Spasticity and autonomic dysreflexia

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Loss of descending inhibition after brain or cord injury makes spinal stretch circuits hyperexcitable. Velocity-dependent resistance, exaggerated reflexes and clonus can coexist with weakness and poor selective control. Secondary shortening and contracture become less reversible with time. The practical question is not whether tone exists but what it does: a flexed hand may impair hygiene, adductor spasm may obstruct care, extensor tone may enable a transfer, and reducing all tone can leave a person unable to stand.

Spasticity management begins with triggers and a goal. Infection, retention, constipation, skin damage, fracture and poorly fitting seating can increase nociceptive input and tone. Physical strategies address posture and range; oral medicines affect the whole body and can worsen sedation or weakness; focal toxin targets selected muscles; intrathecal therapy provides powerful generalised effect with pump-related risk. Review measures pain, sleep, care, walking and participation as well as passive resistance.

Autonomic dysreflexia is a separate emergency of high spinal injury. A noxious stimulus below the lesion produces massive vasoconstriction because inhibitory signals cannot descend. Hypertension activates baroreflex vagal slowing and vasodilation above the lesion, causing headache, flushing and sweating above, with pale cool skin or piloerection below. Cerebral haemorrhage, seizure, retinal injury, arrhythmia and death are preventable through immediate posture, trigger removal and short-acting pressure control.

Key points

Spasticity is a velocity-dependent increase in stretch reflex tone after upper-motor-neurone injury; spasms, clonus, stiffness, dystonia, rigidity and fixed contracture are related but not interchangeable findings.
Tone can help standing, transfers, venous return or continence, so treatment targets pain, sleep, hygiene, skin, gait or care goals rather than a normal tone score.
A sudden increase usually signals a trigger below the neurological level: urinary infection or retention, catheter blockage, constipation, pressure injury, fracture, ingrown nail, tight equipment or pain.
Positioning, stretching, splinting, standing, task practice and equipment review are the foundation, delivered by rehabilitation teams after triggers and biomechanics are assessed.
For generalised spasticity in MS, NICE recommends oral baclofen first line when goals are improved mobility, pain or spasms; titrate slowly to benefit because weakness can worsen function.
Botulinum toxin treats selected focal overactivity, while intrathecal baclofen is considered for severe generalised disease after a successful specialist test and support plan.
Abrupt baclofen withdrawal can cause rebound spasticity, fever, confusion, autonomic instability, rhabdomyolysis and seizures, particularly after pump failure.
Autonomic dysreflexia is uncontrolled sympathetic discharge below a usually T6-or-higher lesion after spinal shock, most often triggered by bladder distension or a blocked catheter.
The person's baseline blood pressure may be low, so a dangerous rise can still appear normal to an unfamiliar observer; compare with their usual value and symptoms.
After sitting upright, examine the catheter and bladder first, then bowel, skin and other triggers; use short-acting antihypertensive treatment under the emergency plan if pressure remains dangerously elevated.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Upper motor-neurone injury

Stroke, multiple sclerosis, spinal cord injury, cerebral palsy and acquired brain injury remove descending control of spinal reflex circuits and cause spasticity.

Peripheral aggravating triggers

Urinary retention, infection, constipation, pressure injury, fracture, tight equipment and pain commonly worsen established tone by increasing afferent input.

High spinal cord lesion

A lesion usually above the mid-thoracic cord disconnects sympathetic reflexes from brain control and creates susceptibility to autonomic dysreflexia.

Visceral or cutaneous trigger

Bladder distension, blocked catheter, rectal loading and skin injury below the lesion commonly initiate dysreflexic episodes.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Loss of descending inhibition
Corticospinal and reticulospinal injury reduces inhibitory control over segmental stretch and flexor reflex circuits below the lesion.
2
Hyperexcitable stretch response
Muscle stretch produces an excessive velocity-dependent contraction, spasms and clonus that may initially retain useful antigravity function.
3
Muscle shortening and fibrosis
Persistent abnormal activation and immobility cause structural shortening, pain and fixed contracture beyond reversible neural tone.
4
Unrestrained sympathetic reflex
In autonomic dysreflexia, afferent input below a high cord lesion triggers widespread vasoconstriction without adequate descending modulation, causing abrupt hypertension.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Functionally harmful spasticity

Velocity-dependent resistance, spasms or clonus causes pain, sleep loss, falls, skin damage, impaired hygiene, contracture or loss of a meaningful task.

Useful tone

Extensor stiffness assists standing or transfer despite abnormal examination, so indiscriminate dose escalation could expose underlying weakness and reduce independence.

Trigger-driven deteriorationRed flag

Previously stable tone suddenly increases with urinary symptoms, blocked catheter, constipation, pressure damage, fracture, tight splint, menstruation or another painful stimulus.

Autonomic dysreflexiaRed flag

A high cord-injured person develops sudden hypertension above baseline, pounding headache, facial flushing, sweating or nasal blockage, sometimes with bradycardia and cool piloerect skin below.

Bladder triggerRed flag

A kinked, blocked or overfull catheter bag, retention, instrumentation or urinary infection precedes the episode; bladder distension is the commonest cause and is checked first.

Baclofen withdrawalRed flag

Abrupt oral cessation or pump interruption causes rapidly escalating generalised tone, pruritus, fever, agitation, hallucination, autonomic instability or seizures and can mimic sepsis.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Goal-based tone and function assessmentFirst step
Why
Separate neural spasticity from contracture and determine which activity, comfort or care outcome treatment should change.
Interpretation and limitations
Examine resistance at different velocities, clonus, active control, range, pain, posture, transfers and gait. A lower Ashworth score without functional gain is not sufficient success.
02
Trigger screen
Why
Find reversible infection, retention, bowel, skin, musculoskeletal and equipment causes of a sudden tone increase.
Interpretation and limitations
Check catheter and bladder volume, urine symptoms, bowel record, skin, nails, seating, splints and limbs for fracture or thrombosis; use bloods and imaging from the findings.
03
Serial blood pressure during dysreflexia
Why
Confirm a rise from the individual's baseline and monitor response to posture, trigger removal and medication.
Interpretation and limitations
Measure every two to five minutes in both arms if needed, recognising that a systolic value normal for the general population may be markedly elevated for a high cord injury.
04
Bladder and catheter assessment
Why
Resolve the commonest autonomic-dysreflexia trigger safely and promptly.
Interpretation and limitations
Inspect the entire drainage system for kinks, fullness and blockage, check position and irrigate or replace only through the person's emergency and local urological protocol with anaesthetic gel.
05
Bowel and skin examination
Why
Find rectal loading, pressure injury, burns, tight clothing, ingrown nails or other noxious stimuli when bladder measures do not resolve hypertension.
Interpretation and limitations
Rectal examination can worsen dysreflexia and should use topical anaesthetic and the established emergency protocol after pressure is controlled or covered.
06
Intrathecal pump assessment
Why
Detect reservoir depletion, catheter disconnection, programming error or infection in severe rebound spasticity.
Interpretation and limitations
Contact the implanting service urgently; pump interrogation and imaging are specialist procedures, and suspected withdrawal requires emergency supportive and baclofen-restoration planning.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Rigidity

Uniform resistance independent of movement speed with bradykinesia favours basal-ganglia rigidity rather than spasticity on examination.

Dystonia

Patterned twisting posture, directional pull and action specificity support dystonia, though both forms of overactivity may coexist.

Fixed contracture

Mechanical range remains limited during slow passive movement and after neural blockade, indicating tissue shortening rather than active reflex tone alone.

Seizure or hyperthermic rigidity

Episodic jerking, altered awareness, fever or autonomic instability may indicate seizure, NMS or serotonin toxicity requiring emergency assessment.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Spasticity reviewTreat trigger, then toneFirst stepTone, spasms or clonus becomes painful, functionally limiting or suddenly worse.

1Define one or more measurable goals and establish whether current tone helps posture or transfer, while distinguishing dynamic spasticity from fixed shortening or dystonia.
2EscalationSearch systematically for bladder, bowel, skin, infection, fracture, pain and equipment triggers and correct these before escalating long-term antispastic treatment.
3Optimise positioning, stretching, orthoses, standing and task practice, then introduce low-dose baclofen or a focal intervention through rehabilitation or neurology review.
4Reassess goal and adverse weakness after each change and refer complex generalised disease for toxin, intrathecal or multidisciplinary options.

02Autonomic emergencySit, monitor and remove the triggerA person with injury at or above T6 has sudden symptoms and a blood-pressure rise from baseline.

1Sit the person upright with legs dependent, loosen restrictive garments, call for urgent help and monitor blood pressure and pulse every two to five minutes.
2Inspect the urinary drainage system immediately; empty the bag, remove kinks and manage blockage or retention using the individual's protocol and topical anaesthetic before catheter manipulation.
3If hypertension persists, search bowel, skin, pressure, fracture, sexual and procedural triggers, avoiding unanaesthetised rectal stimulation that can intensify the episode.
4Give a rapid-onset short-duration antihypertensive under the local emergency plan when pressure remains severe, checking contraindications such as recent PDE5 inhibitor before nitrate.
5Continue until pressure returns near baseline and the cause is resolved, then observe for recurrence and document prevention changes.

03Baclofen crisisRecognise withdrawal or overdoseA person using regular oral or intrathecal baclofen develops abrupt neurological or respiratory change.

1For withdrawal, identify missed doses or pump alarm, provide emergency supportive care and contact the implanting and critical-care services to restore baclofen safely.
2For overdose, recognise flaccidity, somnolence, respiratory depression, hypotension and coma, support airway and circulation and obtain urgent toxicology and pump advice.
3Investigate sepsis, renal dysfunction, rhabdomyolysis and aspiration in parallel and create a future supply, alarm and emergency-contact plan after recovery.

Key medicines and prescribing safety5 treatments · regimens, roles and cautions

First-line oral treatment for generalised spasticity in MS and widely used after spinal cord injury when goals justify systemic therapy.

Oral baclofen

A common adult start is 5 mg three times daily, increased gradually to the lowest effective dose.

Sedation, weakness, dizziness and respiratory risk can impair transfers and falls; reduce for renal impairment and never stop sustained treatment abruptly.

An alternative systemic option when baclofen is ineffective or not tolerated.

Tizanidine

Begin at a low specialist-selected dose and titrate slowly according to daytime and nocturnal goals.

Hypotension, sedation, dry mouth, liver injury and major CYP1A2 interactions occur; monitor liver function under product and local guidance.

Reduces focal overactivity that impairs hygiene, hand use, gait, pain or splint tolerance without treating the whole body.

Botulinum toxin type A

Use product-specific units and targeted muscles at specialist intervals, commonly around twelve weeks.

Products are not interchangeable and local weakness, dysphagia or distant spread can occur; pair injections with therapy and a documented functional target.

Treats severe generalised spasticity when oral adverse effects or inadequate efficacy prevent goal attainment.

Intrathecal baclofen

A specialist performs a test dose, implantation and individual pump titration with scheduled refills.

Overdose causes respiratory depression and withdrawal can be fatal; infection, catheter failure, pump alarms and reliable emergency access require lifelong planning.

Reduces persistent dangerous pressure while the noxious trigger is found and removed.

Short-acting antihypertensive for dysreflexia

Use the individual's emergency plan and local spinal protocol, selecting a rapid and short-duration agent.

Avoid uncontrolled hypotension after trigger relief; nitrates are contraindicated after recent PDE5 inhibitor use, and agent choice must account for pulse and comorbidity.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Pain, contracture and skin injury

Persistent tone impairs sleep, hygiene and positioning and can cause deformity, pressure damage and painful spasms.

Falls and care dependence

Excess tone may obstruct gait and transfers, while indiscriminate reduction can remove useful support and worsen mobility.

Hypertensive cerebral injury

Untreated autonomic dysreflexia can cause intracerebral haemorrhage, seizure, retinal injury, arrhythmia and death during an episode.

Baclofen-withdrawal syndrome

Abrupt oral interruption or pump failure can cause rebound spasticity, fever, confusion, rhabdomyolysis and seizures during baclofen withdrawal.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Track pain, sleep, hygiene, skin, range, transfers, gait and caregiver burden against the agreed goal, including whether reduced tone exposes disabling weakness.
Review bladder, bowel, skin, infection, fractures, menstruation, seating and orthoses whenever spasticity changes unexpectedly.
During autonomic dysreflexia, record pressure and pulse every two to five minutes, interventions, trigger and return to the individual's baseline.
Monitor sedation, falls, renal function and respiratory risk with baclofen and pressure and liver effects with tizanidine under local guidance.
Maintain pump refill dates, alarm education, emergency contact and a rescue plan for every intrathecal baclofen user.
After any dysreflexia episode, revise catheter, bowel, skin or procedural prevention and ensure the person carries accessible emergency information.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Tone may be useful

Extensor spasticity can substitute partly for weak voluntary control during standing, so normalising examination tone may reduce independence.

Triggers speak through tone

Below-level pain may not be consciously felt after cord injury and instead presents as new spasm, dysreflexia or functional decline.

Baseline pressure is low

A rise to an apparently ordinary systolic pressure can represent severe autonomic dysreflexia in someone whose usual value is much lower.

Sit, do not lie

Upright posture uses gravity to lower cerebral pressure; lying flat during dysreflexia can worsen dangerous hypertension.

Bladder comes first

Blocked catheters and distension are the commonest triggers, making visual inspection of the whole drainage system an immediate treatment step.

Pump withdrawal mimics sepsis

Fever, autonomic instability and rising tone can be mislabelled infection; pump failure and baclofen interruption must be checked simultaneously.

11Common pitfallsFrequent interpretation and management errors.

01
Escalating antispastic medicine before checking a blocked catheter, constipation, pressure injury or fracture.
02
Removing useful extensor tone and leaving a patient unable to stand or transfer.
03
Stopping oral or intrathecal baclofen abruptly without a supervised plan.
04
Reassuring during autonomic dysreflexia because the absolute blood pressure looks normal for the general population.
05
Laying the patient flat or performing immediate unanaesthetised rectal examination during severe hypertension.
06
Giving nitrate without checking recent sildenafil, tadalafil or another phosphodiesterase-5 inhibitor.