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PACES > Neurology > Flashcards

Neurology Flashcards

1
Q

UL examination - how to elicit cerebellar signs

A

1) Rebound test:
Arms outstretched, push one arm down, will oscillate back to normal position

2) May see titubation in head/trunk (truncal ataxia)

3) Speech: scanning characteristic

4) Coordination: intention tremor, past pointing DDK

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2
Q

Causes of cerebellar signs:

A

Metabolic causes:
- alcohol excess
- B12 deficiency
- Hypothyroidism

Vascular eg posterior circ stroke

SOL in posterior fossa

Demyelination eg MS

Iatrogenic causes: Phenytoin (gingival hypertrophy)

Genetic causes: Freidrich’s ataxia, ataxia telangiectasia

Also paraneoplastic syndrome: look for signs of lung Ca

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3
Q

Approach to cerebellar examination

A

1) Gait: ataxic

2) Arms:
- Outstretched
- Test for rebound tenderness
- Test for pronator drift

3) Face:
- Nystagmus (fast phase towards side of lesion)
- Loss of smooth pursuit of eye movements
- INO: think MS
- Scanning speech

4) Hands:
- Intention tremor
- DDK

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4
Q

Myotonic dystrophy: UL examination

A

Inspection:
- Face: frontal balding, temporal wasting, bilateral ptosis, expressionless
- Hands: Thenar wasting
- PACEMAKER
- Feeding tube (oesophageal dysmotility)

Tone: Slow hand grip release

Power: Reduced distally > proximally

Coordination: intact

Reflexes: reduced.
- PERCUSSION MYOTONIA (thenar eminence)

Sensation: intact

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5
Q

DDx for ptosis

A

Bilateral ptosis:
- hypothyroidism
- myasthenia pathology: myasthenia gravis, Lambert-Eaton syndrome
- inherited neuromuscular disorders: Myotonic dystrophy, Facioscapulohumeral dystrophy

Unilateral:
- 3rd nerve palsy
- Facial nerve palsy (Bell’s palsy)
- Horner’s syndrome
- Congenital

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6
Q

Pathophysiology of myotonic dystrophy?

A

Autosomal dominant
Trinucleotide expansion results in myotonia.

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7
Q

Investigations for myotonic dystrophy

A

Bedside:
- ECG: cardiomyopathy/conduction delays
- CBG or urine dip: diabetes

Blood tests:
- HbA1c
- CK may be raised

Specialist testing:
- EMG
- Genetic testing
- Echocardiogram (cardiomyopathy)
- If concerns re: swallow - consider a barium meal

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8
Q

Complications of myotonic dystrophy

A

Top to toe:

  • Eyes: cataracts
  • Cardiac: conduction delays, cardiomyopathy
  • GI: impaired swallow, oeseophageal dysmotility
  • QOL: fatigue, psychiatric
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9
Q

Signs of ulnar neuropathy:

A

Inspection:
- Scars at wrists of elbows
- “Ulnar claw”: flexion of 4th and 5th fingers

Power: Weakness of finger abduction
- Thumb abduction maintained if no median nerve involvement

Sensation:
- Split ring finger sensation

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10
Q

Causes of ulnar neuropathy

A

Trauma e.g. fracture

Ulnar nerve nerve entrapment
- Functional e.g. repetitive elbow flexion and extension (builder)
- Associated with other conditions e.g. acromegaly

Iatrogenic e.g. surgery

Inflammatory neuropathy e.g. vasculitis

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11
Q

How to differentiate pure ulnar neuropathy from C8/T1 nerve root lesion?

A

In C8/T1 nerve root lesion, there would be:
- Loss of sensation at T1 (inner upper arm)
- Involvement of radial nerve: wrist extension
- Involvement of median nerve: thumb abduction
- Involvement of posterior interosseous nerve: finger extension

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12
Q

Investigations for ulnar neuropathy

A

Neurophysiology: Electromyography (EMG)
- Can give an indication of prognosis

MRI neck if concerned about cervical radiculopathy

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13
Q

Causes of chorea

A

Basal ganglia

Acute onset: always consider stroke (usually unilateral)

Metabolic: hypoglycaemia, uraemia

Drug-related: dopamine agonists (L-dopa), amphetamines

Post-infection: Sydenham’s chorea

Vasculitis: SLE

Neurogenetic: Huntington’s disease, Wilson’s disease

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14
Q

Complications of Huntington Disease

A
  • Impaired motor function
  • Cognitive impairment
  • Neuropsychiatric disturbance
  • Malnutrition - due to 1) increased calorific requirement secondary to involuntary movements and 2) impaired swallow
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14
Q

Post Polio Syndrome - examination features

A

Look for asymmetric wasting, weakness, arreflexia with usually preserved sensation

Inspection:
- Walking aids, splints
- Possible scars
- Leg length discrepancy
- Muscle wasting

Tone: Hypotonia

Power: Reduced

Reflexes: Absent

Sensation: usually preserved

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14
Q

Management of Huntington Disease

A
  • MDT approach aiming to achieve symptomatic control
  • Led by consultant with special interest
  • Neuropsychiatrist
  • Specialist nurses
  • Dietitian
  • Psychosocial support
  • Genetic counsellors
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15
Q

If there is LMN weakness with sensory involvement, the lesion could be in the…

A

Nerve root
Plexus
Peripheral nerve

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16
Q

If there is LMN weakness with sensory involvement, the lesion CANNOT be…

A

Muscle
NMJ
Anterior horn

(these are all pure motor)

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17
Q

Motor neuron disease - definition

A

Progressive disease characterised by axonal degeneration of both upper and lower motor neurons

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18
Q

Motor neuron disease - examination

A

Inspection: Wasting, fasciculations

Tone: Can be spastic or flaccid (more commonly spastic)

Power: Reduced, often asymmetric

Reflexes: Mixed

Coordination: Intact

Sensation: NORMAL

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19
Q

Motor neuron disease DDx

A

Causes of pure motor pathology (without sensory involvement)
- Demyelination (GBS/CIDP/MS)
- Muscular dystrophy
- NMJ disorders: myasthesia gravis/LEMS

Causes of mixed UMN and LMN signs (but these would all have sensory involvement:
- Cervical Myelopathy (UMN signs from spinal cord involvement + LMN signs from nerve root involvement)
- Dual pathology (eg: cervical myelopathy and peripheral neuropathy)
- Inherited disorders e.g. Friedrich’s ataxia: progressive ataxia with mixed UMN/LMN signs

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20
Q

How does MND present?

A
  • Asymmetric progressive weakness
  • Rapid disease course
  • Cognitive dysfunction - associated with frontotemporal dementia
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21
Q

MND subtypes

A

Amyotrophic lateral sclerosis:
- Both UMN and LMN involvement
- typically spastic paraparesis

Primary lateral sclerosis:
- Predominantly UMN

Progressive muscular atrophy:
- Predominantly LMN

Progressive bulbar palsy:
- Lower cranial nerves and suprabulbar nuclei

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22
Q

Investigations for cerebellar ataxia

A

Acute onset - investigate for stroke
- CT Head in first instance

More chronic onset
- think about Metabolic or Demyelinating causes
- Serum B12, thyroid function
- Alcohol history
- Consider LP for MS

  • In all cases - MRI Brain is the optimal imaging for the cerebellum
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23
Q

How to differentiate sensory ataxia from cerebellar ataxia

A

Cerebellar ataxia will have additional features:
- Scanning speech
- Nystagmus

Sensory ataxia will have positive Romberg’s

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24
Q

Management of ataxic syndromes

A

1) Address underlying cause

2) MDT approach:
- PT/OT
- Neurology

Aiming to preserve functional abilities

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25
Q

Which subtypes of motor neuron disease have the best/worst prognosis?

A

Best prognosis: Primary lateral scleosis (typically UMN only)

Worst prognosis: Progressive bulbar palsy

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26
Q

Motor neuron disease - investigations

A

Electrophysiology: EMG would show fasciculations and fibrillations

MRI spine to rule out cervical myelopathy

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27
Q

Motor neuron disease - management

A

MDT approach led by a consultant with special interest in MND, alongside specialist nurses, physiotherapists etc.

Cause:
- Pharmacological management - Riluzole (adds a few months to prognosis)

Symptoms:
- Pain management

Complications:
- Mobility - PT, OT
- Feeding and minimising aspiration risk e.g. artificial feeding
- Monitor respiratory function +/- ventilatory support
- Neuropsychiatric screening
- Psychosocial support

28
Q

Complications of MND

A
  • Motor functional impairment
  • Cognitive decline (frontotemporal dementia)
  • Impaired swallow - may need artifical feeding
  • Respiratory muscle weakness - may need respiratory support e.g. NIV
29
Q

How does Brown Sequard syndrome present?

A
  • Unilateral spastic paraparesis
  • There is ipsilateral spasticity and loss of dorsal column sensation
  • Contralateral loss of spinothalamic tract

So the affected leg will have:
- spastic weakness
- loss of vibration/proprioception
- preserved pinprick sensation (other leg loses pinprick sensation)

30
Q

Causes of spastic paraparesis

A

Acute spastic paraparesis:
- Cord compression
- Trauma
- Anterior spinal artery occlusion
- Stroke (but usually hemiplegia rather than paraparesis)

Acquired causes with more subacute-chronic onset:

1) Compression of the spinal cord
- Disc herniation
- Spinal stenosis
- Malignant cord compression

2) Demyelination: Multiple sclerosis, transverse myelitis

3) Metabolic: B12 deficiency → SACD

4) Autoimmune: SLE, sarcoidosis

5) Inherited causes: Friedrich’s ataxia

6) Infection: HIV

In general the acquired causes can be asymmetric

31
Q

Causes of absent ankle jerks and upgoing plantars?

A
  • Subacute combined degeneration of the cord
  • Friedrich’s ataxia
  • Conus medullaris syndrome
  • Combined pathology e.g. diabetic neuropathy and stroke
32
Q

Neuropathic pain management

A

1) Tricyclic antidepressant - amitryptilline
2) Anti-epileptic e.g. gabapentin
3) SNRI - duloxetine

33
Q

TCA side effects

A

Drowsiness
Dry mouth
Headache

34
Q

Causes of peripheral sensory neuropathy

A

Metabolic - DBAT
- Diabetic neuropathy
- B12 deficiency
- Alcohol
- Thyroid (Hypothyroidism)
- Uraemia

Drugs
- Chemotherapy
- Isoniazid (TB)

Inflammatory causes
- Vasculitis

Genetic causes e.g. hereditary sensorimotor neuropathy

35
Q

Further bedside tests if you see peripheral neuropathy

A
  • Fundoscopy to assess for diabetic retinopathy
  • CBG
  • Urinalysis to test for glycosuria
36
Q

Investigations for peripheral sensory neuropathy

A

Bedside: fundoscopy, urinalysis, CBG

Bloods:
- FBC, U+Es, LFTs
- HbA1c
- B12
- TFTs
- Autoimmune screen

Special tests:
- EMG
- Nerve conduction studies - assess whether it is demyelinating or axonal

IF UMN signs e.g. in SACD, MRI spine too

37
Q

Management of diabetic neuropathy

A

Treat cause: Tight glycaemic control
- Patient education
- DSN involvement

Treat symptoms:
- Neuropathic pain: stepwise approach (TCA)

Treat complications:
- Regular podiatry/foot clinic for foot care
- Physiotherapy for gait stability

38
Q

Causes of peripheral motor neuropathy (flaccid paraparesis)

A

Think: Nerve, Muscle, NMJ

ACUTE ONSET:
Nerve = Guillain Barre syndrome
- ascending flaccid paralysis
- typically sensory only, but some subtypes have motor involvement

SUBACUTE OR CHRONIC:
Nerve = Chronic Inflammatory Demyelinating Polyradiculopathy

Muscle
- Muscular dystrophy (Becker)
- Polymyositis

NMJ = Myasthenia gravis (would expect fatiguability)

Other:
Hereditary sensorimotor neuropathy (would expect sensory loss, distal wasting and pes cavus)

Diabetic neuropathy (predominantly sensory but can have some motor component)

Vasculitis e.g. polyarteritis nodosa

39
Q

Charcot Marie Tooth - examination

A

Inspection:
- Ankle-foot brace
- Distal wasting
- Pes cavus

Gait: high stepping gait
-Romberg’s +ve

Tone: flaccid

Power: reduced, mainly distal weakness

Reflexes: reduced distally

Coordination: intact

Sensation: Reduced in all modalities

40
Q

Charcot-Marie-Tooth inheritance

A

Autosomal dominant

41
Q

Charcot-Marie-Tooth specific investigations

A

Neurophysiology
- EMG and nerve conduction studies
- Type 1 is demyelinating

Genetic testing

42
Q

Anterior circulation stroke - features

A

Total anterior circulation stroke: 3 H’s
- Hemiplegia (legs > arms)
- Homonymous hemianopia
- Higher cortical dysfunction

Partial anterior circulation stroke:
- 2 of the above

43
Q

Friedrich’s ataxia - inheritance

A

autosomal recessive
frataxin gene mutation

44
Q

Friedrich’s ataxia - examination

A
  • Inspection: mobility aid, distal wasting, truncal ataxia, may notice dysarthria
  • Tone: normal or spastic
  • Power: reduced globally
  • Reflexes: absent with upgoing plantars
  • Coordination: ataxic
  • Sensation: loss of vibration and proprioception
45
Q

Friedrich’s ataxia DDx

A
  • Spinocerebellar ataxia
  • Subacute combined degeneration of the cord*
  • Cervical myelopathy*
  • Combined pathology e.g. spinal cord compression with peripheral neuropathy*

*Wouldnt expect cerebellar signs

46
Q

Friedrich’s ataxia investigations

A

Bedside: ECG (Arrhythmia), urine dip for glycosuria

Bloods: FBC, U+Es, CRP, B12, vitamin E, HbA1c

Imaging: MRI brain and whole spine, echo

Neurophysiology: nerve conduction, EMG

Genetic testing

47
Q

Friedrich’s ataxia management

A
  • No pharmacological management
  • MDT approach: neurology, specialist nurses, PT, OT, orthotics, psychiatry
  • Serial ECGs, echo +/- cardiology reviews
  • Monitor for diabetes
  • Palliative care for symptom control
48
Q

Friedrich’s ataxia complications

A
  • Cardiomyopathy (HOCM leading cause of death)
  • Diabetes mellitus
  • Sensorineural deafness
  • Functional limitations
  • Psychological impact
49
Q

Rinne’s and Weber’s test

A

First do Webers:
Louder in one ear means there is either
- conductive loss in that ear
- sensorineural loss in the other ear (because the louder ear’s nerve is able to compensate)

Then do Rinne’s on the louder ear.
- AC > BC = not conductive hearing loss
- BC > AC = conductive hearing loss

If inconclusive: do Rinne’s on the quieter ear.
- If AC > BC, this is sensorineural hearing loss.

50
Q

Myasthenic gravis - examination

A

Fatiguability testing -

Cranial nerves: sustained upwards gaze leading to diplopia and partial ptosis

Upper limbs: Repeated shoulder abduction/adduction leading to weakness

51
Q

Myasthenia gravis UL examination - differential

A

Proximal myopathy

52
Q

Myasthenia gravis Investigations

A

Bloods:
- anti-acetylcholine receptor antibodies (80%)
- anti-musc antibodies (15%)

Imaging: CT Chest to assess for thymoma

Neurophysiology: Nerve conduction shows fatiguability

FVC (<1.5L needs referral to HDU)

53
Q

Myasthenia gravis management

A

Myasthenic crisis:
- IV steroids
- Measure FVC and ABGs
- FVC <1.5L warrants referral to HDU

Stable patients:
- Pyridostigmine (acetylcholinesterase inhibitor)
- Steroid sparing agents
- Consider referral for monoclonal Abs e.g. rituximab
- Consider thymectomy

54
Q

Multiple sclerosis - examination

A

Patchy, mixed sensory and motor involvement in asymmetric pattern

Inspection; may have mobility aid

Tone: Typically spastic

Power: Asymmetric weakness

Reflexes: Brisk or normal

Coordination: intact, unless cerebellar involvement

Sensation: May have patchy parasthesia

55
Q

Multiple sclerosis: investigations

A
  • MRI brain + whole spine
  • LP: oligoclonal bands
56
Q

Multiple sclerosis management

A

MDT approach

Acute relapse: high dose IV steroids for 5 days
Maintenance: DMARD e.g. beta-interferon or natalizumab

Symptom control e.g. baclofen for spasticity; intermittent self cath for urinary retention

Supportive: PT, OT, psychological

57
Q

Stroke territories

A

Anterior circulation stroke (ACA or MCA)
- TACS: Hemiplegia, Homonymous hemianopia and Higher cortical dysfunction
- PACS: 2/3 of the above
- Anterior cerebral artery: Legs weaker than arms
- Middle cerebral artery: Arms weaker than legs

58
Q

Homonymous hemianopia DDx

A

With macular sparing: Posterior circulation stroke

Without macular sparing: Anterior circulation stroke

(Use Humphreys visual field testing to confirm)

59
Q

Extra-neurological examination in stroke

A

Pulse (AF)
Carotid Bruits
Heart auscultation for murmurs
Blood pressure

60
Q

Stroke investigations

A

Acute:
CT Brain to rule out Haemorrhage

Longer term:
- Blood pressure
- Lipids, HbA1c
- Holter (24 or 72h tape)
- Echocardiogram
- Ultrasound doppler of carotids - stenosis >50% for carotid endarterectomy

61
Q

Stroke management

A

Acute:
- Refer to HASU
- Thrombolysis (within 4.5h)
- Thrombectomy (within 24h including wake up strokes)

Chronic:
- Secondary prevention; Clopidogrel + ACEi + statin
- Manage risk factors: BP, HTN, diabetes, lipids
- Consider carotid endartectomy if >50% stenosis

62
Q

Neurofibromatosis1 features

A

Chromosome 17

CAFE NOIR
- Cafe-au-lait spots: 6 x 15mm
- Axillary freckling
- Fibromas (2+ neurofibromas)
- Eyes: 2x Lisch nodules*(iris harmatomas)
- Neoplasm (CNS tumour/phaeochromocytoma)
- Ortho - scoliosis, kyphosis
- IQ reduced
- Renal artery stenosis

Needs 2 of the above OR
1 + family history

63
Q

Drug induced parkinsonism causes

A

Dopamine antagonists

Neuroleptic agents: Quetiapine, risperidone

Anti emetics: metoclopramide

64
Q

Tuberous sclerosis complex features

A

“Remember Tuberous Sclerosis Complex”

Renal: angiomyoplipoma, RCC

Tumours: brain

Skin: peri-ungual fibromas, ashl-leaf macules, shagreen patches

Cardio: Rhabdomyoma

65
Q

Tuberous sclerosis inheritance

A

Autosomal dominant

66
Q

Tuberous sclerosis investigations

A

Bloods: standard + genetic testing

ECG

Imaging:
- Echo
- MRI brain
- US KUB +/- MRI renal

67
Q

Neurofibromatosis type 2 features

A
  • Acoustic neuromas (hearing aids)
  • Meningiomas
  • Seizures
68
Q

Complications of neurofibromatosis

A

HTN: ‘CPR’
- Coarctation of aorta
- Phaeochromocytoma
- Renal artery stenosis

Neurological:
- Seizures
- Brain tumours
- Hearing loss in type 2

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