Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Manage spasticity by function and triggers, preserve useful tone and recognise autonomic dysreflexia after high spinal injury as a hypertensive emergency requiring immediate trigger removal.
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.
Stroke, multiple sclerosis, spinal cord injury, cerebral palsy and acquired brain injury remove descending control of spinal reflex circuits and cause spasticity.
Urinary retention, infection, constipation, pressure injury, fracture, tight equipment and pain commonly worsen established tone by increasing afferent input.
A lesion usually above the mid-thoracic cord disconnects sympathetic reflexes from brain control and creates susceptibility to autonomic dysreflexia.
Bladder distension, blocked catheter, rectal loading and skin injury below the lesion commonly initiate dysreflexic episodes.
Corticospinal and reticulospinal injury reduces inhibitory control over segmental stretch and flexor reflex circuits below the lesion.
Muscle stretch produces an excessive velocity-dependent contraction, spasms and clonus that may initially retain useful antigravity function.
Persistent abnormal activation and immobility cause structural shortening, pain and fixed contracture beyond reversible neural tone.
In autonomic dysreflexia, afferent input below a high cord lesion triggers widespread vasoconstriction without adequate descending modulation, causing abrupt hypertension.
Velocity-dependent resistance, spasms or clonus causes pain, sleep loss, falls, skin damage, impaired hygiene, contracture or loss of a meaningful task.
Extensor stiffness assists standing or transfer despite abnormal examination, so indiscriminate dose escalation could expose underlying weakness and reduce independence.
Previously stable tone suddenly increases with urinary symptoms, blocked catheter, constipation, pressure damage, fracture, tight splint, menstruation or another painful stimulus.
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.
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.
Abrupt oral cessation or pump interruption causes rapidly escalating generalised tone, pruritus, fever, agitation, hallucination, autonomic instability or seizures and can mimic sepsis.
Uniform resistance independent of movement speed with bradykinesia favours basal-ganglia rigidity rather than spasticity on examination.
Patterned twisting posture, directional pull and action specificity support dystonia, though both forms of overactivity may coexist.
Mechanical range remains limited during slow passive movement and after neural blockade, indicating tissue shortening rather than active reflex tone alone.
Episodic jerking, altered awareness, fever or autonomic instability may indicate seizure, NMS or serotonin toxicity requiring emergency assessment.
Persistent tone impairs sleep, hygiene and positioning and can cause deformity, pressure damage and painful spasms.
Excess tone may obstruct gait and transfers, while indiscriminate reduction can remove useful support and worsen mobility.
Untreated autonomic dysreflexia can cause intracerebral haemorrhage, seizure, retinal injury, arrhythmia and death during an episode.
Abrupt oral interruption or pump failure can cause rebound spasticity, fever, confusion, rhabdomyolysis and seizures during baclofen withdrawal.
Extensor spasticity can substitute partly for weak voluntary control during standing, so normalising examination tone may reduce independence.
Below-level pain may not be consciously felt after cord injury and instead presents as new spasm, dysreflexia or functional decline.
A rise to an apparently ordinary systolic pressure can represent severe autonomic dysreflexia in someone whose usual value is much lower.
Upright posture uses gravity to lower cerebral pressure; lying flat during dysreflexia can worsen dangerous hypertension.
Blocked catheters and distension are the commonest triggers, making visual inspection of the whole drainage system an immediate treatment step.
Fever, autonomic instability and rising tone can be mislabelled infection; pump failure and baclofen interruption must be checked simultaneously.
Escalating antispastic medicine before checking a blocked catheter, constipation, pressure injury or fracture.
Removing useful extensor tone and leaving a patient unable to stand or transfer.
Stopping oral or intrathecal baclofen abruptly without a supervised plan.
Reassuring during autonomic dysreflexia because the absolute blood pressure looks normal for the general population.
Laying the patient flat or performing immediate unanaesthetised rectal examination during severe hypertension.
Giving nitrate without checking recent sildenafil, tadalafil or another phosphodiesterase-5 inhibitor.
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A person with a chronic T4 spinal injury develops a pounding headache, facial flushing and blood pressure 175/100 mmHg from a usual 95/60. Their urinary catheter is in place. What is the best immediate action?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Sedation, weakness, dizziness and respiratory risk can impair transfers and falls; reduce for renal impairment and never stop sustained treatment abruptly.
Hypotension, sedation, dry mouth, liver injury and major CYP1A2 interactions occur; monitor liver function under product and local guidance.
Products are not interchangeable and local weakness, dysphagia or distant spread can occur; pair injections with therapy and a documented functional target.
Overdose causes respiratory depression and withdrawal can be fatal; infection, catheter failure, pump alarms and reliable emergency access require lifelong planning.
Avoid uncontrolled hypotension after trigger relief; nitrates are contraindicated after recent PDE5 inhibitor use, and agent choice must account for pulse and comorbidity.