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MRCP PACES Neurology > Neurology > Flashcards

Neurology Flashcards

1
Q

What are the clinical signs of dystrophia myotonica?

A

Face: long thin expressionless face; wasting of facial muscles; bilateral ptosis; frontal balding; dysarthria
Hands: myotonia; wasting and weakness; percussion myotonia
Cataracts
Cardiomyopathy, arrhythmia (look for PPM)
Diabetes
Dysphagia

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2
Q

What are the common causes of unilateral ptosis?

A

Third nerve palsy

Horner’s syndrome

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3
Q

What are the clinical signs of cerebellar syndrome?

A

DANISH

Dysdiadochokinesis
Ataxia
Nystagmus
Intention tremor
Scanning dysarthria
Hypotonia/hyporeflexia
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4
Q

What are the causes of cerebellar syndrome?

A

PASTRIES

Paraneoplastic cerebellar syndrome
Alcoholic cerebellar degeneration 
Sclerosis (MS)
Tumour (posterior fossa)
Rare (Friedrich’s ataxia)
Iatrogenic (phenytoin toxicity)
Endocrine (hypothyroidism)
Stroke (brain stem)
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5
Q

What are the clinical signs of multiple sclerosis?

A

Internuclear ophthalmoplegia, optic atrophy, reduced visual acuity, any cranial nerve palsy
Upper motor neurone spastictiy, weakness, brisk reflexes, altered sensation
Cerebellar syndrome (DANiSH)

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6
Q

What are the diagnostic criteria for multiple sclerosis?

A

Central nervous system demyelination causing neurological impairment that is disseminated in both space and time

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7
Q

What is the cause of multiple sclerosis?

A

Unknown
But, both genetic and environmental factors appear to play a role

Environmental- increasing latitude, epstein-barr infection
Genetic - HLA-DR2, interlukin 2 and 7

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8
Q

How would you investigate a patient with suspected multiple sclerosis?

A

CSF: oligoclonal IgG bands
MRI: peri ventricular white matter plaques
Visual evoked potentials: delayed velocity but normal amplitude, suggests previous optic neuritis

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9
Q

What are the other (non-neurological) clinical features of multiple sclerosis?

A 
Depression
Urinary retention or incontinence
Impotence 
Bowel problems
Uthoff’s phenomenon - symptoms worse after a hot bath or exercise
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10
Q

How is MS treated?

A

Multidisciplinary team involvement
Disease-modifying treatments -

Interferon beta and glatiramer reduce relapse rate but don’t affect progression
Monoclonal antibody therapy use may be limited by toxicity

Symptomatic treatments - methylprednisolone during acute relapse may shorten duration, anti-spasmodics, carbamazepine, laxatives

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11
Q

What is the definition of a stroke and a transient ischaemic attack?

A

Stroke - rapid onset, focal neurological deficit due to a vascular lesion lasting more than 24 hours

TIA - focal neurological deficit lasting less than 24 hours

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12
Q

What is the Bamford classification of stroke?

A

Total anterior circulation stroke (hemiplegia, homonomous hemianopia, dysphasia, dyspraxia, neglect)

Partial anterior circulation (2/3 of TACS symptoms)

Lacunar (pure hemi- motor or sensory loss)

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13
Q

What is lateral medullary syndrome?

A

Most common brainstem vascular syndrome
Due to occlusion of the posterior inferior cerebellar artery
Variable in it’s presentation

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14
Q

How does lateral medullary syndrome present?

A

Ipsilateral: cerebellar signs, nystagmus, horner’s syndrome, palatal paralysis, loss of trigeminal pain and temperature sensation

Contralateral: loss of pain and temperature sensation

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15
Q

What are the causes of lower limb spasticity?

A

Spinal cord lesions i.e myelopathy

Hyperacute - likely spinal cord infarct/ischaemia, trauma
acute - disc bulge, metastatic cord compression
Sub-acute - MS
Chronic - b12 deficiency, genetic causes (hereditary spastic paraparesis)

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16
Q

What are the clinical signs of syringomyelia?

A

Weakness and wasting of the small muscles of the hands
Loss of reflexes in the upper limbs
Loss of pain and temperature sensation with preservation of joint position and vibration sense
Charcot joints
Pyramidal weakness in legs with upgoing plantars
Kyphoscoliosis
Horner’s syndrome

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17
Q

What is syringomyelia?

A

Caused by a progressively expanding fluid filled cavity within the spinal cord, typically spanning several levels

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18
Q

What are the most important causes of a Charcot joint?

A

Tabes dorsalis (hip and knee)
Diabetes (foot and ankle)
Syringomyelia (shoulder and elbow)

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19
Q

What are the clinical signs of motor neurone disease?

A

Wasting and fasiculation
Usually spastic but may be flaccid
Weakness
Reflexes may be absent or brisk, upgoing plantars
Normal sensory examination
Speech may be bulbar (palatal weakness) or pseudo-bulbar (spastic tongue)

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20
Q

What is the pathophysiology of motor neurone disease?

A

Progressive disease of unknown aetiology

Axonal degeneration of upper and lower motor neurones

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21
Q

What are the types of motor neurone disease?

A

Amyotrophic lateral sclerosis: affects cortico-spinal tracts and predominantly produces spastic parapesis and tetraparesis

Progressive muscular atrophy: affects anterior horn cells, predominantly producing wasting, fasciculation and weakness, has the best prognosis

Progressive bulbar palsy: affecting lower cranial nerves and suprabulbar nuclei producing speech and swallow problems, has the worst prognosis

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22
Q

How would you investigate a patient with suspected motor neurone disease?

A

Clinical diagnosis
EMG: fasiculation
MRI: excludes cord compression and brain stem lesions

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23
Q

What is the management of motor neurone disease?

A

Multidisciplinary approach (including communication aids, PT, OT, SALT, dietetics)

Measure FVC and consider ABG as patients may require NIV

Riluzole slows disease progression but does not improve function or quality of life

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24
Q

What is the prognosis of motor neurone disease?

A

Most die within 3 years of diagnosis from pneumonia and respiratory failure

Worse if elderly at onset, female and with bulbar involvement

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25
What are the causes of wasting of the hand muscles?
``` Motor neurone disease Syringomyelia Cervical cord compression Polio Pancoast’s tumour Trauma Peripheral neuropathy Disuse atrophy ```
26
What are the lumbosacral root levels and corresponding movements?
``` L2/3 - hip flexion L3/4 - knee extension, knee jerk L4/5 - ankle dorsiflexion L5/S1 - knee flexion, hip extension S1/2 - foot plantarflexion, ankle jerk ```
27
What are the cervical roots and corresponding movements?
C5/6 - elbow flexion and supination, biceps and supinator jerks C7/8 - elbow extension, triceps jerk C8/T1 - finger adduction
28
What are the clinical signs of Parkinsonism?
``` Expressionless face Coarse, pill-rolling tremor (usually asymmetrical) Bradykinesia Cog-wheel rigidity Shuffling gait with absent arm swing Slow, faint and monotonous speech ```
29
How would you distinguish Parkinson’s disease from multi-system atrophy?
Parkinsonism with postural hypotension, cerebellar and pyramidal signs
30
What are the causes of Parkinsonism?
``` Parkinson’s disease Parkinson’s plus syndromes Drug-induced (phenothiazines) Anoxic brain injury Post-encephalitis MPTP toxicity ```
31
What are the Parkinson’s plus syndromes?
Multi-system atrophy Progressive supranuclear palsy Corticobasal degeneration (unilateral Parkinsonian signs)
32
What is the pathology of Parkinsonism?
Degeneration of the dopaminergic neurones between the substantia nigra and the basal ganglia
33
What is the treatment of Parkinson’s?
L-Dopa (issues are nausea, dyskinesia, effects of treatment wearing off) Dopamine agonists (bromocriptine - less side effects and delay need to start l-dopa) MAOB inhibitors Anticholinergics (useful in drug induced tremor) Surgery such as deep brain stimulation may be useful in some cases
34
What are the causes of tremor?
Resting - Parkinsonism Postural - benign essential tremor, anxiety, thyrotoxicosis, CO2, hepatic encephalopathy, alcohol Intention - cerebellar disease
35
What are the clinical signs of hereditary sensory motor neuropathy?
Wasting of distal lower limb muscles with preservation of thigh muscles (inverted champagne bottle) ``` Pes cavus Weakness of ankle dorsiflexion and toe extension Stocking sensory loss High stepping gait (foot drop) Stamping (absent proprioception) Wasting of hand muscles ```
36
What are the types of hereditary sensory motor neuropathy?
Also known as Charcot-Marie-Tooth disease ``` HSMN 1 (demyelinating) HSMN 2 (axonal) ``` Autosomal dominant inheritance
37
What is the management of hereditary sensory motor neuropathy?
``` No disease modifying treatments available Multi-disciplinary team approach Orthotics Occupational therapy Analgesia ```
38
What are the causes of pes cavus?
Unilateral: burns, previous compartment syndrome, poliomyelitis, spinal trauma, spinal cord tumours Bilateral: Friedrich’s ataxia, muscular dystrophy, cerebral palsy, syringomyelia, hereditary spastic paraparesis, hereditary sensory motor neuropathy
39
What are the causes of a predominantly sensory peripheral neuropathy?
Metabolic: Diabetes, vitamin deficiencies Toxic: Alcohol, medications (isoniazid), chemotherapy Auto-immune: rheumatoid arthritis, Hypothyroidism, vasculitis, GBS, SLE Infective: herpes zoster, HIV Haematological: MGUS, myeloma, lymphoma Genetic: Charcot-Marie-Tooth disease
40
What are the causes of a predominantly motor peripheral neuropathy?
Acute: Gullian-Barre, botulism Lead toxicity Porphyria HSMN
41
What are the clinical signs of Friedrich’s ataxia?
Young adult with an ataxic gait Pes cavus Bilateral cerebellar ataxia Leg wasting with absent reflexes and bilateral upgoing plantars Posterior column signs (loss of vibration and proprioception) Others: high arched palate, kyphoscoliosis, HOCM, diabetes (check urine glucose)
42
What do you know about Friedrich’s ataxia?
Inheritance is usually autosomal recessive Onset is during teenage years Survival rarely exceeds 20 years from diagnosis Association with HOCM and a mild dementia
43
What are the causes of extensor plantars with absent knee jerks?
Friedrich’s ataxia Subacute combined degeneration of the cord Motor neurone disease
44
What are the clinical signs of a facial nerve palsy?
Unilateral facial droop Absent nasolabial fold Absent forehead crease Inability to raise eyebrows, screw eyes up or smile
45
How can you localise the lesion causing facial nerve palsy?
Pons (MS, stroke) - VI palsy and long tract signs Cerebellar-pontine angle (Acoustic neuroma) - V, VI and VIII and cerebellar signs Auditory/facial canal (Cholesteatoma, abscess) - VIII
46
What are the causes of a unilateral facial palsy?
``` Bell’s palsy is the commonest Herpes-zoster (ramsay hunt syndrome) Mononeuropathy (diabetes, sarcoid, Lyme) Tumour MS/stroke ```
47
What are the causes of a bilateral facial palsy?
``` Guillian Barre Myasthenia gravis Sarcoidosis Bilateral Bell’s palsy Lyme disease ```
48
What is Bell’s palsy?
Rapid onset facial nerve palsy HSV-1 implicated Swelling and compression of the nerve within the facial canal Treatment: prednisolone, aciclovir, eye protection Prognosis: 70-80% make a full recovery, more common and may have poorer outcomes in pregnancy
49
What are the clinical signs of myasthenia gravis?
``` Bilateral ptosis Complicated bilateral extra-ocular muscle palsies Myasthenic snarl Nasal speech Proximal muscle weakness in upper limbs with fatiguability Normal reflexes Sternotomy scars (thymectomy) Assess FVC ```
50
What other conditions may be associated with myasthenia gravis?
``` Diabetes Rheumatoid arthritis Thyrotoxicosis SLE Thymomas ```
51
What is the cause of myasthenia gravis?
Anti-nicotinic acetylcholine receptor antibodies affect motor end plate neurotransmission
52
How would you investigate a patient with suspected myasthenia gravis?
Anti acetlycholine receptor antibodies present in 90% Anti-MuSK often positive if above negative EMG - decreased response to titanic train of impulses Tensilon test CT (thymoma), thyroid function
53
How would you treat a patient with myasthenia gravis?
IV immunoglobulin or plasmapharesis in acute setting Acetylcholine esterase inhibitor (pyridostigmine) Immunosuppression (steroids, azathioprine) Thymectomy usually beneficial even if patient does not have a thymoma
54
What is Lamber-Eaton myasthenic syndrome?
Diminished reflexes that improve after exercise Lower limb girdle weakness Associated with malignancy Antibodies block presynaptic calcium channels “Second wind” on EMG
55
What are the causes of bilateral extra ocular palsies?
Myasthenia gravis Graves disease Miller-Fischer syndrome Cavernous sinus pathology
56
What are the causes of a bilateral ptosis?
``` Congenital Senile Myasthenia gravis Myotonic dystrophy Bilateral Horner’s syndrome ```
57
What are the clinical signs of tuberous sclerosis?
``` Butterfly rash, periingual fibromas, Shagreen patch, Ash leaf macules Cystic lung disease Polycystic kidneys Evidence dialysis or renal transplant White patches on retina Seizures Signs of epileptic treatment ```
58
What is tuberous sclerosis?
Autosomal dominant condition with variable penetrance 80% have epilepsy Cognitive defects in 50%
59
How would you investigate a patient with suspected tuberous sclerosis?
Skull xray - railroad calcifications CT/MRI head - tuberous mass in cerebral cortex Echo Abdominal USS - renal cysts
60
What are the clinical signs of neurofibromatosis?
``` Cutaneous neurofibromas Cafe au lait patches >15 Axillary freckling Lisch nodules in the iris Hypertension (renal artery stenosis, phaeochromocytoma) Fibrosis Neuropathy with large palpable nerves Reduced visual acuity ```
61
What is the inheritance of neurofibromatosis?
``` Autosomal dominant Type 1 (chromosome 17) is classical peripheral form Type 2 (chromosome 22) is central and presents with bilateral acoustic neuromas and deafness ```
62
What conditions is neurofibromatosis associated with?
Phaeochromocytoma | Renal artery stenosis
63
What are the complications of neurofibromatosis?
Epilepsy Sarcomatous change Scoliosis Mental retardation
64
What is a Horner’s pupil?
Ptosis Sunken eye Anhydrosis
65
What are the causes of a Horner’s pupil?
MS, Stroke (Brain stem) Syrinx (Spinal cord) Aneurysm, trauma, Pancoast tumour (neck)
66
What is a Holmes-Adie pupil?
Moderately dilated pupil with a poor response to light and sluggish accommodation May have absent ankle and knee jerks A benign condition that is more common in females
67
What is an Argyll Robertson pupil?
Small, irregular pupil which accommodates but does not react to light Atrophied and depigmented iris Look for sensory ataxia Usually a manifestation of quaternary syphyllis, but may be related to diabetes
68
What are the clinical signs of an oculomotor nerve palsy?
Complete ptosis Dilated pupil Eye points down and out
69
What are the causes of an oculomotor nerve palsy?
Medical: mononeuritis multiplex, midbrain stroke, MS, migraine Surgical: posterior communicating artery aneurysm, cavernous sinus pathology, cerebral uncus herniation
70
What are the clinical signs of optic atrophy?
Relative afferent pupillary defect | Disc pallor
71
What are the causes of optic atrophy?
Glaucoma, tumour, Paget’s and MS most common Retinitis pigmentosa Central retinal artery occlusion Friedrich’s ataxia Tertiary syphyllis
72
What are the clinical signs of age related macular degeneration?
Drusen Fibrosis Neovascularisation
73
What are the causes of age related macular degeneration?
Risk factors: age, white race, family history, smoking | Associated with coronary artery disease and stroke
74
What are the causes of retinitis pigmentosa?
Friedrich’s ataxia Kearns-Sayre syndrome Congenital: usually autosomal recessive Acquired: post-inflammatory retinitis No treatment although vitamin A may slow progression
75
What are the clinical signs of retinal artery occlusion?
Pale fundus with thread like arterioles Cherry red macula May have signs AF or a carotid bruit
76
What are the causes of retinal artery occlusion?
Embolic (carotid plaque rupture) - treat with aspirin, anticoagulation and endarterectomy Giant cell arteritis - high dose steroids
77
What are the clinical signs of retinal vein occlusion?
Flame haemorrhages Swollen optic disc Cotton wool spots Tortuous veins May have visual field defect or signs hypertension and diabetes
78
What are the causes of retinal vein occlusion?
Hypertension Hyperglycemia Hyperviscocity (myeloma) High intraocular pressure (glaucoma)
79
How would you differentiate cerebellar ataxia from sensory ataxia on examination?
Cerebellar ataxia usually has associated nystagmus and dysarthria Sensory ataxia usually has sensory impairment, particularly joint position sense and vibration sense. In sensory ataxia, finger-nose test may be normal with eyes open, but impaired with eyes closed
80
How would you investigate a patient with cerebellar ataxia?
MRI is far superior to CT for looking at brainstem lesions However, CT important in the acute setting to rule out haemorrhage Investigate the cause- LP if ?MS, thyroid function tests
81
What are the causes of sensory ataxia?
Central: spinal cord pathology (dorsal column damage) - cervical myelopathy Peripheral neuropathy - alcohol, diabetes, b12 deficiency, platinum chemotherapies, HIV, Sjorgren’s syndrome, paraneoplastic syndrome Combined peripheral and central: B12 deficiency
82
How would you investigate a patient with peripheral neuropathy?
Look for the cause Urine dip, fundoscopy, blood glucose Bloods: FBC, haemantinics, HbA1c, auto-immune screen, vasculitis screen, HIV tests, paraproteins Nerve conduction studies to distinguish between axonal and demyelinating conditions Full history including social and family history

MRCP PACES Neurology (32 decks)

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