Brachial neuritis

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

Neuralgic amyotrophy is an inflammatory, mechanically influenced peripheral nerve disorder with a distinctive sequence. Pain reaches severe intensity abruptly or over a few days, commonly around the shoulder and scapula, then focal paresis emerges. The lesion may lie within the plexus or appear as separate fascicular mononeuropathies. This patchiness explains why one muscle supplied by a named nerve can be profoundly weak while another supplied by the same root is preserved.

The most important diagnostic competition is cervical radiculopathy. Radicular pain often follows a dermatomal course and is provoked by neck movement, with weakness and sensory change appearing alongside pain. Neuralgic amyotrophy produces much more severe early pain followed by weakness and can involve nerves from multiple root levels. Rotator-cuff tear, calcific tendinopathy, zoster, Lyme disease after relevant exposure, vasculitis, trauma, tumour and motor-neurone disease also require context-specific exclusion.

Recovery reflects axonal regeneration and may take months to years. Some patients retain scapular dyskinesia, fatigue, neuropathic pain and reduced endurance despite partial power return. Early physiotherapy prevents stiffness but must not overload denervated muscle. Once reinnervation appears, graded motor control and strengthening become appropriate. Persistent complete paralysis or imaging-demonstrated fascicular constriction may justify referral to a peripheral nerve surgical service before irreversible muscle loss.

Key points

Brachial neuritis, also called neuralgic amyotrophy or Parsonage-Turner syndrome, typically begins with abrupt severe shoulder or upper-arm pain followed days later by patchy weakness and wasting.
Pain is often relentless, worse at night and not consistently reproduced by neck movement; as pain settles, weakness becomes more apparent and may be mistakenly attributed to guarding.
The upper trunk, long thoracic, suprascapular and anterior interosseous distributions are often affected, but lesions are multifocal and need not respect one plexus segment.
Scapular winging from long-thoracic neuropathy, weak shoulder external rotation and inability to make an OK sign are useful localising examination clues.
Sensory symptoms are variable and sometimes mild despite severe pain; a small lateral forearm or patchy upper-limb deficit is more typical than a clean dermatomal band.
Immune triggers can include recent infection, surgery, strenuous exercise, childbirth and occasionally vaccination, but temporal association alone does not establish causation.
Hereditary neuralgic amyotrophy should be considered with recurrent attacks, childhood onset, affected relatives or dysmorphic features and may involve SEPT9 variants.
Electrodiagnostic testing is most informative after denervation has had time to develop and should sample clinically selected nerves and muscles rather than a generic limb screen.
MRI of the brachial plexus or high-resolution nerve imaging can show multifocal enlargement or hourglass constriction and excludes mass, while cervical MRI addresses a root or cord differential.
Evidence for corticosteroid early in the painful phase is limited; care centres on adequate analgesia, movement preservation, later targeted strengthening and specialist reconstruction for selected non-recovering constrictions.

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

Immune-triggered neuralgic amyotrophy

Many attacks follow infection, surgery, strenuous exertion or childbirth, suggesting immune-mediated fascicular injury; temporal association alone does not prove a specific trigger.

Hereditary neuralgic amyotrophy

Recurrent attacks, childhood onset, affected relatives or dysmorphic features suggest an inherited susceptibility, sometimes involving pathogenic SEPT9 variants.

Idiopathic disease

A substantial group has no identifiable precipitant or family history, so the characteristic pain-then-patchy-weakness sequence remains more informative than an absent trigger.

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

1
Patchy nerve inflammation
Immune injury targets selected fascicles within the brachial plexus or individual nerves, sometimes producing focal swelling or hourglass constriction.
2
Painful axonal damage
Inflammation causes intense neuropathic shoulder or arm pain before axonal interruption reveals patchy weakness, wasting and variable sensory loss.
3
Slow reinnervation
Surviving axons sprout and damaged fibres regenerate towards denervated muscle over months, making recovery uneven and vulnerable to irreversible motor-unit loss.

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

Pain then paresis

Severe unilateral shoulder or upper-arm pain precedes patchy weakness by hours to several weeks, with pain often easing as wasting becomes visible.

Scapular winging

Long-thoracic involvement weakens serratus anterior, producing medial scapular winging during wall push and difficulty elevating the arm smoothly.

Suprascapular pattern

Weak shoulder abduction initiation or external rotation with infraspinatus or supraspinatus wasting suggests suprascapular nerve involvement.

Anterior interosseous palsy

Weak flexor pollicis longus and index profundus prevent a round thumb-index OK sign without cutaneous sensory loss.

Phrenic involvementRed flag

New orthopnoea, sleep-related breathlessness, weak cough or an elevated hemidiaphragm after the pain syndrome indicates potentially important diaphragmatic neuropathy.

Hereditary recurrence

Multiple attacks, bilateral episodes, childhood onset or similarly affected relatives suggests hereditary neuralgic amyotrophy and merits genetic counselling.

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
Detailed motor mapFirst step
Why
Localise weakness across roots, plexus trunks, fascicles and named nerves.
Interpretation and limitations
Compare muscles sharing a root but supplied by different nerves; patchy non-myotomal loss with scapular involvement supports neuralgic amyotrophy.
02
Nerve-conduction studies and electromyography
Why
Confirm axonal plexus or nerve injury and estimate reinnervation.
Interpretation and limitations
Denervation may not appear immediately, so correctly timed targeted sampling after roughly several weeks is more informative than a very early normal study.
03
MRI brachial plexus or MR neurography
Why
Identify nerve enlargement, denervation changes, constriction and structural infiltration.
Interpretation and limitations
Specialist imaging may show focal fascicular torsion or hourglass narrowing; a normal scan does not exclude the clinical syndrome.
04
MRI cervical spine
Why
Evaluate radiculopathy, myelopathy or foraminal compression when examination or pain distribution suggests it.
Interpretation and limitations
Degenerative foraminal narrowing is common and must match the symptomatic root and muscles before being declared causal.
05
Chest imaging
Why
Investigate apical tumour, diaphragmatic elevation or other thoracic pathology when relevant.
Interpretation and limitations
Lower-trunk pain, Horner syndrome, smoking, weight loss or phrenic symptoms should lower the threshold for targeted imaging.
06
Pulmonary function sitting and supine
Why
Assess diaphragmatic weakness when orthopnoea or phrenic involvement is suspected.
Interpretation and limitations
A disproportionate fall when supine supports diaphragm dysfunction and may prompt ultrasound, sleep study and ventilatory support assessment.
07
SEPT9 and inherited neuropathy testing
Why
Confirm hereditary neuralgic amyotrophy in a recurrent familial phenotype.
Interpretation and limitations
Request through clinical genetics after counselling; a negative result does not eliminate every hereditary syndrome and does not alter immediate rehabilitation.

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

Cervical radiculopathy

Dermatomal pain provoked by neck movement with matching myotomal weakness and reflex change supports root disease; brachial neuritis is typically patchier across several root levels.

Rotator-cuff or shoulder disease

Painful restricted passive movement, local tenderness and weakness limited by pain favour musculoskeletal pathology rather than denervation in a named nerve pattern.

Plexus tumour or infiltration

Relentlessly progressive pain, Horner syndrome, mass, weight loss or cancer history raises malignant or structural plexopathy and warrants dedicated imaging.

Motor neurone disease

Painless progressive weakness with widespread fasciculation and upper motor-neurone signs supports motor neurone disease rather than an acute painful monophasic neuropathy.

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

01Acute painRecognise the sequence and exclude dangerFirst stepSevere new shoulder or arm pain appears without a clear joint injury.

1Ask about chest and vascular symptoms, trauma, fever, cancer, rash, neck provocation and recent immune triggers, then perform cardiac, vascular, cervical and neurological examination.
2AlternativeDocument baseline scapular, shoulder, elbow, wrist and finger strength even if pain limits effort, arranging urgent alternative imaging for red flags.
3Provide a short, safe acute analgesic plan and early review because objective weakness may emerge after the first painful consultation.

02Evolving weaknessLocalise patchy nerve injuryPain is followed by focal weakness, winging or muscle wasting.

1Map each weak muscle to root and named nerve, compare sensation and reflexes and look specifically for long-thoracic, suprascapular and anterior interosseous involvement.
2Refer to neurology and arrange appropriately timed neurophysiology, selecting plexus or cervical MRI from the pattern and checking respiratory symptoms.
3Explain that one early normal test does not exclude disease, but reconsider tumour, vasculitis, root compression and hereditary disease when the pattern or course is atypical.

03RehabilitationProtect joints while axons recoverPain is controlled enough for active movement and weakness is established.

1Maintain passive range and scapular mechanics without heavily loading a denervated muscle, using occupational adaptation for work, sleep and self-care.
2Repeat clinical and electromyographic assessment for reinnervation, then progress motor-control and resistance work as recovery becomes physiologically possible.
3Treat residual neuropathic pain separately from weakness and address fear, sleep and prolonged work absence through a coordinated rehabilitation plan.

04Poor recoveryRefer before reconstructive opportunity closesA profoundly weak muscle shows no meaningful clinical or electrophysiological recovery.

1Reconfirm diagnosis and lesion anatomy with high-resolution imaging and repeat neurophysiology, looking for hourglass constriction or complete axonal interruption.
2Discuss the timing of neurolysis, nerve transfer or tendon transfer with a specialist peripheral nerve unit before prolonged denervation limits outcome.
3Continue shoulder protection and functional equipment while setting realistic expectations that pain recovery and motor recovery follow different timelines.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Can reduce severe early nociceptive and inflammatory shoulder pain when not contraindicated.

Naproxen

A time-limited adult oral regimen may be used from the current BNF with the lowest effective dose and gastroprotection selected by gastrointestinal risk.

Avoid or review in kidney disease, ulcer, anticoagulation, heart failure, pregnancy and high cardiovascular risk; analgesia must not mask evolving weakness.

Treats ongoing burning or electric pain after the initial acute phase.

Amitriptyline

Start a low oral night dose, often 10 mg, and titrate slowly under the BNF if persistent neuropathic pain disrupts sleep and function.

Sedation, falls, anticholinergic burden, conduction disease and overdose toxicity require a pre-agreed review and stopping plan.

May shorten the painful phase in selected patients; it is not proven to restore axons or prevent long-term weakness.

Prednisolone considered early

Some specialists offer a short oral corticosteroid course very early in severe pain, but the regimen is not nationally standardised and evidence remains limited.

Exclude infection and review glucose, mood, blood pressure, bone and gastrointestinal risks; uncertainty and off-label or local practice should be explained.

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

Persistent weakness and wasting

Severe axonal loss may leave scapular winging, impaired shoulder rotation, weak pinch or other focal disability that limits work and self-care.

Joint stiffness and abnormal mechanics

Pain avoidance and denervation can produce frozen shoulder, scapular dyskinesia and compensatory overload, adding musculoskeletal restriction to the neurological deficit.

Chronic neuropathic pain

Although the initial severe pain often settles, persistent nerve pain and hypersensitivity can disturb sleep, mood and participation during recovery.

Incomplete functional recovery

Fascicular constriction or failure of reinnervation may require peripheral-nerve surgical assessment before prolonged denervation causes irreversible muscle loss.

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

Re-map strength, scapular motion, range and wasting at serial visits rather than using shoulder pain as the only marker of recovery.
Repeat neurophysiology when the result will demonstrate reinnervation, redirect diagnosis or inform a time-sensitive surgical referral.
Ask about orthopnoea, weak cough, sleep symptoms and exertional breathlessness, obtaining respiratory tests promptly if phrenic involvement is possible.
Review analgesic benefit, sedation, gastrointestinal and renal harm, tapering medicines as the acute pain phase recedes.
Monitor adhesive capsulitis, subluxation and compensatory neck or thoracic pain while exercise intensity is matched to reinnervation.
Track work, driving, sleep and mental wellbeing because residual fatigue and scapular control can remain disabling after headline power improves.

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

Sequence is diagnostic

The defining history is not merely shoulder pain plus weakness, but extreme pain followed by delayed patchy paresis as the pain begins to settle.

Fascicles can be selective

Neuralgic amyotrophy may damage a fascicle within a named nerve, producing isolated anterior interosseous weakness without the rest of median neuropathy.

Early EMG can be normal

Wallerian degeneration and denervation potentials take time to develop, so test timing and correct muscle selection determine diagnostic yield.

Scans show constrictions

Modern high-resolution imaging may reveal hourglass fascicular narrowing that identifies selected patients for peripheral nerve surgical review.

Diaphragm involvement hides

Unilateral phrenic neuropathy may present as orthopnoea or sleep disturbance rather than obvious daytime respiratory failure.

11Common pitfallsFrequent interpretation and management errors.

01
Calling the initial pain a rotator-cuff disorder without follow-up for weakness.
02
Assuming a cervical MRI abnormality is causal without matching localisation.
03
Excluding brachial neuritis after one very early normal electromyogram.
04
Strengthening a fully denervated muscle aggressively during the painful phase.
05
Missing phrenic neuropathy in a patient with new orthopnoea.
06
Attributing temporal association with vaccination as proof of causation.
07
Waiting years to refer a non-recovering fascicular constriction.