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Year 3 > Neuro > Flashcards

Neuro Flashcards

1
Q

What are glaucomas

A

optic neuropathies associated with raised intraocular pressure
can be classified:
whether peripheral iris is coverin the trabecular meshwork

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2
Q

primary open-angle glaucoma

A

iris is clear of trabecular network

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3
Q

Risk factors for primary open-angle glaucoma

A

-increasing age
-genetics
-afro caribbean ethnicity
myopia
-HTN
-DM
-Corticosteroids

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4
Q

Presentation of primary open-angle glaucoma

A

peripheral visual field loss - nasal scotomas progressing to ‘tunnel vision’
decreased visual acuity
optic disc cupping

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5
Q

Fundoscopy signs of primary open angle glaucoma

A
  1. optic disc cupping (cup to disc ratio >0.7): occurs as loss of disc substance makes optic cup widen and deepen
  2. optic disc pallor - indicating optic atrophy
  3. Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
  4. Additional features - cup notching (usually inferior where vessels enter disc), disc haemorrhages
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6
Q

Cranial nerve I functions and pathway/foramen

A

olfactory
smell
cribiformplate

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7
Q

Cranial nerve II: name, functions, pathway/foramen

A

Optic
sight
optic canal

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8
Q

Cranial nerve III: name, functions, clinical sign, pathway/foramen

A

Oculomotor
Functions - eye movement (MR, IO, SR, IR), pupil constriction, accomodation, eyelid opening
Clinical - palsy results in ptosis, down and out eye, dilated fixed pupil
pathway - superior orbital fissure (SOF)

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9
Q

Cranial nerve IV: name, functions,, clinical sign, pathway

A

Trochlear
eye movement (SO)
clinical sign - palsy results in defective downward gaze (vertical diplopia)
Pathway - superior orbital fissure (SOF)

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10
Q

Cranial nerve V name, functions, clinical signs, pathway

A

Trigeminal
functions - facial sensation, mastication
Clinical sign - lesions may cause: trigeminal neuralgia, loss of corneal reflex (afferent), loss of facial sensation, paralysis of mastication muscles, deviation of jaw to weak side
pathway: V1; superior orbital fissure, V2: foramen rotundum, V3: foramen ovale

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11
Q

Cranial nerve VII: name, functions, clinical signs, pathway

A

facial
Functions - facial movements, taste (anterior 2/3rd tongue), lacrimation, salivation
Clinical signs: lesions may result in: flaccid paralysis of upper + lower face, loss of corneal reflex (efferent), loss of taste, hyperacusis
pathway - internal auditory meatus

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12
Q

Cranial nerve VI: name, functions, clinical signs, pathway

A

Abducens
functions: eye movements (LR)
Clinical signs: palsy results in defective abduction (horizontal diplopia)
pathway: Superior orbital fissure (SOF)

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13
Q

Cranial nerve VIII name functions, clinical signs, pathway

A

Vestibulocochlear
Functions - hearing, balance
clinical signs - hearing loss, vertigo, nystagmus, acoustic neuromas are schwann cell tumours of the cochlear nerve
pathway - internal auditory meatus

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14
Q

Cranial nerve IX name, function, clinical signs, pathways

A

glossopharyngeal
functions - taste (posterior 1/3 tongue), salivation, swallowing, mediates input from carotid body and sinus
clinical signs - lesions may result in: hypersensitivie carotid sinus reflex, loss of gag reflex (afferent)
pathway - jugular foramen

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15
Q

Cranial nerve X name, function, clinical signs, pathways

A

vagus
functions - phonation, swallowing and innervates viscera
clinical signs - lesions may result in uvula deviates away from site of lesion, loss of gag reflex (efferent)
Pathway - jugular foramen

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16
Q

Cranial nerve XI name, function, clinical signs, pathways

A

Accessory
functions - head and shoulder movement
clinical signs - lesions may result in weakness turning head to contralateral side
pathway - jugular foramen

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17
Q

Cranial nerve XII name, function, clinical signs, pathway

A

hypoglossal
functions - tongue movement
clinical signs - tongue deviated towards the side of the lesion
pathway - hypoglossal canal

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18
Q

corneal reflex afferent and efferent limbs

A

aff - opthalmic nerve (V1)
eff - facial nerve (VII)

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19
Q

Jaw jerk reflex afferent and efferent limbs

A

afferent - mandibular nerve (V3)
eff - mandibular nerve (V3)

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20
Q

Gag reflex afferent and efferent limb

A

afferent - glossopharyngeal (IX)
eff - Vagal nerve (X0

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21
Q

Carotid sinus reflex afferent and efferent limbs

A

Aff - glossopharyngeal (IX)
eff - vagal nerve (X)

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22
Q

Pupillary light reflex afferent and efferent limbs

A

aff - optic nerve (II)
eff - oculomotor nerve (III)

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23
Q

lacrimation reflex afferent and efferent limbs

A

aff - opthalmic nerve (v1)
eff - facial nerve (VII)

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24
Q

Typical presentation of epilepsy occuring in the temporal lobe

A

hallucinations (auditory/gustatory/olfactory), epigastric rising/emotional,
automatisms (lip smacking, grabbing, plucking), deja vu/dysphasia post ictal

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25
Q

typical presentation of epilepsy occuring in the frontal lobe

A

head/leg movements, posturing, poct-ictal weakness, jacksonian march

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26
Q

Typical presentation of epilepsy occuring in the parietal lobe

A

paraesthesia

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27
Q

typical presentation of epilepsy occuring in the occipital lobe

A

floaters/flashers

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28
Q

motor neuron disease

A

neurological condition of unknown cause which can present with upper and lower motor neuron signs
rarely present before 40 and various patterns of disease are recognised : amyotrophic lateral scleorsis, progressive muscular atrophy and bulbar palsy

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29
Q

clues which point towards diagnosis of motor neurone disease

A

fasciculations
absence of sensory signs/symptoms
mixture of lower motor neuron and upper motor neuron signs
wasting of the small hand muscles/tibilias anterior is common

other features:
Does not affect external ocular muscles
no cerebellar signs
abdominal reflexes are usually preserved and sphincter dysfunction if present is a late feature

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30
Q

What is Guillain barre syndrome

A

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

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31
Q

Pathogenesis of guillain barre syndrome

A

cross-reaction of antibodies with gangliosides in the peripheral nervous system
correlation between anti-ganglioside antibody and clinical features has been demonstrated
anti-GM1 antibodies in 25% patients

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32
Q

Miller Fisher syndrome

A

variant of Guillain Barre syndrome
associated with ophthalmoplegia, areflexia and ataxia
eye muscles are usually affected first
usually presents as a descending paralysis rather than ascending (guillain barre other variants)
anti-GQ1b antibodies are seen in 90% cases

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33
Q

What does a congruous defect mean

A

complete or symmetrical visual field loss

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34
Q

What does an incongrous defect mean

A

defect is incomplete or asymmetric

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35
Q

Homonymous hemianopia

A

incongruous defects : lesion of optic tract
congrous defects: lesion of optic radiation or occipital cortex
macula sparing: lesion of occipital cortex

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36
Q

Homonymous quadrantanopias

A

superior = lesion of inferior optic radiations in the temporal lobe (meyes loop)
inferior = lesion of superior optic radiations in the parietal lobe
nmemonic = PITS (parietal - inferior, temporal - superior)

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37
Q

Bitemporal hemianopia

A

lesion of optic chiasm
upper quadrant defect> lower quadrant defect = infeiror chiasmal compression, commonly a pituitary tumour
lower quadrant defect > upper quadrant defect = superior chiasma compression, commonly a craniophayrngioma

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38
Q

what is thoracic outlet syndrome

A

disorder involving compression of brachial plexus, subclavian artery or vein at the site of the thoracic outlet
can be neurogenic or vascular (more likely neurogenic)

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39
Q

Risk factors for alzheimers disease

A

increasing age
FH
5% cases inherited as autosomal dominant trait
Apoprotein E allele E4- encodes a cholesterol transport protein
caucasian ethnicity
Down’s syndrome

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40
Q

Pathological changes in alzhiemers disease

A

macroscopic: widespread cerebral atrophy, particularly involving the cortex and hippocampus
Microscopic: cortical plaques due to deposition of type A Beta amyloid protein and intraneuronal neruofibrillary tangles caused by abnormal aggregation of the tau protein ; hyperphosphylation of tau protein

biochemical: defeict of acetylcholine from damage to an ascending forebrain projection

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41
Q

Empty sella syndrome overview and features

A

overview - pituitary gland is flattened and on the posterior aspect of the sella tucica
cause unknown
more common in multiparous (having borne more than one child) obese women

Features - headaches, HTN, rhinorrhoea

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42
Q

Arnold chiari malformation

A

describes downward displacement or herniation of cerebellar tonsils through the formane magnum
malformations may be congenital or acquired through trauma

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43
Q

Features of arnold-chiari malformation

A

non-communicating hydrocephalus may develop as a result of obstruction of cerebrospinal fluid(CSF) outflow
headache
syringomyelia ( a disorder in which a fluid-filled cyst (called a syrinx) forms within the spinal cord)

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44
Q

Huntington’s disease

A

inherited neurodegenerative condition
progressive and incurable that typically results in death 20 years after initial symptoms develop

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45
Q

Genetic components of huntingtons disease

A

autosomal dominant
trinucleotide repeat disorder: repeat expansion of CAG (phenomenon of anticipation may be seen, where disease presents at an earlier age in successive generations
results in degeneration of cholinergic and GABAergic neruons in the striatum of the basal ganglia
due to defect in huntington gene on chromosome 4

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46
Q

Features of huntington’s disease

A

typically develop after 35 years of age
chorea - abnormal involuntary movement disorder
personality changes (irritability, apathy, depression) and intellectual impairment
dystonia (causes muscles to contract involuntarily)
saccadic eye movements

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47
Q

Difference between nystagmus and saccadic eye movements

A

Nystagmus can be congenital or acquired; it tends to be rhythmic and regular and, if present in central gaze, continuous and sustained. Saccadic intrusions are more often nonrhythmic, intermittent, and unsustained.

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48
Q

Difference between chorea and dystonia

A

Dystonia is a movement disorder in which involuntary sustained or intermittent muscle contractions cause twisting and repetitive movements, abnormal postures, or both. Chorea is an ongoing random-appearing sequence of one or more discrete involuntary movements or movement fragments.

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49
Q

What is phenytoin

A

used in management of seizures
binds to sodium channels increasing their refractory period

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50
Q

Acute adverse effects of phenytoin

A

dizziness, diplopia, nystagmus, slurred speech, ataxia
confusion, seizure

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51
Q

why is phenytoin teratogenic

A

it is associated with cleft palate and congenital heart disease

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52
Q

Cerebral palsy

A

disorder of movement and posture due to a non-progressive lesion of the motor pathways developing in the brain

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53
Q

antenatal causes of cerebral palsy

A

accounts for 80% cases
cerebral malformation and congenital infection (rubella, toxoplasmosis, CMV)

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54
Q

intrapartum causes of cerebral palsy

A

account for 10% cases
birth asphyxia/trauma

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55
Q

post natal causes of cerebral palsy

A

10 % cases
intraventricular haemorrhage
meningitis
head trauma

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56
Q

manifestations of cerebral palsy

A

abnormal tone early infancy
delayed motor milestones
abnormal gait
feeding difficulties

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57
Q

non motor problems in cerebral palsy

A

learning difficulties
epilepsy
squints
hearing impariment

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58
Q

Four classifications of cerebral palsy

A

spastic
dyskinetic
ataxic
mixed

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59
Q

spastic cerebral palsy

A

subtypes of hemiplegia, diplegia or quadriplegia
increased tone resulting from damage to upper motor neurons

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60
Q

dyskinetic cerebral palsy

A

caused by damage to basal ganglia and the substantia nigra
athetoid movements and oro motor problems
( slow, writhing movements of the distal extremities.)

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61
Q

ataxic cerebral palsy

A

caused by damage with typical cerebellar signs

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62
Q

Management of cerebral palsy

A

multidisciplinary approach is needed
treatment for spasticity include oral diazepam, oral and intrathecal baclofen, botulinum toxin type A, orthopedic surgery and selective dorsal rhizotomy
anticonvulsants and analgesia as required

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63
Q

A shaft fracture of the humerus is likely to damage which nerve

A

the radial nerve

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64
Q

what happens if you damage the radial nerve

A

wrist drop
sensory loss to small area between dorsal aspect of 1st and 2nd metacarpals

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65
Q

Wernickes (receptive) aphasia

A

due to lesion of superior temporal gyrus
typically supplied by inferior division of left middle cerebral artery

‘forms’ speech before sending it to brocas area
lesions result in sentences that make no sense, word substitution and neologisms but speech remains fluent (called word salad)
comprehension is impaired

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66
Q

Brocas (expressive) aphasia

A

due to a lesion of the inferior frontal gyrus
typically supplied by superior division of left middle cerebral artery

speech is non fluent laboured an dhalting
repetition is impaired

comprehension is normal

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67
Q

Conduction aphasia

A

due to stroke affecting arcuate fasiculus (connection between wernickes and brocas)

speech is fluent but repetition is poor
aware of errors they ar emaking

comprehension is normal

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68
Q

global aphasia

A

large lesion affecting wernickes, brocas and connection between resulting in severe expressive and receptive aphasia
may still be able to communicate using gestures

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69
Q

subtypes of vascular dementia

A

stroke related VD - multi infarct or single infarct dementia
subcortical VD - caused by small vessel disease
mixed dementia - presence of both VD and alzheimers

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70
Q

Risk factors for developing vascular dementia

A

history of stroke of TIA
AF
HTN
DM
Hyperlipidaemia
Smoking
Obesity
CHD
FH of stroke of CVS disease

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71
Q

How do patients present with vascular dementia

A

several months or several years of history of a sudden or stepwise deterioration of cognitive function

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72
Q

Symptoms of vascular dementia

A

focal neurological abnormalities (visual disturbance, sensory or motor)
Difficulty with attention and concentration
Seizures
memory disturbance
gait disturbance
speech disturbance
emotional disturbance

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73
Q

How is a diagnosis for vascular dementia made

A

comprehensive history and physical exam
formal screen for cognitive impairment
medical review to exclude medication cause
MRi scan to show infarcts and extensive white matter changes

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74
Q

Management of vascular dementia

A

mainly symptomatic
include - cognitive stimulation programmes, etc.
Consider AChE inhibitors or memantine if they have comorbid Alzheimers, parkinsons, or dementia with Lewy bodies

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75
Q

Features of horner’s syndrome

A

miosis (small pupil)
ptosis
enophthalmos (sunken eye)
anhidrosis (loss of sweating on one side)

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76
Q

How can apraclonidine eye drops be used to distinguish horners syndrome

A

cause pupillary dilation in Horners syndrome due to denervation supersensitivity but produces mild pupillary constriction in normal pupil by down regulating the norepinephrine release at the synaptic cleft

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77
Q

Causes of Horners syndrome

A

remember as 4 Ss, 4Ts, and 4Cs,
(S for central, T for torso (pre ganglionic) and C for cervical (post ganglionic))

Central lesions ( 4Ss)
Stroke
MS
Swelling (tumours)
Syringomyelia (cyst in spinal cord)

Pre ganglionic lesions (4Ts)
Tumour (pancoast’s)
Trauma
Thyroidectomy
Top rib (cervical rib growing above first rib above clavicle)

Post ganglionic (4Cs)
Carotid aneurysm
carotid artery dissection
cavernous sinus thrombosis
cluster headache

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78
Q

What is congenital horner’s syndrome associated with

A

heterochromia
difference in colour of the iris on the affected side

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79
Q

Parathyroid hormone (PTH) actions on calcium and phosphate

A

-increase calcium levels and decrease phosphate levels

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80
Q

parathyroid hormone actions on bones

A

increases bone resorption
immediate action on osteoblasts to increase calcium in the ECF]
osteoblasts produce a protein signaling molecule that activate osteoclast s which cause the bone resoprtion

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81
Q

Renal actions of parathyroid hormone

A

increases renal tubular resorption of calcium
increases synthesis of active form of vit D (1,25(OH)2D)
decreases renal phosphate reabsorption

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82
Q

active form of vit d actions on plasma calcium and phosphate

A

increases plasma calcium and phosphate

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83
Q

active form of vit d action on bone and renal system

A

increases renal tubular reabsorption and gut absorption of calcium
increases renal phosphate reabsorption in the proximal tubule
increases osteoclastic activity

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84
Q

calcitonin actions

A

secreted by C cells of thyroid
inhibits osteoclast activity
inhibits renal tubular absorption of calcium

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85
Q

three clinically relevant groups of opioid receptors

A

Mu receptors
kappa receptors
delta receptors

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86
Q

mu opioid receptors

A

three types which have different actions and are located within the brain, brainstem and spinal cord
mu1 - present on neurons responsible for transmitting pain signals within the CNS and molecules which activate these receptors have analgesic effects on the body
mu2&3 - present in brainstem and activation of them causes respiratory depression, reduced gastro-intestinal motility and vasodilation
also responsible for the pupillary constriction seen in opioid overdose

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87
Q

kappa opioid receptors

A

three types located throughout the brain, brainstem and spinal cord
responsible for the cognitive effects of opioid drugs and activation causes dysphoria, hallucinations and depressed consciousness

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88
Q

delta opioid receptors

A

two types located exclusively in the brain and brainstem
potentiation action upon mu receptors and make the effects of analgesia, respiratory depression and dependence more pronounced when activated together

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89
Q

delta opioid receptors

A

two types located exclusively in the brain and brainstem
potentiation action upon mu receptors and make the effects of analgesia, respiratory depression and dependence more pronounced when activated together

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90
Q

examples of weak opioids and their common side effects

A

codeine or tramadol
constipation, urinary retention , addiction

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91
Q

3 examples of strong opioids, administration, common use and effects

A

morphine, oxycodone, methadone
oral/s/c
postoperative pain, major trauma

sedation, respiratory depression, constipation, addiction

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92
Q

2 examples of very strong opioids and effects

A

fentanyl or dihydrocodeine
oral, Iv, sc, transdermal
intra-operative analgesia. critical care, palliative care
significant sedation, respiratory depression, highly addictive

93
Q

hemiparesis

A

is weakness or the inability to move on one side of the body

94
Q

how do lacunar strokes present

A

isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
strong association with HTN
common sites include basal ganglia, thalamus and internal capsule

95
Q

anterior cerebral artery stroke symptoms

A

contralateral hemiparesis and sensory loss
lower extremity > upper

96
Q

middle cerebral artery stroke symptoms

A

contralateral hemiparesis and sensory loss
upper limb > lower
contralateral homoymous hemianopia
aphasia

97
Q

posterior cerebral artery stroke symptoms

A

contralateral homonymous hemianopia with macular sparing
visual agnosia
( an impairment in recognizing visually presented objects, despite otherwise normal visual field, acuity, color vision, brightness discrimination, language, and memory. )

98
Q

Weber’s syndrome symptoms (stroke of posterior cerebral artery that supply the midbrain)

A

ipsilateral CN III palsy (An enlarged pupil that does not react normally to light.
Double vision (diplopia)
Droopy eyelid (ptosis)
Eye misalignment (strabismus)
Tilted head to compensate for binocular vision difficulties.)
contralateral weakness of upper and lower extremities

99
Q

posterior inferior cerebellar artery stroke (wallenberg syndrome)

A

ipsilateral: facial pain and temperature loss
contralateral:limb/torso pain and temperature loss
ataxia and nystagmus

100
Q

anterior inferior cerebellar artery (lateral pontine syndrome) stroke

A

similar to wallenbergs but ipsilateral facial paralysis and deafness

101
Q

retinal/opthalmic artery stroke

A

amaurosis fugax (s a temporary loss of vision in one or both eyes due to a lack of blood flow to the retina)

102
Q

basilar artery stroke

A

locked in syndrome (a rare neurological disorder characterized by complete paralysis of voluntary muscles, except for those that control the eyes.)

103
Q

extradural haematoma

A

bleeding into space between dura mater and the skull
often results from acceleration to deceleration trauma or a blow to the side of the head
majority occur in temporal region where skull fractures cause a rupture of the middle meningeal artery

features: raised ICP
exhibit a lucid interval (some)

104
Q

Subdural haematoma

A

bleeding into outermost meningeal layer
most commonly around the frontal and parietal lobes
can be acute or chronic
risk factors - old age and alcoholism
slower onset of symptoms than extradural

105
Q

Subarachnoid haemorrhage

A

occurs spontaneously in the context of a ruptured cerebral aneurysm but can be seen in association with other injuries when a patient has sustained a traumatic brain injury

106
Q

Subarachnoid haemorrhage

A

occurs spontaneously in the context of a ruptured cerebral aneurysm but can be seen in association with other injuries when a patient has sustained a traumatic brain injury

107
Q

minimum of cerebral perfusion pressure in adults

A

70mmHg

108
Q

unilaterally dilated pupils with a sluggish or fixed light response means

A

3rd nerve compression secondary to tentorial herniation

109
Q

bilaterally dilated pupils with a sluggish or fixed light response means

A

poor CNS perfusion
bilateral 3rd nerve palsy

110
Q

unilaterally dilated pupils or equal with a cross reaction light response means

A

optic nerve injury

111
Q

bilaterally constricted pupils with difficult to assess light response means

A

opiates
pontine lesions
metabolic encephalopathy

112
Q

unilaterally constricted pupils with preserved light response means

A

sympathetic pathway disruption

113
Q

subacute combined degeneration of spinal cord

A

due to vitamin b12 deficiency
dorsal columns and lateral coritcospinal tracts are affected
joint position and vibration sense lost first then distal paraesthesia
upper motor neuron signs typically develop in the legs, classically extensor plantars, brisk knee reflexes, absent ankle jerks
if untreated stiffness and weakness persist

114
Q

TSH receptor antibodies are present in 90-100% patients with what

A

Graves disease - thyrotoxicosis

115
Q

anti-TPO antibodies mean

A

Hashimotos - hypothyroidism

116
Q

Non motor problems in parkinsons

A

Depression
Memory loss
Pain
Anxiety
Sleep
Balance issues

117
Q

normal intracranial pressure

A

7-15 mmHg

118
Q

Motor response GCS scoring

A
  1. none
  2. extending to pain
  3. abnormal flexion to pain (decorticate posture)
  4. withdraws from pain
  5. localises to pain
  6. obeys comands
119
Q

Verbal response GCS scoring

A
  1. none
  2. sounds
  3. words
  4. confused
  5. orientated
120
Q

Eye response GCS scoring

A
  1. none
  2. to pain
  3. to speech
  4. spontaneous
121
Q

Roof of oral cavity formed by

A

2/3 maxilla bone and 1/3 horizontal plane of palatine bone

122
Q

Anterior nucleus of hypothalamus

A

cooling by stimulation of parasympathetic nervous system
A/c -> anterior/cooling

123
Q

Lateral nucleus of hypothalamus (stimulation and lesion)

A

stimulation -> increased appetite
lesions -> anorexia

124
Q

Posterior nucleus of hypothalamus

A

Heating (conservation and increased production)
Damage results in poikilothermia
stimulates sympathetic nervous system
(posterior - poikillothermia)

125
Q

Septal nucleus of hypothalamus

A

Regulates sexual desire
(septal = sex)

126
Q

Suprachiasmatic nucleus function in hypothalamus

A

regulates circadian rhythm

127
Q

Supraoptic nucleus function in hypothalamus

A

produces ADH
lesions = diabetes insipidus

128
Q

Paraventricular nucleus function in hypothalamus

A

produces oxytocin and ADH
lesions = diabetes insipidus

129
Q

Ventromedial nucleus function in hypothalamus

A

Satiety centre
lesions = hyperphagia

130
Q

Dorsomedial nucleus function in hypothalamus

A

stimulation = savage behaviour

131
Q

Long thoracic nerve derived from

A

ventral rami c5,c6 and c7

132
Q

Where does long thoracic nerve innervate

A

tip of serratus anterior muscle

133
Q

What happens in injury to long thoracic nerve

A

winging of scapula

134
Q

Which cranial nerve has the longest intracranial length

A

trochlear nerve (CN IV)

135
Q

Parasympathetic stimulation of penis

A

(Points)
causes erection

136
Q

Sympathetic stimulation of penis

A

(shoots)
causes ejaculation

137
Q

Wests syndrome

A

infantile spasms (epilepsy)
brief spasm beginning in the first few months of life
usually secondary to serious neurological abnormality or may be idiopathic

138
Q

Features of Wests syndrome

A

flexion of head,trunk limbs, extension of arms (Salaam attack) last 1-2 secs, repeat up to 50 times
progressive mental handicap
EEg: hyperaarhythmia

139
Q

Treatments and prognosis of Wests syndrome

A

vigabatrin and steroids
has a poor prognosis

140
Q

(petit mal) absence seizures onset and features

A

onset 4-8years
duration few -30 seconds
no warnings
quick recovery
often many per day

141
Q

Treatment for (petit mal) absence seizures

A

sodium valproate or ethosuximide

142
Q

Lennox-Gastaut syndrome onset and features and treatment

A

(may be an extension of infantile spasms)
onset 1-5 years
features: atypical absences, falls, jerks, 90% moderate-severe
treatment = ketogenic diet might help

143
Q

Benign rolandic epilepsy

A

most common in childhood, more common in males
features = paraesthesia usually on waking up

144
Q

Juvenile myoclonic epilepsy

A

typical onset in the teenage years more common in girls
features: infrequent generalised seizures, often in morning/following sleep deprivation
day time absences
sudden shock-like myoclonic seizure

treatment = good response to sodium valproate

145
Q

First line medication for tonic clonic seizures in males

A

sodium valproate

146
Q

First line medication for generalised tonic clonic seizures in females

A

lamitrigine or levetiracetam

147
Q

First and second line management for focal seizures

A

first line: lamotrigine or levetiracetam
second line: carbamazepine, oxcarbazepine or zonisamide

148
Q

What drug might exacerbate absence seizures

A

carbamezapine

149
Q

First and second line management for absence seizures

A

first line: ethosuximide
second line:
male: sodium valproate
female: lamotrigine or levetiracetam

150
Q

Management for monoclonic seizures

A

males: sodium valproate
females: levetiracetam

151
Q

Management for tonic or atonic seizures

A

males: sodium valproate
females: lamotrigine

152
Q

Guillian Barre syndrome

A

describes an immune-mediated demyelination of the peripheral nervous system often triggered by an infection (classically Campylobacter jejuni).

153
Q

Characteristic features of Gullian barre syndrome

A

progressive, symmetrical weakness of all the limbs.
the weakness is classically ascending i.e. the legs are affected first
reflexes are reduced or absent
sensory symptoms tend to be mild (e.g. distal paraesthesia) with very few sensory signs

there may be a history of gastroenteritis
respiratory muscle weakness
cranial nerve involvement
(diplopia, bilateral facial nerve palsy, oropharyngeal weakness is common)
autonomic involvement (urinary retention, diarrhoea)

154
Q

Investigations for Gullian Barre syndrome

A

LP (Rise in protein with a normal WCC count)
Nerve conduction studies (Decreased motor nerve conduction velocity, prolonged distal motor latency)

155
Q

Another name for motor neurone disease
and describe it

A

Amyotrophic lateral sclerosis
affects both upper (corticospinal tracts) and lower motor neurons
results in a combination of upper and lower motor neuron signs

156
Q

Spinal tracts affected in Brown-Sequard syndrome (spinal cord hemisection)

A
  1. Lateral corticospinal tract
  2. Dorsal columns
  3. Lateral spinothalamic tract
157
Q

Clinical findings in Brown-sequard syndrome (spinal cord hemisection)

A
  1. Ipsilateral spastic paresis below lesion
  2. Ipsilateral loss of proprioception and vibration sensation
  3. Contralateral loss of pain and temperature sensation
158
Q

Clinical findings in Brown-sequard syndrome (spinal cord hemisection)

A
  1. Ipsilateral spastic paresis below lesion
  2. Ipsilateral loss of proprioception and vibration sensation
  3. Contralateral loss of pain and temperature sensation
159
Q

Spinal tracts affected in Subacute combined degeneration of the spinal cord (vitamin B12 & E deficiency)

A
  1. Lateral corticospinal tracts
  2. Dorsal columns
  3. Spinocerebellar tracts
160
Q

Clinical findings in subacute combined degeneration of the spinal cord

A
  1. Bilateral spastic paresis
  2. Bilateral loss of proprioception and vibration sensation
  3. Bilateral limb ataxia
160
Q

Clinical findings in subacute combined degeneration of the spinal cord

A
  1. Bilateral spastic paresis
  2. Bilateral loss of proprioception and vibration sensation
  3. Bilateral limb ataxia
161
Q

Clinical findings in Friedrich’s ataxia

A
  1. Bilateral spastic paresis
  2. Bilateral loss of proprioception and vibration sensation
  3. Bilateral limb ataxia
  4. Cerebellar axtaxia (like an intention tremor)
162
Q

Clinical findings in an anterior spinal artery occlusion

A
  1. Bilateral spastic paresis
  2. Bilateral loss of pain and temperature sensation
163
Q

Syringomyelia clinical findings

A
  1. Flacid paresis (typically affecting the intrinsic hand muscles)
  2. Loss of pain and temperature sensation
164
Q

Another name for vestibular schwanoma and its classical history

A

acoustic neuroma

Classical history of vertigo, hearing loss, tinnitus (all CN VIII) and an absent corneal reflex (CN V), facial palsy (VII)

165
Q

Where are bilateral vestibular schwanomas seen

A

neurofibromatosis type 2

166
Q

Investigation and management of a vestibular schwanoma

A

MRI of the cerebellopontine angle
surgery, radiotherapy or observation

167
Q

First line management for a patient with parkinsons whos motor symptoms ARE affecting their quality of life
and if they ARE NOT affecting quality of life

A

levodopa

NOT affecting = dopamine agonist, levodopa or monoamine oxidase B inhibitor

168
Q

some adverse effects that are due to the difficulty in achieving a steady dose of levodopa

(parkinsons)

A

end-of-dose wearing off: symptoms often worsen towards the end of dosage interval. This results in a decline of motor activity
‘on-off’ phenomenon: large variations in motor performance, with normal function during the ‘on’ period, and weakness and restricted mobility during the ‘off’ period
dyskinesias at peak dose: dystonia, chorea and athetosis (involuntary writhing movements)

169
Q

Features of a cluster headache

A

pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours
clusters typically last 4-12 weeks
intense sharp, stabbing pain around one eye (recurrent attacks ‘always’ affect same side)
patient is restless and agitated during an attack
accompanied by redness, lacrimation, lid swelling
nasal stuffiness
miosis and ptosis in a minority

170
Q

Management of cluster headache

A

acute: 100% oxygen (80% response rate within 15 minutes), subcutaneous triptan (75% response rate within 15 minutes)
prophylaxis: verapamil is the drug of choice. There is also some evidence to support a tapering dose of prednisolone

171
Q

Lacunar infarct

A

presents with 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis

172
Q

Myasthenia gravis

A

Autoimmune disorder resulting in insufficient functioning acetylcholine receptors
More common in women

173
Q

Key features of myasthenia gravis

A

muscle fatigability - muscles become progressively weaker during periods of activity and slowly improve after periods of rest:
extraocular muscle weakness: diplopia
proximal muscle weakness: face, neck, limb girdle
ptosis
dysphagia

174
Q

Investigations for myasthenia gravis

A

1.single fibre electromyography: high sensitivity (92-100%)
2.CT thorax to exclude thymoma
3.CK normal
4.autoantibodies: around 85-90% of patients have antibodies to acetylcholine receptors. In the remaining patients, about about 40% are positive for anti-muscle-specific tyrosine kinase antibodies
5.Tensilon test: IV edrophonium reduces muscle weakness temporarily - not commonly used any more due to the risk of cardiac arrhythmia

175
Q

Management of myasthenia gravis

A

1.long-acting acetylcholinesterase inhibitors
pyridostigmine is first-line
2. immunosuppression is usually not started at diagnosis, but the majority of patients eventually require it in addition to long-acting acetylcholinesterase inhibitors:
prednisolone initially
azathioprine, cyclosporine, mycophenolate mofetil may also be used
3. thymectomy

176
Q

Management of myasthenic crisis

A

plasmapheresis
intravenous immunoglobulins

177
Q

Migraine criteria

A

At least 5 attacks following the criteria below:
1. headache lasting 4-72hrs
2.headache has two of following characteristics
a. unilateral location
b. pulsating quality
c. moderate or severe pain intensity
d. aggravation by or causing avoidance of routine physical activity
3. During headache at least one of following:
a. nausea/ vomiting
b. photophobia and phonophobia
4. not attributed to another disorder

178
Q

arnold chiari malformation

A

Arnold-Chiari malformation describes the downward displacement, or herniation, of the cerebellar tonsils through the foramen magnum. Malformations may be congenital or acquired through trauma.

179
Q

Features of arnold chiari malformation

A

non-communicating hydrocephalus may develop as a result of obstruction of cerebrospinal fluid (CSF) outflow
headache
syringomyelia

180
Q

First line migraine medication

A

offer combination therapy with an oral triptan and an NSAID, or an oral triptan and paracetamol

181
Q

Prophylaxis of migraines medication

A

topiramate or propranolol ‘according to the person’s preference, comorbidities and risk of adverse events’. Propranolol should be used in preference to topiramate in women of child bearing age as it may be teratogenic and it can reduce the effectiveness of hormonal contraceptives

182
Q

Bell’s palsy

A

an acute, unilateral, idiopathic, facial nerve paralysis. The aetiology is unknown although the role of the herpes simplex virus has been investigated previously. The peak incidence is 20-40 years and the condition is more common in pregnant women.

183
Q

Management of bell’s palsy

A

oral prednisolone within 72 hrs of onset

eye care is important to prevent exposure keratopathy

184
Q

Follow up for Bell’s palsy

A

if the paralysis shows no sign of improvement after 3 weeks, refer urgently to ENT
a referral to plastic surgery may be appropriate for patients with more long-standing weakness e.g. several months

185
Q

Causes of brain abscesses

A

extension of sepsis from middle ear or sinuses, trauma or surgery to the scalp, penetrating head injuries and embolic events from endocarditis

186
Q

Symptoms of a brain abscess

A

headache - often dull, persistent
fever- may be absent and usually not the swinging pyrexia seen with abscesses at other sites
focal neurology - e.g. oculomotor nerve palsy or abducens nerve palsy secondary to raised intracranial pressure
other features consistent with raised intracranial pressure
- nausea
-papilloedema
-seizures

187
Q

Management of brain abscess

A

surgery
a craniotomy is performed and the abscess cavity debrided
the abscess may reform because the head is closed following abscess drainage.
IV antibiotics: IV 3rd-generation cephalosporin + metronidazole
intracranial pressure management: e.g. dexamethasone

188
Q

Temporal arteritis

A

Typically patient > 60 years old
Usually rapid onset (e.g. < 1 month) of unilateral headache
Jaw claudication (65%)
Tender, palpable temporal artery
Raised ESR

189
Q

Risk factors for idiopathic intracranial hypertension

A

obesity
female sex
pregnancy
Drugs:
-combined oral contraceptive
-steroids
-tetracyclines
-vitamin A
-lithium

190
Q

Features of idiopathic intracranial hypertension

A

headache
blurred vision
papilloedema
enlarged blind spot
sixth nerve palsy (maybe)

191
Q

Management of idiopathic intracranial hypertension

A

weight loss
diuretics e.g. acetazolamide
Topiramate
repeated LPs
surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure

192
Q

How does an extradural haematoma appear on imaging

A

biconvex (or lentiform), hyperdense collection around the surface of the brain
limited by the suture lines of the skull

193
Q

What could happen if you start a combination therapy of sodium valproate and lamotrigine to control generalised epilepsy

A

serious skin rashes such as steven -johnson syndrome

194
Q

Nerve root for ankle reflex

A

S1-S2

195
Q

Nerve root for knee reflex

A

L3-L4

196
Q

Nerve root for biceps reflex

A

C5-C6

197
Q

Nerve root for triceps reflex

A

C7-C8

198
Q

Most common presentation of MS

A

optic neuritis

199
Q

What is malaria spread by

A

female anopheles mosquitos

200
Q

How is malaria spread

A

Female mosquito takes in blood from infected person and malaria is then reproduced in the mosquitos gut into sporozoites
Mosquito bites another person and and sporozites are injected into them
sporozoites mature in the liver into merozoites
which enter blood and infect RBCs which eventually rupture and cause release of more merozoites (haemolytic anaemia)
In RBCs merozoites reproduce every 48hrs (why temperature spikes every 48hrs)

201
Q

Non specific symptoms of malaria

A

fever, sweat, rigors
malaise
myalgia
headache
vomiting

202
Q

Signs of malaria

A

pallor due to anaemia
hepatosplenomegaly
Jaundice as bilirubin is released during destruction of RBCs

203
Q

How to diagnose malaria

A

Blood film
sent on 3 consecutive days to exclude diagnosis (because of 48hr window where the merozoites reproduce)

204
Q

Most dangerous type of malaria

A

plasmodium falciparum - accounts for 75% of UK cases

205
Q

3 types of antimalarials

A

Malarone (Proguanil and atovaquone) - best for side effects but most expensive

Mefloquine
doxycycline

206
Q

Should patients with falciparum malaria be admitted

A

yes always as they can deteriorate rapidly

207
Q

How long to cluster headache attacks last

A

between 15 mins and 3 hrs

208
Q

What can cluster headache attacks be triggered by

A

alcohol
strong smells
exercise

209
Q

Acute management for cluster headaches

A

sumatriptan 6mg s/c
High flow oxygen for 15-20 mins

210
Q

Prophylaxis for cluster headache

A

verapamil
lithium
prednisolone (short course for 2-3 weeks)

211
Q

Presentation of trigeminal neuralgia

A

intense facial pain
comes on spontaneously
can last from seconds to hours
attacks often worse over time

212
Q

Triggers of trigeminal neuralgia

A

cold weather
spicy food
caffeine
Citrus fruits

213
Q

First line treatment for trigmeinal neuralgia

A

carbamazepine

if it doesnt work surgery can be done to decompress or intentionally damage the trigeminal nerve

214
Q

What is a subarachnoid haemorrhage

A

Bleeding into the subarachnoid space between the pia mater and the arachnoid membrane. Usually a result of a ruptured cerebral aneurysm

215
Q

Causes of spontaneous subarachnoid haemorrhages

A

Saccular berry aneurysms (adult polycystic kidney disease, Ehlers danlos syndrome)
AV malformation
Aortic dissection

216
Q

Subarachnoid haemorrhages are more common in?

A

black patients
female patients
aged 45-70

217
Q

Subarachnoid haemorrhages are associated with what

A

Neurofibromatosis
Cocaine use
sickle cell anaemia
connective tissue disorders
Autosomal dominant polycystic kidney disease

218
Q

Investigations for subarachnoid haemorrhage

A

Ct head - first line
LP - if CT head is negative, done 12 hours after onset of symptoms
Angiography (CT or MRI) used to confirm source of bleeding

219
Q

Management of subarachnoid haemorrhage

A

managed by specialist neurosurgical team
surgery - clipping or coiling

Nimodipine - calcium channel blocker used to prevent vasospasm

LP or insertion of shunt to treat hydrocephalus

antiepileptics to treat seizures

220
Q

What is a subdural haematoma and what is it caused by

A

occurs between dura mater and arachnoid mater
caused by rupture of bridging veins in the outermost meningeal layer

221
Q

What shape is a subdural haematoma on a head CT

A

Crescent / banana

222
Q

What is a crescendo TIA

A

two+ TIAs in one week
carries an increased risk of developing into a stroke

223
Q

RF for stroke

A

AF
diabetes
Atherosclerosis
HTN
smoking
previous stroke or TIA
vasculitis
thrombophilia
combined oral contraceptive pill

224
Q

What score do you use in ED for stroke

A

ROSIER

225
Q

Management of stroke

A
  1. Immediate CT brain to exclude primary intracerebral haemorrhage
  2. Admit to specialist stroke centre
  3. Exclude hypoglycaemia
  4. Aspirin (anti-platelet) 300mg STAT after CT and continued for 2 weeks
  5. Blood pressure should not be lowered in acute phase unless there are complications (hypertensive encephalopathy)
    1. So as not to worsen ischaemic strokes
  6. If cholesterol >3.5mmol/l patients should be commenced on a statin

< 4.5 hours since first symptom = ****Alteplase**** (thrombolysis)

  • Tissue plasminogen activator → rapidly breaks down clots and can reverse the effects of a stroke if given in time
  • Should be monitored post administration for intracranial or systemic haemorrhage

< 6 hours since first symptom = ******Thrombectomy******

    • IV thrombolysis <4.5 hours
226
Q

Absolute CI to thrombolysis

A
  • Previous intracranial haemorrhage
  • Seizure at onset of stroke
  • Intracranial neoplasm
  • Suspected subarachnoid haemorrhage
  • Stroke or traumatic brain injury in preceding 3 months
  • Lumbar puncture in preceding 7 days
  • Gastrointestinal haemorrhage in preceding 3 weeks
  • Active bleeding
  • Pregnancy
  • Oesophageal varices
  • Uncontrolled hypertension >200/120mmHg
227
Q

Haemorrhagic stroke management

A
  1. Supportive care plus monitoring
  2. Immediate referral for neurosurgery assessment
    1. Requires surgery if:
      1. Small deep haemorrhage
      2. GCS < 8
      3. Posterior fossa haemorrhage
  3. Rapid blood pressure control
    1. Aim for systolic 140 while ensuring that the magnitude drop does not exceed 60 mmHg within 1 hour of starting treatment
  4. Urgent reversal of anticoagulation
    1. If on warfarin → give prothrombin complex concentrate (4-factor) and vitamin K
    2. If on Dabigatran → reverse with idarucizumab
    3. If on Factor Xa inhibitor → treat with prothrombin complex concentrate (4-factor).
  5. Venous thromboembolism prophylaxis plus early mobilisation
228
Q

Secondary prevention of stroke

A
  • Clopidogrel 75mg OD
  • aspirin plus MR dipyridamole is now recommended after an ischaemic stroke only if clopidogrel is contraindicated or not tolerated,
  • Carotid artery endartectomy → patient has suffered stroke or TIA in the carotid territory and are not severely disabled OR if carotid stenosis > 70%
  • Treat modifiable risk factors

Year 3 (14 decks)

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