Neurology Flashcards
Distribution of peripheral sensory nerves hand
Radial nerve - snuff box
Median nerve - lateral first finger
Ulnar nerve - medial hand
Upper limb dermatomes/peripheral nerves
Lateral biceps - C5 musculocutaneous
Lateral forearm - C6 lateral cutaneous (from MC)
Snuff box - C6/radial
Radial first finger - C6/median
Middle finger - C7, variable nerve
Ulnar hand - C8/ulnar
Medial forearm - C8, medial cutaneous nerve
Medial biceps - T1
Upper limb reflex nerves/roots
Biceps - Musculocutaneous. C5/6
Brachioradialis - radial. C6(5)
Triceps - Radial. C7 (C6-8)
Differentiating ulnar from C8/T1 lesion
Abductor pollicis brevis C8/T1, median nerve
Medial forearm C8 not ulnar
Ulnar neuropathy signs
Inspection: flexion 4th/5th fingers. First dorsal and hypothenar wasting.
Power: Weak finger abduction
Altered sensation little finger/half ring palmar
Ulnar nerve nerve injury sites
- At elbow in ulnar groove from repetitive flexion/extension
- Wrist fracture/surgery
Parkinsonism definition
Triad:
- Tremor - resting, low freq
- Hypertonia - rigidity>spasticity, cogwheel
- Bradykinesia - slow initiation, reduced amplitude with repetition, micrographia
Parkinson’s plus syndromes
Progressive supranuclear palsy - early postural instability, vertical gaze palsy, trunkal rigidity, speech/swallow issues
Multisystem atrophy - early autonomic features, cerebellar signs
Cortico-basal degeneration - akinetic rigidity of one limb, alien limb, sensory loss/change
LBD
Parkinson’s investigations
Bedside
- OBS /postural BP
- DHx
- MOCA/cognitive assessment for dementia
Imaging:
- Consider MRI to exclude structural pathology
- Consider DaT scan
Parkinson’s treatment
- L- Dopa with Dopa carboxylase inhibitor (madopar/co-beneldopa). SEs - Nausea, dyskinesia, on/off, waning over years. Inhibitor prevents peripheral metab from prodrug to dopamine -> fewer peripheral SEs
- Dopamine agonists (rotigotine) - less waning, more SEs inc disinhibition
- MAOB inhibition (selegiline) - prevents dopamine breakdown
Others: - COMT inhibition - prevents L dopa breakdown to reduce off periods
- Apomorphine - SC for severe off rescue
- DBS
30 year old woman
Visual loss with pain on movement
Worse in bath
Episodes urinary incontinence 2 months ago
MS
Explain INO
Lésion in médian longitudinal fasciculus in pons causes ipsilateral failure of adduction with contralateral nystagmus on abduction
Causes
- MS
- Vascular
(Lyme’s, HIV, syphilis)
MS pathophysiology/prognosis
Inflammatory plaques leading to demyelination disseminated in space and time. Episodes >1h, >30/7 between.
Poor healing leads to secondary progression in >80%
10% no improvement between relapses - primary progressive
Small no - no progression
MS management
Lifestyle: stop smoking, exercise, avoid stress
DMDs: demethyl fumarate, anti t cell MAbs
Methylpred for relapses 3-5/7 affects duration but not freq/prog, use <2 per year
Symptomatic: spasticity- baclofen/gabapentin. Botox for tremor.
MS Signs
CNs: INO (often bilateral), optic atrophy, reduced acuity, other CN palsy
PNS: UMN lesions - spasticity, weakness, brisk reflexes, altered sensation
Cerebellar lesions
Lhermittes sign - electric shock sensation on cervical flexion
MS investigations
Bedside:
Bloods:
Imaging:
MRI for spatially disseminated lesions - >2 over > 2 attacks sufficient for diagnosis
Special tests:
CSF - IgG oligoclonal bands on electrophoresis, not seen in plasma
Evoked potentials - e.g. visual, sensory, auditory - evidence of e.g. optic neuritis
MS investigations
Bedside:
Bloods:
Imaging:
MRI for spatially disseminated lesions - >2 over > 2 attacks sufficient for diagnosis
Special tests:
CSF - IgG oligoclonal bands on electrophoresis, not seen in plasma
Evoked potentials - e.g. visual, sensory, auditory - evidence of e.g. optic neuritis
Peripheral primarily sensory neuropathy causes
Metabolic:
- Diabetes
- B12 deficiency
- Uraemia
- Hypothyroidism
Toxic:
- Alcohol
- Chemotherapy (vincristine)
Inflammatory:
- CIPD (chronic inflammatory )
- Sarcoidosis, RA
- Amyloidosis
Paraneoplastic:
- Solid cancer, e.g. lung
- Paraproteinaemia
Peripheral neuropathy investigations
Bedside:
- Blood glucose
- Urine dip for glucose
- Fundoscopy
Bloods
- U&E (uraemia)
- FBC (macrocytosis)
- Hba1c
- TFTs
- ESR +/- vasculitis screen
Special tests
- Electrophysiology
How does electrophysiology aid with differentiating causes of peripheral neuropathy
- Length dependent (metabolic) vs equal/mononeuritis multiplex (inflammatory)
- Demyelination vs axonal
Axonal vs demyelinating causes peripheral neuropathy
Most are axonal
Demyelinating = inflammatory e.g. GBS, CIDP
Median neuropathy signs
Inspection: Thenar wasting
Sensory: thumb-middle of ring finger palmar
Motor:
- Abductor pollicis brevis weakness
- Poor precision grip
Differentiating sites of median neuropathy
Carpal tunnel:
- Palm sensation intact
Anterior interosseous nerve (forearm)
- Distal phalanx of thumb and index weakness
- Other muscles intact
Proximal (elbow)
- Combined
Caused carpal tunnel syndrome
Oedema in carpal tunnel
Arthritis:
- RSI
- RA
Endocrine
- Myxoedema
- Acromegaly
- Diabetes/obesity increases risk
Tumours
- Ganglion/lipoma
- Myeloma -> amyloidosis
Radial neuropathy signs
Inspection
Motor
- Wrist/finger drop
- Supinator weakness
(BEAST - brachioradialis, extensors, abductor pillicis longus, supinator, triceps)
Sensory
- Most reliably anatomical snuff box
Mononeuritis multiplex causes
Generally systemic, most commonly vasculitis
Endocrine - diabetes
Mononeuritis multiplex definition
- asymmetrical
- asynchronous
- sensory and motor
- peripheral neuropathy
isolated damage to at least two separate limb or cranial nerves.
Multiple nerves in random areas of the body can be affected simultaneously or sequentially. As the condition worsens, it becomes less multifocal and more symmetrical, mimicking distal dying-back symmetrical polyneuropathy.
Nerve conduction demyelinating vs axonal findings
Ulnar nerve - axonal >38m/s, demyelinating <38
Charcot Marie Tooth epidemiology
Most common inherited neurological disorder. No ethnic etc. predisposition
AD and AR inheritance forms exist.
Charcot Marie Tooth forms
Most commonly demyelinating and AD.
Multiple forms including AR and axonal.
Type 1 - AD, demyelinating
Type 2 - AD/R, axonal degeneration
Type 4 - AR
Type X - X-linked recessive
Charcot Marie Tooth examination
Inspection:
- Pes cavus
- Pernoeal/peripheral muscle wasting
- Possible palpable nerve thickening
- Length dependent peripheral neuropathy - peripheral weakness and reduced sensation. Motor > sensory
- Hypo/arreflexia
- High-stepping/slapping gait
Bells palsy signs
- Unilateral face weakness including failure to raise eyebrow
- Numbness/pain around the ear
- Hypersensitivity to sounds (stapedius palsy)
- Bell’s phenomenon - up/out movement of eye on attempt to close
Bells palsy management
If withing 72h - High dose prednisolone for 5/7 then wean
No evidence for antivirals (although some evidence of association with HSV1)
Protect the eye - drops, sunglasses, taping at night
Facial nerve lesion site localising features
- Pons - VI nerve signs (failure to abduct eye) (e.g. stroke, tumour)
- Cerebellar-pontine angle - V, VI, VIII, cerebellar signs. (e.g. acoustic neuroma)
- Auditory canal - VIII signs (e.g. cholesteatoma/abscess)
- Face/neck - Scars or parotid mass
Causes of facial nerve palsy
- Bell’s
Infective - Ramsay Hunt (Herpes Zoster)
- Lyme
- Chronic otitis media/abscess/necrotising OE
Tumour
MS
Stroke
Diabetic mononeuropathy
Sciatic neuropathy signs
L4-S3
Hamstring weakness
Weakness all muscles below the knee
Lateral sensory loss below the knee
Common peroneal neuropathy signs
Branch of sciatic nerve above knee, L4-S1
Weakness of anterior muscles:
- Foot drop/weak dorsiflexion
- Weak ankle eversion
Dorsal foot sensory loss
Tibial neuropathy signs
Branch of sciatic nerve above knee, L4-S3
Weakness of posterior muscles:
- Weak plantarflexion (unable to stand on toes)
- Weak inversion
- Weak toe flexion
Foot sole sensory loss
Lower limb reflexes nerves/roots
Knee jerk - Femoral, L3/4
Ankle jerk - Tibial, S1/2
Cranial nerve nucleus sites
2/2/4/4
I, II - forebrain
III, IV - midbrain
V - VIII - pons
IX - XII - medulla
Causes of myelopathy
Cervical spondylosis most common
DDx:
Inflammatory:
- MS
- Ank spond
Nutritional:
- B12 -> subacute combined degeneration of the cord
Cord compression:
- Malignant - primary or bone/met
- Disc protrusion
- Neurofibroma
Vascular:
- Anterior spinal artery thrombus (usually preserves dorsal column modalities)
Infective:
- Tabes dorsalis
Myelopathy localisation on examination
Radiculopathy at level:
- LMN features
- Reduced reflexes
Myelopathy below level:
- UMN features
- Hyperreflexia
May also have sensory level
Myelopathy management
- Urgent focussed MRI (consider whole brain/spine if inflammatory cause considered)
- Analgesia
- Neurosurgical referral if spondylosis
Stroke cortical features
RSW often with dysphasia
LSW often with neglect
TACS triad
Hemianopia
Hemiparesis
Higher cortical sign
PACS présentation by vessel
MCA arm/face prédominant
ACA leg
TACS tends to be MCA
Types of MS
- Relapsing-remitting most common F:M 3:1
- Secondary progressive next - RR first, then changes over a few months
- Primary progressive - steady decline, male and female equal
MS DDx
Inflammatory:
- NMO (aquaporin 4)
- MOGAD (MOG antibodies)
- Sjogrens, lupus, sarcoid
- CNS vasculitis
Metabolic
- B12
- Copper
Infection
- Syphilis
- Lyme
Compressive
- Cervical spondylosis (if all below the neck)
- Disc prolapse
- Neoplasm
MS key areas of inflammation (4)
- Periventricular
- Juxtacortical/cortical
- Infratentorial
- Spinal cord
Distinguishing sensory and cerebellar ataxia
Sensory:
- Sensory disturbance especially dorsal column
- Pseudoathetosis
- Usually able to finger-nose with eyes open, worse with eyes closed
Cerebellar
- Nystagmus
- Dysarthria
4 main types of motor neurone disease in prevalence
- Amyotrophic lateral sclerosis
- Progressive bulbar palsy
- Progressive muscular atrophy
- Primary lateral sclerosis
ALS presentation
- 70% limbs first. Usually a limb, then to contralateral same limb, or ipsilateral contiguous limb. Rarely diagonally.
- 25% bulbar first - often speech. Then usually progresses to neck/head drop.
- Mixed UMN (spasticity) & LMN (wasting, fasciculation)
Dysphagia later, and symptoms of orthopnoea/hypoventilation
ALS prognosis
3-5 years
Primary lateral sclerosis
UMN only
Affects speech and limbs
Occasionally develop LMN signs later (then becomes UMN-dominant ALS)
Without conversion, prognosis good - 10 years
Progressive muscular atrophy
MND form with LMN symptoms/signs only
ALS neurophysiology findings
Nerve conduction to exclude alternative dx (multifocal motor neuropathy)
Electromyography - fibrillation, fasciculation
ALS management
- Riluzole only treatment to slightly affect prognosis
- Then supportive/MDT care - nutrition, ventilation, ACP, vaccines, etc
Bulbar vs pseudobulbar palsy
Bulbar - LMN
Pseudobulbar - UMN
LMN - fasciculation, tongue wasting, absent palate movement, absent gag/jaw jerk reflexes
UMN - tongue spasticity, absent palate movement, increased gag/jaw jerk reflexes
Multifocal motor neuropathy
DDx for motor neurone disease
- Tends to affect distal muscles
- LMN only
Kennedy disease
X-linked spinobulbar muscular atrophy
- MND DDx
- LMN disease only
- limb and bulbar involvement
- Sometimes slight sensory deficit
