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MRCP PACES > Neurology > Flashcards

Neurology Flashcards

1
Q

What are the features of spastic paraparesis?

A

Increased tone bilaterally
Pyramidal weakness bilaterally
Increased reflexes
Upgoing plantars and clonus
Spastic scissoring gait

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2
Q

What extra things would you look for in spastic paraparesis (if doing LL exam)? - not in normal LL exam

A

Eyes - INO, nystagmus, RAPD

Mouth - fasciculations

Hands/arms - small muscle wasting, fasciculations, co-ordination, tone, power, reflexes

UL - sensory level

Back - spinal surgery scars, tenderness

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3
Q

Spastic paraparesis + cerebellar signs + dorsal column involvement?

A

Friedreich’s Ataxia

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4
Q

Completing Lower Limb Exam

A

PR - anal tone + saddle anaesthesia
Examine UL and Cranial nerves
Take Hx

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5
Q

What are the main causes of spastic paraparesis?

A

Demyelination

Cord Compression

Trauma

Anterior Horn Cell Disease

Cerebral Palsy

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6
Q

Spastic paraparesis + sensory level

A

Cord compression
- disc disease - spinal stenosis
- tumour
- trauma
- infection - epidural abscess, TB
- Vascular issue - haematoma/haemorrhage

Cord infarction

Transverse myelitis

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7
Q

What are the causes of transverse myelitis?

A

Infection - HSV, VZV, HIV
Autoimmune
Paraneoplastic
Sarcoid
Neuromyelitis optica

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8
Q

Spastic Paraparesis and dorsal column loss?

A

Demyelination
Friedrich’s ataxia
Subacute combined degeneration of cord
Syphilis
Parasagittal meningioma
Cervical myelopathy

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9
Q

Spastic paraparesis and spinothalamic loss

A

Syringomyelia
Anterior spinal artery infarction

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10
Q

Spastic paraparesis and cerebellar signs

A

Demyelination
Friedrichs ataxia
Spinocerebellar ataxi
Arnold Chiari malformation
Syringomyelia

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11
Q

Spastic paraparesis and small hand muscle wasting

A

Cervical myelopathy
Anterior horn cell disease
Syringomyelia

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12
Q

Spastic paraparesis and UMN signs

A

Cervical myelopathy
Bilateral strokes

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13
Q

Spastic paraparesis and absent ankle jerk

A

MND
Friedrich’s ataxia
Subacute combined degeneration of cord
Syphilis
Cervical myelopathy and peripheral neuropathy
Conus medullaris

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14
Q

Other causes of spastic paraparesis

A

Hereditary spastic paraparesis
Tropical - HTLV1
Cerebral Palsy

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15
Q

Spastic paraparesis without any sensory involvement

A

Consider MND and HSP

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16
Q

Classic case for cerebral palsy?

A

Birth injury/illness in neonatal period
Intellectual impairment
Spastic paraparesis
Brisk reflexes
Upgoing plantars

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17
Q

Classic case for hereditary spastic paraparesis

A

Spastic paraparesis
Upgoing plantars
Brisk reflexes

ABSENT sensory signs

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18
Q

Classic case for Friedrich’s ataxia

A

Pes cavus
Cerebellar signs
Wasting
Spastic paraparesis
?Absent reflexes
Dorsal column loss
Peripheral sensory neuropathy

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19
Q

Classical case for MS

A

Spastic paraparesis
Brisk reflexes
Upping plantars
Cerebellar signs
Hx of visual or sphincter disturbance

Poss sensory - dorsal column >spinothalamic

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20
Q

Classical case for anterior spinal artery occlusion

A

Spastic paraplegia
Brisk reflexes
Upgoing plantars
Loss of pain and temperature with sensory level
Dorsal columns spared

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21
Q

Classical case for MND

A

Spastic paraparesis
Brisk reflexes
Upgoing plantars
Wasting
Fasciculations
No sensory signs

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22
Q

Demyelinating causes for spastic paraparesis

A

MS
Neuromyelitis optica
Subacute degeneration of cord
Transverse myelitis

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23
Q

Asymmetric spastic paraparesis

A

Think Brown-Sequard

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24
Q

Compressive causes of myelopathy

A

Disk herniation
Tumours
Spinal stenosis

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25
Q

Autoimmune causes of myelopathy

A

MS
Lupus
Sarcoid

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26
Q

Infectious causes of myelopathy

A

HIV
Varicella

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27
Q

Nutritional causes of myelopathy

A

Vitamin deficiency - B12
Copper deficiency

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28
Q

Genetic causes of myelopathy

A

Hereditary spastic paraparesis

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29
Q

Acute causes of spastic paraparesis (minutes to 1-2 days)

A

Minutes - Likely vascular cause

1-2 days
- Trauma
- Disc herniation

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30
Q

Subacute causes of spastic paraparesis - days to weeks

A

Autoimmune:
- Lupus
- Demyelination

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31
Q

Causes of spastic paraparesis that occur over weeks to months

A

Nutritional deficiencies - B12, copper
Slow growing tumour

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32
Q

Chronic causes of spastic paraparesis - month to years

A

Genetic causes

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33
Q

How would you investigate spastic paraparesis?

A

Bedside
- Blood pressure (autonomic involvement)
- Vital capacity - resp muscle involvement

Bloods
- Bone profile
- LFT
- Immunoglobulin and protein electrophoresis
- FBC, CRP, ESR - malignancy, infection, inflammation
- Virology - HIV, HTLV1, syphilis
- Anti NMO, AMA - autoimmune
- Haematinics - B12

Imaging
- MRI spine - help find cause, localise lesion and assess for intervention
- MRI brain - ?MS

Special
- Visual evoked potentials - ?MS
- LP - ?oligoclonal bands
- EMG - fibrillation and fasciculation in MND

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34
Q

How is spastic paraparesis managed?

A

Non pharmacological:
- Education
- PT/OT
- Orthotics
- Social services
- DVLA

Medical
- steroids - IV methylpred/PO dex
- Radiotherapy

Surgical
- Decompress/fix depending on cause

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35
Q

Which malignancies commonly metastasise to bone?

A

Solid organ - Breast, Prostate, Lung, Kidney, Thyroid

Haem - myeloma

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36
Q

What are differentials for flaccid paraparesis?

A

Myopathies - inflammatory, toxic, inherited

NMJ disorder - botulism, myasthenia

Neuropathy - Hereditary sensory motor neuropathy, alcohol, lead poisoning, porphyria

Anterior horn cells - MND

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37
Q

How is MS defined

A

Demyelinating disease of the CNS which is disseminated in time and space

Doesn’t affect peripheral nerves

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38
Q

What investigation findings are seen in MS?

A

Visual evoked potentials - reduced - slow conduction

CSF - increased proteins and lymphocytes. Unmatched oligoclonal bands

MRI - active inflammation, hyperintense on T2 imaging. Periventricular white matter lesions, corpus callosum, brainstem, cerebellar, spinal cord and optic nerve

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39
Q

Stocking distribution of sensation loss with reduced/absent reflexes?

A

Peripheral polyneuropathy

Usually soft touch
± pin prick
± vibration

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40
Q

How do you test for sensory ataxia?

A

If UL - do finger nose with eyes closed
LL - Rhombergs positive only with eyes closed = sensory

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41
Q

If thinking peripheral polyneuropathy, what should you look for on examination?

A

Pes cavus/charcot joint

High stepping gate - foot drop

Thickened nerves - leprosy, Charcot Marie tooth, amyloidosis, neurofibromatosis

Arms - fistula

Abdo - renal, insulin injection sites

Thyroid

Conjunctival pallor

Hands - Dupeytrens contracture, finger prick marks, clubbing, vasculitic signs, muscle wasting

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42
Q

When you have detected a peripheral neuropathy, what should you try to work out?

A

Sensory, motor or sensorymotor

Distal or proxima

Small or large fibre

Focal, multifocal or polyneuropathy

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43
Q

Motor causes of peripheral neuropathy?

A

CIDP
GBS
Hereditary sensorimotor polyneuropathy
Multifocal motor neuropathy and conduction block
Porphyria
Lead/Dapsone
Anterior Horn Cell - Progressive muscular atrophy
Botulism
Muscle issues - inclusion body myositis

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44
Q

Predominant sensory peripheral neuropathy?

A

B12, B1, B6
Alcohol
Diabetes
Isoniazid
Vincristine
Vasculitis
Uraemia

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45
Q

Splitting sensory peripheral neuropathy Ddx into categories:

A

Metabolic:
- Diabetes
- Hypothyroidism

Nutritional deficiency:
- B1, B6, B12

Toxic:
- Alcohol
- Drugs - chemo, antibiotics, antivirals - TB drugs, phenytoin, metronidazole, gold, amiodarone, ciclosporin, hydralazine

Immune mediated:
- RA
- GPA
- CIDP
- GBS

Others:
- Genetic
- Infection - HIV, Lyme

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46
Q

How would you investigate a patient with suspected diabetic neuropathy?

A

Bedside:
- LS BP - ?autonomic dysfunction
- Fundoscopy
- Urinalysis

Bloods
- Renal function
- Hb1AC

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47
Q

How would you investigate sensory polyneuropathy

A

Bedside - fundoscopy, finger prick glucose, urinalysis

Bloods:
- FBC - anaemia, WCC, macrocytosis
- B12
- U&E - uraemia
- Hb1AC
- TFT
- LFT
- ESR/CRP
- Can do connective tissue screen - ANA, ccp, RF, ANCA, Ig, ACE, paraneoplastic
- Virology

Imaging/Special - if req.
- nerve conduction studies ?demyelinating ?axonal
- EMG
- Nerve biopsy
- LP - raised protein + normal cell in GBS. cytology if ?lymphoma
- Genetic testing - Charcot Marie Tooth

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48
Q

How can you interpret nerve conduction studies?

A

Reduced amplitude = axonal pathology

Slower conduction = demyelinating pathology

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49
Q

What are the non-pharmacological management options for peripheral neuropathy?

A

OT/PT
Orthotics
Social needs assessment
DVLA considerations
CBT - chronic pain
TENS machine
Stop drinking - if contributing
DSN/Podiatry if diabetic
Dietician

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50
Q

What is the pharmacological management of peripheral neuropathy?

A

Pain management
- Amitriptyline, Duloxetine
- Gabapentin/Pregablin
- Consider topical capsaicin
- Chronic pain team input

Tight glycaemic control

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51
Q

What is Charcot joint?

A

A neuropathic joint where impaired joint position sense and sensation of pain leads to chronic damage to joints such as the ankle and mid-foot, often accompanied by poor healing responses related to peripheral vascular changes or autonomic neuropathies.

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52
Q

How would you clinically distinguish between neuropathy and myopathy?

A

Myopathy
- Proximal muscle weakness
- No fasciculations + reflexes preserved until late in disease course
- Contractures

Neuropathy
- Distal
- Fasiculations and reflexes lost early
- No contractures
- Sensory signs

If myopathy - consider cardiac involvement

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53
Q

What medications cause neuropathy - consider type of neuropathy too

A

Sensory - Isoniazid

Sensorymotor - Vincristine, amiodarone

Motor - Dapsone

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54
Q

What is Charcot Marie Tooth Disease?

A

Hereditary Sensory Motor Neuropathy

Inherited - typically autosomal dominant

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55
Q

What would you look for on inspection in Charcot Marie Tooth?

A
  • B/L Pes Cavus
  • Muscle wasting - more prominent distally
  • Inverted Champagne Bottle
  • B/L Clawed hands/toes
  • High steppage gait
  • Scoliosis
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56
Q

What examination features would make you think Charcot Marie Tooth?

A

LMN signs:
- Reduced Tone
- Reduced reflexes

Reduced Power - distal>proximal
Normal co-ordination

Mildly impaired sensation - all modalities.

Positive Romberg’s
Can palpate thicker nerves

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57
Q

What are the main differentials for Charcot Marie Tooth disease?

A
  • Diabetes
  • Alcohol
  • Vasculitis with mononeuritis multiplex
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58
Q

Acquired neuropathies which are differentials for Charcot Marie Tooth?

A

Immune - CIDP, multifocal motor neuropathy with conduction block

Metabolic - diabetes

Toxic - alcohol, meds

Nutrition - B12

Paraneoplastic

Amyloidosis

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59
Q

Investigations to consider in Charcot Marie Tooth

A

Bedside
- Basic jobs - L/S for autonomic involvement
- Blood glucose
- Urine dip - glucose/amyloid
- Fundoscopy - CMT types 6 - optic atrophy

Bloods - r/o alternatives - inflammatory markers, deficiency, Diabetes etc.

Special
- Genetic testing
- Nerve conduction studies
- Nerve biopsy

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60
Q

How is Charcot Marie Tooth managed?

A

MDT Approach:
- PT
- OT
- Genetic counselling
- Support groups

Med - analgesia

Sure - orthopaedic procedures

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61
Q

Types of Charcot Marie Tooth?

A

Based on clinical findings, inheritance, nerve conduction studies and genetic testing:

Thickened peripheral nerves T1/3

Weak arm>leg = T2D

Pyramidal tract signs - T5

Optic atrophy - T6

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62
Q

What are some pyramidal tract signs

A

Hyperreflexia
Spasticity
Upgoing plantars
Slowed alternating movements

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63
Q

Thrombolysis contraindications

A

Significant head trauma within 3months
Ischaemic stroke within 3 months
Intracranial malignancy
Bleeding: active, disorders, recent
Recent surgery - esp brain/spine
HTN 200/100
Pregnancy

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64
Q

Inflammatory causes of motor neuropathy

A

Guillian Barre
Chronic Inflammatory Demyelinating Polyneuropathy
Multifocal motor neuropathy
Sarcoid
Vasculitis
Paraprotein
Amyloidosis

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65
Q

Infectious causes of motor neuropathy

A

HIV
Diptheria
Lyme disease
HTLV-1
West nile virus
Rabies
Enteroviruses

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66
Q

Toxin causes of motor neuropathy

A

Lead
Arsenic
Thallium
Mercury
Shellfish poisoning

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67
Q

Metabolic causes of motor neuropathy?

A

Diabetic amyotrophy
Porphyria

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68
Q

Drug causes of motor neuropathy?

A

Penicillamine
Gold
Ciclosporin

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69
Q

Congenital causes of motor neuropathy

A

Charcot-Marie Tooth

70
Q

Neuromuscular junction disorders associated with flaccid paraparesis?

A

Myasthenia gravis
Lambert Eaton Syndrome
Botulism
Organophosphate poisoning
Tick paralysis
Snake venom

71
Q

Features of Guillian Barre Syndrome

A

Acute inflammatory demyelinating neuropathy

Ascending paralysis

Onset over days - weeks, typically after an infection - chest (Mycoplasma) or GI - Campylobacter

72
Q

Symptoms of Guillain Barre

A

Spine pain
Distal paraesthesia - sensory loss is patchy
Fatigue
Ascending flaccid paralysis
Absent reflexes

73
Q

What are the other features of Guillian Barre (apart from flaccid paralysis)

A

Cranial nerves - ptosis, ophthalmoplegia, facial nerve and bulbar weakness

Autonomic - tachycardia, labile BP, arrhythmia, bladder/bowels

Resp - SOB, fatigue

74
Q

What is Miller Fischer Syndrome?

A

Proximal variant of GBS

Ataxia
Ophthalmoplegia
Areflexia

anti-GQ1b antibodies

75
Q

How would you investigate Guillian Barre

A

CSF Cytology - raised protein, normal WCC

Nerve conduction study - reduced velocity + conduction block

Anti GM1 antibodies

FVC

ECG

76
Q

How is Guillian Barre managed?

A

IVIG

Methylpred

Plasma exchange

ITU - if FVC <1.3L or Bulbar dysfunction - may need tracheostomy/ventilationW

77
Q

What is spina bifida

A

Neural tube defect with incomplete closure of the vertebral canal

78
Q

How does spina bifida present?

A

Asymmetrical flaccid paraparesis with sensory loss (usually L5/S1)

Bladder and bowel involvement

Cutaneous - tufts of here/dimples

79
Q

What would you expect with old polio?

A

Flaccid mononeuropathy

Often associated limb shortening

Limb hypoplasia and wasting

Reduced reflexes

No sensory loss

80
Q

What is a differential for old polio?

A

Infantile hemiplegia
Motor neurone disease

81
Q

What is polio, how is it transmitted?

A

Enterovirus transmitted via faecal oral route

Causes predilection of anterior horn cells

82
Q

Clinical signs of Parkinson’s Disease

A

Expressionless face
Coarse, pill rolling resting tremor - 3-5hz
Bradykinesia
Absence of arm swing
Stooped, shuffling gait + postural instability
Cog-wheel rigidity + lead pipe rigidity
Slow monotonous faint speech
Micrographia

83
Q

How is it best to illicit cogwheel rigidity?

A
  • Best felt at wrist
    At elbow - felt on extension motion

Ask patient to do somehting with other hand - tap on knee

84
Q

Screening tests to do in UL neuro exam?

A

Pronator drift - help detect UMN lesion

Tap arms - over shoot on bounce back = cerebellar

Extension of fingers rapidly - difficult = myotonic dystrophy

Tap index finger and thumb - small = Parkinson’s

Shoulder abduct against resistance one side. Then ask pt. to hold up both arms in shoulder abduction. If one side falls - myasthenia

85
Q

What other tests would you do to assess for Parkinsons Plus syndromes?

A

BP - MSA or cerebellar syndromes - Parkinsonism with postural hypo + cerebellar and pyramidal signs

Verticle eye movements - impaired in PSP

Dementia + PD = Lewy body dementia

Visual or cognition - Lewy body

Gait failure/LL impairment - vascular dementia

Medication hx - drugs can cause parkinsonism - metoclopramide, haloperidol, chlorpromazine

86
Q

Causes of Parkinsonism?

A

Parkinsons disease

PP syndromes - MSA, PSP, Corticobasal degeneration (unilateral)

Drug induced

Anoxic brain injury

Post encephalitis

MPTP toxicity

87
Q

Pathophysiology of Parkinson’s disease?

A

Degeneration of dopaminergic neurones in the substantia nigra and basal ganglia.

88
Q

Non motor manifestations of Parkinsons Disease?

A

Constipation
Urinary incontinence
Autonomic instability - postural hypotension
Mood disorders
Anosmia
Cognitive effects
Pain
Sleep disorders - REM, broken sleep

89
Q

How is PD investigated?

A

Referral to specialist for diagnosis

Clinical diagnosis - need 3 core features - bradykinesia, rigidity and tremor + r/o other causes

Some Ix may include:
- CT/MRI head
- SPECT - differentiate between PD and essential tremor
- Caeruloplasmin and urinary copper

90
Q

How is Parkinson’s Disease managed?

A

MDT - neurology, psych, PD nurses, PT/OT, GP, SALT, Social care

Medications:
- Dopamine agonist - Ropinirole, Rotigotine, Apomorphine
- Levodopa - usually with carbidopa
- MAO-i - Selegiline, Phenelzine
- COMT inhibitory - Entacapone
- Amantadine

Surgical
- Pallidotomy - create scar in globus pallidus to reduce activity
- Thalmic surgery
- Deep brain stimulation - in subthalmic nucleus or globus pallidus

91
Q

How is medication therapy chosen in Parkinson’s Disease?

A

Early disease - MAOI or Dopamine agonists

Less side effects
Spare L-DOPA for later in disease course

92
Q

Important complications of Levodopa therapy?

A

Weaning off
On-off fluctuations
Dyskinesia
Hallucinations and psychosis
Compulsive behaviours

93
Q

What are the symptoms associated with post polio syndrome?

A

Fatigue
Cramps
Progressive muscle weakness

94
Q

How would you investigate a patient with suspected post polio syndrome?

A

Exclude concurrent or alternative pathologies:
- MRI lumbosacral spine
- Nerve conduction studies
- EMG

95
Q

How is post polio syndrome managed?

A

MDT approach:
- Neurology - symptom management
- PT/OT
- Neuropsychologist

Regular review
Assess patient function and help make adjustments for maintaining independence

96
Q

What does pet cavus indicate and give some causes?

A

Suggests chronic neuromuscular disease

Charcot-Marie Tooth
Freidreich’s Ataxia
Old polio
Syringomyelia
Cerebral Palsy

97
Q

Features of Horners Syndrome?

A

Partial ptosis
Apparent enopthalmos
Miosis (constricted) - causes anisocoria (not equal)
Anhidrosis and flushing

98
Q

What should you mention if you mention ptosis

A

unilateral/bilateral
complete or partial
fatiguable or not

99
Q

How can you try localise lesion in Horners Syndrome based on clinical signs?

A

Using presence of anhidrosis/flushing

1st order - ipsilateral body and face affected
2nd order - Ipsilateral face only affected
3rd order - No anhidrosis or flushing

100
Q

Things to examine when suspecting Horners syndrome?

A

General - hemiparesis, hearing aids

Face - heterochromia, eye movements

Neck - scars/signs of trauma, lymphadenopathy, aneurysm, thyroid nodules, tracheal deviation, carotid bruits

Upper thorax - scars (superior/posterior), lung bases, vocal resonance

Ipsilateral arm - wasting, fasciculations, claw hand

Neuro UL - motor, cerebellar, sensory

101
Q

Possible causes for Horners Syndrome

A

Congenital - birth injury - Klumpke’s, Hereditary

First order (from hypothalamus, to midbrain, to spinal cord) - often associated with other neurological signs
- Trauma
- Stroke - Wallenberg syndrome
- Tumour
- Demyelination
- Syringomyelia

Second order - spinal cord, exit C8-T2, top of lung, into neck
- Trauma
- Pancoast tumour
- Schwannoma

Third Order - neck into face
- Trauma
- Carotid artery dissection
- Cavernous sinus thrombosis or inflammation
- Cluster headache
- Migraine

102
Q

How would you investigate Horners Syndrome?

A

Bedside - review old photos

Bloods - depend on cause. Consider LFT/Bone profile for malignancy

Imaging
- MRI Brain
- CXR - ?Pancoast
- MRA/Carotid doppler
- MRI cavernous sinus and orbit

Special tests
- Apraclonidine test - reverse anisociria by dilating affected pupil - ptosis may resolve
- Cocaine test - exacerbate anisocoria - dilate normal pupil but not affected
- Hydroxyamphetamine test - localise lesion - if absent or poor dilation –> 3rd order

103
Q

How is Horners syndrome managed?

A

Education
Treat underlying cause

104
Q

How is hereditary Horners syndrome inherited?

A

Autosomal Dominant

105
Q

What is Wallenberg’s Syndrome?

A

Lateral Medullary syndrome:
- Posterior inferior cerebellar artery infarct

Dysphagia
Sensory loss - ipsilateral face and contralateral trunk and limbs
Rotatory Nystagmus

106
Q

If a patient has face or neck pain prior to onset of Horners, what should you consider?

A

Carotid artery dissection –> need urgent CTA or MRA

107
Q

What is pseudoathetosis and what does it represent?

A

Involuntary slow writing movements when eyes are shut

Evidence of sensory ataxia secondary due to loss of proprioception

108
Q

What are some red flags that a lower motor neurone neuropathy is not a typical length dependent neuropathy?

A

Non-length discrepancy

Marked asymmetry

Prominent sensory ataxia

109
Q

Common causes of peripheral neuropathy?

A

Diabetes
Alcohol
Hypothyroidism

110
Q

Common causes of inflammatory peripheral neuropathy?

A

Acute - Guillain-Barre

Chronic - CIDP

111
Q

Key features of Guillain-Barre syndrome

A

Ascending bilateral weakness
Loss of reflexes
Reduced sensation

112
Q

How would you investigate a patient with a concerning peripheral neuropathy?

A

Bloods
- FBC, UE, LFT, CRP, ESR
- HbA1C/TFT/B12/Virology (rule out common causes)
- Paraneoplastic screen

EMG - ?axonal or demyelinating
Nerve conduction studies

CSF - raised protein, normal cell count in GBS/CIDP

113
Q

How would Guillain-Barre be managed?

A

A-E approach in acute setting

Mostly supportive

Frequent FVC monitoring - if <1.5 - consider whether ventilatory failure present - ABG’s/discuss with ITU

Severe Sx - may need Plasma Exchange or IVIG

114
Q

How would CIDP be managed?

A

MDT approach - PT, OT, Orthotics

Regular neurology review

Symptomatic therapies:
- Neuropathic pain

Disease modifying:
- Plasma exchange
- IVIG
- Steroids
- Immunosuppression

115
Q

What are the symptoms of spastic paraparesis due to myelopathy?

A

Weakness
Upgoing plantars
Increased tone
Brisk reflexes
Reduced Sensation

116
Q

What things should you do as screening tests for an UL examination?

A

Pronator drift
Myotonic dystrophy
Parkinsons
Winging of scapula
Cerebellar - past pointing/push arms down

117
Q

How is spinocerebellar ataxia inherited?

A

Autosomal dominant
Has anticipation - present earlier throughout generations

118
Q

Tips for checking co-ordination on UL/LL exam

A

Ask patient to extend finger as far as possible. Put finger at end of reach to look for tremor. Then move a little closer for past pointing

LL
- Tap feet against hands - look for irregularity
- Put finger at maximal foot reaching distance - get them to touch toe to finger –> past pointing/tremor

119
Q

How would you test the key nerves in UL examination?

A

Radial - finger extension
Ulnar - abductor digiti minimi
Medial - thumb abduction

120
Q

How does pattern of weakness help you localise the cause?

A

Proximal - myopathic cause

Distal - neuropathic cause

121
Q

What are the key differentials for distal weakness with preserved reflexes, normal sensation and normal tone?

A

This indicates a muscle pathology:
- Myotonic dystrophy
- Inclusion body myositis

122
Q

What are some features of inclusion body myositis?

A

Elderly male patients
Long finger flexors affected
Proximal impairment in legs - quads

123
Q

Features of myotonic dystrophy

A

Distal weakness
Atrophic temples
Partial ptosis
Frontal balding

Percussion myotonia
Look for PPM - associated with conduction delay (heart block/Long QT)
Listen to lungs - bibasal creps

Associated with diabetes, peripheral oedema and gonadal atrophy

124
Q

What is percussion myotonia?

A

Tap on thenar eminence - thumb move inwards

125
Q

Important when testing UL tone?

A

Do full 180 degree motion
Fast and slow - look for catch.
Catch is often late. If throughout –> cogwheel rigidity

126
Q

What is pyramidal weakness?

A

Flexors stronger than extensors

127
Q

Key things to look and comment on in diabetic neuropathy?

A

Neurologically impairment - sensory motor but predominantly sensory

Vasculature - check pulses and listen for femoral bruit

Look for ulcers and infections

Look and comment on toes - ?amputations

Charcot joint

128
Q

What order is sensation lost in diabetic neuropathy?

A

Temperature first then proprioception and vibration

Dorsal columns protected by myelin sheath

129
Q

Causes of dystonia?

A

Idiopathic
Parkinsons
Parkinsons plus

If a patient is dystonic - ask r.e. signs of PD

130
Q

What are some features of dystonia?

A

Botox is helpful
Symptoms resolve with rest
Worse when stressed or tired

Develop neck flexion and head drop

131
Q

How would you differentiate between neurofibromatosis type 1 and 2?

A

NF1 - childhood. Many cutaneous features

NF2 - hearing loss. minimal cutaneous. early adulthood

132
Q

Features of a Parkinsons Gait?

A

Slow shuffling
Reduced arm swing
Stooped posture
Reduced stride length

133
Q

Important additional examination things in suspected Parkinson’s?

A

Clasp fingers - big and fast as possible - screening test
Use synkinesis - look for tremor. Worse when doing other things
If have paper - draw spiral/write sentence
Ask for BP - considering autonomic features of MSA

Mention but don’t do
- Globolar tap - lose blink suppression
- Pull test - take many steps back in PSP/MSA

134
Q

What would a symmetrical tremor in a patient with Parkinsonian features make you think?

A

Less likely to be PD

  • Parkinson’s plus
  • Vascular parkinson’s
  • Drug related - antipsychotic
135
Q

What can cause a cranial nerve VII palsy?

A

Bells
Ramsay Hunt
Cerebellopontine angle tumour
Lyme disease
Sarcoidosis - bilateral bells palsy
Guillain Barre - bilateral
Lupus - bilateral

136
Q

What is important about aciclovir use?

A

Nephrotoxic - needs regular U&E monitoring

137
Q

If a patient has double vision, how should you approach this?

A

Check eye movements
- Look for clear CN III, IV or VI palsy

If not fitting into clear nerve pathology –> complex ophthalmoplegia. Need to consider other causes

138
Q

If cranial nerve VI is affected, what should you check and why?

A

Assess CN VII –> ?cerebellopontine angle tumour

139
Q

How can cranial nerve III pathologies be categorised?

A

Compressive vs Vascular

If evidence of pupil dilation –> need urgent admission
Vascular has no pupil involvement

140
Q

When checking eyelids, what should you be looking for?

A

Drooping - ?MG ?myotonic dystrophy

Lid lag - ?thyroid eye disease
Proptosis

141
Q

If a patient has sudden loss of vision and a RAPD, what should you always consider?

A

GCA

142
Q

What can cause tunnel vision?

A

Glaucoma
Retinitis Pigments

Tunnel vision crosses the midline

143
Q

How can eye pathologies be split into eye vs systemic issues?

A

If unilateral –> optic nerve/retinal issue.

If B/L
- Hemianopic –> vascular/cranial issue
- If cross midline –> Eye issue

144
Q

What can cause angioid streaks on fundoscopy?

A

Pseudoxanthoma elasticum
Ehler’s Danlos

145
Q

Additional things to examine in a patient with proximal myopathy

A

Fatiguability
Inspect eyes - ?ptosis
Fasciculations - ?MND
Check skin - ?dermatomyositis
Look for cushingoid appearance - ?steroid use
Wasting - ?Hereditary/MND/Long Standing

146
Q

What are some causes of proximal myopathy?

A

Inflammatory - dermatomyositis/polymyositis

Connective tissue - SLE, RA, Systemic sclerosis, Mixed, vasculitis

Cancer

Drugs - statins, steroids

Infections - HIV, EBV, CMV, Hepatitis, Bacterial

Endocrine - thyroid, acromegaly, Addisons, cushings, diabetic

Toxins - alcohol

Metabolic - liver/renal failure, electrolyte abnormalities

Misc - mitochondrial, rhabdo, sarcoidosis

147
Q

Investigations for proximal myopathy

A

Bloods
- FBC, U&E, Ca, Phosphate, Mg, LFT
- CK, extended LFT’s
- TFT, Vit D, HbA1C, cortisol
- HIV/Hepatitis screen/CMV/EBV/Serum ACE
- Rheum screen

Urine dip/PCR
Nerve conduction studies and EMG
Muscle MRI
Muscle biopsy
Ca screen if dermatomyositis/polymyositis
Systemic assessment - CXR, ECG, Echo, Lung function etc.

148
Q

When would a patient with a proximal myopathy need admission?

A

Evidence of respiratory involvement
Evidence of rhabdomyolysis

149
Q

What increase risk of myopathy in patient’s taking statins?

A

CYP450 inhibitors:
- Fibrates
- Ciclosporin
- Amiodarone
- Macrolides (clarithromycin)
- Protease inhibitors

Old age
ETOH XS
Renal/liver failure
Hypothyroid
Strenuous exercise

150
Q

What factors predispose to vitamin D deficiency?

A

Dark skin
Low exposure to sunlight
Old age
Renal failure
Poor absorption - coeliac
Meds - reduce breakdown - Rifampicin, Phenytoin

151
Q

What can cause a raised CK?

A

Rhabdo
Afro-caribbean ethnicity
IM injections
Exercise
MND
Hypothyroid

152
Q

What would you expect on examination in a cerebellar syndrome?

A

Tone - REDUCED - if increased ?corticospinal tract involvement
Power - Normal - if reduced ?corticospinal
Reflexes - pendular (less brisk)
Intention tremor
Dysdiadocokinesia
Nystagmus
Past pointing
Scanning/slurred speech
Gait - broad based. Struggle with tandem

153
Q

What should you test if you detect unilateral cerebellar signs?

A

CN V, VI, VII, VIII - CP angle tumour

154
Q

What should you consider if you detect BL cerebellar signs?

A

Spinocerebellar ataxia
Freidrichs ataxia - look for pacemaker, dorsal columns, pes cavus, Diabetes

155
Q

Differentials for unilateral cerebellar signs

A

Demyelination
Vascular
Space occupying lesions

156
Q

Differentials for B/L cerebellar signs

A

Inherited:
- Spinocerebellar ataxia
- Friedreich’s ataxia
- Ataxic Telangiectasia

Metabolic - alcohol, B12 deficiency, Wilson’s

Iatrogenic - phenytoin, carbemazepine

Paraneoplastic (anti hu/yo)
Endocrine - hypothyroid

157
Q

Important professionals in management of Friedreich’s ataxia

A

Cardiologist - HCM, HF, Arrhythmia
Diabetes
Orthopaedics
Neurologist

PT/OT/Social workers/Genetic counsellors, Orthotics
GP

158
Q

How does Huntington’s disease present?

A

Chorea - hyperkinetic movements. Large movements. Jerky, Unpredictable

Hemiballism - violent flinging movements. Single arm +-ipsilateral leg

Athetosis - slow writhing

Dysarthria

Facial grimace

159
Q

Differentials for Huntington’s Disease?

A

Inherited - Huntington’s, Wilsons

Vascular - stroke, polycythaemia rubra vera

Immune - Sydenham’s chorea, SLE, antiphospholipid

Hormonal - Pregnancy (Gravidarum chorea), OCP, Hyperthyroid

Toxic - antipsychotics, dopaminergic in PD, anti epileptics

Infectious - HIV, lyme’s

Paraneoplastic

160
Q

How is Huntington’s disease managed?

A

Non Medical:
- Education, genetic counselling etc.
- PT/OT + SALT
- DVLA considerations

Medical:
- Tetrabenazines - anti-choretic
Treat complications:
- Depression - SSRI
- Rigidity - dopamine agonist, baclofen
- psychosis - atypical antipsychotics

161
Q

What is the inheritance of Huntington’s?

A

Autosomal dominance with anticipation
Trinucleoside repeat of CAG on chromosome 4

162
Q

What are some complications of Huntington’s?

A

Seizures
Psychosis
Depression
Rigidity
Progressive dementia
Aspiration pneumonia

163
Q

What happens in internuclear ophthalmoplegia?

A

Medial longitudinal fasciculus (heavily myelinated tract) normally allow communication between contralateral CN III and CN VI for co-ordinated lateral gaze.

In INO - loss of MLF unilaterally or bilaterally –> lose of conjugate adduction.
- R MLF loss = R adduction loss - nystagmus of L eye when looking left. No issues when looking right. (L MLF still working).

If left eye covered, then R eye should be able to abduct and adduct without issues - muscles and nerves unaffected, just the communication for conjugate gaze

164
Q

Causes of internuclear ophthalmoplegia?

A

MS and Stroke are most common

Others:
- Sarcoid/SLE
- Infections
- Wernicke’s
- Fabry’s

165
Q

Examples of stroke mimics

A

Hypoglycaemia
Hemiplegic migraines
Seizures
Hyponatraemia
SOL
Intoxication/Infection
MS
Todd’s Paresis

166
Q

Completing examination with hemiparetic signs?

A

Examine cranial nerves, UL and LL (whichever haven’t done)
Urine dip
Fingerprick glucose

167
Q

How can different strokes be classified?

A

Bamford classification:
Anterior - partial/total
Posterior
Lacunar

168
Q

Classical case of anterior circulation stroke?

A
  • Motor sensory deficit affecting 2/3 of face, arm and leg
  • Higher cortical dysfunction
  • Visual field defect

Total = 3/3, Partial = 2/3

169
Q

Classical case for posterior circulation stroke?

A

Cranial nerve loss with contralateral motor sensory deficit

Conjugate eye movement disorder

Bilateral motor-sensory deficit

Cerebellar dysfunction

Isolated homonymous hemianopia

170
Q

Classical case for a lacunar stroke?

A

Discrete symptoms affecting 2/3 arm, leg or face (NO HIGHER CORTICAL SIGNS OR VISUAL FIELD IMPAIRMENT)

Pure sensory
Pure motor
Sensory motor
Ataxic hemiparesis

171
Q

How can you assess speech?

A

1 - Simple commands

2 - 2 step commands

3 - Expressive dysphasia/dysarthria - baby hippopotamus

4 - Speech production e.g. what did you have for breakfast?

5 - Test naming - hold up pen and ask them to identify/what use it for

172
Q
A

MRCP PACES (6 decks)

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