Station 3: Neuro Flashcards
Scars in neurology?
- Muscle biopsy scar - triceps, deltoid, lateral quadriceps
- Nerve biopsy scar - lateral ankle (sural nerve)
- Sternotomy scar - thymectomy in MG
- Anterior or posterior neck scar - cervical decompression
- Lumbar scar - laminectomy
- Scalp or behind ear - previous burrhole surgery or craniotomy
Approach to gait?
- Observe surrounding for walking aids, ankle foot orthoses
- Always ask if patients can stand or walk first
- Observe base: narrow or wide?
- If abnormal: symmetrical or asymmetrical?
- If normal: ask to tandem-walk (could you walk heel-to-toe, as if on a tight-rope?) -> brings out subtle gait ataxia
- If normal: walk on tip toes, then on heels -> assess distal power
- Romberg’s test (test of proprioception - peripheral nerves/dorsal column): stable with eyes open, unstable with eyes closed whilst standing in narrow base -> positive Romberg’s -> sensory ataxia
*If in BCC - ask about ADL: How far can they walk? Can they climb stairs? Can they get out of a chair? Can they dress or feed themselves?
Describe different types of abnormal gait?
- Spastic: narrow-based, stiff, scissoring, toe-scuffing
- Diplegic: extensor and adductor spasm, walking on tip toe, scissoring if no adductor release
- Hemiplegic: circumducting with scuffing of one foot (UL flexor hypertonia, LL extensor hypertonia, distal weakness > proximal)
- Extrapyramidal: shuffling, festinant, poor arm swing, freezing, slow turning
- Ataxic: broad-based, wide staggering quality, titubation, falling towards side of lesion
- Sensory ataxic: stomping, more evident in the dark (loss of proprioception)
- Apraxic: gait ignition failure, difficulty walking, walk of little steps but with upright stance (marche a petit pas) -> frontal lobe pathology (stroke, NPH, MS)
- Neuropathic: high-stepping, stomping
- Myopathic: waddling, hip on the side of weakness drops when stepping forward, and trunk sways to other side to compensate (trendelenburg - pelvis sags down when hip on the affected side is lifted)
Approach to cerebellar examination?
Ataxia: presence of truncal ataxia if lesion is at cerebellar vermis
Nystagmus
Dysmetric saccades
Impaired smooth pursuit
Scanning or slurred speech
Dysmetria (past-pointing)
Dysdiadochokinesia
Rebound phenomenon - arms outstretched with palms upwards, apply pressure on forearm with sudden release (arms will oscillate or past original position in cerebellar dysfunction)
Hypotonia
Gait - wide based, staggering, falling towards side of lesion
Tandem-gait - subtle ataxia
Romberg’s test - not really cerebellar, actually tests for proprioception
Approach to upper limb examination?
Inspection, tone, power, reflexes, coordination, sensation (STT pin prick, DCML soft touch, vibration and position sense)
Upper limb
Inspection - muscle biopsy scar on deltoid or triceps, muscle wasting, fasciculations, tremors at rest
Stretch out hands, palms upwards and close eyes - postural tremors, pronator drift (weakness), upward drift (cerebellar), rebound phenomenon (cerebellar)
Turn hands over - pseudoathetosis (sensory ataxia)
Tone - pronator catch for spasticity, cogwheel rigidity at wrist, lead pipe rigidity at elbow
Power - according to nerve root, stabilize proximal joint, test for fatiguability if indicated
Reflexes - supinator, biceps, triceps
Inverted supinator: elbow flexion absent but instead there is finger flexion (C5/C6 cervical myelopathy)
Hoffman reflex: flicking distal middle finger will cause thumb and index finger flexion
Coordination
Dysmetria, intention tremor, rebound phenomenon
Sensation
Depending on earlier findings - if UMN, find sensory level
If LMN - assess for whether there is nerve root or specific nerve problem
If peripheral neuropathy - assess glove distribution
Pin prick
Soft touch
Vibration and joint position sense
Approach to lower limb examination?
Inspection, tone, power, reflexes, coordination, sensation (STT pin prick, DCML soft touch, vibration and joint position sense)
Lower limb
Inspection - muscle biopsy scars on quadriceps, nerve biopsy scar at lateral ankle (sural), wasting, fasciculations
Tone - move hips and look at foot, lift knee rapidly and look at foot - foot off bed indicates hypertonic, check clonus
Power - according to nerve root, stabilize proximal joint, test fatiguability if indicated
Reflexes - knee, ankle, plantar
Coordination - heel-shin test
Sensation
Depending on earlier findings - if UMN, find sensory level
If LMN - assess for whether there is nerve root or specific nerve problem
If peripheral neuropathy - assess stocking distribution
Gait
Causes of absent ankle jerks + extensor plantar responses?
Caused by a combination of pyramidal and peripheral nerve lesions
- Stroke + peripheral neuropathy
- Cervical myelopathy + peripheral neuropathy
- Cervical and lumbar myelopathy
- Friedreich’s ataxia
- Subacute combined degeneration
- Neurosyphilis
- MND
- Conus medullaris lesion
Spasticity vs rigidity?
Spasticity
- Increased muscle tone, velocity-dependent
- More pronounced at the onset of movement
- Decreased with continuous passive movement
- Clasp-knife phenomenon
- Caused by enhanced stretch reflex activity, this is activated whenever there is rapid stretching of muscles, so the muscle will contract to resist the force that is stretching it
- In UMN lesion, inhibitory inputs are lost and so during normal movement there is also enhanced stretch reflex activity
Rigidity
- Increased muscle tone throughout ROM
- Velocity-independent
- Lead-pipe/cogwheel rigidity
Spastic paraparesis - approach and clinical signs?
Approach:
Spastic gait -> UMN! (brain, cerebellum, spinal cord)
Localise the lesion:
- UMN findings in upper limbs -> C4 or above (spastic quadriparesis)
- LMN signs -> one level indicates lesion at the level (cervical spondylosis), diffuse signs indicate MND
- Cerebellar signs
- Sensory level
- Eyes -> RAPD, INO, optic atrophy suggest MS
- Pseudobulbar signs (brisk jaw jerk, dysarthria) -> brainstem or bilateral cerebral
- Look for surgical scars -> craniotomy or spinal procedure
Clinical signs:
- Stiff, narrow based gait
- Legs longer due to postural change -> toe-scuffing, circumducting
- Hips drawn together due to increased adductor tone (scissoring)
- Pyramidal weakness
- Hyper-reflexia
- Clonus
- Extensor plantar responses
- Wasting and contractures -> in long-standing cases, due to disuse atrophy
Spastic paraparesis - causes?
Brain
- MS/demyelination (young, INO, RAPD, optic atrophy, cerebellar)
- Bilateral cerebral infarcts
- Parasagittal meningioma (features of parietal lobe - contralateral impaired proprioception, 2 point discrimination)
- Cerebral palsy
Spinal cord
- MND (fasciculations, wasting)
- Friedreich’s ataxia (young, cerebellar, dorsal column, pes cavus)
- Spinal cord compression (cervical spondylosis, trauma, tumour)
- Anterior spinal cord infarction (impaired pain and temperature)
- Transverse myelitis (sensory level)
- Syringomyelia (impaired pain and temperature, UL wasting and hypo-reflexia)
- Hereditary spastic paraparesis (upper limbs normal, no sensory signs)
- Tropical spastic paraparesis (HTLV-1 myelopathy, Afro-Caribbean, proximal > distal weakness, dorsal column, peripheral neuropathy)
Spastic paraparesis - how to differentiate the cause?
Rapidity of onset:
Seconds to minutes - vascular, trauma (although would not expect to present with spasticity at acute phase)
Hours - compressive (trauma), inflammatory (transverse myelitis - MS, NMO), infective (epidural abscess TB, staph)
Days - compressive (degenerative, slow growing tumours), inflammatory, nutritional (B12, copper)
Weeks to months - degenerative/hereditary (HSP), compressive, infective (HIV/HTLV-1), nutritional
*HSP slowly progressive walking difficulties, with positive FHx
Causes of spastic paraparesis + cerebellar signs?
- Friedreich’s ataxia
- SCA
- MS
- Syringomyelia
- Lesion at craniospinal junction
- Arnold-Chiari malformation (herniation of cerebellar tonsils into foramen magnum)
- Neurosyphilis
Causes of spastic paraparesis + dorsal column signs?
- Cervical myelopathy
- Friedreich’s ataxia
- MS
- Subacute combined degeneration
- Neurosyphilis
Cerebellar syndromes - approach and clinical findings?
- Is it cerebellar or ataxic syndrome?
- Ataxic: combination of cerebellar and sensory
- Cerebellar: scanning speech, eyes (nystagmus, impaired smooth pursuit, dysmetric saccade)
- Sensory: joint position and vibration impairment, Romberg’s, pseudoathetosis (worse when eyes are closed), distal weakness
- Associated features that can help differentiate cause: eye signs (INO, RAPD), pyramidal weakness, peripheral neuropathy - Cerebellar features:
- Head titubation
- Gaze-evoked nystagmus fast phase towards side of lesion (or bidirectional if bilateral lesions)
- Scanning speech
- Truncal ataxia (cerebellar vermis lesion)
- Rebound phenomenon (failure of calibration of muscle forces)
- Hypotonia
- Dysdiadochokinesis (clapping hands, tapping on thigh, rapid pronation/supination of hands)
- Dysmetria
- Intention tremor esp closer to target
- Impaired heel-shin test
- Pendular jerks
- Wide-based staggering gait - Sensory ataxia: is it central or peripheral?
- Central: spinal cord (dorsal column pathology)
- Peripheral: peripheral neuropathy
- Joint position impairment and pseudoathethosis (can be both)
- Distal weakness (peripheral)
- Stomping gait
Cerebellar syndromes - causes?
Cause is evident in history + cadence of onset
Unilateral
- Vascular: infarct or haemorrhage (acute)
- SOL: tumour, abscess (chronic)
- Demyelination (acute or relapsing-remitting)
Bilateral
- Nutritional: B12, vit E deficiency, coeliac disease (chronic)
- Toxic: alcohol (chronic)
- Hypothyroidism (chronic)
- Demyelination
- Degenerative/hereditary: SCA, Friedreich (chronic)
- Paraneoplastic (acute/subacute and progressive)
- Drugs: phenytoin, carbamazepine, barbiturates (acute or chronic)
Cerebellar syndromes - investigations?
Cause is evident in history + cadence of onset
Ix guided by history but all with cerebellar ataxia will require brain imaging
- MRI is superior to CT to look at the posterior fossa
- CT has important role in hyperacute presentations when haemorrhage needs to be rapidly excluded
Other targeted Ix
- Alcohol and drug history
- B12, FBC, TFT, VDRL, anti-tissue transglutaminase, anti-endomysial (coeliac)
- Paraneoplastic antibodies
- Lumbar puncture for protein and oligoclonal bands (MS)
- VEP
Cerebellar syndromes - management?
- Address underlying aetiology
- Manage reversible factors
- MDT: physio, OT to maintain function, preserve strength, provide adaptation
- Review medications: any that are exacerbating or influencing things such as dizziness and unsteadiness?
- Social history: occupation risk, alcohol history (whilst may not be caused by alcohol intake, it may exacerbate the symptoms and so advising to limit intake or stop altogether)
Cerebellar syndromes - paraneoplastic cerebellar syndrome, which cancer is most frequently associated?
Paraneoplastic cerebellar syndrome:
- Subacute and progressive
- Lose mobility within 1 year
- Antibodies against tumour but cross-react with CNS cells
- Small cell lung Ca, breast, gynaecological, Hodgkin lymphoma
- Anti-Yo (breast, gynae), anti-Hu (SCLCa)
Cerebellar syndromes - genetic causes and the features?
- SCA (AD): UMN, extrapyramidal, peripheral neuropathy, ophthalmoplegia
- Friedreich’s ataxia (AR): DM, cardiomyopathy, arrhythmia
- Ataxia telangiectasia (AR): skin and eye telangiectasia, dystonia, chorea
- VHL: cerebellar haemangioblastoma, RCC
SCA - the genetics?
- Autosomal dominant inheritance
- The known mutation is trinucleotide repeat and demonstrate anticipation (earlier onset and more severe disease in subsequent generations)
- More than 25 types described, commonest is SCA1, SCA2, SCA3, SCA6
Friedreich’s ataxia - clinical features, investigations and management?
Clinical features:
- Onset 10-15yrs, degenerative, wheelchair bound < 25yrs
- Spinocerebellar tract: cerebellar ataxia
- Posterior column: loss of proprioception + vibration sense
- Corticospinal tract: spastic paraparesis, pyramidal weakness, extensor plantars
- Dorsal root: absent reflexes
- Peripheral nerves: pes cavus
- Associations: DM, cardiomyopathy/arrhythmia, kyphoscoliosis, hearing impairment
Investigation:
- Genetic testing ultimately
- Exclude reversible causes: B12, vit E deficiency
- Exclude compressive causes: MRI brain and spinal cord
- Nerve conduction study to investigate for peripheral neuropathy
Management:
- Genetic counselling and patient education
- MDT: OT, physio, neurology, cardiology
- OT: adaptation at home or work, walking aids, devices or orthotics
- Physio: preserve function and strength
- Correction of pes cavus or scoliosis
- Regular ECG and ECHO (important cause of early mortality!)
- Meds for diabetes
Friedreich’s ataxia - the genetics?
- Autosomal recessive
- Mutation trinucleotide GAA repeat
- Problems with frataxin gene that leads to iron accumulation in mitochondria, oxidative damage, cell death
- Affects spinal cord (corticospinal, posterior column, spinocerebellar tracts), roots and peripheral nerves
HINTS exam - when do you perform it and what does it indicate?
- Persistent vertigo over hours or days
- Nystagmus
- Normal neurological exam
- Differentiates between central or peripheral cause of vertigo
Central cause: posterior circulation stroke, MS, tumour, trauma, medication
Peripheral cause: BPPV, vestibular neuronitis, Meniere’s disease
HINTS exam - describe the components
Head impulse
Focus on nose and turn head left to right, and then rapidly back to midpoint
Central: no corrective saccade (also normal)
Peripheral: corrective saccade (eyes move past the midpoint then saccade back)
Nystagmus
Central: bidirectional
Peripheral: none or unidirectional
Test of skew
Focus on nose and cover one eye, then quickly move hand to cover other eye
Central: vertical skew
Peripheral: no vertical skew
Multiple sclerosis - approach and clinical signs?
Use term ‘demyelinating disease’ when presenting
Characterised by lesions separated in space and time
- Eyes - RAPD, optic atrophy
- Brainstem - INO (impaired adduction + nystagmus in abducting eye but not necessarily), cranial nerves
- Cerebellum - nystagmus, dysmetric saccades, impaired smooth pursuit, dysarthria, incoordination, rebound phenomenon
- Spinal cord (corticospinal tract) - pyramidal weakness, hypertonia, hyperreflexia, spastic paraparesis
- Spinal cord (dorsal column tract) - pseudoathetosis, sensory ataxia, Romberg’s positive, loss of vibration and proprioception
Other signs:
Lhermitte’s sign - electrical shock sensation down neck to upper and lower limbs with neck flexion
Uhtoff’s phenomenon - worsening of symptoms with heat e.g. exercise, hot bath
Multiple sclerosis - investigations?
Diagnosis by 2017 McDonald’s criteria
- Allows diagnosis of MS after CIS, without need for 2nd clinical episode
MRI brain demyelination protocol, most useful:
- Periventricular and juxtacortical white matter/brainstem/cerebellum/spinal cord T2 hyperintense lesions
- Gadolinium-enhancing lesions reflect active disease
Visual/auditory evoked potential
- Look at lesions in eyes and brainstem
CSF
- Usually normal
- Unmatched oligoclonal bands (reflect inflammation limited to CNS; if matched with serum suggests spillover into CSF due to systemic disease e.g SLE)
Labs
- Exclude mimics if presence of atypical features: ESR, CRP, autoimmune screen, vasculitis screen, B12, VDRL
- Atypical features: raised inflammatory markers, matched serum/CSF oligoclonal bands, unusual radiological findings
Multiple sclerosis - treatment?
Acute relapse:
- Steroids, hastens recovery and reduces duration of relapse, but does not change overall clinical course
- Screen for infection that might trigger relapse
Disease-modifying:
- Mainly reserved for RRMS with evidence of active disease
- B-IFN and glatiramer acetate (subcutaneous or IM), reduce relapse rate by 1/3, associated with injection-site reactions, flu-like symptoms
- B-IFN associated with nAb which reduces efficacy over time
- Natalizumab (monoclonal ab), reduce relapse rate by 2/3, reserved for severe active disease, associated with hypersensitivity and PML
- Mitoxantrone (cytotoxic agent), reduce relapse rate by 2/3, reserved for very aggressive active disease, associated with cardiac failure, bone marrow suppression, leukaemia
- Oral fingolimod
- ALL DMTs should be withdrawn if patient plans to become pregnant, or during pregnancy
Others:
- Physiotherapy, OT, speech and language therapy
- Anti-spastic agents: baclofen, botox
- Laxatives for constipation
- Analgesia
Multiple sclerosis - causes?
- Complex aetiology
- Genetic susceptibility - increased risk of MS if there is MS in 1st degree relatives
- Environmental factors - increases with increasing latitude, possible EBV/HHV-6/chlamydia infections
Multiple sclerosis - clinical course?
- Relapsing-remitting (80-85%): short acute attacks with remission and steady baseline state
- Secondary progressive (30-40%): RR pattern initially then becomes progressive after years (usually 20yrs), with gradual neurological decline but no clear relapse
- Primary progressive (10-15%): gradually progressive deterioration from onset of symptoms
- Progressive-relapsing (5-10%): gradually progressive deterioration from onset, with superimposed relapses
Multiple sclerosis - 2017 McDonald criteria?
Allows diagnosis of MS after a single CIS, without the need to wait for a 2nd clinical episode
Evidence of lesions disseminated in time and space
Dissemination in time:
- New T2 hyperintense or gadolinium-enhancing lesions on follow-up MRI, compared to baseline scan
- Simultaneous asymptomatic gadolinium-enhancing and non-enhancing lesions at any time
Dissemination in space: > 1 T2 lesion in at least 2 of: - Juxtacortical - Periventricular - Infratentorial - Spinal cord
Multiple sclerosis - MS mimics?
Many mimics, suspect if atypical features:
Systemic symptoms, raised inflammatory markers, matched CSF/serum oligoclonal bands, unusual radiological findings
- Vasculitis/autoimmune: NMO, SLE, Sjogren, sarcoidosis
- Vascular: TIA, stroke, CADASIL, APLS
- Metabolic: B12 deficiency
- Infection: HIV, syphilis, PML
Neuromyelitis Optica (NMO) - clinical features and treatment?
- Autoimmune mediated: aquaporin-4 antibody
- More severe optic neuritis and more extensive spinal cord involvement > 3 vertebral segments
- Recovers less well
- Treatment with IVIg or plasma exchange in acute setting, steroids and immunosuppressants long-term
Upper limb - root, nerve, muscle, sensory, reflex distribution?
Shoulder abduction: C5-C6 (lateral arm, forearm, thumb, index finger), axillary nerve (regimental badge over shoulder), deltoid
Shoulder adduction: C6-C8 (lateral arm, forearm, entire hand), thoracodorsal nerve (purely motor), lat dorsi and pec major
Elbow flexion: C5-C6, musculocutaneous nerve (lateral forearm), biceps, biceps reflex
Elbow extension: C6-C8, radial nerve (extensor forearm, back of hand), triceps, triceps and brachioradialis reflex
Wrist flexion: C6-C7, median and ulnar nerves, flexor carpi radialis and ulnaris
Wrist extension: C5-C8, radial and posterior interosseous nerves, extensor carpi radialis longus and ulnaris
Finger flexion: C8 (little finger, ulnar 1/2 of ring finger and hand), median (FDS) and ulnar (FDP) nerves
Finger extension: C7-C8, posterior interosseous nerve (purely motor), extensor digitorum
Finger abduction: C8-T1, ulnar nerve, 1st dorsal interosseous and abductor digiti minimi
Finger adduction: C8-T1, ulnar nerve, palmar interosseous
Thumb abduction: C8-T1, median nerve, abductor pollicis brevis
Thumb opposition: C8-T1, median nerve, opponens pollicis
Thumb flexion: C8-T1, median nerve, flexor pollicis brevis
Median nerve - motor and sensory distribution?
C5-T1
Motor: Pronator teres Flexor carpi radialis Flexor digitorum superficialis Opponens pollicis Abductor pollicis brevis Flexor pollicis brevis
Sensory:
1st 3 and 1/2 digits + thenar eminence
Median nerve palsy - features, causes, Ix and treatment?
Proximal median nerve palsy (damage at elbow, pronator teres muscle, anterior interosseous nerve)
Benediction sign (try to make a fist) - weakness of flexion of 1st and 2nd digits
Weakness:
- Thumb opposition (also powered by flexor pollicis longus supplied by ant interosseous nerve, proximal)
- Distal thumb flexion (flexor pollicis longus)
- Wrist flexion (flexor carpi radialis)
- Arm pronation (pronator teres)
Sensory deficit 1st 3 1/2 digits + thenar eminence (palmar cutaneous branch, proximal)
Distal median nerve palsy (damage at wrist or carpal tunnel)
Ape hand sign - wasting thenar eminence, sparing hypothenar eminence
Weakness:
- Thumb abduction (abd pollicis brevis)
- Thumb opposition (opponens pollicis)
- Flexion at MCP joint (flexor pollicis brevis)
Sensory deficit 1st 3 1/2 digits, thenar eminence spared
Special tests
- Tinel’s sign: percussion over flexor retinaculum
- Phalen’s sign: wrist flexion for 1 min
Causes
- Idiopathic
- Work-related
- Pregnancy
- Endo: hypothyroidism, DM, acromegaly
- MSK: RA, degenerative, gout
- Neuro: HNPP, inflammatory e.g. CIDP/MMN
- ESRF, uraemia, regular dialysis
- Amyloidosis
Ix
- NCS: localise lesion -> median motor and sensory latencies and conduction velocities
- EMG: provide prognosis in terms of recovery -> abductor pollicis brevis denervation
Treatment
- Physiotherapy
- Wrist splint
- Local steroid injections
- Carpal tunnel decompression surgery
Ulnar nerve - motor and sensory distribution?
C8-T1
Motor: Flexor carpi ulnaris Flexor digitorum profundus Dorsal interosseous Palmar interosseous
Sensory:
1/2 ring finger, little finger, hypothenar eminence
Ulnar nerve palsy - features, causes, Ix and treatment?
Proximal ulnar nerve palsy (elbow) -> most common
Hypothenar wasting
Ulnar border of forearm wasting
Weakness:
- Wrist flexion in ulnar direction (flexor carpi ulnaris)
- Finger abd/adduction (palmar and dorsal interossei)
- 4&th & 5th MCP flexion (lumbricals)
- 4th & 5th DIPJ flexion (flexor digitorum profundus)
Sensory deficit 5th and adjacent medial 4th fingers, palmar and dorsal surfaces of medial portion of hand
Distal ulnar nerve palsy (wrist)
Claw hand (4th & 5th extension MCP joint, flexion IP joint)
Hypothenar and 1st dorsal interosseous wasting
Weakness:
- Finger abd/adduction (palmar and dorsal interossei)
- 4&th & 5th MCP flexion (lumbricals)
Sensory deficit 5th and adjacent medial 4th fingers
Special tests
- Froment’s sign: testing adductor pollicis -> pinching paper between thumb and index fingers, with thumb in adduction, will lead to thumb flexion (flexor pollicis longus compensating, innervated by median nerve)
Causes
- Compression at elbow: arthritis, fracture, perioperative, mass
- Lesion at wrist: ganglion, tumour, fracture
- DM
- Vasculitis
- HNPP, CIDP, MMN
Ix
- NCS: localise lesion
- EMG: provide prognosis in terms of recovery
Treatment
- Physiotherapy
- Arm or wrist splint
- Manage neuropathic pain: TCA, gabapentin/pregabalin, topical capsaicin
- Decompression surgery
Median, ulnar, T1 radiculopathy - how to differentiate?
Abductor pollicis brevis (APB)
First dorsal interosseous (FDIO)
Median nerve lesion: APB weak, FDIO normal
Ulnar nerve lesion: APB normal, FDIO weak
T1 lesion: APB and FDIO weak
Radial nerve - motor and sensory distribution?
C5-T1
Motor: Triceps Brachioradialis Extensor carpi radialis longus Extensor carpi ulnaris Extensor digitorum
Sensory:
Extensor forearm, back of hand, dorsum of 1st 4 fingers
Radial nerve palsy - features, causes, Ix and treatment?
Axilla lesion (tricep) Wrist drop Weakness: - Finger extension at MCP joint - Wrist extension - Forearm supination - Elbow extension Sensory deficit tricep, posterior forearm, 1st dorsal interosseous Absent tricep reflex
Spiral groove lesion (brachioradialis) Wrist drop Weakness: - Finger extension at MCP joint - Wrist extension - Forearm supination - Elbow flexion with forearm held between supination and pronation Sensory deficit 1st dorsal interosseous
Proximal forearm lesion Wrist drop Weakness: - Finger extension at MCP joint - Wrist extension No sensory deficit (post interosseous nerve purely motor)
Wrist lesion
No wrist drop, no weakness
Sensory deficit 1st dorsal interosseous
Causes
- Trauma or fractures
- Compression: crutches, Saturday night palsy
- Tumour, ganglion
Ix
- NCS: localise lesion
- EMG: provide prognosis in terms of recovery
Treatment
- Physiotherapy
- Wrist or elbow splint
- Decompression surgery
Radial and C7 radiculopathy - how to differentiate?
C7 radiculopathy affect both median and radial nerves, so weakness at:
- Shoulder adduction
- Elbow extension
- Wrist flexion and extension
Radial nerve lesion, weakness:
- Spares shoulder abduction (C5, axillary nerve) and wrist flexion (C7, median and ulnar nerves)
