Neurology Flashcards

1
Q

What are the types of strokes ?

A

Ischaemia or infarction
Intracranial haemorrhage - haemorrhagic

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2
Q

How can blood supply to the brain be disrupted ?

A

A thrombus
Atherosclerosis
Shock
Vasculitis

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3
Q

What is a TIA ?

A

Temporary neurological dysfunction caused by ischaemia but without infarction.
Symptoms have a rapid onset and often resolve before the patient is seen.

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4
Q

What are some symptoms of strokes ?

A

Asymmetrical
Limb weakness
Facial weakness
Dysphasia
Visual field defects
Sensory loss
Ataxia and vertigo ( PCA infarction )

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5
Q

What are some risk factors for a stroke ?

A

Previous TIA or stroke
AF
Carotid artery stenosis
HTN
DM
Raised cholesterol
FH
Smoking
Obesity
Vasculitis
COCP

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6
Q

What are some examples of 5-HT3 antagonists ?

A

Ondansetron

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7
Q

When are 5-HT3 antagonists used ?

A

Chemotherapy - related nausea

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8
Q

Where do 5-HT3 antagonists act ?

A

They mainly act in the chemoreceptor trigger zone area of the medulla oblongata.

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9
Q

What are some adverse effects of 5-HT3 antagonists ?

A

Prolonged QT interval
Constipation

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10
Q

What are some features of Wernicke’s aphasia ?

A

A lesion of the superior temporal gyrus
The lesion results in sentences that make no sense, word substitution and neologisms but speech remains fluent.
Comprehension is impaired

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11
Q

What are some features of broca’s aphasia ?

A

A lesion of inferior frontal gyrus
Speech is non-fluent, laboured and halting
Repetition is impaired
Comprehension is normal

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12
Q

What is a conduction aphasia ?

A

Classically due to a stroke affecting the arcuate fasiculus - the connection between wernicke’s and Broca’s area
Speech is fluent but repetition is poor
Comprehension is normal

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13
Q

What is Arnold-chiari malformation ?

A

Describes the downward displacement or herniation of the cerebellar tonsils through the foramen magnum.

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14
Q

What are some features of Arnold-chiari malformation ?

A

Non-communicating hydrocephalus
Headache
Syringomyelia

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15
Q

Where would a lesion that causes peripheral ataxia be ?

A

Cerebellar hemisphere lesions

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16
Q

Where would the lesion be to cause gait ataxia ?

A

Cerebellar vermis lesion

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17
Q

What is ataxia telangiectasia ?

A

An autosomal recessive disorder caused by a defect in the ATM gene which encodes for DNA repair enzymes.
It typically presents in early childhood with abnormal movements.

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18
Q

What are some features of ataxia telangiectasia ?

A

Cerebellar ataxia
Telangiectasia
Recurrent chest infections ( IgA deficiency )

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19
Q

What is Bell’s palsy ?

A

May be defined as an acute, unilateral, idiopathic facial nerve paralysis.

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20
Q

What are some features of Bell’s palsy ?

A

Lower motor neuron facial nerve palsy - forehead affected
Post-auricular pain
Altered taste
Dry eyes
Hyperacusis

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21
Q

What is the management of Bell’s palsy ?

A

No treatment
Prednisolone only
Combination of antivirals and prednisolone

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22
Q

Where is the origin of the brachial plexus ?

A

Anterior rami of C5 to T1

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23
Q

What are the sections of the brachial plexus ?

A

Roots
Trunks
Divisions
Cords
Branches

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24
Q

What is Erb-Duchenne paralysis ?

A

Damage to the C5-C6 roots caused by a breech presentation.

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25
Q

What is Klumpke’s paralysis ?

A

Caused by damage to T1 due to traction causing loss of intrinsic hand muscles.

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26
Q

What can cause a brain abscess ?

A

Extension of sepsis from middle ear or sinuses
Trauma or surgery to the scalp
Penetrating head injuries
Embolic events from endocarditis

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27
Q

What are some features of brain abscesses ?

A

Headache - dull, persistent
Fever
Focal neurology - oculomotor or abducens nerve palsy
Nausea
Papilloedema
Seizures

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28
Q

What are the investigations for brain abscesses ?

A

CT scans

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29
Q

What is the management of brain abscesses ?

A

Surgery - craniotomy
IV abx - cephalosporin + metronidazole
Dexamethasone for intracranial pressure management

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30
Q

If a lesion is present in the parietal lobe what features are present ?

A

Sensory inattention
Apraxia
Tactile agnostic
Inferior homonymous quadrantanopia

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31
Q

If a lesion is present in the occipital lobe what features are present ?

A

Homonymous hemianopia
Cortical blindness
Visual agnosia

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32
Q

If a lesion is present in the temporal lobe what features are present ?

A

Wernicke’s aphasia
Superior homonymous quadrantanopia
Auditory agnosia
Difficulty recognising faces

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33
Q

If a lesion is present in the frontal lobe what features are present ?

A

Broca’s aphasia
Disinhibition
Perseveration
Anosmia

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34
Q

If a lesion is present in the cerebellum what features are present ?

A

Gait
Truncal ataxia
Intention tremor
Past pointing
Dysdiadokinesis
Nystagmus

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35
Q

What area is affected in Parkinson’s disease ?

A

Substantia nigra of the basal ganglia

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36
Q

What area is affected in Huntington’s disease ?

A

Striatum ( caudate nucleus ) of the basal ganglia

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37
Q

What tumours commonly spread to the brain ?

A

Lung
Breast
Bowel
Skin
Kidney

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38
Q

What is the management of glioblastoma ?

A

Surgical with postoperative chemotherapy and/or radiotherapy.

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39
Q

What is the most common primary brain tumour ?

A

Glioblastoma

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40
Q

What is a meningioma ?

A

Typically benign, extrinsic tumours of the CNS.
Arising from the arachnoid cap cells of the meninges

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41
Q

What is the management of meningiomas ?

A

Observation
Radiotherapy
Surgical resection

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42
Q

What is a vestibular schwannoma ?

A

A benign tumour arising from the 8th cranial nerve

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43
Q

What are some features of vestibular schwannomas ?

A

Hearing loss
Facial nerve palsy
Tinnitus

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44
Q

What is the management of a vestibular schwannoma ?

A

Observation
Radiotherapy
Surgery

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45
Q

What is a pituitary adenoma ?

A

Benign tumours of the pituitary gland which either secretory or non-secretory.

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46
Q

What is brown - sequard syndrome ?

A

Caused by lateral hemisection of the spinal cord

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47
Q

What are some features of brown - sequard syndrome ?

A

Ipsilateral weakness below lesion
Ipsilateral loss of proprioception and vibration sensation
Contralateral loss of pain and temperature sensation

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48
Q

What is carbamazepine the first line treatment for ?

A

Partial seizures - epilepsy

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49
Q

What is the mechanism of action of carbamazepine ?

A

It binds to sodium channels increases their refractory period.

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50
Q

What are the adverse effects of carbamazepine ?

A

P450 enzyme inducer
Dizziness and ataxia
Drowsiness
Headache
Visual disturbance
Steven-Johnson syndrome

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51
Q

What is cataplexy ?

A

The sudden and transient loss of muscular tone caused by strong emotion ( laughter and being frightened ).

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52
Q

What conditions are associated with cataplexy ?

A

Narcoplexy

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53
Q

What are the features of cataplexy ?

A

Buckling knees to collapse

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54
Q

Where are the cavernous sinuses located ?

A

On the body of the sphenoid bone
It runs from the superior orbital fissure to the petrous temporal bone.

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55
Q

Are unilateral cerebellar lesions contra or ipsilateral ?

A

Ipsilateral

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56
Q

What are the symptoms for cerebellar lesions ?

A

Dysdiadochokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia

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57
Q

What are some causes of cerebellar lesions ?

A

Friedreich’s ataxia
Stroke
Alcohol
MS
Hypothyroidism
Phenytoin, lead poisoning

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58
Q

Where is the CSF located ?

A

Arachnoid mater and pia mater

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59
Q

How is the CSF reabsorbed back into the circulation ?

A

3rd ventricle
-
Cerebral aqueduct
-
4th ventricle
-
Subarachnoid space
-
Into venous system via arachnoid granulations

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60
Q

What are some risk factors for cluster headaches ?

A

Men
Smokers
Alcohol

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61
Q

What are some features of cluster headaches ?

A

Intense sharp, stabbing pain around one eye
- pain once or twice a day
- redness, lacrimation, lid swelling
- nasal stuffiness

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62
Q

What are the investigations for cluster headaches ?

A

Neuroimaging - to see if there are underlying brain lesions
MRI with gadolinium

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63
Q

What is the management of cluster headaches ?

A

Acute - 100% oxygen, subcut triptan
Prophylaxis - verapamil

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64
Q

In paediatric practice what are the most common CNS tumours ?

A

Astrocytomas

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65
Q

What is the most characteristic feature of a common peroneal nerve lesion ?

A

Foot drop

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66
Q

What are some other features of common peroneal nerve lesion ?

A

-Weakness of foot dorsiflexion
-Weakness of foot eversion
-Weakness of the extensor hallucis longus
-Sensory loss over the dorsum of the foot and lower lateral part of the leg

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67
Q

What is the function of cranial nerve 1 ( Olfactory nerve ) ?

A

Smelling

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68
Q

What is the function of cranial nerve 2 ( optic nerve ) ?

A

Sight

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69
Q

Which muscles are innervated by the 3rd cranial nerve ( oculomotor nerve ) ?

A

Medial rectus
Inferior oblique
Superior rectus
Inferior rectus

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70
Q

What is the function of cranial nerve 3 ( Oculomotor nerve ) ?

A

Eye movement
Pupil constriction
Accommodation
Eyelid opening

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71
Q

How does a 3rd cranial nerve lesion present ?

A

Ptosis
‘Down and out’ eye
Dilated fixed pupil

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72
Q

What is the function of cranial nerve 4 ( trochlear nerve ) ?

A

Eye movement

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73
Q

What muscle is innervated by the trochlear nerve ?

A

Superior oblique

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74
Q

How does an injury to the trochlear nerve present ?

A

Defective downward gaze
Vertical diplopia

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75
Q

What is the function of cranial nerve 5 ( trigeminal nerve ) ?

A

Facial sensation
Mastication

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76
Q

How does an injury to the 5th cranial nerve present ?

A

Trigeminal neuralgia
Loss of corneal reflex
Loss of facial sensation
Paralysis of mastication muscles

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77
Q

What is the function of cranial nerve 6 ( abducens nerve ) ?

A

Eye movement

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78
Q

What muscle is innervated by the abducens nerve ?

A

Lateral rectus

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79
Q

How does a abducens nerve palsy present ?

A

Palsy results in defective abduction
Horizontal diplopia

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80
Q

What is the function of cranial nerve 7 ( facial nerve ) ?

A

Facial movement
Taste ( anterior 2/3rds of tongue )
Lacrimation
Salivation

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81
Q

How can a facial nerve palsy present ?

A

Flaccid paralysis of upper + lower face
Loss of corneal reflex
Loss of taste
Hyperacusis

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82
Q

What is the function of cranial nerve 8 ( vestibulocochlear nerve ) ?

A

Hearing
Balance

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83
Q

How does an 8th nerve palsy present ?

A

Hearing loss
Vertigo
Nystagmus

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84
Q

What is the function of cranial nerve 9 ( glossopharyngeal nerve ) ?

A

Taste ( posterior 1/3 of tongue )
Salivation
Swallowing

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85
Q

How can lesions of the glossopharyngeal nerve present ?

A

Hypersensitive carotid sinus reflex
Loss of gag reflex

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86
Q

What is the function of cranial nerve 10 ( vagus nerve ) ?

A

Phonation
Swallowing

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87
Q

How can a vagus nerve palsy present ?

A

Uvula deviates away from site of lesion
Loss of gag reflex

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88
Q

What is the function of cranial nerve 11 ( accessory nerve ) ?

A

Head and shoulder movement

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89
Q

how does a lesion of the accessory nerve present ?

A

Weakness turning head to contralateral side

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90
Q

What is the function of cranial nerve 12 ( hypoglossal nerve ) ?

A

Tongue movement

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91
Q

How does a hypoglossal nerve palsy present ?

A

Tongue deviates towards the side of lesion

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92
Q

How does the 1st cranial nerve exit the skull ?

A

Cribriform plate

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93
Q

How does the 2nd cranial nerve exit the skull ?

A

Optic canal

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94
Q

How does the 3rd cranial nerve exit the skull ?

A

Superior orbital fissure

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95
Q

How does the 4th cranial nerve exit the skull ?

A

Superior orbital fissure

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96
Q

How does the 5th cranial nerve ( V1, V2 & V3 ) exit the skull ?

A

V1 - superior orbital fissure
V2 - foramen rotundum
V3 - foramen ovale

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97
Q

How does the 6th cranial nerve exit the skull ?

A

Superior orbital fissure

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98
Q

How does the 7th cranial nerve exit the skull ?

A

Internal auditory meatus

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99
Q

How does the 8th cranial nerve exit the skull ?

A

Internal auditory meatus

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100
Q

How does the 9th cranial nerve exit the skull ?

A

Jugular foramen

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101
Q

How does the 10th cranial nerve exit the skull ?

A

Jugular foramen

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102
Q

How does the 11th cranial nerve exit the skull ?

A

Jugular foramen

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103
Q

How does the 12th cranial nerve exit the skull ?

A

Hypoglossal canal

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104
Q

Which nerves are involved in the corneal reflex ( afferent and efferent limbs ) ?

A

Afferent - ophthalmic nerve ( V1 )
Efferent - facial nerve

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105
Q

Which nerves are involved in the gag reflex ( afferent and efferent limbs ) ?

A

Afferent limb - glossopharyngeal nerve
Efferent limb - vagus

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106
Q

Which nerves are involved in the pupillary light reflex ( afferent and efferent limbs ) ?

A

Afferent limb - optic nerve
Efferent limb - oculomotor

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107
Q

What is Creutzfeldt-Jakob disease ?

A

A rapidly progressive neurological condition caused by prion proteins. These proteins induce the formation of amyloid folds resulting in tightly packed beta-pleated sheets resistant to proteases.

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108
Q

How does Creutzfeldt-Jakob disease present ?

A

Dementia
Myoclonus

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109
Q

What investigations are there for diagnosing Creutzfeldt-Jakob disease ?

A

CSF is usually normal
EEG - biphasic high amplitude sharp waves
MRI

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110
Q

What are some symptoms of degenerative myelopathy ?

A

pain
loss of motor function
loss of sensory function causing numbness
loss of autonomic function

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111
Q

what is the management of degenerative cervical myelopathy ?

A

decompressive surgery
close observation is an option for mild stable disease

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112
Q

what is the gold standard investigation for degenerative cervical myelopathy ?

A

MRI of the cervical spine

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113
Q

what drugs can cause peripheral neuropathy ?

A

amiodarone
isoniazid
vincristine
ntrofurantoin
metrondiazole

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114
Q

what are the features of encephalitis ?

A

fever
headache
psychiatric symptoms
seziures
vomiting
focal features - aphasia
peripheral lesions

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115
Q

what are some investigations for encephalitis ?

A

CSF - LP
neuroimaging
EEG

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116
Q

what is the management of encephalitis ?

A

IV aciclovir if suspected encephalitis

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117
Q

what are infantile spasms ?

A

brief spasms beginning in the first few months of life

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118
Q

what are the possible treatments of infantile spasms ?

A

vigabatrin and steroids

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119
Q

what are some features of juvenile myoclonic epilepsy ?

A

infrequent generalised seizures
daytime absences
usdden, shock like myoclonic seizure

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120
Q

what is the treatment of juvenile myoclonic epilepsy ?

A

good response to sodium valproate

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121
Q

what are some features of febrile convulsions ?

A

ages between 6 months - 5 years
occurs due to a viral infection
brief - tonic or tonic clonic

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122
Q

what are some features of alcohol withdrawal seizures ?

A

history of alcohol excess
benzos given to reduce the risk
occur in patients with excessive alcohol intake who suddenly stop

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123
Q

what is a focal seizure ?

A

( partial seizures )
start in a specific area - on one side of the brain

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124
Q

what is a generalised seizure ?

A

these engage or involve networks on both sides of the brain at the onset
consciousness is completely lost

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125
Q

what are some specific types of generalised seizures ?

A

tonic clonic
tonic
clonic
typical absence
myoclonic
atonic

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126
Q

what are some other features to ask about in patients who are having a seizure ?

A

biting their tongue
urinary incontinence
post-ictal period for around 15 minutes

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127
Q

what are some investigations for patients having seizures ?

A

EEG
MRI

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128
Q

what is the management of epilepsy ?

A

start anti-epileptics after the second seizure
driving advice - cant drive for 6 months following a seizure, for established epilepsy they must be seizure for 12 months
women should be placed on contraception

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129
Q

what is the mechanism of sodium valproate ?

A

increases GABA activity

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130
Q

what are the indications for sodium valproate ?

A

generalised seizures

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131
Q

what are some adverse side effects of sodium valproate ?

A

increased appetite and weight gain
P450 inhibitor
alopecia
ataxia
tremor
hepatitis
pancreatitis
teratogenic - neural tube defect

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132
Q

what is the mechanism of action for carbamazepine ?

A

binds to sodium channels increasing their refractory period

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133
Q

when is carbamazepine indicated ?

A

second line for focal seizures

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134
Q

what are some adverse effects for carbamazepine ?

A

P450 inducer
dizziness and ataxia
drowsiness
leucopenia
visual disurbance

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135
Q

what is the mechanism of action of lamotrigine ?

A

sodium channel blocker

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136
Q

what are the indications for lamotrigine ?

A

generalised seizures
focal seizures

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137
Q

what are mechanism of aciton of lamotrigine ?

A

binds to sodium channels increasing their refractory period

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138
Q

what are the adverse effects of phenytoin ?

A

p450 inducer
dizziness and ataxia
drowsiness
megaloblastic anaemia
peripheral neuropathy

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139
Q

what are some features of a focal seizure in the temporal lobe ?

A

with or without impairment of consciousness
aura - rising epigastric sensation
last around 1 minute
automatisms are common ( lip smacking )

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140
Q

what are some features of focal seizures in the frontal lobe ?

A

head/leg movements
posturing
post-ictal weakness

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141
Q

what are some features of focal seizures in the parietal lobe ?

A

paraesthesia

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142
Q

what are some features of focal seizures in the occipital lobe ?

A

floaters / flashes

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143
Q

what is the medication management for generalised tonic-clonic seizures ?

A

males = sodium valproate
females - lamotrigine / levetiracetam

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144
Q

what is the medication management for focal seizures ?

A

first line - lamotrigine or levetiracetam
second line - carbamazepine

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145
Q

what is the medication management for absence seizures ?

A

first line - ethosuximide
second line :
- males - sodium valproate
-females - lamotrigine or levetiracetam

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146
Q

what is the medication management for myoclonic seizures ?

A

males - sodium valproate
females - levetiracetam

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147
Q

what is the medication management for tonic or atonic seizures ?

A

males - sodium valproate
females - lamotrigine

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148
Q

what is an essential tremor ?

A

an autosomal dominant condition which usually affects both upper limbs

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149
Q

what are some features of essential tremor ?

A

postural tremor - worse if arms are outstretched
improved by alcohol and rest

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150
Q

what is the management of essential tremor ?

A

propanolol - first line
primidone is sometimes used

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151
Q

what is an extradural haematoma ?

A

a collection of blood that is between the skull and the dura

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152
Q

what is the main cause of an extradural haemotoma ?

A

trauma - low impact ( blow to the head or fall )

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153
Q

where is a extradural haematoma usually located ?

A

temporal region - at the pterion which overlies the middle meningeal artery

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154
Q

what is the classical presentation of an extradural haematoma ?

A

a patient who initially loses then briefly regain consciousness after a low impact head injury
as the haematoma expands the uncus of the temporal lobe herniates around the tentorium cerebello causing fixed dilated pupils

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155
Q

what is seen on imaging in an extradural haematoma ?

A

it appears as a biconvex hyperdense collection around the surface of the brain
they are limited by the suture lines of the skull

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156
Q

what is the management of an extradural haematoma ?

A

craniotomy and evacuation of the haematoma is defintive treatment

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157
Q

what does the facial nerve supply ?

A

muscles of facial expression
nerve to stapedius ( ear )
supplies anterior 2/3 of tongue
parasympathetic fibres to lacrimal glands and salivary glands

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158
Q

what can cause a bilateral facial nerve palsy ?

A

sarcoidosis
guillain-barre syndrome
lyme disease
bilateral acosutic neuromas

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159
Q

what can cause a unilateral facial nerve palsy ?

A

bell’s palsy
ramsey hunt syndrome
acoustic neuroma
parotid tumour
HIV
DM
MS
stroke

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160
Q

what is the difference between bell’s palsy and a stroke ?

A

LMN or a bell’s palsy isnt forehead sparing while a stroke is

161
Q

what are the 3 branches of the facial nerve ?

A

greater petrosal nerve
nerve to stapedius
chorda tympani

162
Q

what is foot drop ?

A

a result from weakness of the foot dorsiflexors

163
Q

what are some causes of foot drop ?

A

common peroneal nerve lesion
L5 radiculopathy
sciatic nerve lesion
superficial or deep peroneal nerve lesion

164
Q

what is suggestive of L5 radiculopathy on examination ?

A

weakness of hip abduction

165
Q

what is the management of foot drop if examination indicates a peroneal neuropathy ?

A

conservative management - avoid leg crossing, squatting and kneeling

166
Q

how long does foot drop usually take to resolve ?

A

2-3 months

167
Q

what are some features of a fourth nerve palsy ?

A

vertical diplopia
subjective tilting of objects
head tilt
eyes deviate upwards and routed outwards

168
Q

what is friedreich’s ataxia ?

A

an early onset hereditary ataxia
autosomal recessive, trinucleotide repeat disorder characterised by a GAA repeat on chromosome 9.

169
Q

what is the typical age of onset of friedreich’s ataxia ?

A

10-15 years old

170
Q

what are the most common presenting features of friedreich’s ataxia ?

A

gait ataxia
kyphoscoliosis

171
Q

what are some neurological features of friedreich’s ataxia ?

A

absent ankle jerk / extensor plantars
cerebellar ataxia
optic atrophy

172
Q

what are the modalities of the GCS ?

A

motor response
verbal response
eye opening

173
Q

what are the different options in the motor response of the GCS ?

A

6 - obeys command
5 - localised to pain
4 - withdraws from pain
3 - abnormal flexion to pain
2 - extending to pain
1 - none

174
Q

what are the different options in the verbal response of the GCS ?

A

5 - orientated
4 - confused
3 - words
2 - sounds
1 - none

175
Q

what are the different options in the eye opening of the GCS ?

A

4 - spontaneous
3 - to speech
2 - to pain
1 - none

176
Q

what is guillain barre syndrome ?

A

an immune mediated demyelination of the peripheral nervous system often triggered by an infection

177
Q

what is the pathogenesis of guillain barre syndrome ?

A

cross - reaction of antibodies in the peripheral nervous system

178
Q

what are the initial symptoms of guillain barre syndrome ?

A

back/leg pain

179
Q

what are the characteristic features of guillain barre syndrome ?

A

progressive symmetrical weakness of all limbs
usually ascending
reduced or absent reflexes

180
Q

what are some other features ( less common ) of guillain barre syndrome ?

A

history of gastroenteritis
resp muscle weakness
cranial nerve involvement
urinary retention

181
Q

what are some investigations of guillain barre syndrome ?

A

LP - rise in protein with a normal WBC count
nerve conduction studies

182
Q

what are some features of a migraine ?

A

recurrent severe headache - unilateral and throbbing
associated with aura, nausea and photosensitivity

183
Q

what are some features of a tension headache ?

A

recurrent non-disabling bilateral headache
tight band

184
Q

what is a cluster headache ?

A

pain occurs once or twice a day lasting 15 mins to 2 hours
intense pain behind the eye
restless during attack
accompanied by redness, lacrimation and lid swelling

185
Q

what are some features of temporal arteritis ?

A

typically affects the over 60s
rapid onset
unilateral
tender palpable temporal artery
raised ESR

186
Q

what are some causes of an acute single episode of headache ?

A

meningitis
encephalitis
subarachnoid haemorrhage
head injury
sinusitis
glaucoma

187
Q

what are some causes of a chronic headache ?

A

chronically raised ICP
Paget’s disease
psychological

188
Q

what are some features of a headache history that would prompt further investigations ?

A

immunocompromised
under 20 with history of malignancy
vomiting
worsening headache with fever
thunderclap headache
new onset neurological/cognitive deficit
recent head trauma

189
Q

what is herpes simplex encephalitis ?

A

virus characteristically affects the temporal lobes

190
Q

what are some features of herpes simplex encephalitis ?

A

fever, headache, seizures, vomiting
aphasia
cold sores

191
Q

what is seen on investigations in herpes simplex encephalitis ?

A

CSF - elevated proteins and lymphocytosis
CT - medial temporal and inferior frontal changes
MRI is better
EEG

192
Q

what is the management of herpes simplex encephalitis ?

A

IV aciclovir

193
Q

what is huntington’s disease ?

A

an autosomal dominant neurogenerative condition.
progressive and incurable
trinucelotide repeat disorder

194
Q

what are some features of huntington’s disease ?

A

develops after 35 years old
chorea
personality changes and intellectual impairment
dystonia
saccadic eye movements

195
Q

what is idiopathic intracranial hypertension ?

A

a condition classically seen in young overweight females

196
Q

what are some risk factors for idiopathic intracranial hypertension ?

A

obesity
female
pregnancy
drugs - COCP, steroids

197
Q

what are some features of idiopathic intracranial hypertension ?

A

headache
blurred vision
papilloedema
enlarged blind spot
6th nerve palsy may be present

198
Q

what is the management of idiopathic intracranial hypertension ?

A

weight loss
carbonic anhydrase inhibitor
topiramate

199
Q

what are some general features of intracranial venous thrombosis ?

A

headache
nausea and vomiting
reduced consciousness

200
Q

what investigations should be performed when suspecting intracranial venous thrombosis ?

A

MRI venography
non-contrast CT head
d-dimers elevated

201
Q

what is the management of intracranial venous thrombosis ?

A

anticoagulation - low molecualr weight heparin ( acutely ), warfarin ( longer use )

202
Q

what are some causes of cavernous sinus syndrome ?

A

cavernous sinus thrombosis
local infection
neoplasia
trauma

203
Q

what are some features of cavernous sinus thrombosis ?

A

peri-orbital oedema
ophthalmoplegia

204
Q

what is lambert-eaton syndrome ?

A

autoimmune disorder caused by an antibody directed against presynaptic voltage gated calcium channel in the PNS.

205
Q

what is lambert-eaton syndrome associated with ?

A

small cell lung cancer
lesser extent breast cancer

206
Q

what are the features of lambert-eaton syndrome ?

A

repeated muscle contractions
limb-girdle weakness
hyporeflexia
autonomic symptoms - dry mouth, impotence,

207
Q

what is the treatment of lambert-eaton syndrome ?

A

treatment of underlying cancer
immunosuppression
IV immunoglobulin

208
Q

what is the mechanism of action of levodopa ?

A

prevents peripheral metabolism of L-dopa to dopamine

209
Q

what are some adverse effects of levodopa ?

A

dyskinesia
on-off effect
postural hypotension
cardiac arrythmias
nausea and vomiting
psychosis

210
Q

what features are present if there is damage to the median nerve at the wrist ?

A

paralysis and wasting of thenar eminence muscles and opponens pollicis
sensory loss - palmar aspect of lateral 2.5 fingers

211
Q

what features are present if there is damage to the median nerve at the elbow ?

A

features of the damage of the wrist
+
unable to pronate forearm
weak wrist flexion
ulnar deviation of wrist

212
Q

what are the features of medication overuse headache ?

A

present for 15 days or more per month
worsened by symptomatic medication
patients using opioids or triptans most at risk

213
Q

what is the management of medication overuse headache ?

A

simple analgesics and triptans withdrawn abruptly
opioids withdrawn gradually

214
Q

what are the symptoms of meningitis ?

A

headache
fever
nausea / vomiting
photophobia
drowsiness
seizures

215
Q

in bacterial meningitis what is seen on LP ?

A

cloudy
low glucose
high protein
high neutrophils

215
Q

what are the signs of meningitis ?

A

neck stiffness
purpuric rash

215
Q

in viral meningitis what is seen on LP ?

A

clear
high glucose
normal / raised protein
high lymphocytes

216
Q

in TB meningitis what is seen on LP ?

A

slightly cloudy , fibrin web
low glucose
high protein

217
Q

what are some complications of meningitis ?

A

sensorineural hearing loss
seizures
focal neurological deficit
sepsis
intracerebral abscess
brain herniation
hydrocephalus

218
Q

what are some triggers of a migraine ?

A

tiredness
stress
alcohol
COCP
lack of food
dehydration
menstruation
bright lights

219
Q

what is the management of migraines ?

A

acute - oral triptans + NSAID or paracetamol

prophylaxis - propanolol, topiramate

220
Q

what is motor neuron disease ?

A

a neurological condition of unknown cause which can present with both UMN and LMN signs.

221
Q

what are some features that would suggest motor neuron disease ?

A

asymmetrical limb weakness
wasting of small hand muscles
fasciculations

222
Q

how is a diagnosis of motor neuron disease made ?

A

clinically
MRI to exclude cervical cord compression

223
Q

what are some management options for motor neuron disease ?

A

riluzole
respiratory care - BiPAP
nutrition - PEG tube

224
Q

what is the mechanism of action for riluzole ?

A

prevents stimulation of glutamate receptors

225
Q

what is multiple sclerosis ?

A

a chronic cell-mediated autoimmune disorder characterised by demyelination in the CNS.

226
Q

what is the most common sub-type of multiple sclerosis ?

A

relasping-remitting disease

227
Q

what are some features of multiple sclerosis ?

A

optic neuritis
optic atrophy
sensory changes - pins/needles, numbness
trigeminal neuralgia
spastic weakness
ataxia
tremor
urinary incontinence

228
Q

what is seen on investigation in multiple sclerosis ?

A

MRI - high signal T2 lesions, periventricular plaques
CSF - oligoclonal bands

229
Q

what is the management of multiple sclerosis ?

A

acute relapse - high dose steroids
DMARDs - reduce the risks

230
Q

what is myasthenia gravis ?

A

an autoimmune disorder resulting in insufficient functioning ach receptors.

231
Q

what are the features of myasthenia gravis ?

A

fatigability
extra-ocular weakness - diplopia
proximal muscle weakness
ptosis
dysphagia

232
Q

what conditions are associated with myasthenia gravis ?

A

thymomas
autoimmune disorders - pernicious anaemia, thyroid disorders, rheumatoid, SLE

233
Q

what are some investigations for myasthenia gravis ?

A

single fibre electromyography
CT thorax to exclude thymoma
antibodies to ach receptors

234
Q

what is the management of myasthenia gravis ?

A

long acting ach inhibitors - pyridostigmine
thymectomy

235
Q

what is the management of myasthenic crisis ?

A

plasmapheresis
IV immunoglobulins

236
Q

what drugs can exacerbate myasthenia gravis ?

A

penicillamine
quinidine
beta blockers
lithium
phenytoin
abx

237
Q

what is narcolepsy ?

A

a condition where there are low levels of orexin - a protein responsible for controlling appetite and sleep patterns

238
Q

what are some features of narcolepsy ?

A

typical onset in teenage years
hypersomnolence
cataplexy
sleep paralysis

239
Q

what is the investigation for narcolepsy ?

A

multiple sleep latency EEG

240
Q

what is the management for narcolepsy ?

A

daytime stimulants - modafinil

241
Q

what is neuroleptic malignant syndrome ?

A

a rare but dangerous condition seen in patients taking anti-psychotic medication. it may occur with dopaminergic drugs for Parkinsons usually when the drug is suddenly stopped or dose reduced.

242
Q

what are the typical features of neuroleptic malignant syndrome ?

A

pyrexia
muscle rigidity
autonomic lability - hypertension, tachycardia and tachypnoea
delirium

243
Q

what are some complications of neuroleptic malignant syndrome ?

A

AKI secondary to rhabdomyolysis
leucocytosis

244
Q

what is the management of neuroleptic malignant syndrome ?

A

stop antipsychotics
IV fluids to prevent renal failure
dantrolene may be useful

245
Q

what is neuropathic pain ?

A

defined as pain which arises following damage or disruption of the nervous system.

246
Q

what are some examples were neuropathic pain occurs ?

A

diabetic neuropathy
post-herpetic neuralgia
trigeminal neuralgia
prolapsed intervertebral disc

247
Q

what is the management of neuropathic pain ?

A

first line - amitriptyline, duloxetine, gabapentin or pregabalin

248
Q

what is normal pressure hydrocephalus ?

A

a reversible cause of dementia seen in elderly patients.

249
Q

what is the pathogenesis of normal pressure hydrocephalus ?

A

secondary to reduced CSF absorption at the arachnoid villi.
these changes may be secondary to ehad injury, subarachnoid haemorrhage or meningitis.

250
Q

what is the classical triad of features of normal pressure hydrocephalus ?

A

urinary incontinence
dementia and bradyphrenia
gait abnormality
( develop over a few months )

251
Q

what is seen on imaging in normal pressure hydrocephalus ?

A

hydrocephalus with ventriculomegaly in the absence of, or out of proportion to, sulcal enlargement

252
Q

what is the management of normal pressure hydrocephalus ?

A

ventriculoperitoneal shunting

253
Q

what is parkinsons disease ?

A

a progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra.

254
Q

what is the classical triad of parkinsons disease ?

A

bradykinesia
tremor
rigidity

255
Q

what is bradykinesia ?

A

poverty of movement
short shuffling steps with reduced arm swinging
difficulty in initiating movement

256
Q

what is the tremor like in parkinsons disease ?

A

worse when stressed or tired
improves with voluntary movement
typically pill rolling

257
Q

other than the classic triad of parkinson’s disease what are some other features are present ?

A

mask like facies
flexed posture
micrographia
drooling of saliva
depression
impaired olfaction
fatigue

258
Q

what are the features of drug induced parkinsonism ?

A

motor symptoms are generally rapid onset and bilateral
rigidity and rest tremor are uncommon

259
Q

how is a diagnosis of parkinson’s disease made ?

A

clinically

260
Q

what is the first line management of parkinson’s disease ?

A

levodopa

261
Q

why is levodopa usually prescribed with a decarboxylase inhibitor ?

A

it prevents the peripheral metabolism of levodopa to dopamine outside of the brain and hence can reduce the side effects

262
Q

what are some common adverse effects of levodopa ?

A

dry mouth
anorexia
palpitations
postural hypotension
psychosis

263
Q

what are some examples of dopamine receptor agonists ?

A

bromocriptine
cabergoline

264
Q

what are some adverse effects of dopamine receptor agonists ?

A

pulmonary fibrosis
cardiac fibrosis
hallucinations
postural hypotension

265
Q

what is an example of a MAOI ?

A

selegiline

266
Q

what is the management of drug induced parkinsonism ?

A

anti-muscarinics

267
Q

what are some causes of parkinsonism ?

A

parkinson’s disease
drug induced
wilson’s disease
post-encephalitis
toxins - CO

268
Q

what are some conditions that cause predominately motor loss peripheral neuropathy ?

A

guillain-barre syndrome
porphyria
lead poisoning

269
Q

what are some conditions that cause predominately sensory loss peripheral neuropathy ?

A

diabetes
uraemia
alcoholism
leprosy
vitamin b12 deficiency
amyloidosis

270
Q

how does alcohol cause neuropathy ?

A

secondary to both direct toxic effects and reduced absorption of B vitamins

271
Q

if phenytoin is taken during pregnancy what conditions can develop ?

A

cleft palate
congenital heart disease

272
Q

what is pituitary apoplexy ?

A

sudden enlargement of a pituitary tumour ( usually non-functioning macroadenoma ) secondary to haemorrhage or infarction.

273
Q

what are some precipitating factors for pituitary apoplexy ?

A

hypertension
pregnancy
trauma
anticoagulation

274
Q

what are the features of pituitary apoplexy ?

A

sudden onset headache
vomiting
neck stiffness
visual field defect
extraocular nerve palsy
features of pituitary insufficiency - hypotension

275
Q

what is the investigation for diagnosing pituitary apoplexy ?

A

MRI

276
Q

what is the management of pituitary apoplexy ?

A

urgent steroid replacement due to loss of ACTH
careful fluid balance
surgery

277
Q

what are some typical features of post-LP headache ?

A

develops within 24-48 hours
last several days
worse in upright position

278
Q

what is the normal ICP ?

A

7-15mmHg

279
Q

what are the causes of raised ICP ?

A

idiopathic intracranial hypertension
traumatic head injury
infection - meningitis
tumours
hydrocephalus

280
Q

what are the features of raised ICP ?

A

headache
vomiting
reduced levels of consciousness
papilloedema
cushing’s triad

281
Q

what is the cushing’s triad ?

A

widening pulse pressure
bradycardia
irregular breathing

282
Q

what investigations are needed for raised ICP ?

A

CT/MRI

283
Q

what is the management of raised ICP ?

A

investigate and treat the underlying cause
head elevation to 30 degrees
IV mannitol
controlled hyperventilation
shunts

284
Q

how does controlled hyperventilation lower ICP ?

A

reduce pCO2 causing vasoconstriction of the cerebral arteries reducing ICP

285
Q

what nerve roots are tested in the ankle reflex ?

A

S1-S2

286
Q

what nerve roots are tested in the knee reflex ?

A

L3-L4

287
Q

what nerve roots are tested in the biceps reflex ?

A

C5-C6

288
Q

what nerve roots are tested in the triceps reflex ?

A

C7-C8

289
Q

what is restless legs syndrome ?

A

a syndrome of spontaneous continuous lower limb movement that may be associated with paraesthesia.

290
Q

what are some clinical features of restless leg syndrome ?

A

uncontrollable urge to move legs
worse at rest
paraesthesia - crawling or throbbing sensation

291
Q

what are some causes and associations of restless legs syndrome ?

A

family history
iron deficiency anaemia
uraemia
DM
pregnancy

292
Q

what is the management of restless leg syndrome ?

A

simple measures - walking, stretching
treat any iron deficiency
dopamine agonist
benzodiazepines
gabapentin

293
Q

what is Reye’s syndrome ?

A

a severe, progressive encephalopathy affecting children that is accompanied by fatty infiltration of the liver, kidneys and pancreas.

294
Q

what is the aetiology of reye’s syndrome ?

A

association with aspirin use and viral cause

295
Q

what are some features of reye’s syndrome ?

A

preceding illness
encephalopathy - confusion, seizures
hypoglycaemia
fatty infiltration of the liver, kidneys and pancreas

296
Q

what is the management of reye’s syndrome ?

A

supportive

297
Q

what is the injury causing brown-sequard syndrome ?

A

spinal cord hemisection

298
Q

what tracts are affected in brown-sequard syndrome ?

A

lateral corticospinal tract
dorsal columns
lateral spinothalamic tract

299
Q

what are the features of brown-sequard syndrome ?

A

ipsilateral spastic paresis below lesion
ipsilateral loss of proproception and vibration sensation
contralateral loss of pain and temperature sensation

300
Q

what tracts are affected in an anterior spinal artery occlusion ?

A

lateral corticospinal tracts
lateral spinothalamic tract

301
Q

what are the features of anterior spinal artery occlusion ?

A

bilateral spastic paresis
bilateral loss of pain and temperature sensation

302
Q

what tracts are affected in syringomyelia ?

A

ventral horns
lateral spinothalamic tract

303
Q

what are the features of syringomyelia ?

A

flaccid paresis
loss of pain and temperature sensation

304
Q

what functions does the dorsal column medial lemniscus pathway carry ?

A

fine and discriminative touch
proprioception

305
Q

what functions does the spinothalamic tract carry ?

A

coarse touch
pressure sensation
temperature sensation

306
Q

which matter does the motor pathway travel through ?

A

white

307
Q
A
308
Q

what function does the corticospinal tract carry ?

A

speed and agility of voluntary movements

309
Q
A
310
Q

what is status epilepticus ?

A

a single seizure lasting longer than 5 minutes
or
2 seizures within 5 minute period without the person returning to normal between them

311
Q

what is the management of status epilepticus ?

A

ABC - airway adjunct, oxygen and check glucose

first line - benzodiazepines
second line - levetiracetam ( if non resolving )

312
Q

what are the features associated with a stroke of the anterior cerebral artery ?

A

contra-lateral hemiparesis and sensory loss

313
Q

what are the features associated with a stroke of the middle cerebral artery ?

A

contra-lateral hemiparesis and sensory loss
contra-lateral homonymous hemianopia
aphasia

314
Q

what are the features associated with a stroke of the posterior cerebral artery ?

A

contralateral homnoymous hemianopia with macular sparing
visual agnosia

315
Q

what are the features present in a retinal / ophthalmic artery lesion ?

A

amaurosis fugax

316
Q

what is the presentation of a basilar artery lesion ?

A

locked in syndrome

317
Q

how does a lacunar stroke present ?

A

either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia

318
Q

where are the common sites for lacunar strokes ?

A

basal ganglia
thalamus
internal capsule

319
Q

what is a stroke ?

A

( cerebrovascular accident )
represents a sudden interruption in the vascular supply of the brain.

320
Q

what are the 2 main types of a stroke ?

A

ischaemic
haemorrhagic

321
Q

what is the essential problem in ischaemic strokes ?

A

blockage in the blood vessel stops blood flow

322
Q

what is the essential problem in haemorrhagic strokes ?

A

blood vessel bursts leading to reduction in blood flow

323
Q

what are the 2 subtypes of ischaemic stroke ?

A

thrombotic stroke
embolic stroke

324
Q

what are the subtypes of haemorrhagic strokes ?

A

intracerebral haemorrhage
subarachnoid haemorrhage

325
Q

what are the risk factors for ischaemic strokes ?

A

age
hypertension
smoking
hyperlipidaemia
DM
AF

326
Q

what are some risk factors for haemorrhagic stroke ?

A

age
hypertension
arteriovenous malformation
anticoagulation therapy

327
Q

what are some features of a stroke ?

A

motor weakness
speech problems
swallowing problems
visual field defects - homonymous hemianopia
balance problems

328
Q

what are some symptoms of cerebral hemisphere infarcts ?

A

contra-lateral hemiplegia
contra-lateral sensory loss
homnoymous hemianopia
dysphagia

329
Q

what are some symptoms of a brainstem infarct ?

A

quadriplegia
locked in syndrome

330
Q

what is the criteria for the oxford stroke classification ?

A

unilateral hemiparesis and/or hemisensory loss of the face, arm and leg

homonymous hemianopia

higher cognitive dysfunction - dysphasia

331
Q

which arteries are involved in a TACs infarct ?

A

middle and anterior cerebral arteries

332
Q

how may of the oxford stroke classification is needed for a TACs stroke ?

A

all 3

333
Q

what arteries are affected in a PACs stroke ?

A

smaller arteries of the anterior circulation ( upper or lower division of the middle cerebral artery )

334
Q

how many of the oxford stroke is required for a PACs stroke ?

A

2

335
Q

according to the oxford stroke classification what criteria is needed for a diagnosis of a lacunar infarct ?

A

1 of the following :
- unilateral weakness ( and/or sensory deficit ) of face and arm, leg
- pure sensory troke
- ataxic hemiparesis

336
Q

what arteries are involved in a POC infarct ?

A

vertebrobasilar arteries

337
Q

according to the oxford stroke classification what features are required for a POCs stroke ?

A

cerebellar or brainstem syndromes
loss of consciousness
isolated homonymous hemianopia

338
Q

what does the FAST campaign stand for ?

A

Face - has their face fallen on one side ?
Arms - can they raise both arms and keep them there ?
Speech - slurred ?
Time - 999

339
Q

what investigations are required when suspecting a stroke ?

A

CT - non contrast head
MRI

340
Q

why is neuroimaging an urgency in strokes ?

A

to determine whether a patient is suitbale for thrombolytic therapy to treat early ischaemic strokes.

341
Q

what is the management of ischaemic strokes ?

A

once haemorrhagic strokes are excluded patients should be given aspirin 300 mg as soon as possible
thrombolysis with alteplase

342
Q

what is a TIA ?

A

stroke symptoms that resolve within 24 hours

343
Q

what is the immediate antithrombotic therapy for a TIA ?

A

give aspirin 300mg immediately

344
Q

what is the management of a haemorrhagic stroke ?

A

supportive
stop anticoagulants and anti-thrombotic
lower BP

345
Q

what are some contraindications for thrombolysis ?

A

previous intracranial haemorrhage
seizure at onset of stroke
intracranial neoplasm
suspected subarachnoid haemorrhage
LP in preceding 7 days
active bleeding
oesophageal varices
uncontrolled HTN

346
Q

what is the secondary prevention for a stroke ?

A

first line - clopidogrel
second line - aspirin plus modified release dipyridamole

347
Q

what is the time frame to offer someone thrombolysis after a stroke ?

A

4.5 hours

348
Q

what is a subdural haemorrhage ?

A

a collection of blood deep to the dural layer of the meninges.

349
Q

what are the neurological symptoms of a subdural haemorrhage ?

A

altered mental state
weakness on one side
aphasia
visual field defect
headache
seizures

350
Q

what are the physical examination findings for subdural haemorrhage ?

A

papilloedema
pupil changes
gait abnormalities
hemiparesis or hemiplegia

351
Q

what are the behavioural and cognitive changes in a subdural haemorrhage ?

A

memory loss
irritability
apathy
depression
cognitive impairment - difficulty focusing

352
Q

what is the investigation of choice for a subdural haemorrhage and what are the findings ?

A

CT imaging
crescentic collection not limited by suture lines

353
Q

what is the management of subdural haemorrhages ?

A

if small can be observed and managed conservatively
surgical - decompressive craniectomy

354
Q

what causes a chronic subdural haemorrhage ?

A

rupture of the small bridging veins within the subdural space and cause slow bleeding

355
Q

who are most at risk of developing a chronic subdural haemorrhage ?

A

elderly and alcoholic patients
due to brain atrophy and fragile taut veins

356
Q

how does a chronic subdural haematoma present ?

A

typically several week to month progressive history of either confusion, reduced consciousness or neurological deficit.

357
Q

what is the management chronic subdural haematoma ?

A

if no neurological deficit - conservatively
if there is a neurological deficit - decompression with burr holes

358
Q

what is syringomyelia ?

A

describes a collection of cerebrospinal fluid within the spinal cord.

359
Q

what are some causes of syringomyelia ?

A

chiari malformation
trauma
tumours
idiopathic

360
Q

what are some features of syringomyelia ?

A

loss of sensation to temperature but preservation of light touch, proprioception and vibration
spastic weakness
neuropathic pain
ungoing plantars

361
Q

what investigations should be performed when suspecting syringomyelia ?

A

full spine MRI with contrast - exclude a tumour
brain MRI - exclude chiari malformation

362
Q

what is the management of syringomyelia ?

A

treat the cause of the syrinx
a shunt into the syrinx can be placed if persistent

363
Q

what are the characteristic features of a tension headache ?

A

tight band around the head
bilateral
lower intensity than a migraine
may be related to stress

364
Q

what is chronic tension type headache defined as ?

A

15 or more days per month

365
Q

what is the management of a tension headache ?

A

acute - aspirin, NSAIDs, paracetamol
prophylaxis - amitriptylline

366
Q

what are some features of a third nerve palsy ?

A

eyes deviated down and out
ptosis
pupil may be dilated

367
Q

what are some causes of third nerve palsy ?

A

DM
vasculitis - temporal arteritis, SLE
PCA aneursym
cavernous sinus thrombosis

368
Q

what is a TIA ?

A

a brief period of neurological deficit due to a vascular cause typically lasting less than an hour.

369
Q

what are some features of TIA ?

A

sudden onset
unilateral weakness or sensory loss
aphasia or dysarthria
ataxia, vertigo or loss of balance
visual problems - amaurosis fugax, diplopia and homonymous hemianopia

370
Q

what is amaurosis fugax ?

A

sudden transient loss of vision in one eye

371
Q

what is the immediate management of TIA ?

A

give aspirin 300mg immediately

372
Q

what is the secondary prevention of a TIA ?

A

clopidogrel is first line
aspirin + dipyridamole - second line
high intensity statin - atorvastatin 20-80

373
Q

what investigations are performed for a TIA ?

A

MRI
carotid imaging - urgent carotid doppler

374
Q

what tremor is present in Parkinson’s disease ?

A

resting, pill rolling tremor

375
Q

how is the tremor described in essential tremor ?

A

postural tremor - worse if arms are outstretched
improved by rest and alcohol

376
Q

what is trigeminal neuralgia ?

A

a pain syndrome characterised by severe unilateral pain. usually idiopathic

377
Q

what is the management of trigeminal neuralgia ?

A

carbamazepine is first line
failure to respond to treatment should prompt referral to neurology

378
Q

what are some adverse effects of triptans ?

A

triptan sensation - tingling, heat, tightness, heaviness and pressure

379
Q

what is the classical history of vestibular schwannoma ?

A

a combination of vertigo, hearing loss, tinnitus and absent corneal reflex.
facial palsy

380
Q

what investigations should be performed for vestibular schwannoma ?

A

MRI of the cerebellopontine angle

381
Q

what is the management of vestibular schwannoma ?

A

surgery
radiotherapy
observation

382
Q

what is an incongruous defect + example?

A

incomplete or asymmetric visual field loss
optic tract lesion

383
Q

what is a congruous defect + example ?

A

complete or symmetrical visual field loss
optic lesion or occipital cortex lesion

384
Q

where is the lesion in a bitemporal hemianopia ?

A

lesion of the optic chiasm

385
Q

where is the lesion in a superior homonymous quadrantanopia ?

A

inferior optic radiation in the temporal lobe - Meyer’s loop

386
Q

where is the lesion in a inferior homonymous quadrantanopia ?

A

superior optic radiations in the parietal lobe

387
Q

if there is macular sparing in homonymous hemianopia where is the lesion ?

A

lesion of the occipital cortex

388
Q

what is von Hippel-Lindau syndrome ?

A

an autosomal dominant condition predisposing to neoplasia.
it is due to an abnormality in the VHL gene located on short arm of chromosome 3.

389
Q

what are some features of von Hippel-Lindau syndrome ?

A

cerebellar haemangioma
retinal cyst
phaechromocytoma
extra-renal cysts
endolymphatic sac tumours
clear cell renal cell carcinoma

390
Q

what is wernicke’s encephalopathy ?

A

a neuropsychiatric disorder caused by thiamine deficiency which is most commonly seen in alcoholics.

391
Q

what is the classic triad of wernicke’s encephalopathy ?

A

ophthalmoplegia/nystagmus
ataxia
encephalopathy

392
Q

what are some features of wernicke’s encephalopathy ?

A

oculomotor dysfunction - nystagmus
gait ataxia
encephalopathy - confusion, disorientation
peripheral neuropathy

393
Q

what investigations should be performed when suspecting wernicke’s encephalopathy ?

A

decreased red cell transketolase
MRI

394
Q

what is the management of wernicke’s encephalopathy ?

A

urgent replacement of thiamine

395
Q

if wernicke’s encephalopathy isn’t treated what can develop ?

A

korsakoff syndrome

396
Q

how does korsakoff syndrome present ?

A

antero and retrograde amnesia
confabulation

397
Q
A