Diabetes-induced microangiopathy → mononeuritis multiplex ^[3], classically affecting:

The nerve is compressed where it passes through a tight anatomical space. Any process that reduces the space (swelling, inflammation, anatomical variant) or increases the contents (oedema, tumour, ganglion) will compress the nerve.

Double crush syndrome: peripheral entrapment syndromes often associated with cervical/lumbar spondylosis — proximal compression of a peripheral nerve renders it more susceptible to the effects of a second, more distal injury (e.g. cubital tunnel syndrome & Guyon's canal syndrome) ^[5]

• Direct nerve transection (lacerations, surgical injury)
• Fractures: e.g. radial nerve injured in mid-shaft humeral fractures (spiral groove); axillary nerve injured in shoulder dislocations; common peroneal nerve in fibular neck fractures
• Injection injury: sciatic nerve from improper intramuscular injection
• Traction injuries: brachial plexus during birth (Erb's palsy C5-6, Klumpke's palsy C8-T1) or motorcycle accidents

• Diabetes-induced microangiopathy → ischaemic damage to vasa nervorum → acute mononeuropathy or mononeuritis multiplex ^[3]
• Classical presentations: CN III palsy (pupil-sparing), CN VI palsy, CN V involvement, foot drop (CPN palsy) ^[3]
• Can present as "mix and match" — i.e., a patient can get a 3rd nerve palsy and a foot drop at a similar time ^[3]
• Diabetes also predisposes to entrapment neuropathies (CTS is 2-3× more common in diabetics) due to nerve oedema and glycosylation of connective tissue

• Vasculitis: polyarteritis nodosa (PAN), granulomatosis with polyangiitis (GPA), eosinophilic granulomatosis with polyangiitis (EGPA), rheumatoid vasculitis
  • Mechanism: inflammation of vasa nervorum → nerve infarction → typically presents as mononeuritis multiplex but can start as single nerve
• Atherosclerotic disease: rare as isolated cause

• Focal neuropathy in sarcoidosis: granulomatous inflammation of nerve (e.g., facial nerve palsy in neurosarcoidosis)
• Leprosy (Mycobacterium leprae): still relevant in SE Asian context — predilection for superficial nerves (ulnar, median, common peroneal, greater auricular) → thickened, palpable nerves with sensory loss and weakness

• Direct tumour infiltration or compression (e.g., Pancoast tumour → lower brachial plexus/thoracic outlet)
• Paraneoplastic
• Schwannoma, neurofibroma — benign nerve sheath tumours causing focal compression

• Herpes zoster: reactivation in dorsal root ganglion → can cause motor nerve palsy in addition to dermatomal pain/rash (e.g., Ramsay Hunt syndrome = CN VII palsy + vesicles in ear)
• HIV: can cause various mononeuropathies
• Lyme disease: facial nerve palsy (bilateral in some cases)
• Leprosy: as above

• Surgical injury (e.g., accessory nerve during lymph node biopsy in posterior triangle)
• Tourniquet palsy
• Positioning during anaesthesia (e.g., radial nerve compression against operating table)

1. Compression / Ischaemia: Nerve compression impairs epineural blood flow & axonal conduction ^[5]

   • Acute: conduction block (neurapraxia) → reversible
   • Chronic: progressive demyelination → axonal degeneration → irreversible
   • This is why early decompression is important

2. Ischaemia (Vasa Nervorum Infarction): In diabetes and vasculitis, occlusion of the tiny blood vessels supplying the nerve (vasa nervorum) → nerve infarction → acute onset, often painful

3. Wallerian Degeneration: When the axon is severed, the distal segment degenerates completely (the "severed cable" dies). The proximal stump can regenerate (at ~1 mm/day or ~1 inch/month) if the connective tissue scaffold is intact.

4. Demyelination: Loss of Schwann cell myelin → slowed/blocked conduction. If the axon itself is preserved, remyelination can occur → better prognosis.

The sequence in chronic entrapment:

1. Intermittent compression → transient ischaemia → intermittent symptoms (e.g., nocturnal paraesthesia in CTS)
2. Sustained compression → focal demyelination → conduction slowing across the entrapment site (detectable on NCS)
3. Prolonged compression → axonal degeneration → muscle wasting, persistent weakness, and sensory loss (harder to reverse)

• Cranial mononeuropathy: CN III, IV, VI, VII most commonly affected
• Upper limb: Median, ulnar, radial nerve
• Lower limb: Common peroneal, femoral, sciatic, lateral cutaneous nerve of thigh, tibial
• Trunk: Intercostal, phrenic

Clinical features of peripheral neuropathy (including mononeuropathy) ^[1][2]:

• Motor: weakness, wasting, fasciculation, hyporeflexia (LMN signs) ^[1][2]

  • Why LMN signs? Because peripheral nerves are the final common pathway (lower motor neuron). Damage → loss of tonic input to muscle → flaccidity, wasting, reduced reflexes. Fasciculations occur because denervated muscle fibres become hyperexcitable and fire spontaneously.
  • Distal: difficulty in tip-toeing, foot drop, ↓manual dexterity ^[2]
  • Proximal: difficulty in climbing stairs, combing hair, standing up from sitting ^[2] — rare in mononeuropathy (more typical of myopathy or polyradiculopathy), but femoral neuropathy can cause proximal weakness

• Sensory ^[2]:

  • Large, myelinated fibres: loss of touch/proprioception (–ve) or pins-and-needle (+ve) ^[2]
  • Small, unmyelinated fibres: loss of pain/temperature (–ve) or pain (+ve) ^[2]
  • The sensory deficit follows the territory of the specific nerve, not a dermatomal pattern (which follows nerve roots) — this is a key distinction for localization

• Autonomic: rarely occurs alone ^[2]:

  • Postural hypotension, disturbance in sweating, cardiac rhythm, GI/bladder functions, sexual function ^[2]
  • In isolated mononeuropathy, autonomic features are usually subtle (e.g., local sweating changes, vasomotor changes in the affected territory)

• Others ^[2]:

  • Skeletal deformity: claw hand, pes cavus, kyphoscoliosis — from chronic denervation and unopposed muscle action
  • Trophic changes: disuse atrophy, hair loss, brittle nails, trophic ulcers, Charcot's joints — from loss of sensation (protective sensation) and autonomic denervation
  • Nerve thickening in leprosy, acromegaly, HMSN, CIDP, neurofibromatosis ^[2]

• Why it can mimic: A small cortical stroke in the "hand knob" area can cause isolated hand weakness that superficially looks like a peripheral nerve palsy
• How to differentiate: UMN signs (hyperreflexia, spasticity, upgoing plantar, no wasting early on) vs. LMN signs in mononeuropathy (hyporeflexia, flaccidity, wasting, fasciculation). Sensory loss in UMN lesions follows dermatomal/cortical patterns, not peripheral nerve distributions.

• Why it can mimic: A C8-T1 radiculopathy can mimic ulnar neuropathy (both cause hand weakness + medial hand numbness); an L5 radiculopathy can mimic common peroneal nerve (CPN) palsy (both cause foot drop)
• How to differentiate:
  • Radiculopathy affects all muscles in that myotome regardless of which peripheral nerve they belong to, plus follows a dermatomal sensory pattern
  • In CPN palsy: foot eversion is weak (superficial peroneal) + dorsiflexion weak (deep peroneal), but inversion is preserved (tibialis posterior = tibial nerve, L5 root). In L5 radiculopathy, inversion is ALSO weak (because tibialis posterior receives L5 via the tibial nerve) and hip abduction is weak (gluteus medius, L5) ^[1]
  • Radiculopathy often has back/neck pain radiating in a dermatomal distribution
  • Cervical spondylosis (esp. C6/7): neck pain + neck movement exacerbates ^[5]

• Why it can mimic: A lower trunk brachial plexopathy (C8-T1) mimics combined median + ulnar neuropathy
• How to differentiate: Plexopathy affects multiple nerves arising from the same trunk/cord, so motor and sensory deficits cross nerve boundaries but stay within the plexus distribution
• Thoracic outlet syndrome affects the lower brachial plexus → paraesthesia / weakness along ulnar distribution but may also involve median-innervated muscles — this "too much for one nerve" pattern suggests plexopathy ^[5]
• Causes: cervical rib, fracture clavicle, Pancoast tumour ^[5]
• Degenerative (cervical myelopathy / radiculopathy, carpal tunnel syndrome) — note how degenerative cervical pathology can coexist with or mimic peripheral entrapment ^[8]

• Pure motor involvement, NO sensory loss
• Mixed UMN + LMN signs (fasciculation + wasting + hyperreflexia + upgoing plantars) — this combination is virtually diagnostic of MND/ALS
• Typically progressive and multifocal rather than confined to one nerve

• Myasthenia gravis ^[8][9]: Fatigable weakness (worsens with repeated use, improves with rest), often affects ocular muscles (ptosis, diplopia) first. No sensory involvement, no wasting early on.
• How to differentiate from mononeuropathy: The weakness in MG does NOT follow a single nerve distribution — it follows the muscles with the highest density of NMJ receptors (ocular > bulbar > proximal limbs). Fatigability is the hallmark.
• Botulinum toxin: toxins from Clostridium botulinum directed at pre-synaptic receptors in the NMJ ^[10]

• Proximal weakness (difficulty climbing stairs, combing hair, standing from sitting) — not in a nerve distribution ^[11]
• Preserved or reduced reflexes but NO fasciculation
• No sensory involvement
• CK often elevated
• Differential diagnosis of myopathies: infection (viral, bacterial), inflammation (PM, DM, IBM), congenital (DMD, BMD, FSHMD, limb-girdle), endocrine (Cushing's, thyroid), drug-induced (corticosteroids, statins), channelopathy (myotonic dystrophy, periodic paralysis) ^[11]

• Inconsistent examination findings; e.g., weakness of ankle dorsiflexion on direct testing but normal gait
• Hoover's sign: weakness of hip extension that returns to normal when the contralateral hip is flexed against resistance (involuntary synergistic movement)
• Distribution does not conform to any anatomical pattern
• Normal reflexes, no wasting

CTS is primarily a clinical diagnosis ^[5]. The diagnostic confidence increases with the combination of:

Differential diagnosis of CTS: cervical spondylosis (esp. C6/7), pronator teres syndrome, thoracic outlet syndrome, peripheral neuropathy ^[5]

CTS is a clinical diagnosis. Nerve conduction studies (normal conduction does not r/o CTS) ^[5]

Clinical diagnosis supported by:

• Symptoms in ulnar nerve territory (medial 1½ digits)
• Positive Tinel's sign at the medial epicondyle
• Positive elbow flexion test (sustained elbow flexion 60s → reproduces symptoms)
• Examine elbow: cubitus valgus deformity, limited ROM, Tinel sign, ulnar nerve subluxability, elbow flexion test ^[5]
• Differentiate from distal compression: less prominent claw hand (FDP 4/5 also affected), dorsal sensory also affected ^[5]
• NCS: reduced conduction velocity across the elbow segment

Diagnosed clinically in the appropriate setting:

• Known diabetes mellitus
• Acute onset of cranial nerve deficit (CN III, VI, V, or CPN)
• CN III palsy: pupil-sparing (differentiates from compressive lesion)
• Mix and match presentations ^[3]
• Imaging (MRI brain, MRA/CTA) performed primarily to exclude compressive causes (e.g., PComA aneurysm for CN III palsy)

Baseline bloods: CBC, LRFT, glucose, B12/folate, TFT, ESR/CRP, autoimmune (ANA, RF, ANCA), SPE Ig ^[1]

MRI for denervation changes — how it works:

• When a muscle is acutely denervated, it develops intracellular oedema → T2 hyperintensity on MRI (within days to weeks)
• Chronically denervated muscle undergoes fatty infiltration → T1 hyperintensity (weeks to months)
• This allows you to estimate the chronicity of denervation and identify which muscles are affected (confirming nerve territory)

Not routinely performed for simple entrapment mononeuropathy, but indicated when considering:

• GBS (albuminocytological dissociation: ↑protein, normal cell count)
• CIDP (similarly elevated protein)
• Infection (Lyme, HIV, syphilis)
• Infiltrative causes (lymphoma, carcinomatous meningitis)

Nerve biopsy: last resort for inflammatory / infective / infiltrative disorders ^[1]

• Usually sural nerve (purely sensory nerve at the ankle — minimizes motor deficit from biopsy)
• Indications:
  • Suspected vasculitis (nerve + muscle biopsy — look for necrotizing arteritis of vasa nervorum)
  • Leprosy (granulomatous inflammation, acid-fast bacilli)
  • Amyloidosis (Congo red staining → apple-green birefringence under polarized light)
  • Infiltrative tumours
• NOT indicated for routine entrapment neuropathies

These are effectively part of the clinical examination but function as diagnostic tests:

Management depends on the Seddon classification of nerve injury:

Key management points in trauma:

• Closed injuries (compression, traction): observe first; most are neurapraxia or axonotmesis and will recover. Perform NCS/EMG at 2–3 weeks (to establish baseline) and repeat at 3 months (to assess recovery).
• Sharp transection (laceration, surgical injury): immediate or early surgical repair (primary neurorrhaphy within 72 hours if wound is clean; delayed primary repair within 2–3 weeks if wound is contaminated)
• Fracture-associated (e.g., radial nerve in humeral shaft fracture): Most are neurapraxia from stretching/contusion → observe. If no clinical or EMG signs of recovery by 3–4 months → surgical exploration
• Splinting to prevent contractures during recovery: e.g., wrist splint in extension for radial nerve palsy (prevents flexion contracture of wrist), AFO for foot drop

Management is generally supportive ^[18]:

• Usually transient → management directed to controlling underlying hyperglycaemia ^[18]
• 60% with good functional recovery in 12–24 months but mild residual weakness may remain ^[18] (this figure specifically refers to diabetic amyotrophy/proximal diabetic neuropathy, but the principle of spontaneous recovery applies to acute diabetic mononeuropathy generally)
• Glycaemic control: This is the single most important intervention. Tight glucose control (HbA1c < 7%) reduces the risk of further microvascular complications and may improve nerve recovery. Prefer SGLT2i and GLP-1 receptor agonists ^[18] (for T2DM) as they have additional cardiovascular and renal benefits.
• Neuropathic pain management: Gabapentin/pregabalin/amitriptyline ^[18]
• Eye protection in CN III/VI palsy: Patching the affected eye to prevent diplopia; lubricating eye drops if lagophthalmos; prism glasses for persistent diplopia
• MRI brain to rule out stroke if CN III palsy (and also to exclude PComA aneurysm) ^[18]
• Ankle-foot orthosis for foot drop due to CPN palsy
• No role for immunosuppression in diabetic mononeuropathy (it is ischaemic, not inflammatory)

When mononeuropathy (or mononeuritis multiplex) is caused by vasculitis, the treatment targets the underlying inflammatory process:

• High-dose corticosteroids (e.g., prednisolone 1 mg/kg/day or IV methylprednisolone pulse for severe cases): Rapidly suppresses vasa nervorum inflammation → prevents further nerve infarction
• Steroid-sparing immunosuppressants:
  • Cyclophosphamide (for severe systemic vasculitis — GPA, EGPA, PAN)
  • Azathioprine (for maintenance after remission induction)
  • Rituximab (anti-CD20, increasingly used in ANCA-associated vasculitis)
  • Mycophenolate mofetil (alternative maintenance agent)
• Treat the underlying condition: e.g., treat SLE, RA, hepatitis B/C-associated vasculitis

• Schwannoma / neurofibroma: Surgical excision — microsurgical enucleation (schwannoma can often be shelled out from the nerve without sacrificing it; neurofibromas are more integrated and may require nerve sacrifice + grafting)
• Extrinsic tumour compression (e.g., Pancoast tumour → brachial plexus): Treat the primary tumour (surgery, radiotherapy, chemotherapy) + neuropathic pain management
• Paraneoplastic: Treat the underlying malignancy; immunotherapy (IVIG, steroids) may have limited benefit

Bell's palsy is the most common cranial mononeuropathy and has its own specific management:

1. Corticosteroids (within 72 hours of onset): Prednisolone 25 mg BD × 10 days or 60 mg daily × 5 days then taper. Mechanism: reduces oedema within the facial canal → reduces compression of CN VII → improves recovery rate.
2. Eye care (critical — because orbicularis oculi weakness → incomplete eye closure → exposure keratopathy):
   • Artificial tears during the day
   • Lubricating ointment + tape eyelid shut at night
   • Moisture chamber (glasses/goggles)
   • If severe: temporary tarsorrhaphy (surgical partial closure of eyelid)
3. Antivirals: Valaciclovir 1g TDS or aciclovir 400 mg 5×/day — added to steroids in severe palsy (House-Brackmann grade IV–VI), though evidence is debated
4. Physiotherapy: Facial muscle exercises once recovery begins
5. Prognosis: ~70% complete recovery; worse prognosis if complete paralysis, age > 60, diabetes, hypertension, Ramsay Hunt syndrome

• Genetic: Autosomal dominant, PMP22 gene deletion on chromosome 17p (the same gene duplicated in Charcot-Marie-Tooth type 1A — deletion vs. duplication)
• Presentation: Recurrent, episodic mononeuropathies at typical entrapment sites, often with trivial compression. Episodes resolve spontaneously over days to weeks.
• Management: Avoidance of nerve compression (ergonomic modifications, avoid prolonged pressure on nerves), genetic counselling. No specific pharmacological treatment.

• Can develop after any mononeuropathy, especially traumatic or post-surgical
• Features: Disproportionate burning pain, allodynia (pain from normally non-painful stimulus), swelling, colour and temperature changes, later atrophic changes
• Management: Multidisciplinary — physiotherapy (graded motor imagery, mirror therapy), neuropathic pain agents (gabapentin, amitriptyline), psychological support, nerve blocks in refractory cases

• Mechanism: When axonal degeneration occurs (axonotmesis or neurotmesis), the muscle fibres supplied by the damaged axons lose their trophic support and undergo denervation atrophy. If reinnervation does not occur within ~12–18 months, the muscle fibres are progressively replaced by fibrous tissue and fat → irreversible weakness.
• Clinical relevance: This is why early referral when motor deficit is present is so important ^[5]. In CTS with established thenar wasting, even successful carpal tunnel release may not fully restore muscle bulk or strength because the motor endplates have degenerated.
• Prognosis: usually recover after primary cause is removed unless axonal loss occurred ^[2] — this statement encapsulates the key prognostic principle. Demyelinating injury (neurapraxia) recovers fully; axonal loss may not.

• Mechanism: When muscles are paralysed, the unopposed action of their antagonists and the effect of gravity gradually pull the joint into a fixed position. Without active movement through full range of motion, the joint capsule, ligaments, and tendons shorten → fixed contracture.
• Examples:
  • Wrist drop (radial nerve palsy): Wrist stuck in flexion from unopposed wrist flexors → if not splinted in extension, a flexion contracture develops within weeks
  • Foot drop (CPN palsy): Ankle stuck in plantarflexion from unopposed gastrocnemius/soleus → equinus contracture → unable to achieve plantargrade foot even if nerve recovers
  • Claw hand (ulnar nerve palsy): MCP hyperextension + IP flexion deformity becomes fixed
• Prevention: Splinting in the functional position (wrist extension splint for radial palsy, AFO in neutral for foot drop), regular passive range of motion exercises, physiotherapy
• Contractures > 15° at major joints significantly impair function and may require surgical release if established

• Foot drop → steppage gait (high-stepping gait to clear the foot from the ground): increased risk of tripping and falls, particularly on uneven surfaces and stairs
• Falls → secondary injuries (fractures, head injury) — especially dangerous in elderly or diabetic patients who may also have visual impairment and peripheral sensory loss
• Management: Ankle-foot orthosis (AFO) to maintain dorsiflexion during swing phase; gait training with physiotherapy

• Hand mononeuropathies (CTS, ulnar, radial nerve): Loss of fine motor skills → difficulty with buttons, writing, opening jars, using tools → occupational disability, loss of independence
• Lower limb mononeuropathies: Difficulty walking, climbing stairs, driving → reduced mobility, social isolation
• These functional consequences can be devastating, particularly in patients whose livelihood depends on manual dexterity or mobility

• Mechanism: Loss of protective sensation means the patient cannot feel pain from pressure, friction, heat, or sharp objects → repeated unrecognized microtrauma to the anaesthetic skin → tissue breakdown → ulceration
• Classic example: Diabetic foot ulcer — the combination of peripheral sensory neuropathy (cannot feel the injury), microangiopathy (poor blood supply → impaired healing), and autonomic neuropathy (dry cracked skin from loss of sweating, altered blood flow) creates the "perfect storm" for chronic non-healing ulcers ^[3][19]
  • Worsened healing: damaged microvasculature, less nutrients for good healing to occur. Prone to infection due to the higher glucose content. Peripheral neuropathy → unknown injury ^[19]
• In isolated mononeuropathy (e.g., posterior tibial nerve → sole of foot is anaesthetic): pressure ulcers can develop under the metatarsal heads from walking
• Prevention: Patient education about foot care, daily foot inspection, appropriate footwear, regular podiatry, avoidance of walking barefoot

• Neuropathic ulcers are prone to bacterial colonization and deep infection
• If infection penetrates to bone → osteomyelitis → may require prolonged antibiotics or even amputation
• Non-healing foot ulcer in a diabetic is a common presentation — always examine the feet for neuropathy, ischaemia, and infection ^[19]

• Mechanism: Loss of proprioception and pain sensation → the joint is subjected to repeated microtrauma without the protective pain response → progressive joint destruction with fractures, dislocations, and deformity → Charcot's joints ^[2]
• Most commonly affects the foot and ankle in diabetic neuropathy
• Presents as a warm, swollen, deformed foot — often misdiagnosed as cellulitis or gout
• Can occur in any mononeuropathy with significant sensory loss affecting a weight-bearing joint
• Trophic changes: disuse atrophy, hair loss, brittle nails, trophic ulcers, Charcot's joints ^[2]

• Loss of temperature and pain sensation → inability to detect hot surfaces, sharp objects, or chemical exposure → burns, cuts, and injuries that go unnoticed until tissue damage is established

• Mechanism: Nerve injury causes upregulation of sodium channels at the injury site and in the dorsal root ganglion → ectopic firing of damaged nerve fibres → spontaneous burning pain, shooting/lancinating pain, allodynia (pain from light touch), and hyperalgesia (exaggerated pain from mildly painful stimulus)
• Can be severely disabling and resistant to conventional analgesics
• Develops in a significant proportion of patients with mononeuropathy, especially traumatic and post-surgical nerve injuries
• Management: gabapentin/pregabalin, amitriptyline, duloxetine; refractory cases may need nerve blocks or neuromodulation

• Previously known as: Reflex sympathetic dystrophy (Type I) or causalgia (Type II)
• Mechanism: Maladaptive neuroplastic response to nerve injury → regional pain far out of proportion to the inciting event + autonomic dysfunction + trophic changes. The exact pathophysiology involves peripheral sensitization, neurogenic inflammation, sympathetic-afferent coupling, and central sensitization.
• Clinical features (three stages):

• Management: Early physiotherapy (graded motor imagery, mirror therapy), neuropathic pain agents, psychological support, bisphosphonates for bone changes, sympathetic nerve blocks in refractory cases

Specific complications of carpal tunnel release ^[5]:

• Persistent CTS symptoms (inadequate release) — incomplete division of the flexor retinaculum
• Nerve injury: palmar cutaneous branch — this sensory branch can be damaged during dissection, causing a painful neuroma or numbness over the thenar eminence (so-called "pillar pain")
• Vascular injury: superficial palmar arch — runs deep to the retinaculum; laceration causes haematoma or ischaemia to digital arteries

Additional surgical complications (any nerve decompression):

• Wound infection
• Haematoma
• Scar-related nerve tethering (the nerve becomes adherent to scar tissue → recurrence of symptoms)
• Painful neuromas at sites of nerve transaction or biopsy: The cut nerve ending sprouts disorganized axonal processes that form a tender nodule → tingling and pain on palpation. Management: socket modification, lignocaine and steroid injection, or surgical resection ^[20]
• CRPS (as described above)

• Tendon weakening/rupture: Repeated steroid injections near tendons can cause collagen degradation → tendon rupture (especially in the carpal tunnel where flexor tendons run adjacent to the injection site)
• Skin atrophy and depigmentation: Subcutaneous fat loss and hypopigmentation at injection site
• Infection: Introduction of bacteria during injection (rare if aseptic technique used)
• Transient hyperglycaemia: In diabetic patients — steroids cause insulin resistance → blood glucose may spike for 24–48 hours after injection. Important to warn diabetic patients and adjust their insulin accordingly.
• Nerve injury: Direct injection into the nerve (patient reports electric shock pain during injection → stop immediately)

• Joint stiffness: Paradoxically, the splint intended to protect the nerve can cause joint stiffness if worn continuously without range of motion exercises
• Skin breakdown: Under the splint, especially in diabetic patients with poor sensation
• Muscle deconditioning: Prolonged immobilization → disuse atrophy of muscles beyond the nerve territory
• DVT risk: Particularly in lower limb splinting/immobilization

Diabetic mononeuropathy rarely occurs in isolation — it is a marker of established microvascular disease. The patient almost certainly has or will develop other chronic diabetic complications ^[3][19]:

• Microvascular: retinopathy, nephropathy (glomerulosclerosis), neuropathy (peripheral, autonomic, mononeuropathy, amyotrophy) ^[3]
• Macrovascular: stroke, coronary artery disease, peripheral artery disease ^[3]
• This is why screening for chronic complications is essential: retinopathy, nephropathy, neuropathy — "Big 3" ^[19]
• Good control of blood glucose delays complications ^[3]

If mononeuropathy is the presenting feature of systemic vasculitis (PAN, GPA, EGPA), the untreated disease will progress to:

• Further nerve infarctions → mononeuritis multiplex → confluent neuropathy
• Renal involvement → glomerulonephritis → renal failure
• Other organ damage (lung haemorrhage, GI ischaemia, cardiac involvement)
• Hence the urgency of immunosuppression

• In the context of chronic neuropathic ulcers, malignant transformation to squamous cell carcinoma (Marjolin's ulcer) can occur in long-standing, non-healing wounds — though this is rare and more associated with burn scars than typical neuropathic ulcers