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FRACP clinical exam > Neurology > Flashcards

Neurology Flashcards

1
Q

Where is increased jaw jerk seen in?

A

Pseudobulbar palsy.

Remember:
A bulbar palsy is a lower motor neuron lesion of cranial nerves IX, X and XII. A pseudobulbar palsy is an upper motor neuron lesion of cranial nerves IX, X and XII.

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2
Q

Horner’s syndrome and its 6 causes

A

Partial ptosis and a constricted pupil which reacts normally to light, absence of sweating

  1. Lung apex carcinoma - usually SCC
  2. Thyroid malignancy
  3. Carotid artery lesion - aneurysm or dissection or pericarotid tumour
  4. Brainstem lesions such as lateral medullary syndrome, syringobulbia
  5. Retroorbital lesion
  6. Syringomyelia - usually causes bilateral Horner’s syndrome

Therefore important to check for lateral medullary syndrome in assessing horner’s syndrome

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3
Q

Features of lateral medullary syndrome

A
  1. Nystagmus to the side of lesion
  2. Ipsilateral 5, 9, and 10th CN lesion
  3. Ipsilateral cerebellar signs
  4. Contralateral pain and temperature loss over trunks and limbs
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4
Q

6 Causes of bilateral anosmia

A
  1. URTI
  2. Meningioma of the olfactory groove
  3. Ethmoid tumour
  4. Trauma to the cribriform plate fracture
  5. Hydrocephalus
  6. Congenital - Kallmann’s syndrome
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5
Q

6 Causes of pupil constriction

A
  1. Horner’s syndrome
  2. Argyll Robertson pupil
  3. Pontine lesion
  4. Narcotics
  5. Pilocarpine drops
  6. Old age
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6
Q

4 Causes of dilated pupils

A
  1. Mydriatics, atropine, cocaine
  2. Third nerve lesion
  3. Adie’s pupil - lesion in the efferent parasympathetic pathway
  4. Congenital
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7
Q

4 Causes of absent light reflex but intact accommodation reflex

A
  1. Midbrain lesion - eg: Argyll Robertson pupil
  2. Ciliary ganglion lesion - Adie’s pupil
  3. Parinaud’s syndrome - dorsal midbrain syndrome caused by compression of the vertical gaze center at the rostral interstitial nucleus of medial longitudinal fasciculus (riMLF) resulting in vertical gaze palsy
  4. Bilateral anterior visual pathway lesion (ie, bilateral afferent pupil deficits)
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8
Q

4 causes of Argyll Robertson pupil

A

Lesion of the iridodilator fibres in the midbrain, resulting in intact accommodation but does not react

  1. Neurosyphilis
  2. DM
  3. Alcoholic midbrain degeneration
  4. Other midbrain lesions
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9
Q

Causes of ptosis with:

  1. Normal pupils
  2. Constricted pupils
  3. Dilated pupils
A
  1. Normal pupils:
    a. Myotonic dystrophy
    b. thyrotoxic myopathy
    c. myasthenia gravis
    d. botulism
    e. fascioscapulohumeral dystrophy
  2. Constricted pupils - tabes dorsalis, horner’s syndrome
  3. With dilated pupils: third cranial nerve lesion
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10
Q

Name 4 central and peripheral causes of third cranial nerve palsy

A

Central

  1. Brainstem infarction
  2. Tumour
  3. Demyelination
  4. Trauma

Peripheral

  1. Compression: Pcom aneurysm, nasopharyngeal carcinoma, Tolosa Hunt syndrome (superior orbital fissure syndrome causing painful lesion of the third, fourth, sixth and first division of the 5th cranial nerve)
  2. Infarction due to DM, arteritis
  3. Trauma
  4. Cavernous sinus lesions
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11
Q

How do you test for fourth cranial nerve palsy in presence of 3rd cranial nerve palsy?

A

Tilt the patient’s head to the same side as the lesion. The affected eye will INTORT if the fourth nerve is intact.

OR, you can ask the patient to look down and across to the opposite side from the lesion and look for intortion - remember SIN (Superior oblique, supplied by IV, INtorts the eye)

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12
Q

Name 4 causes of bilateral 6th cranial nerve palsy

A
  1. Head injury
  2. Wernicke’s encephalopathy
  3. Raised ICP
  4. Mononeuritis multiplex
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13
Q

Name 4 central and peripheral causes of unilateral 6th cranial nerve palsy

A

Central:

  1. Vascular
  2. Tumour
  3. Wernicke’s encephalopathy
  4. MS

Peripheral

  1. Diabetes
  2. Trauma
  3. Raised ICP
  4. Idiopathic
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14
Q

Where is the lesion in the following?

Upbeat nystagmus
Downbeat nystagmus

A

Upbeat nystagmus - floor of the fourth ventricle

Downbeat nystagmus - foramen magnum lesion (eg, meningioma, Arnold Chiari type I malformation, trauma, spinocerebellar degeneration)

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15
Q

Name 4 UMN lesion causes of 12th CN palsy

A
  1. Vascular
  2. Motor neuron disease
  3. Tumour
  4. Multiple sclerosis
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16
Q

Name 3 central and peripheral LMN causes of hypoglossal nerve palsy

A

Central:

  1. Vascular - thrombosis of the vertebral artery
  2. Motor neuron disease
  3. Syringobulbia

Peripheral:

  1. Aneurysm involving posterior fossa
  2. Tumour
  3. Arnold-Chiari malformation (protrusion of the cerebellar tonsils through the foramen magnum, causing basilar compression with lower cranial nerve palsies, cerebellar limb signs and UMN signs of legs)
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17
Q

Name 5 causes of multiple cranial nerve palsies

A

Think CANCERS first

  1. Nasopharyngeal carcinoma
  2. Lesion at the base of the skull (eg: meningioma, metastasis)
  3. Arnold-Chiari malformation - involves lower CNs
  4. Chronic meningitis due to TB, sarcoid, carcinomas
  5. Gullaine Barre syndrome (spares I, II, VIII)
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18
Q

Features of lateral medullary syndrome

A

Usually due to the occlusion of PICA.

Dysphagia, hoarseness and diminished gag reflex due to CN 9/10 deficit

Ipsilateral cerebellar deficits (spinocerebellar tract)

Ipsilateral deficit of pain and temperature from face (spinal trigeminal area of sensory nucleus of V affected)

Contralateral deficit of pain and temperature of rest of the body (lateral spinothalamic tract affected)

Horner’s syndrome (affecting Sympathetic pathway)

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19
Q

4 features of Gerstmann’s syndrome

A

Dominant parietal lobe deficit - AALF

Acalculia
Agraphia (inability to write)
L/R disorientation
Finger agnosia - inability to name individual fingers, caused by L angular gyrus lesion in the R handed and about half of left handed patients

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20
Q

How would you test the frontal lobe function?

A
  1. Primitive reflexes - palmar-mental reflex, pout reflex, grasp reflex
  2. Interpretation of proverb
  3. Test for anosmia
  4. Gait apraxia - feet typically behave as if glued to the floor, resulting in a hesitant shuffling gait with freezing
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21
Q

Three causes of drifting of arm

A
  1. UMN (pyramidal) weakness due to weakness and causes downward drift of the affected upper limb
  2. Cerebellar disease - generally upward drift with slow pronation of the wrist and the elbow
  3. Loss of proprioception resulting in drift in any direction, usually affects the fingers only
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22
Q

Motor supply of median nerve

A

All the muscles of the forearm except flexor carpi ulnaris and ulnar half of the flexor digitorum profundus

Also LOAF:
Lateral two lumbricals
Opponens pollicis
Abductor pollicis brevis
Flexor pollicis brevis
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23
Q

Motor supply of the ulnar nerve

A

Motor supply to all the muscles of the hand except LOAF, plus flexor carpi ulnaris and ulnar half of the flexor digitorum profundus.

FDP - flexor of wrist, MCP, IPJ

Deficit results in clawing of the little and ring finger (clawing is hyperextension at the MCPJ and flexion of the IPJ)

Clawing is more pronounced with an ulnar nerve lesion at the wrist as a lesion at or above the elbow also causes loss of the flexor digitorum profundus therefore less flexion of the IPJ - ie so called ulnar paradox.

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24
Q

5 features of cervical rib syndrome

A
  1. Weakness and wasting of the small muscles of the hand
  2. C8/T1 sensory loss
  3. Unequal radial pulses and blood pressure
  4. Subclavian bruit on arm manoeuvring
  5. Palpable cervical rib in the neck
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25
Q

Describe upper brachial plexus lesion (C5-6)

A

Called Erb Duchenne.

  1. Loss of shoulder movement and elbow flexion - the hand is held in the waiter’s tip position
  2. Sensory loss over the lateral aspect of the arm and forearm
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26
Q

Describe lower brachial plexus lesion (C8-T1)

A
  1. True claw hand with paralysis of all the intrinsic muscles
  2. Sensory loss along the ulnar side of the hand and forearm
  3. Horner’s syndrome
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27
Q

Causes of proximal weakness

A
  1. NMJ disorders - MG
  2. Neurogenic - MND, polyradiculopathy
  3. Myopathy

Causes of myopathy includes

  1. Hereditary muscular dystrophies
  2. Congenital myopathies (rare)
  3. Acquired - PACEPODS
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28
Q

Causes of myopathy

A

PACE PODS

Polymyositis/dermatomyositis
Alcohol, AIDS
Carcinoma
Endocrine - hyper/hypothyroidism, acromegaly, cushing

Periodic paralysis
Osteomalacia
Drugs - steroids mainly
Sarcoidosis

29
Q

5 major causes of muscular dystrophies

A
  1. Duchennes - affects only males, hypertrophied calves and deltoids, proximal muscle weakness, dilated cardiomyopathy
  2. Beckers - similar to Duchennes but less cardiac disease, later onset and less rapid progression
  3. Limb girdle - can affect males and females (AR), shoulder or pelvic girdle affected, face and heart usally spared
  4. facioscapulohumeral - facial and pectoral weakness with hypertrophy of deltoids (AD)
  5. Dystrophica myotonica (AD)
30
Q

9 Clinical features of dystrophia myotonica

A
  1. Frontal baldness
  2. Triangular facies
  3. Atrophy of temporalis muscle
  4. Cataracts
  5. Atrophy of SCM with weak neck flexion (extension is normal)
  6. Percussion myotonica
  7. Muscle wasting and weakness distally and proximally
  8. Cardiomyopathy
  9. Testicular atrophy
31
Q

Tests for cerebellar disease

A
  1. Nystagmus
  2. Jerky speech with “British Constitution”
  3. Arm drift
  4. Intention tremor and/or pass pointing
  5. Dysdiadochokinesis
  6. Rebounding - inability to stop the arms when lifted quickly from the side
  7. Difficulty with heel shin test
  8. Truncal ataxia
  9. Gait - staggers towards the affected side if unilateral cerebellar hemisphere lesion

If obvious unilateral cerebellar lesion is found, then examine the cranial nerves for evidence of cerbellopontine angle tumour (5, 7, 8) or lateral medullary syndrome.

32
Q

Muscles supplied by C5-6 nerve root

A 
Deltoid
Biceps
Brachioradialis
Supra/infraspinatus
Serratus anterior - scapular fixation and rotation (supplied by long thoracic nerve C5-7)
33
Q

How do you distinguish between C5/6 cord, root or plexus lesion?

A

In cord lesion, biceps and brachioradialis reflexes are decreased, while other reflexes below that level such as triceps and lower limb reflexes are increased.

In C5/6 root or plexus lesion, biceps and brachioradialis reflexes are absent but triceps and leg reflexes are normal.

To distinguish between root and plexus lesion of C5/6, test the muscles in order which they arise - ie, very proximal lesion will involve all C5/6 muscles (including serratus anterior and supraspinatus/infraspinatus).

If all muscles of the arm are weak with absent reflexes of the arm, then the patient probably has a brachial plexus lesion.

34
Q

Differential diagnosis for bilateral proximal arm and leg weakness

A

Depends on reflex findings

  1. Reflexes preserved or reduced - myopathy (MD or PM) or myasthenia gravis (check for fatigability)
  2. Reflexes are lost - consider spinal muscular atrophy or myasthenic syndrome
  3. Reflexes are increased - motor neuron disease (check for fasciculation, wasting and fasciculation of the tongue, sensation), cervical myelopathy, multilacunar state
35
Q

Weakness and wasting of the quadriceps can be due to a femoral nerve lesion or L2-4 root or plexus lesion. How would you distinguish between the two?

A

Test the hip adductors which have the same nerve root (L2-4) however supplied by obturator nerve.

36
Q

Describe features of the femoral nerve lesion

A
  1. Weakness of ilipsoas and weakness and wasting of the quadriceps
  2. Reduced knee jerk
  3. Power in the hip adductors normal
  4. Sensory impairment over thigh and medial aspect of the shin

Commonly caused by diabetic amyotrophy, haemorrhage into the psoas, traction during hip surgery.

37
Q

What causes foot drop?

A

Weakness of tibialis anterior, which is supplied by common peroneal nerve and L4/5 nerve root.

To distinguish between common peroneal nerve lesion and L4/5 nerve root lesion, test for inversion/eversion of the foot:

L4/5- also supplies tib posterior which inverts the foot

common peroneal nerve - also supplies peroneal muscles which EVERTS the foot

38
Q

3 causes of pes cavus

A
  1. Charcot Marie Tooth disease
  2. Friedreich’s ataxia
  3. Spina bifida
39
Q

3 differential diagnosis of dissociative sensory loss (touch spared, pain/temperature pathway affected)

A
  1. Syringomyelia
  2. Hemicord lesion (Brown-Sequard syndrome)
  3. Lateral medullary syndrome
40
Q

5 aspects of gait to observe

A
  1. Posture of head, trunk and limbs
  2. Arm swing
  3. Stride length
  4. Base or stance
  5. Involuntary movements
41
Q

2 causes of high stepping gait bilaterally

A
  1. CMT disease

2. Motor neuron disease

42
Q

Shuffling gait, but with wide base

A

Seen in:

  1. Normal pressure hydrocephalus
  2. Vascular dementia due to multi-lacunar state
  3. Progressive supranuclear palsy
43
Q

Risk factors for MS

A
  1. EBV infection at older age (disease is rare in seronegative patients)
  2. HLA-DRB1
  3. Lived as children in regions far from the equator
  4. Family history (7x more common in immediate relatives)
  5. Smoking
44
Q

What proportion of patients with RRMS develop SPMS?

A

After about 10 years of RRMS, 50% develop SPMS, and eventually 80% enter this stage.

45
Q

Charcot’s triad in MS

A
  1. Nystagmus
  2. Intention tremor
  3. Scanning speech
46
Q

5 differential diagnosis of multiple CNS lesions

A
  1. MS
  2. Vasculitis such as SLE, Behcet’s disease
  3. Small vessel ischaemia
  4. Paraneoplastic syndrome
  5. Multiple embolic infarcts from any source
47
Q

5 common sites of demyelinating lesions on MRI scanning

A
  1. Corpus callosum
  2. Juxtacortical white matter
  3. Spinal cord
  4. Optic nerve
  5. Periventricular white matter
48
Q

Explain how visual evoked response works in diagnosis of MS

A

Delayed in 80% of established cases and indicates previous optic neuritis.

Basically tests the afferent visual pathway by recording the discrete light stimulated evoked potential at the occipital lobe amongst the background EEG pattern.

49
Q

Investigations in myasthenia gravis

A
  1. Anti-AChR, or if seronegative for this, anti-MuSK (which are present 40% of ACh antibody negative patients)
  2. EMG to test for reduction in muscle potential with repetitive stimulation
  3. Thymoma investigation - CXR, CT chest
  4. Screen for other associated conditions (hyperthyroidism, autoimmune diseases such as ANA, RF)
  5. Respiratory function test if severe
50
Q

Drugs to avoid in myasthenia gravis

A

Drugs which interfere with NMJ transmission

  1. Quinidine
  2. Procainamide
  3. Gentamicin
51
Q

Management of acute myasthenia gravis

A
  1. Anticholinesterase for mild symptomatic cases
  2. Steroids - may initially aggravate the disease therefore inpatient monitoring is important
  3. Azathioprine if steroid refractory
  4. Rituximab if desperate
  5. Thymectomy in seropositive ACh-Ab positive patients
  6. Plasmapheresis if myasthenic crisis.
52
Q

How is lambert-eaton syndrome different from MG?

A
  1. PRE-synaptic failure of RELEASE of ACh
  2. Caused by small cell carcinoma of the lung in 50% or other autoimmune causes
  3. Increased power with repetitive stimulatin
  4. Sparing of ocular/bulbar muscles
53
Q

Features of radial nerve lesion

A

C5-8 lesion

  1. Wrist and finger drop (normal wrist flexion)
  2. Triceps loss (if the lesion is above the spiral groove)
  3. Sensory loss over the anatomical snuff box
  4. Finger abduction ‘appears’ to be wear because of the difficult y of spreading the fingers when they cannot be straightened.
54
Q

Features of median nerve lesion

A

C6-T1 lesion

Supplies all the muscles on the front of the forearm except flexor carpi ulnaris and half of the digitorum profundus. Also supplies LOAF.

  1. Loss of thumb abduction
  2. Positive Ochsner’s clasping test - ask the patient to clasp the hands firmly together - the index finger on the affected side fails to flex. Due to loss of flexor digitorum sublimis with alesion in/above the cubital fossa
  3. Sensory loss over the palmar aspect of thumb, index, middle and lateral half of the ring finger
55
Q

5 causes of carpal tunnel syndrome

A
  1. Idiopathic
  2. Arthopathy such as RA
  3. Endocrine disease - acromegaly, hypothyroidism
  4. Pregnancy
  5. Trauma, overuse
56
Q

5 causes of unilateral cerebellar signs

A
  1. Space occupying lesion (abscess, tumours)
  2. Ischaemia (vertebrobasilar disease)
  3. paraneoplastic syndrome
  4. Multiple sclerosis
  5. Trauma
57
Q

6 causes of BILATERAL cerebellar signs

A
  1. Drugs: phenytoin
  2. Friedrich’s ataxia
  3. Hypothyroidism (rare)
  4. Multiple sclerosis
  5. Trauma
  6. Hypothyroidism
58
Q

Features of a midline cerebellar lesion

A

Truncal ataxia, abnormal heel-toe walking or abnormal speech.

Consider:

  1. Paraneoplastic syndrome
  2. Midline tumour
59
Q

Clinical features of Friedriech’s ataxia

A

Usually a young person with:

  1. Bilateral cerebellar signs including nystagmus
  2. Posterior column loss in the limbs
  3. UMN signs in the limbs (although ankle reflexes are absent)
  4. Peripheral neuropathy
  5. Optic atrophy
  6. Pes cavus, cocking of the toes and kyphoscoliosis
  7. Cardiomyopathy
  8. Diabetes mellitus
60
Q

Causes of spastic and ataxic paraparesis (UMN signs and cerebellar signs combined)

A
  1. MS
  2. Spinocerebellar degeneration
  3. Syphilitic meningomyelitis
  4. Lesion at the craniospinal junction (eg: meningioma)
61
Q

Myasthenia gravis findings

A
  1. Muscle fatigue, particularly involving the elevators of the eyelids and the oculomotor muscles, bulbar muscles and proximal limb girdles
  2. Peek sign (orbicularis oculi weakness) - close the eyelids, within 30s they will begin to separate
  3. Weakness of neck flexion
  4. Thymectomy scar
  5. Preserved reflexes, no sensory loss or muscle wasting
62
Q

Tests for myasthenia gravis

A
  1. Acetylcholine receptor antibodies - positive 80-90%, and false positives are rare. Titre is not directly related to disease severity
  2. Anti-striated muscle antibody - detectable in 90% of patients with a thymoa
  3. MuSK antibodies - present in 40% of ‘seronegative’ patients
  4. EMG - repetitive stimulation leading to reduction in muscle potential amplitude
  5. CXR/CT chest to look for thymoma
  6. Respiratory function test
  7. Check for other associated conditions - (TFTs, RF, ANA)
63
Q

Examination findings in AIDP

A
  1. Distal muscle weakness without atrophy, although 25% can have proximal > distal weakness
  2. Upper limbs may be more affected than the lower limbs
  3. Reduced/absent tendon reflexes
  4. Muscle tenderness
  5. Signs of autonomic neuropathy
  6. Sensory loss is usually minimal but may affect posterior columns more than the spinothalamic tract
64
Q

Causes of AIDP

A
  1. Mycoplasma pneumonia
  2. HIV
  3. Campylobacter infection
  4. Acute viral hepatitis
  5. Glandular fever
65
Q

DDx of acute ascending motor paralysis

A
  1. AIDP
  2. Diphtheria
  3. Polio
  4. Botulism
  5. Critical illness myopathy or polyneuropathy

Remember that diphtheria, botulism and MG usually begins with bulbar symptoms.

66
Q

Causes of peripheral neuropathy

A

DAMIT BITCH

Drugs - isoniazid, bortezomib, vinka alkaloids
Alcohol
Metabolic - diabetes, thyroid
Infection - HIV, syphilis
Tumour
B vitamins
Infiltrative - sarcoid, amyloid
Toxins - heavy metals
Connective tissue diseases
Hereditary including friedrich's ataxia
67
Q

Causes of predominantly motor peripheral neuropathy

A
  1. AIDP and CIDP
  2. CMT disease
  3. Acute intermittent porphyria
  4. Diabetes
  5. Lead poisoning
  6. Multifocal motor neuropathy
68
Q

Features of sub acute combined degeneration of the cord

A

Most distinct pattern is that of UMN signs causing an extensor plantar response plus peripheral neuropathy causing loss of knee and ankle jerks

  1. Symmetrical posterior column loss (vibration, position sense) causing ataxic gait
  2. Symmetrical UMN signs of lower limbs with ABSENT ankle reflexes, knee reflexes can be variable
  3. Peripheral sensory neuropathy
  4. Optic atrophy
  5. Dementia
69
Q

Clinical triad of syringomyelia

A
  1. Loss of pain and temperature over the neck, shoulders and arms (cape distribution)
  2. Weakness, atrophy and areflexia of arms
  3. UMN lesion of the lower limbs

FRACP clinical exam (8 decks)

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