drive is disproportionately lost. Now the accelerator has less opposition and reflex excitability rises.

Oliver Hart

So spasticity is not simply "the corticospinal tract broke."

Claire Brooks

Correct. It is about the broader descending network controlling spinal reflex excitability.

Oliver Hart

True or false: a completely isolated corticospinal lesion is expected to produce severe spasticity.

Claire Brooks

False according to the model presented in the chapter.

Oliver Hart

Loss of descending inhibitory control contributes to-HOST B: Increased spinal reflex excitability.

Oliver Hart

Major brainstem pathway implicated?

Claire Brooks

Reticulospinal system. SEGMENT 6 - WHY SPASTICITY OFTEN APPEARS LATER

Oliver Hart

If inhibitory pathways are damaged during the original stroke or SCI, why is everyone not immediately spastic?

Claire Brooks

Because the nervous system changes over time. Immediately after major CNS injury, patients may pass through a period of shock and decreased reflex activity. Then reflexes gradually return and hyperreflexia and muscle overactivity may emerge later. This evolution supports the idea of plastic rearrangement in the brain and spinal cord, often becoming evident within the first several weeks after injury.

Oliver Hart

So spasticity is partially a story about neuroplasticity.

Claire Brooks

Exactly-but not necessarily good neuroplasticity. The chapter asks whether it may represent maladaptive plasticity. SEGMENT 7 - BRUNNSTROM: SPASTICITY CAN RISE AND THEN FALL

Oliver Hart

Let's use stroke. Patient starts flaccid. Then tone increases. Later the tone may decrease as selective movement returns.

Claire Brooks

That is the classic Brunnstrom-type progression: flaccidity; then synergies with some spasticity; marked spasticity; movement beginning out of synergy with less spasticity; then increasingly selective and coordinated control if recovery continues.

Oliver Hart

So getting more spastic early in recovery does not automatically mean neurologic deterioration.

Claire Brooks

Correct. Context matters. SEGMENT 8 - SPASTICITY IS DYNAMIC

Oliver Hart

Does spasticity stay constant through the day?

Claire Brooks

Not necessarily. Muscle overactivity can vary with posture, pain, temperature, emotion, time of day, breathing, and noxious stimuli.

Oliver Hart

Which explains the classic inpatient call: "He was fine yesterday and suddenly his tone is terrible."

Claire Brooks

Exactly. Before increasing baclofen, ask about UTI, constipation, pressure injury, ingrown toenail, pain, catheter issues, or a new neurologic problem. Increased tone can be a signal, not merely a treatment THING

Oliver Hart

Let's distinguish some terminology. Clonus.

Claire Brooks

Rhythmic involuntary contraction that produces oscillation-classically at the ankle. It is conceptualized as recurrent activation of stretch reflexes.

Oliver Hart

Flexor spasm?

Claire Brooks

A withdrawal-type response often triggered by sensory input, particularly important after spinal cord injury. With loss of descending inhibition, relatively ordinary stimuli may trigger an exaggerated flexor response.

Oliver Hart

Tonic spasticity?

Claire Brooks

Sustained exaggerated stretch-reflex activity when the muscle is held under prolonged stretch.

Oliver Hart

Does spasticity look the same after stroke and SCI?

Claire Brooks

No. Supraspinal lesions often produce stereotyped antigravity postures and synergies; after stroke, upper-extremity flexor patterns are common. Spinal cord lesions can produce more prominent spasms and flexor-reflex activity. In complete SCI, both excitatory and inhibitory descending influences are absent, leaving spinal networks disinhibited in a different way.

Claire Brooks

Beyond the Diagnosis - Episode 4: Spasticity | 5

Oliver Hart

So far everything sounds neural. But chronic paresis changes muscle mechanically too.

Claire Brooks

Exactly. If a weak muscle remains shortened, it adapts: sarcomeres are lost, muscle fibers stiffen, and tendon and muscle compliance change. Eventually mechanical resistance becomes part of the clinical picture.

Oliver Hart

Meaning neural spasticity and structural stiffness can coexist.

Claire Brooks

Exactly. And botulinum toxin cannot chemically reverse a mature fixed contracture.

Oliver Hart

We finally reach the patient. What is question number one?

Claire Brooks

Not "What is the Ashworth score?" Ask: What is the problem? What is the main cause of the problem? What other factors contribute to the problem?

Oliver Hart

That may be the whole chapter.

Claire Brooks

Pretty close. SEGMENT 13 - PATIENTS DO NOT COME IN SAYING MY SPASTICITY IS WORSE

Oliver Hart

What do they actually say?

Claire Brooks

"My arm is tight." "My fist will not open." "My foot turns in." "I trip." "I cannot reach." "I cannot clean my hand." "My leg kicks at night." "I cannot get my brace on." These complaints often reflect multiple SEGMENT 14 - THE CLASSIC TRAP: WEAKNESS MASQUERADING AS SPASTICITY

Oliver Hart

Patient has a flexed elbow posture. What is your first thought?

Claire Brooks

Many people think overactive elbow flexors. But the posture could result from hypertonic flexors, weak extensors, both flexors and extensors being overactive with flexors predominating, or a fixed contracture.

Oliver Hart

So posture does not tell you mechanism.

Claire Brooks

Exactly. SEGMENT 15 - CASE 1: WHY BACLOFEN MADE THE PATIENT TRIP MORE

Oliver Hart

The chapter gives a middle-aged man with remote brain injury, trouble reaching, foot drop, and baclofen that makes the arm looser but causes more tripping.

Claire Brooks

The exam suggested his reaching problem was not simply flexor spasticity. During elbow extension he had abnormal agonist-antagonist cocontraction and associated finger flexion. In the leg he had dorsiflexor weakness plus plantar-flexor contracture. Baclofen may reduce tone while simultaneously exposing-or worsening the impact of-underlying weakness.

Oliver Hart

High-yield point: tone can occasionally be functionally useful.

Claire Brooks

Exactly. If someone with incomplete SCI relies on extensor tone to stand, aggressively reducing that tone may impair transfers or walking.

Oliver Hart

WHAT IS ACTUALLY CAUSING THE PROBLEM?

Oliver Hart

Flexed elbow that cannot passively extend even with slow sustained stretch.

Claire Brooks

Think contracture or mechanical restriction.

Oliver Hart

Full passive range slowly, but catch with rapid stretch.

Claire Brooks

Spasticity.

Oliver Hart

Patient extends elbow and fingers suddenly flex.

Claire Brooks

Associated reaction or synkinesis.

Oliver Hart

Elbow extension jerks because flexors and extensors fire together.

Claire Brooks

Abnormal cocontraction.

Oliver Hart

Patient cannot dorsiflex despite minimal plantar-flexor tone.

Claire Brooks

Weakness may be the primary problem.

Oliver Hart

Even if I prove spasticity exists, that still does not tell me why the patient cannot perform the task.

Claire Brooks

Correct. Motor performance may also be impaired by weakness, loss of dexterity, sensory loss, visual-field cut, neglect, pain, cognitive impairment, apraxia, and coordination deficits. Successful THE JOINT

Oliver Hart

If focal treatment is appropriate, now you need anatomy. Shoulder adduction?

Claire Brooks

Pectoralis major and minor, latissimus dorsi, and sometimes coracobrachialis depending on posture.

Oliver Hart

Shoulder internal rotation?

Claire Brooks

Subscapularis, teres major, pectoralis major and minor.

Oliver Hart

Elbow flexion?

Claire Brooks

Brachialis, biceps, brachioradialis, with pronator teres sometimes contributing.

Oliver Hart

Forearm pronation?

Claire Brooks

Pronator teres and pronator quadratus.

Oliver Hart

Finger flexion?

Claire Brooks

Flexor digitorum superficialis and profundus.

Oliver Hart

Thumb flexion?

Claire Brooks

Flexor pollicis longus and brevis depending on the pattern.

Oliver Hart

Hip adduction?

Claire Brooks

Adductor complex.

Oliver Hart

Knee flexion?

Claire Brooks

Hamstrings, with gastrocnemius potentially contributing.

Oliver Hart

Equinovarus?

Claire Brooks

Often some combination of gastrocnemius, soleus, tibialis posterior, and other invertor or toe-flexor contributions depending on the exact posture.

Claire Brooks

SEGMENT 18 - GOALS BEFORE NEEDLES

Oliver Hart

Now we are getting to management. What comes first?

Claire Brooks

Goals. Before oral medication. Before botulinum toxin. Before phenol. Before a pump. The patient and clinician need to agree on what successful treatment would actually look like. SEGMENT 19 - SMARTER GOALS

Oliver Hart

Make SMARTER useful.

Claire Brooks

Specific. Measurable and meaningful. Agreed upon. Realistic. Time-bound. Evaluated. Revised.

Oliver Hart

Bad goal: "Reduce spasticity."

Claire Brooks

Terrible.

Oliver Hart

Better?

Claire Brooks

"Allow the caregiver to open the hand sufficiently for palm hygiene without pain within six weeks." Or "Improve active elbow extension enough to place the forearm on the keyboard." Or "Reduce nocturnal spasms so the patient sleeps at least six uninterrupted hours."

Oliver Hart

Those goals tell you whether treatment worked.

Claire Brooks

Exactly. TREAT

Oliver Hart

Woman with right finger tightness after basal ganglia hemorrhage. She cannot lift her index finger off the keyboard while typing. Ashworth score of the finger flexors? Zero.

Claire Brooks

Yet the finger flexors are still functionally implicated during the task. Passive tone testing did not reproduce the movement-dependent problem. Meanwhile her shoulder had an Ashworth score of one, but shoulder tightness was not interfering with hygiene, dressing, or function. The clinician targeted the muscles causing the meaningful task limitation rather than the muscles with the higher score.

Oliver Hart

That is such a PM&R lesson.

Claire Brooks

The score is a data point. The patient is the outcome.

Oliver Hart

What is the fundamental problem with Ashworth?

Claire Brooks

It measures resistance to passive movement. That resistance can arise from reflex activity, mechanical stiffness, contracture, other forms of hypertonia, and examiner technique. So it is not a pure measure of spasticity.

Oliver Hart

Which is why someone can have meaningful task-triggered overactivity with an Ashworth zero.

Claire Brooks

Correct. SEGMENT 22 - TARDIEU: BRING VELOCITY BACK INTO THE EXAM

Oliver Hart

Why does the chapter like the Tardieu conceptually?

Claire Brooks

Because the defining physiology of spasticity involves velocity-dependent stretch responses. Tardieu evaluates muscle response at different stretch velocities and pays attention to the angle of catch.

Claire Brooks

Comparing fast versus slow stretch helps separate dynamic reflex overactivity from fixed mechanical shortening. SEGMENT 23 - THE FOUR-PART CLINICAL EXAM

Oliver Hart

Give me a bedside sequence.

Claire Brooks

Observation: look at posture at rest and how it changes with position. Active examination: watch movement, active range, strength, coordination, cocontraction, associated reactions, and pain. Passive examination: assess passive ROM, resistance, velocity-dependent catch, clonus, rigidity, and contracture. Functional examination: watch gait and actual tasks-reach, type, transfer, walk, pour water-whatever reproduces the real problem. SEGMENT 24 - HISTORY QUESTIONS THAT ACTUALLY MATTER

Oliver Hart

Let's make a practical spasticity history.

Claire Brooks

Ask whether the limb is always tight or only sometimes; whether position or movement triggers it; whether spasms or pain are present; whether there is skin breakdown; whether hygiene, splints, dressing, reaching, hand use, transfers, or walking are affected; what treatments were tried and what happened; SEGMENT 25 - BEFORE TREATMENT: SPASTICITY OR CONTRACTURE?

Oliver Hart

Treatment decision one: spasticity or contracture?

Claire Brooks

Exactly. If the primary limitation is fixed joint deformity or mature soft-tissue shortening, reducing neural reflex activity may not restore motion. If the limitation is predominantly dynamic overactivity, pharmacologic treatment may be much more useful. Often both coexist.

Oliver Hart

Next decision?

Claire Brooks

Distribution. A single muscle group is focal. Multiple groups in one or two limbs may be multifocal or regional. More generalized involvement makes systemic or intrathecal strategies more relevant. Focal problems often pair with chemodenervation, generalized problems with oral or intrathecal therapies, and rehabilitation interventions continue across all levels. SEGMENT 27 - THERAPY IS NOT THE WEAK OPTION

Oliver Hart

Before drugs.

Claire Brooks

Physical modalities: stretching, positioning, splinting, casting, orthoses, strengthening, motor retraining, task practice, and adaptive devices. These are commonly used first-line strategies because they are widely available and generally lower risk than medication. SEGMENT 28 - ORAL MEDICATIONS: THE FIRST BIG TRADEOFF

Oliver Hart

Oral drugs. What is the central problem?

Claire Brooks

They are systemic. You may want to relax one problematic limb, but the medication reaches the entire nervous system or body. Common limitations include sedation, drowsiness, weakness, dizziness, and hypotension depending on the drug. Reducing tone can unmask weakness and impair mobility in some patients. SEGMENT 29 - BACLOFEN

Oliver Hart

Baclofen.

Claire Brooks

GABA-B agonist. It reduces spinal reflex activity and is one of the most widely used oral antispastic agents. Important adverse effects include drowsiness and weakness. Do not abruptly discontinue it: withdrawal can produce rebound spasticity, hallucinations, and seizures.

Oliver Hart

Board pearl: baclofen withdrawal is not just "tone comes back."

Claire Brooks

Correct. It can be dangerous.

Oliver Hart

Tizanidine.

Claire Brooks

Alpha-2 adrenergic agonist. It decreases excitatory interneuronal signaling and can reduce tonic and phasic reflex activity. Tradeoffs include sedation, hypotension, and dry mouth. Someone with painful nocturnal spasms may benefit from the combination of spasm reduction, analgesic effect, and sedation, but orthostatic hypotension can make it a poor choice for another patient. SEGMENT 31 - DANTROLENE

Oliver Hart

Different mechanism.

Claire Brooks

Very. Dantrolene acts directly on skeletal muscle by reducing calcium release from the sarcoplasmic reticulum. Weakness remains an issue, and potential hepatotoxicity makes liver-function monitoring important. SEGMENT 32 - BENZODIAZEPINES AND GABAPENTIN

Oliver Hart

Benzodiazepines.

Claire Brooks

GABA-A activity. They can reduce muscle overactivity, but sedation limits use, and abrupt cessation carries withdrawal risk.

Oliver Hart

Gabapentin.

Claire Brooks

More often used for neuropathic pain and seizures, but it may have spasmolytic effects. Sedation and dizziness matter. RAPID-FIRE MEDICATION ROUND

Oliver Hart

Baclofen receptor?

Claire Brooks

GABA-B.

Oliver Hart

Tizanidine?

Claire Brooks

Alpha-2 adrenergic agonist.

Claire Brooks

Skeletal muscle.

Oliver Hart

Major dantrolene toxicity?

Claire Brooks

Hepatotoxicity.

Oliver Hart

Oral spasmolytic problem shared by several drugs?

Claire Brooks

Sedation and weakness.

Oliver Hart

Never abruptly stop?

Claire Brooks

Baclofen-and benzodiazepines also require caution with withdrawal. SEGMENT 33 - WHEN FOCAL TREATMENT MAKES MORE SENSE

Oliver Hart

If the problem is two finger flexors, why sedate the entire patient?

Claire Brooks

Exactly. If the problem is focal, treatment should often be focal. This is where chemodenervation becomes attractive.

Oliver Hart

Give me botulinum toxin without the molecular biochemistry exam.

Claire Brooks

It inhibits acetylcholine release at the neuromuscular junction. The toxin interferes with SNARE proteins required for synaptic vesicle release. Less acetylcholine means less muscle activation. Clinical effect develops over several days and lasts on the order of months.

Oliver Hart

Botox lowers tone. Does that automatically improve hand function?

Claire Brooks

No. Reducing muscle overactivity does not automatically translate into better activity and participation. If the goal is palm hygiene, orthotic fit, pain reduction, or passive ROM, success may be SEGMENT 36 - THERAPEUTIC WEAKNESS

Oliver Hart

Botulinum toxin literally weakens muscle. Why would weakening a muscle ever improve active movement?

Claire Brooks

Sometimes the overactive antagonist blocks the movement you want. Weakening it can reduce abnormal cocontraction and permit the agonist to express remaining voluntary control. The weakness is SEGMENT 37 - GUIDANCE MATTERS

Oliver Hart

Do you just palpate the muscle and inject?

Claire Brooks

Guidance strategies include EMG, electrical stimulation, and ultrasound. Anatomic localization alone is less reliable in many situations. The key is getting toxin into the correct muscle, because no amount of dosing sophistication rescues a wrong target.

Oliver Hart

Patient says: "Botox did not work." What questions do you ask?

Claire Brooks

Was the diagnosis correct? Was spasticity actually the problem? Was the right muscle selected? Was the dose appropriate? Was injection technique adequate? Were the goals realistic? Was there a

Claire Brooks

contracture? Did the patient need therapy afterward? Was there true biologic nonresponse or immunoresistance? Poor response can be patient-related, injector-related, or drug-related.

Oliver Hart

So "toxin failure" may really be clinical-reasoning failure.

Claire Brooks

Exactly. SEGMENT 39 - PHENOL AND ALCOHOL NEUROLYSIS

Oliver Hart

Before botulinum toxin, what did people use for focal treatment?

Claire Brooks

Phenol and alcohol nerve blocks. These agents chemically injure neural tissue and block transmission. Potential targets include the obturator nerve for adductor overactivity, tibial branches for plantar-flexor patterns, and musculocutaneous branches for elbow flexors.

Oliver Hart

Big difference from botulinum toxin?

Claire Brooks

Phenol is neurolytic; botulinum toxin produces reversible neuromuscular blockade. Phenol can work quickly and be cost-effective, but carries particular risks-especially when mixed sensory-motor nerves PILL OR NEEDLE

Oliver Hart

Now the pump. Who is the patient?

Claire Brooks

Usually someone with severe, more generalized spasticity or spasms that remain problematic despite less invasive management. Intrathecal baclofen delivers baclofen directly into CSF near spinal targets, allowing powerful spinal effect at much smaller doses than oral therapy, though pump therapy SEGMENT 41 - THE ITB TRIAL

Oliver Hart

You do not just implant the pump.

Claire Brooks

Correct. A screening trial is typically performed first. But you are not merely asking whether the Ashworth score dropped. You may ask whether painful spasms improved, positioning improved, transfers became easier, caregivers gained better hygiene access, or the patient tolerated therapy better.

Oliver Hart

And if the patient becomes weak during the trial?

Claire Brooks

That may mean the spasticity was masking weakness. It does not necessarily mean ITB is impossible; it may mean the eventual dose should be lower.

Oliver Hart

Pump goes in. Done?

Claire Brooks

Definitely not. Ongoing dose titration, pump refills, system maintenance, patient and caregiver education, and monitoring for complications make this a longitudinal treatment relationship. SEGMENT 43 - ITB WITHDRAWAL: KNOW THIS COLD

Oliver Hart

This is one of the most important safety sections in the chapter. Intrathecal baclofen withdrawal.

Claire Brooks

Absolutely. Early clues may include sudden recurrence or dramatic worsening of spasticity, increased spasms, agitation, and change from baseline. Severe manifestations can include hyperthermia, seizures, autonomic instability, rhabdomyolysis, multiorgan complications, and death.

Oliver Hart

Which can look like sepsis.

Claire Brooks

Exactly. Sudden recurrent spasticity plus systemic deterioration in a patient dependent on intrathecal baclofen should raise immediate concern for withdrawal.

Oliver Hart

Young woman with chronic anoxic brain injury, ITB pump, previously controlled seizures. Family notices she is suddenly much tighter and not herself. Then fever, seizures, extreme hyperthermia, and status epilepticus.

Claire Brooks

The initial concern for infection is understandable, but the combination of sudden recurrent spasticity plus systemic deterioration should prompt urgent evaluation of pump and catheter integrity and restoration of baclofen delivery. Supportive medications may help, but they do not replace restoring intrathecal baclofen.

Oliver Hart

ITB patient suddenly much tighter than baseline. First thought?

Claire Brooks

Look for common noxious triggers-but also immediately consider pump or catheter dysfunction.

Oliver Hart

Severe withdrawal plus fever and seizures can imitate?

Claire Brooks

Sepsis or another hypermetabolic syndrome.

Oliver Hart

Definitive treatment?

Claire Brooks

Restoration of intrathecal baclofen delivery. SEGMENT 45 - CONTRACTURE IS A DIFFERENT PROBLEM

Oliver Hart

If the patient has a fixed ankle equinus contracture, what happens if you keep escalating antispastic medication?

Claire Brooks

You may reduce neural tone without changing the fixed mechanical deformity. At some point, the treatment has to match the tissue problem: serial casting, orthotic management, or sometimes surgical

Oliver Hart

What role does surgery play?

Claire Brooks

Primarily treatment for fixed deformity and contracture rather than spasticity itself. Options include tendon lengthening, tendon transfer, peripheral neurotomy, and dorsal rhizotomy in selected populations. Tendon procedures change joint mechanics and resting alignment; they do not eliminate the abnormal CNS stretch reflex.

Oliver Hart

So once again: posture and spasticity are not synonymous.

Oliver Hart

Do we ever intentionally leave spasticity alone?

Claire Brooks

Absolutely. If tone helps the patient stand, helps transfers, maintains limb bulk, assists venous return, or simply is not causing pain, hygiene problems, skin problems, deformity, or functional limitation, there may be no reason to treat it aggressively.

Oliver Hart

A tone score is not an indication for treatment.

Claire Brooks

Exactly. SEGMENT 48 - WHEN SHOULD WE TREAT?

Oliver Hart

Give me practical indications.

Claire Brooks

Treatment becomes more compelling when muscle overactivity contributes to pain, skin compromise, poor hygiene, difficulty dressing, difficulty fitting orthoses, loss of ROM, progressive contracture risk, sleep disruption, caregiver burden, impaired gait, impaired transfers, impaired upper-extremity function, SEGMENT 49 - THE MANAGEMENT ALGORITHM

Oliver Hart

Give me the mental algorithm.

Claire Brooks

One: What is the patient's actual problem? Two: Is spasticity really the main cause? Three: Is there a fixed contracture? Four: Is the problem focal, regional, multifocal, or generalized? Five: What function or complication are we trying to change? Six: What is the least burdensome treatment capable of achieving that goal? Seven: How will we know whether it worked?

Oliver Hart

That is much better than Ashworth two equals Botox.

Claire Brooks

Much better.

Oliver Hart

Patient after stroke has a clenched fist. Caregiver cannot clean the palm. No meaningful active hand function. Passive finger extension is possible, but fast stretch produces marked resistance. What is the goal?

Claire Brooks

Probably not restoring fine motor hand function if none exists. A realistic goal may be improving hand opening enough for hygiene, preventing skin maceration, improving splint tolerance, or reducing pain.

Oliver Hart

Treatment?

Claire Brooks

Potentially focal chemodenervation of relevant finger and thumb flexors combined with stretching,

Oliver Hart

Incomplete SCI. Patient has strong extensor tone and uses it to stand and transfer. They complain the legs feel stiff. Do you eliminate the tone?

Claire Brooks

Not automatically. First determine whether the stiffness actually impairs function. Aggressively reducing tone may expose underlying weakness and worsen transfers or ambulation. Maybe the correct target is nocturnal spasms rather than daytime extensor tone. CLINICAL CASE - THE FOOT THAT TURNS IN

Oliver Hart

Poststroke patient walks with equinovarus. Is that plantar-flexor spasticity?

Claire Brooks

Maybe. Examine plantar-flexor overactivity, tibialis posterior, tibialis anterior, toe flexors, dorsiflexor weakness, contracture, selective motor control, knee position, hip strategy, and then observe gait.

Oliver Hart

Again: treat the gait pattern, not a presumed muscle. MASTER RAPID-FIRE ROUND

Oliver Hart

Spasticity is one feature of what larger syndrome?

Claire Brooks

Upper motor neuron syndrome.

Oliver Hart

Defining stretch characteristic?

Claire Brooks

Velocity-dependent increase in resistance or stretch-reflex activity.

Oliver Hart

Isolated corticospinal damage causes classic spasticity?

Claire Brooks

Not necessarily; the chapter emphasizes weakness and loss of dexterity rather than spasticity.

Oliver Hart

Major descending pathway implicated in spasticity?

Claire Brooks

Reticulospinal system.

Oliver Hart

Fixed resistance at slow and fast stretch?

Claire Brooks

Think contracture or nonreflex mechanical stiffness.

Oliver Hart

Rhythmic stretch-induced oscillation?

Claire Brooks

Clonus.

Oliver Hart

Task-triggered involuntary movement elsewhere?

Claire Brooks

Associated reaction or synkinesis.

Oliver Hart

Passive tone score tells you function?

Claire Brooks

No.

Oliver Hart

Scale that better captures velocity dependence?

Claire Brooks

Tardieu.

Oliver Hart

First clinical question?

Claire Brooks

What is the actual problem?

Oliver Hart

Baclofen receptor?

Claire Brooks

GABA-B.

Oliver Hart

Tizanidine receptor?

Claire Brooks

Alpha-2 adrenergic.

Oliver Hart

Dantrolene acts primarily where?

Claire Brooks

Skeletal muscle.

Oliver Hart

Dantrolene lab concern?

Claire Brooks

Liver toxicity.

Oliver Hart

Focal problem affecting two muscles?

Claire Brooks

Consider focal treatment rather than automatically using systemic medication.

Oliver Hart

Botulinum toxin action?

Claire Brooks

Blocks acetylcholine release at the neuromuscular junction.

Oliver Hart

Does Botox guarantee improved activity?

Claire Brooks

No.

Oliver Hart

Why might intentional muscle weakness improve movement?

Claire Brooks

By reducing an overactive antagonist or abnormal cocontraction.

Oliver Hart

Chemical neurolysis agents?

Claire Brooks

Phenol and alcohol.

Oliver Hart

Generalized severe refractory spasticity?

Claire Brooks

Consider intrathecal therapy in appropriate patients.

Oliver Hart

Sudden severe tone increase in an ITB patient?

Claire Brooks

Consider withdrawal or pump/catheter malfunction.

Oliver Hart

ITB withdrawal can cause seizures and hyperthermia?

Claire Brooks

Yes.

Oliver Hart

Fixed deformity?

Claire Brooks

Think contracture and mechanical management, sometimes surgery.

Oliver Hart

Tone can sometimes be functional?

Claire Brooks

Yes.

Oliver Hart

Most important treatment outcome?

Claire Brooks

Achievement of a meaningful patient- or caregiver-centered goal. SEGMENT 50 - THE FIVE QUESTIONS TO ASK BEFORE YOU INJECT ANYTHING

Oliver Hart

I want something residents can carry into Botox clinic tomorrow. Five questions.

Claire Brooks

One: What specific activity, symptom, or care problem are we trying to improve? Two: Is muscle overactivity actually causing that problem? Three: Which muscle or muscles are responsible for the unwanted posture or movement? Four: Is the limitation dynamic, or is there a fixed contracture? Five: How will we objectively know if the injection worked?

Oliver Hart

And "Ashworth went from two to one" may not be enough.

Claire Brooks

Correct. If the patient still cannot accomplish the intended task, the physiologic effect may not equal clinical success.

Oliver Hart

Three things. Everything else disappears. What stays?

Claire Brooks

Takeaway One: Tightness does not equal spasticity-and spasticity does not equal disability. Spasticity exists within a much larger upper motor neuron syndrome. Weakness, contracture, cocontraction, motor-control deficits, sensory impairment, and other abnormalities may contribute more to the patient's problem than tone itself.

Oliver Hart

Number two?

Claire Brooks

Takeaway Two: Treat a meaningful problem, not an examination score. An Ashworth score does not tell you whether treatment is necessary. Start with the patient's functional complaint. Set a specific goal. Then select the treatment that fits the distribution and mechanism of the problem.

Oliver Hart

And number three?

Claire Brooks

Takeaway Three: Spasticity treatment is a toolbox, not a ladder. Stretching. Casting. Orthoses. Task-specific therapy. Oral medication. Botulinum toxin. Phenol. Intrathecal therapy. Surgery. These can be combined. The right treatment depends on whether the problem is focal or generalized, dynamic or fixed, helpful or harmful-and what the patient is actually trying to accomplish.

Oliver Hart

So do not ask: "How do I reduce the tone?"

Claire Brooks

Ask: "What is preventing this person from functioning-and which part of that problem is actually treatable?"

Oliver Hart

That is Spasticity.

Claire Brooks

And please stop injecting every muscle with an Ashworth score of one.

Oliver Hart

Somewhere an insurance reviewer just felt a disturbance in the Force.

Oliver Hart

What distinguishes spasticity from fixed stiffness?

Claire Brooks

Velocity dependence.

Oliver Hart

What larger syndrome includes spasticity?

Claire Brooks

Upper motor neuron syndrome.

Oliver Hart

Name three other features.

Claire Brooks

Weakness, hyperreflexia, clonus, impaired coordination, or impaired motor control-any three.

Oliver Hart

Resistance at all velocities with loss of passive ROM?

Claire Brooks

Think contracture or mechanical stiffness.

Oliver Hart

Why may oral baclofen worsen walking?

Claire Brooks

Tone reduction may expose underlying weakness.

Oliver Hart

What does an Ashworth score primarily reflect?

Claire Brooks

Resistance to passive movement.

Oliver Hart

Which bedside method better incorporates stretch velocity?

Claire Brooks

Tardieu.

Oliver Hart

What should precede treatment selection?

Claire Brooks

Identification of the specific problem and meaningful treatment goal.

Oliver Hart

Focal finger-flexor problem?

Claire Brooks

Consider focal management such as chemodenervation rather than automatically using systemic medication.

Oliver Hart

Botulinum toxin mechanism?

Claire Brooks

Inhibition of acetylcholine release at the neuromuscular junction.

Oliver Hart

Phenol mechanism?

Oliver Hart

Beyond the Diagnosis - Episode 4: Spasticity | 17

Claire Brooks

Chemical neurolysis.

Oliver Hart

Severe generalized spasticity refractory to other management?

Claire Brooks

Intrathecal baclofen may be considered in selected patients.

Oliver Hart

Sudden severe spasticity plus fever and seizures in an ITB patient?

Claire Brooks

Intrathecal baclofen withdrawal should be among the urgent possibilities.

Oliver Hart

Does tendon lengthening eliminate the abnormal CNS stretch reflex?

Claire Brooks

No. It primarily changes mechanical alignment and tendon length.

Oliver Hart

And the most important question in spasticity management?

Claire Brooks

What meaningful problem are we trying to solve? management should be individualized to the patient and clinical setting.