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Neurology Flashcards

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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
How to differentiate sensory ataxia from cerebellar ataxia
Cerebellar ataxia will have additional features: - Scanning speech - Nystagmus Sensory ataxia will have positive Romberg's
24
Management of ataxic syndromes
1) Address underlying cause 2) MDT approach: - PT/OT - Neurology Aiming to preserve functional abilities
25
Which subtypes of motor neuron disease have the best/worst prognosis?
Best prognosis: Primary lateral scleosis (typically UMN only) Worst prognosis: Progressive bulbar palsy
26
Motor neuron disease - investigations
Electrophysiology: EMG would show fasciculations and fibrillations MRI spine to rule out cervical myelopathy
27
Motor neuron disease - management
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
Complications of MND
- Motor functional impairment - Cognitive decline (frontotemporal dementia) - Impaired swallow - may need artifical feeding - Respiratory muscle weakness - may need respiratory support e.g. NIV
29
How does Brown Sequard syndrome present?
- 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
Causes of spastic paraparesis
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
Causes of absent ankle jerks and upgoing plantars?
- Subacute combined degeneration of the cord - Friedrich's ataxia - Conus medullaris syndrome - Combined pathology e.g. diabetic neuropathy and stroke
32
Neuropathic pain management
1) Tricyclic antidepressant - amitryptilline 2) Anti-epileptic e.g. gabapentin 3) SNRI - duloxetine
33
TCA side effects
Drowsiness Dry mouth Headache
34
Causes of peripheral sensory neuropathy
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
Further bedside tests if you see peripheral neuropathy
- Fundoscopy to assess for diabetic retinopathy - CBG - Urinalysis to test for glycosuria
36
Investigations for peripheral sensory neuropathy
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
Management of diabetic neuropathy
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
Causes of peripheral motor neuropathy (flaccid paraparesis)
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
Charcot Marie Tooth - examination
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
Charcot-Marie-Tooth inheritance
Autosomal dominant
41
Charcot-Marie-Tooth specific investigations
Neurophysiology - EMG and nerve conduction studies - Type 1 is demyelinating Genetic testing
42
Anterior circulation stroke - features
Total anterior circulation stroke: 3 H's - Hemiplegia (legs > arms) - Homonymous hemianopia - Higher cortical dysfunction Partial anterior circulation stroke: - 2 of the above
43
Friedrich's ataxia - inheritance
autosomal recessive frataxin gene mutation
44
Friedrich's ataxia - examination
- 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
Friedrich's ataxia DDx
- 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
Friedrich's ataxia investigations
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
Friedrich's ataxia management
- 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
Friedrich's ataxia complications
- Cardiomyopathy (HOCM leading cause of death) - Diabetes mellitus - Sensorineural deafness - Functional limitations - Psychological impact
49
Rinne's and Weber's test
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
Myasthenic gravis - examination
Fatiguability testing - Cranial nerves: sustained upwards gaze leading to diplopia and partial ptosis Upper limbs: Repeated shoulder abduction/adduction leading to weakness
51
Myasthenia gravis UL examination - differential
Proximal myopathy
52
Myasthenia gravis Investigations
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
Myasthenia gravis management
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
Multiple sclerosis - examination
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
Multiple sclerosis: investigations
- MRI brain + whole spine - LP: oligoclonal bands
56
Multiple sclerosis management
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
Stroke territories
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
Homonymous hemianopia DDx
With macular sparing: Posterior circulation stroke Without macular sparing: Anterior circulation stroke (Use Humphreys visual field testing to confirm)
59
Extra-neurological examination in stroke
Pulse (AF) Carotid Bruits Heart auscultation for murmurs Blood pressure
60
Stroke investigations
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
Stroke management
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
Neurofibromatosis1 features
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
Drug induced parkinsonism causes
Dopamine antagonists Neuroleptic agents: Quetiapine, risperidone Anti emetics: metoclopramide
64
Tuberous sclerosis complex features
"Remember Tuberous Sclerosis Complex" Renal: angiomyoplipoma, RCC Tumours: brain Skin: peri-ungual fibromas, ashl-leaf macules, shagreen patches Cardio: Rhabdomyoma
65
Tuberous sclerosis inheritance
Autosomal dominant
66
Tuberous sclerosis investigations
Bloods: standard + genetic testing ECG Imaging: - Echo - MRI brain - US KUB +/- MRI renal
67
Neurofibromatosis type 2 features
- Acoustic neuromas (hearing aids) - Meningiomas - Seizures
68
Complications of neurofibromatosis
HTN: 'CPR' - Coarctation of aorta - Phaeochromocytoma - Renal artery stenosis Neurological: - Seizures - Brain tumours - Hearing loss in type 2

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