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Neurology Flashcards

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1
Q

Distribution of peripheral sensory nerves hand

A

Radial nerve - snuff box
Median nerve - lateral first finger
Ulnar nerve - medial hand

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2
Q

Upper limb dermatomes/peripheral nerves

A

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

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3
Q

Upper limb reflex nerves/roots

A

Biceps - Musculocutaneous. C5/6
Brachioradialis - radial. C6(5)
Triceps - Radial. C7 (C6-8)

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4
Q

Differentiating ulnar from C8/T1 lesion

A

Abductor pollicis brevis C8/T1, median nerve
Medial forearm C8 not ulnar

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5
Q

Ulnar neuropathy signs

A

Inspection: flexion 4th/5th fingers. First dorsal and hypothenar wasting.
Power: Weak finger abduction
Altered sensation little finger/half ring palmar

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6
Q

Ulnar nerve nerve injury sites

A
  • At elbow in ulnar groove from repetitive flexion/extension
  • Wrist fracture/surgery
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7
Q

Parkinsonism definition

A

Triad:
- Tremor - resting, low freq
- Hypertonia - rigidity>spasticity, cogwheel
- Bradykinesia - slow initiation, reduced amplitude with repetition, micrographia

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8
Q

Parkinson’s plus syndromes

A

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

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9
Q

Parkinson’s investigations

A

Bedside
- OBS /postural BP
- DHx
- MOCA/cognitive assessment for dementia
Imaging:
- Consider MRI to exclude structural pathology
- Consider DaT scan

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10
Q

Parkinson’s treatment

A
  • 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
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11
Q

30 year old woman
Visual loss with pain on movement
Worse in bath
Episodes urinary incontinence 2 months ago

A

MS

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12
Q

Explain INO

A

Lésion in médian longitudinal fasciculus in pons causes ipsilateral failure of adduction with contralateral nystagmus on abduction
Causes
- MS
- Vascular
(Lyme’s, HIV, syphilis)

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13
Q

MS pathophysiology/prognosis

A

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

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14
Q

MS management

A

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.

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15
Q

MS Signs

A

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

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16
Q

MS investigations

A

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

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17
Q

MS investigations

A

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

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18
Q

Peripheral primarily sensory neuropathy causes

A

Metabolic:
- Diabetes
- B12 deficiency
- Uraemia
- Hypothyroidism
Toxic:
- Alcohol
- Chemotherapy (vincristine)
Inflammatory:
- CIPD (chronic inflammatory )
- Sarcoidosis, RA
- Amyloidosis
Paraneoplastic:
- Solid cancer, e.g. lung
- Paraproteinaemia

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19
Q

Peripheral neuropathy investigations

A

Bedside:
- Blood glucose
- Urine dip for glucose
- Fundoscopy
Bloods
- U&E (uraemia)
- FBC (macrocytosis)
- Hba1c
- TFTs
- ESR +/- vasculitis screen
Special tests
- Electrophysiology

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20
Q

How does electrophysiology aid with differentiating causes of peripheral neuropathy

A
  • Length dependent (metabolic) vs equal/mononeuritis multiplex (inflammatory)
  • Demyelination vs axonal
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21
Q

Axonal vs demyelinating causes peripheral neuropathy

A

Most are axonal
Demyelinating = inflammatory e.g. GBS, CIDP

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22
Q

Median neuropathy signs

A

Inspection: Thenar wasting
Sensory: thumb-middle of ring finger palmar
Motor:
- Abductor pollicis brevis weakness
- Poor precision grip

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23
Q

Differentiating sites of median neuropathy

A

Carpal tunnel:
- Palm sensation intact
Anterior interosseous nerve (forearm)
- Distal phalanx of thumb and index weakness
- Other muscles intact
Proximal (elbow)
- Combined

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24
Q

Caused carpal tunnel syndrome

A

Oedema in carpal tunnel
Arthritis:
- RSI
- RA
Endocrine
- Myxoedema
- Acromegaly
- Diabetes/obesity increases risk
Tumours
- Ganglion/lipoma
- Myeloma -> amyloidosis

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25
Radial neuropathy signs
Inspection Motor - Wrist/finger drop - Supinator weakness (BEAST - brachioradialis, extensors, abductor pillicis longus, supinator, triceps) Sensory - Most reliably anatomical snuff box
26
Mononeuritis multiplex causes
Generally systemic, most commonly vasculitis Endocrine - diabetes
27
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.
28
Nerve conduction demyelinating vs axonal findings
Ulnar nerve - axonal >38m/s, demyelinating <38
29
Charcot Marie Tooth epidemiology
Most common inherited neurological disorder. No ethnic etc. predisposition AD and AR inheritance forms exist.
30
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
31
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
32
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
33
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
34
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
35
Causes of facial nerve palsy
- Bell's Infective - Ramsay Hunt (Herpes Zoster) - Lyme - Chronic otitis media/abscess/necrotising OE Tumour MS Stroke Diabetic mononeuropathy
36
Sciatic neuropathy signs
L4-S3 Hamstring weakness Weakness all muscles below the knee Lateral sensory loss below the knee
37
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
38
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
39
Lower limb reflexes nerves/roots
Knee jerk - Femoral, L3/4 Ankle jerk - Tibial, S1/2
40
Cranial nerve nucleus sites
2/2/4/4 I, II - forebrain III, IV - midbrain V - VIII - pons IX - XII - medulla
41
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
42
Myelopathy localisation on examination
Radiculopathy at level: - LMN features - Reduced reflexes Myelopathy below level: - UMN features - Hyperreflexia May also have sensory level
43
Myelopathy management
- Urgent focussed MRI (consider whole brain/spine if inflammatory cause considered) - Analgesia - Neurosurgical referral if spondylosis
44
Stroke cortical features
RSW often with dysphasia LSW often with neglect
45
TACS triad
Hemianopia Hemiparesis Higher cortical sign
46
PACS présentation by vessel
MCA arm/face prédominant ACA leg TACS tends to be MCA
47
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
48
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
49
MS key areas of inflammation (4)
- Periventricular - Juxtacortical/cortical - Infratentorial - Spinal cord
50
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
51
4 main types of motor neurone disease in prevalence
- Amyotrophic lateral sclerosis - Progressive bulbar palsy - Progressive muscular atrophy - Primary lateral sclerosis
52
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
53
ALS prognosis
3-5 years
54
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
55
Progressive muscular atrophy
MND form with LMN symptoms/signs only
56
ALS neurophysiology findings
Nerve conduction to exclude alternative dx (multifocal motor neuropathy) Electromyography - fibrillation, fasciculation
57
ALS management
- Riluzole only treatment to slightly affect prognosis - Then supportive/MDT care - nutrition, ventilation, ACP, vaccines, etc
58
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
59
Multifocal motor neuropathy
DDx for motor neurone disease - Tends to affect distal muscles - LMN only
60
Kennedy disease
X-linked spinobulbar muscular atrophy - MND DDx - LMN disease only - limb and bulbar involvement - Sometimes slight sensory deficit

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