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Neurology Flashcards

1
Q

What are risk factors for IHH?

A

obesity
female sex
pregnancy
drugs
combined oral contraceptive pill
steroids
tetracyclines
retinoids (isotretinoin, tretinoin) / vitamin A
lithium

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2
Q

What are the treatments for IHH?

A

Weight loss and carbonic anhydrase

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3
Q

What is syringomyelia?

A

Syringomyelia classically presents with cape-like loss of pain and temperature sensation due to compression of the spinothalamic tract fibres decussating in the anterior white commissure of the spine

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4
Q

What are two causes of pinpoint pupils?

A

Pontine haemorrhage
Opioid overdose

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5
Q

How is a stroke managed?

A

ROSIER (recognition of stroke in the emergency room)
FAST survey
Blood glucose check
CT head non contrast
If ischaemic offer thrombolysis within 4.5 hours or thrombectomy 4-6 h
Admit to stroke ward for rehabilitation

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6
Q

How is TIA managed?

A
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7
Q

When is thrombectomy considered?

A

Thrombectomy is considered in patients with a confirmed blockage of the proximal anterior circulation or proximal posterior circulation. It may be considered within 24 hours of the symptom onset and alongside IV thrombolysis.

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8
Q

What is given for secondary prevention of stroke?

A

Clopidogrel 75mg once daily (alternatively aspirin plus dipyridamole)
Atorvastatin 20-80mg (not started immediately – usually delayed at least 48 hours)
Blood pressure and diabetes control
Addressing modifiable risk factors (e.g., smoking, obesity and exercise)

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9
Q

Who is involved in the MDT for stroke?

A

Stroke physicians
Nurses
Speech and language (SALT) to assess swallowing
Dieticians in those at risk of malnutrition
Physiotherapy
Occupational therapy
Social services
Optometry and ophthalmology
Psychology
Orthotics

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10
Q

What is the ROSIER score?

A
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11
Q

What is the Oxford Bamford classification?

A

Homonymous hemianopia
Unilateral
Higher symptoms

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12
Q

What is the features of epidural haematoma?

A

bi-convex shape and limited by the cranial sutures
Lucid period
Might seem to get better then worse

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13
Q

What are the features of subdural haematoma?

A

Crescent shape
Slow developing
Bridging veins
Seen in alcoholics and atrophy, older patients

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14
Q

What is the treatment for haemorrhagic stroke?

A

Immediate imaging (e.g., CT head) is required to establish the diagnosis.
Bloods should include a full blood count (for platelets) and a coagulation screen.

Admission to a specialist stroke centre
Discuss with a specialist neurosurgical centre to consider surgical treatment
Consider intubation, ventilation and intensive care if they have reduced consciousness
Correct any clotting abnormality (e.g., platelet transfusions or vitamin K for warfarin)
Correct severe hypertension but avoid hypotension

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15
Q

What is the guideline for warfarin?

A

Major bleeding - stop warfarin, vitamin K and PCC
>8 (mild bleeding) IV vitamin K
>8 (no bleeding) oral vitamin k
<5-8 (some bleeding) IV vitamin K
<5-8 (no bleeding) - withhold 1-2 doses and recheck

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16
Q

What are the symptoms of SAH?

A

Sudden thunderclap occipital headache
Neck stiffness
Photophobia
Vomiting
Neurological symptoms (e.g., visual changes, dysphasia, focal weakness, seizures and reduced consciousness)

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17
Q

What are some associated for SAH?

A

Family history
Cocaine use
Sickle cell anaemia
Connective tissue disorders (e.g., Marfan syndrome or Ehlers-Danlos syndrome)
Neurofibromatosis
Autosomal dominant polycystic kidney disease

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18
Q

What investigations are done for SAH?

A

CT

Lumbar puncture

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19
Q

When is a CT less reliable for SAH?

A

6 hours after symptoms for SAH

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20
Q

When should a lumbar puncture be done for SAH?

A

12 hours after onset of symptoms to check for xanthochromia

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21
Q

How is SAH managed?

A

Nimodipine
NORSE
Neurosurgery = coiling

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22
Q

What is key for MS?

A

A characteristic feature of MS is that lesions vary in location and are “disseminated in time and space”.

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23
Q

How is MS managed?

A

MDT support
DMT
Steroids for relapses

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24
Q

How is MS investigated?

A

MRI
Evoked potentials
Lumbar punctures - oligoclonal bands

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25
Q

What are some of the symptoms of MS?

A

Intranuclear ophthalmoplegia
Marcus Gunn

Lhermitte’s sign
Uthoff sign
Diplopia
Oscillopsia
Nystagmus

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26
Q

What is intranuclear opthalmoplegia?

A

Internuclear ophthalmoplegia is caused by a lesion in the medial longitudinal fasciculus. The nerve fibres of the medial longitudinal fasciculus connect the cranial nerve nuclei (“internuclear”) that control eye movements (the 3rd, 4th and 6th cranial nerve nuclei). These fibres are responsible for coordinating the eye movements to ensure the eyes move together.

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27
Q

What is the triad of symptoms in Parkinson’s?

A

Pill rolling tremor
Bradykinesia
Cogwheel rigidity

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28
Q

What is the frequency of tremor in Parkinson’s?

A

4-6 Hz

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29
Q

What is the frequency of tremor in Essential tremor?

A

6-12Hz

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30
Q

What are the features of Essential tremor?

A

Fine tremor (6-12 Hz)
Symmetrical
More prominent with voluntary movement
Worse when tired, stressed or after caffeine
Improved by alcohol
Absent during sleep

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31
Q

How is Essential tremor managed?

A

Propranolol (a non-selective beta blocker)
Primidone (a barbiturate anti-epileptic medication)

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32
Q

What is complex regional pain?

A
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33
Q

What is LEMS and how is it normally managed?

A

Excluding underlying malignancy (e.g., small-cell lung cancer) is essential.

Amifampridine works by blocking voltage-gated potassium channels in the presynaptic membrane, which in turn prolongs the depolarisation of the cell membrane and assists calcium channels in carrying out their action.

Other options include:

Pyridostigmine (cholinesterase inhibitor)
Immunosuppressants (e.g., prednisolone or azathioprine)
IV immunoglobulins
Plasmapheresis

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34
Q

What are the causes of myasthenia gravis?

A

Anti AchR antibodies
Anti - Muscle-specific kinase (MuSK) antibodies
Anti- Low-density lipoprotein receptor-related protein 4 (LRP4) antibodies

MuSK and LRP4 are important proteins for the creation and organisation of the acetylcholine receptor. Destruction of these proteins leads to inadequate acetylcholine receptors.

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35
Q

What are the features of myasthenia gravis?

A

The symptoms most affect the proximal muscles of the limbs and small muscles of the head and neck, with:

Difficulty climbing stairs, standing from a seat or raising their hands above their head
Extraocular muscle weakness, causing double vision (diplopia)
Eyelid weakness, causing drooping of the eyelids (ptosis)
Weakness in facial movements
Difficulty with swallowing
Fatigue in the jaw when chewing
Slurred speech

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36
Q

What tests are done for myaesthenia gravis?

A

Antibody tests look for:

AChR antibodies (around 85%)
MuSK antibodies (less than 10%)
LRP4 antibodies (less than 5%)

A CT or MRI of the thymus gland is used to look for a thymoma.

The edrophonium test can be helpful where there is doubt about the diagnosis.

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37
Q

What would be expected in the endrophonium test?

A

Relieving the problem temporarily

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38
Q

What does the ice test show for myasthenia gravis?

A
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39
Q

How is myastenia gravis treated + myasthenic crisis?

A

ment options include:

Pyridostigmine is a cholinesterase inhibitor that prolongs the action of acetylcholine and improves symptoms
Immunosuppression (e.g., prednisolone or azathioprine) suppresses the production of antibodies
Thymectomy can improve symptoms, even in patients without a thymoma
Rituximab (a monoclonal antibody against B cells) is considered where other treatments fail

Myasthenic Crisis
Myasthenic crisis is a potentially life-threatening complication of myasthenia gravis. It causes an acute worsening of symptoms, often triggered by another illness, such as a respiratory tract infection. Respiratory muscle weakness can lead to respiratory failure. Patients may require non-invasive ventilation or mechanical ventilation.

Treatment is with IV immunoglobulins and plasmapheresis.

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40
Q

What are some features of tuberous sclerosus?

A
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41
Q

What is the pathophysiology of tuberous sclerosus?

A
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42
Q

What are the characteristics of neurofibromatosis?

A

Cafe au lait
Relative affected
Axillary freckles
Bone dysplasia
Iris harmatomas (Lisch nodules)
Neurofibromas
Gliomas

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43
Q

How is neurofibromatosis inherited?

A

Autosomal dominant
Chromosome 17 Von Recklinhausen
Chromosome 22

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44
Q

How is neurofibromatomas managed?

A

Bevacizumab antiVEGF

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45
Q

How is MS investigated?

A

VEPs
MRI brain with diffusion-weighted imaging
Oligoclonal bands

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46
Q

What is a red flag for SAH?

A

A sudden-onset headache, reaching maximum intensity within 5 minutes, is a red flag requiring further evaluation to exclude a subarachnoid haemorrhage

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47
Q

What is Janz syndrome?

A

Juvenile myoclonic epilepsy (Janz syndrome)
typical onset is in the teenage years, more common in girls
features:
infrequent generalized seizures, often in morning//following sleep deprivation
daytime absences
sudden, shock-like myoclonic seizure (these may develop before seizures)
treatment: usually good response to sodium valproate

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48
Q

What is a benign rolandic seizure?

A

Benign rolandic epilepsy
most common in childhood, more common in males
features: paraesthesia (e.g. unilateral face), usually on waking up

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49
Q

What is West Syndrome?

A

Jack knife or Salaam seizure
Hyparrythmias
Steroids and vigabatrin

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50
Q

What are the features of Normal Pressure Hydrocephalus?

A

Dementia, incontinence, gait disturbance

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51
Q

What is Weber’s syndrome?

A

Weber’s syndrome is a form of midbrain stroke characterised by the an ipsilateral CN III palsy and contralateral hemiparesis

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52
Q

How is a TIA managed?

A

A patient who presents to their GP within 7 days of a clinically suspected TIA should have 300mg aspirin immediately (and be referred for specialist review within 24h)

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53
Q

What is a lacunar stroke?

A

involves perforating arteries around the internal capsule, thalamus and basal ganglia
pure motor or sensory loss

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54
Q

What is CVST?

A
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55
Q

What are the symptoms of CSVT?

A

Common features
headache (may be sudden onset)
nausea & vomiting
reduced consciousness

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56
Q

What investigations are done for CSVT?

A

Investigation
MRI venography is the gold standard
CT venography is an alternative
non-contrast CT head is normal in around 70% of patients
D-dimer levels may be elevated

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57
Q

What is the management for CVST?

A

anticoagulation
typically with low molecular weight heparin acutely
warfarin is still generally used for longer term anticoagulation

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58
Q

What are the types of sinus venous thrombosis?

A

Sagittal sinus thrombosis
may present with seizures and hemiplegia
parasagittal biparietal or bifrontal haemorrhagic infarctions are sometimes seen
‘empty delta sign’ seen on venography

Cavernous sinus thrombosis
other causes of cavernous sinus syndrome: local infection (e.g. sinusitis), neoplasia, trauma
periorbital oedema
ophthalmoplegia: 6th nerve damage typically occurs before 3rd & 4th
trigeminal nerve involvement may lead to hyperaesthesia of upper face and eye pain
central retinal vein thrombosis

Lateral sinus thrombosis
6th and 7th cranial nerve palsies

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59
Q

Why is cyclizine sometimes contraindicated in people with Parkinson’s?

A

dry mouth, blurred vision and urinary retention. Moreover, Cyclizine may potentially worsen cognitive function i

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60
Q

What are the features of Miller Fisher syndrome?

A

ophthalmoplegia, areflexia and ataxia.

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61
Q

What type of consciousness is associated with subdural haematoma?

A

Fluctuating consciousness = subdural haemorrhage

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62
Q

How should a TIA be managed in a patient on DOAC or warfarin?

A

Admission for a non-contrast CT head, only aspirin and 24 hours if not on medication

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63
Q

What is AICA?

A

Sudden onset vertigo and vomiting, ipsilateral facial paralysis and deafness - anterior inferior cerebellar artery

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64
Q

What are the complications of meningitis?

A

sensorineural hearing loss (most common)
seizures
focal neurological deficit
infective
sepsis
intracerebral abscess
pressure
brain herniation
hydrocephalus

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65
Q

How is paroxysmal hemicrania managed?

A

Paroxysmal hemicrania is completely responsive to treatment with indomethacin

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66
Q

What is paroxsymal hemicrania?

A

Paroxysmal hemicrania (PH) is defined by attacks of severe, unilateral headache, usually in the orbital, supraorbital or temporal region. These attacks are often associated with autonomic features, usually last less than 30 minutes and can occur multiple times a day.

PH sits within the group of disorders called trigeminal autonomic cephalgias which also contains cluster headache, a condition which shares many features with PH.

Importantly, PH is completely responsive to treatment with indomethacin.

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67
Q

What is given if a patient cannot tolerate clopidogrel as second line?

A

If clopidogrel is contraindicated or not tolerated, given aspirin and modified release dipyramidole for secondary prevention following stroke

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68
Q

What are the features of Shy Drager syndrome?

A

Shy-Drager syndrome is a type of multiple system atrophy.

Features
parkinsonism
autonomic disturbance
erectile dysfunction: often an early feature
postural hypotension
atonic bladder
cerebellar signs

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69
Q

What is foot drop associated with?

A

‘Foot drop’ - ?common peroneal nerve lesion

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70
Q

What is a surgical cranial nerve III palsy linked to?

A

Painful third nerve palsy = posterior communicating artery aneurysm

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71
Q

What are the features of CJD?

A

Creutzfeldt-Jakob disease is characterised by rapid onset dementia and myoclonus

72
Q

What is first like investigation for narcolepsy?

A

The investigation of choice for narcolepsy is multiple sleep latency EEG

73
Q

How long do cluster headaches last?

A

The correct answer is 15 minutes to 2 hours.

74
Q

What can be used to differentiate between seizures and pseudoseizures?

A

Prolactin can be used to differentiate between a true seizure and a pseudoseizure

75
Q

What is the main prophylaxis in migraine?

A

PTA - propanolol, topirimate and amytriptalline

76
Q

What is the driving restriction following TIA?

A

TIA = T1A = 1 MONTH

77
Q

How are AEDs reduced or stopped?

A

Seizure free for 2 years and reduce AEDs over 2-3 months

78
Q

What are the effects of valproate?

A

P450 inhibitor
gastrointestinal: nausea
increased appetite and weight gain
alopecia: regrowth may be curly
ataxia
tremor
hepatotoxicity
pancreatitis
thrombocytopaenia
hyponatraemia

79
Q

What is amaurosis fugax?

A

Amaurosis fugax is a form of stroke that affects the retinal/ophthalmic artery

80
Q

What sign might be seen in acute ischaemic stroke?

A

In acute ischaemic stroke, a ‘hyperdense artery’ sign may be seen on CT - this is usually visible immediately in contrast to changes in the parenchyma

81
Q

When is the empty delta sign seen?

A

Sagittal sinus thrombosis - ‘empty delta sign’ seen on venography

82
Q

How is Bell’s palsy managed?

A

All patients with a Bell’s palsy should be given oral prednisolone within 72 hours of onset

83
Q

What are causes of facial nerve palsy?

A

AIDS (A)
Lyme disease (LEXANDER graham)
Bell’s palsy (BELL)
Sarcoidosis (S)
Tumour (T)
Diabetes (D)
Surgery (s)

84
Q

What is used first line in MS for stiffness?

A

Baclofen and gabapentin are first-line for spasticity in multiple sclerosis

85
Q

Name the medications that exacerbate mysasthenia gravis

A

penicillamine
quinidine, procainamide
beta-blockers
lithium
phenytoin
antibiotics: gentamicin, macrolides, quinolones, tetracyclines

86
Q

What is the management of ischaemic stroke?

A

CT - dark and hypodense
Thrombolysis 4.5 hours
The standard target time for thrombectomy in acute ischaemic stroke is 6 hours

87
Q

What is Wallenburg syndrome?

A

Lateral medullary syndrome (posterior inferior cerebellar artery)
aka Wallenberg’s syndrome
ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
contralateral: limb sensory loss

88
Q

At what level and above does autonomic dysreflexia occur at?

A

Autonomic dysreflexia can only occur if the spinal cord injury occurs above the T6 level

89
Q

What nerves are found at the cerebellopontine angle?

A

Cranial nerves V, VII and VIII are affected in vestibular schwannomas

90
Q

What does a posterior circulation stroke cause?

A

Contralateral homonymous hemianopia with macular sparing and visual agnosia - posterior cerebral artery

91
Q

What is used in patients that cannot swallow levodopa with PD?

A

If a patient with Parkinson’s disease cannot take levodopa orally, they can be given a dopamine agonist patch as rescue medication to prevent acute dystonia

92
Q

How is NMS treated?

A

stop antipsychotic
patients should be transferred to a medical ward if they are on a psychiatric ward and often they are nursed in intensive care units
IV fluids to prevent renal failure
dantrolene may be useful in selected cases
thought to work by decreasing excitation-contraction coupling in skeletal muscle by binding to the ryanodine receptor, and decreasing the release of calcium from the sarcoplasmic reticulum
bromocriptine, dopamine agonist, may also be used

93
Q

What is a side effect of triptans?

A

Triptans may cause tightness of the throat and chest

94
Q

What are the side effects of phenytoin?

A

common: gingival hyperplasia (secondary to increased expression of platelet derived growth factor, PDGF), hirsutism, coarsening of facial features, drowsiness
megaloblastic anaemia (secondary to altered folate metabolism)
peripheral neuropathy
enhanced vitamin D metabolism causing osteomalacia
lymphadenopathy
dyskinesia

95
Q

What are some symptoms of IIH?

A

headache
blurred vision
papilloedema (usually present)
enlarged blind spot
sixth nerve palsy may be present

96
Q

Suggest how to assess what side has been affected in internuclear opthalmoplegia.

A

failure to adduct on the affected side and nystagmus on the contralateral side i.e. right sided opthalmoplegia = right sided inability to adduct eye and contralateral nystagmus

97
Q

What is Weber’s syndrome?

A

Ipsilateral cranial nerve three palsy along with contralateral weakness.

98
Q

What is the most common cause of a lower motor neurone lesion of the facial nerve?

A

ALexander Graham Bell has STDs. Remember
AIDS
Lyme disease
Bell’s palsy (most likely)
Sarcoidosis
Tumours
Diabetes

99
Q

What are the symptoms of facial nerve palsy?

A

Acute (but not sudden) onset of unilateral lower motor neuron facial weakness
Mild to moderate postauricular otalgia, which may precede the paralysis.
Hyperacusis
Nervus intermedius symptoms, such as altered taste and dry eyes/mouth.
Patients may subjectively describe “numbness” or “heaviness” without objective facial somatosensory disturbances.

100
Q

How does a C6 nerve palsy present?

A

Motor symptoms as most often reduced power with elbow flexion, wrist extension and forearm supination

101
Q

What needs to be monitored in GBS?

A

Forced vital capacity

102
Q

What are the symptoms of anterior spinal artery infarct?

A

Loss of pain sensation (analgesia)
Loss of temperature sensation (thermoanesthesia)
Motor function impairment
Loss of autonomic functions

103
Q

What does the management of ASAI involve?

A

Pain control
Physiotherapy for motor function improvement
Management of autonomic dysfunctions
Skin care for preventing pressure sores

104
Q

What are the causes of autonomic neuropathy?

A

Alcohol, amyloidosis, HIV
B12 deficiency
Chemotherapies
Diabetes (50%)
Everything else: lyme disease, sarcoidosis, amyloidosis

105
Q

How is autonomic neuropathy/ peripheral neuropathy treated and investigated?

A

Investigate and treat the cause
Supportive management such as better blood pressure control, pain relief

106
Q

Define Bell’s palsy

A

Bell’s palsy is an idiopathic syndrome characterized by unilateral, lower motor neuron facial weakness, without sparing the extraocular muscles and muscles of mastication. It presents with mild-moderate postauricular otalgia, hyperacusis (rare), and nervus intermedius symptoms such as altered taste and dry eyes/mouth.

107
Q

What is thought to be the cause of Bell’s palsy?

A

HSV, EBV and VZV re-activation

108
Q

How is Bell’s palsy investigated?

A

Full blood count (FBC)
Erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP)
Viral serology (e.g. HSV-1, EBV, VZV)
Lyme serology (if suggestive symptoms or exposure)
Otoscopy to see if any vesicular lesions in external auditory meatus
Electromyography (EMG)
Imaging studies (e.g., magnetic resonance imaging (MRI) or computed tomography (CT))

109
Q

What causes Erb’s palsy and Klumpke’s palsy?

A

Erb’s palsy: Involving damage to the C5-C6 nerve roots. Traumatic birth
Klumpke’s palsy: Involving damage to the C8-T1 nerve roots. Radiotherapy in axilla for breast cancer

110
Q

What are the features of Brown Seqard?

A

Ipsilateral hemiplegia
Ipsilateral loss of proprioception and vibration
Contralateral loss of pain and temperature sensation

111
Q

What are the features of pseudobulbar palsy?

A

Upper motor neurone disease
Brisk reflex, breathy speech
Emotional lability
No nasal speech (because weaker in LMN)
Spastic speech

112
Q

What is a bulbar palsy?

A

Concerned with CN IX, X, XI

113
Q

What are the causes of bulbar palsy?

A

Motor neurone disease: Notably, the progressive bulbar palsy variant.
Myasthenia gravis: An autoimmune neuromuscular disorder.
Guillain-Barré syndrome: An acute inflammatory demyelinating polyradiculoneuropathy.
Brainstem stroke: Particularly the lateral medullary syndrome or Wallenberg’s syndrome.
Syringobulbia: A rare neurologic condition characterized by a fluid-filled cavity (syrinx) within the spinal cord.

114
Q

What are the causes of cerebellar disease?

A

Inherited i.e. Fredrich’s ataxia, ataxia telangietasia and Joubert’s
MS
Alcohol
Vascular
Infection
Space occupying lesion

115
Q

What are the symptoms for cerebellar disease?

A

Dysdiadokinesia
Ataxia
Nystagmus
Intention tremor
Stocatto speech
Hypotonia

116
Q

What are the symptoms of cervical spondylosis?

A

Neck pain
Radiculopathy resulting from compression of nerve roots at the site of foraminal exit, leading to flaccid upper limb paresis
Myelopathy, thought to be due to the dynamic stretch of the spinal cord over impinging spinal osteophytes, manifesting as variable sensory changes (sometimes including the Lhermitte phenomenon) and spastic paraparesis
Bladder and bowel disturbance, though this is rare

117
Q

What is another name for Hereditary Motor and Sensory Neuropathy?

A

hereditary motor and sensory neuropathy (HMSN) is also known as Charcot Mary Tooth
PMP22
Longest nerves affected first - hence feet
AD
Champagne bottle leg, pes cavus and claw hand

118
Q

What are the features of CJD?

A

Dementia, psychiatric impairment and myoclonus
PRNP gene

119
Q

What are the 6 D’s of charcot’s arthropathy?

A

Destruction, Deformity, Degeneration, Dense bones, Debris, and Dislocation

120
Q

What are some causes of dystonias?

A

Rare genetic disease like Flatau Sterling
Cervical torticollis
Anti-dopaminergic medications

121
Q

What are the symptoms of encephalitis?

A

Fever
Flu-like prodromal illness
Seizures
Focal neurological deficits
Headaches
Behavioural changes

122
Q

What is the most common cause of encephalitis?

A

HSV-1

123
Q

What are the driving restriction/ DVLA guidelines for those with seizures or epilepsy?

A

6 months - 1 off seizure
12 months - epilepsy

5 years - 1 off seizure as a lorry driver
10 years - epilepsy

124
Q

What is associated with an extradural haematoma?

A

Lentiform
Lucid
Lemon shape

125
Q

What is L5 rAdIculopathy characterised by?

A

Loss of inversion of ankle inversion and hip abduction

126
Q

What is the ulnar paradox?

A
127
Q

What is Freidrich’s ataxia?

A
128
Q

Compare and contrast ataxia telangitasia and Freidrich’s ataxia

A
129
Q

What is Devic’s disease?

A

Neuromyelitis optica

130
Q

What are the variants of GBS?

A
131
Q

Describe the testing for GBS

A

Monitoring of forced vital capacity (FVC) for respiratory muscle involvement
Cardiac monitoring for autonomic instability
Blood tests, including arterial blood gas (ABG)
Serological tests: Anti-ganglioside antibodies
Lumbar puncture: may show albuminocytological dissociation
Nerve conduction studies: may show prolongation or loss of the F wave
Identification of the underlying cause: stool cultures, serology, CSF virology

132
Q

How is GBS managed?

A

Intravenous immunoglobulin (IVIG) over a 5-day course
Plasmapheresis, which has similar efficacy to IVIG but is associated with more side effects.

133
Q

What is the criteria for a CT head after 1 hour?

A

<13 GCS
<15 GCS after 2 hours
1 episode of vomiting
Open or depressed skull fracture
Focal neurology

134
Q

What is the criteria for a CT after 6 hours?

A

4A’s

age
anticoagulant
amnesia
a worrying mechanism of fall

135
Q

Outline the contraindications for LP

A

Focal neurology
Instability
Neoplasm
Coagulation disorder
ICP raised
Skin infection

136
Q

What is HSP?

A

Hereditary spastic paresis is a spectrum of conditions that cause UMN and LMN disease
The main clinical features involve progressive spasticity and weakness of the legs due to degeneration of the axonal tracts of the corticospinal pathway in the spinal cord.
Requires botulinum and baclofen for spasticity

137
Q

What is Horner’s syndrome?

A

Horner’s syndrome is a lesion that affects the sympathetic chain. It can either be central (first-order) like a CVA, (second-order) or third order. Pancoast for example, only cause unilateral Horner’s and do not affect the limbs or upper body.

138
Q

Which type of Horner’s syndrome does not involve anhidrosis?

A

Carotid dissection or third order neurones.

In third order neurone lesions, there is miosis and ptosis but no anhydrosis, as the nerves supplying the sweat glands in the face have exited before reaching the internal carotid plexus. Therefore lesions affecting the carotid plexus, as in this case with internal carotid artery dissection, will have the clinical presentation of a third order Horner’s lesion.

(Prince Andrew has pancoast, but not carotid dissection)

139
Q

How can localisation of the lesion be identified in Horner’s syndrome?

A

First order = upper limb, and unilateral PAM
Second order = unilateral PAM
Third order = ptosis and anhidrosis, but not anhidrosis

140
Q

Give examples of the pathologies involved in first order neurone Horner’s syndrome?

A

First order neurone -
stroke or tumour
Syringomyelia
Multiple sclerosis
Encephalitis
Brain tumors
Lateral medullary syndrome

141
Q

Give examples of the pathologies involved in second order neurone Horner’s syndrome?

A

Second order
Pancoast

Cervical rib traction on stellate ganglion
Thyroid carcinoma
Thyroidectomy
Goiter
Bronchogenic carcinoma of the superior fissure (Pancoast tumor) on apex of lung
Klumpke paralysis
Trauma - base of neck, usually blunt trauma, sometimes surgery.
As a complication of tube thoracostomy
Thoracic aortic aneurysm

142
Q

What causes third order Horner’s?

A

Carotid artery dissection, stenting
Cluster headache - combination termed Horton’s headache
An episode of Horner’s syndrome may occur during a migraine attack and be relieved afterwards[6]
Cavernous sinus thrombosis
Middle ear infection

143
Q

What is involved in the treatment of hydrocephalus?

A

This is called a ventriculoperitoneal or ventriculoatrial shunt.

144
Q

Discuss IIH

A

IIH is also known as pseudotumor cerebrii
Opening pressure >25
Lithium, OCP, steroids, tetracyclines, lymecycline, vitamin A are risk factors
Headaches are worse in the morning
Bilateral, non pulsatile headaches
Bending forward
False localising sign
Visual disturbances which can result in blindness
Treat with weight loss, azetolzolamide, topirimate, shunting

145
Q

What changes are seen in paplidema?

A

Affected eye cannot adduct
Other eye undergoes nystagmus

146
Q

What are some associations with migraine?

A

Unilateral throbbing headache, potentially preceded by an aura (visual or sensory)
Headache duration of 4-72 hours
Association with photophobia and phonophobia
Possible triggers such as oral contraceptives or specific foods (e.g., chocolate)

147
Q

What is the false localising sign?

A

Cranial nerve VI palsy due to its location

148
Q

What is IVT?

A

Intracerebral venous thrombosis
Hypercoagulable states like pregnancy, COCP, dehydration and smoking are risk factors.
Sagittal sinus thrombosis = empty delta sign
Cavernous sinus thrombosis = chemosis, exopthalmos

149
Q

When is thrombectomy indicated?

A

Certain posterior and anterior circulation strokes

150
Q

What is Vernet’s syndrome?

A
151
Q

What is thoracic outlet syndrome?

A
152
Q

How is LEMS managed?

A

Underlying cause management: Cancer treatment options (chemotherapy, radiation, surgery) are required if LEMS is associated with a malignancy.

Symptom management: Amifampridine can be used, which blocks pre-synaptic potassium channels in the nerve terminals, augmenting the release of acetylcholine.

Severe respiratory or bulbar weakness: Management includes intubation and ventilation, along with plasma exchange or intravenous immunoglobulin (IVIG).

153
Q

How is a head injury managed?

A
154
Q

What is the Munro Kellie doctrine?

A

Monro–Kellie doctrine when understanding raised intracranial pressure. It states that the sum of the volume of brain tissue, cerebrospinal fluid and intracranial blood is constant (due to the fixed volume of the skull)

155
Q

What is the Brudisnki and Kernig’s sign?

A
156
Q

What are the signs of meningitis?

A

Headache
Fever
Neck stiffness
Photophobia
Nausea and vomiting
Focal neurology
Seizures
Reduced conscious level
Features of overwhelming sepsis, such as non-blanching petechial rash indicative of impending Disseminated Intravascular Coagulation (DIC).

157
Q

What is meralgia parasthetica?

A

Compression or entrapment of the lateral femoral cutaneous nerve under the inguinal ligament.
Direct injury to the nerve.
Conditions or factors that increase pressure on the nerve such as obesity, tight clothing or belts, pregnancy, ascites, and surgical procedures or trauma involving the inguinal area.

158
Q

What is mononeuritis multiplex?

A

Mononeuritis multiplex, occasionally termed polyneuritis multiplex, is a type of peripheral neuropathy which is characterized by simultaneous or sequential involvement of individual non-contiguous nerve trunks

159
Q

What are the causes of mononeuritis multiplex?

A

Diabetes mellitus
Vasculitis: polyarteritis nodosa, granulomatosis with polyangitis, and eosinophilic granulomatosis with polyangitis
Immune-mediated diseases, such as rheumatoid arthritis and systemic lupus erythematosus
Infections: leprosy, Lyme disease, Parvovirus B19, HIV
Sarcoidosis
Cryoglobulinaemia
Reactions to exposure to chemical agents, including trichloroethylene and dapsone
Rarely, following the sting of certain jellyfish, such as the sea nettle

160
Q

What is the pathophysiology of MND?

A

MND is associated with misfolding of the TDP-43 protein in many cases.
It can be an inherited condition, with several associated genes yet to be identified.
About 2% of total cases are associated with a mutation in the SOD-1 gene.

161
Q

How is MND managed?

A

Riluzole
NIV
MDT.
Providing pain relief with simple analgesia and treating spasticity and contractures with baclofen and botox injections.
Using anticholinergics to manage drooling.
Supporting feeding via an NG or PEG tube as bulbar disease progresses.
Discussing advanced care planning early in disease progression to minimise distress and complications.

162
Q

What is myotonic dystrophy?

A
163
Q

What is the difference between jugular outlet and pseudobulbar palsy?

A

Jugular outlet affects 9, 10, 11
Pseudobular affects 9, 10 and 12

164
Q

What are the causes of sensory neuropathy?

A

Alcohol
B12/Folate
Chronic Renal Failure
Diabetes Mellitus
Everything Else (!) - encompassing Vasculitis and Paraneoplastic syndromes

165
Q

What is pyramidal weakness?

A
166
Q

What are the types of gait?

A
167
Q

What are some types of paresis?

A
168
Q

How is SCC managed?

A

Radiation therapy to reduce the tumour burden and alleviate pressure on the spinal cord.
Surgical decompression: This should be performed urgently, typically within 48 hours.
Administration of dexamethasone: Indicated in patients with demonstrated malignancy on MRI or those with high clinical suspicion, given at 16 mg daily in divided doses, along with proton pump inhibitors (PPI)

169
Q

Contraindications to thrombolysis

A
170
Q

What is the main area for thrombectomy to work?

A

Proximal middle cerebral artery

171
Q

T or F, in cerebellar disease, a Romberg’s test is negative?

A

T

172
Q

What is the treatment for CSVT/ IVT?

A

LMWH

173
Q

T or F, urinary copper is high in wilsons?

A

T

174
Q

What makes the three antibodies are often seen: anti-Yo, anti-Tr and mGluR1.

A

SCLC. These cause cerebellar degeneration

175
Q

How should triptans be taken in migraine?

A

Sumatriptan only once the headache starts and not during the aura phase
Avoid in heart disease

176
Q

What should be used if a patient cannot have IV ceftriaxone?

A

Give IV chloramphenicol

Finals (24 decks)

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