Neuro Flashcards
(229 cards)
1
Q
What are glaucomas
A
optic neuropathies associated with raised intraocular pressure
can be classified:
whether peripheral iris is coverin the trabecular meshwork
2
Q
primary open-angle glaucoma
A
iris is clear of trabecular network
3
Q
Risk factors for primary open-angle glaucoma
A
-increasing age
-genetics
-afro caribbean ethnicity
myopia
-HTN
-DM
-Corticosteroids
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
5
Q
Fundoscopy signs of primary open angle glaucoma
A
- optic disc cupping (cup to disc ratio >0.7): occurs as loss of disc substance makes optic cup widen and deepen
- optic disc pallor - indicating optic atrophy
- Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
- Additional features - cup notching (usually inferior where vessels enter disc), disc haemorrhages
6
Q
Cranial nerve I functions and pathway/foramen
A
olfactory
smell
cribiformplate
7
Q
Cranial nerve II: name, functions, pathway/foramen
A
Optic
sight
optic canal
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)
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)
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
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
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)
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
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
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
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
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
18
Q
corneal reflex afferent and efferent limbs
A
aff - opthalmic nerve (V1)
eff - facial nerve (VII)
19
Q
Jaw jerk reflex afferent and efferent limbs
A
afferent - mandibular nerve (V3)
eff - mandibular nerve (V3)
20
Q
Gag reflex afferent and efferent limb
A
afferent - glossopharyngeal (IX)
eff - Vagal nerve (X0
21
Q
Carotid sinus reflex afferent and efferent limbs
A
Aff - glossopharyngeal (IX)
eff - vagal nerve (X)
22
Q
Pupillary light reflex afferent and efferent limbs
A
aff - optic nerve (II)
eff - oculomotor nerve (III)
23
Q
lacrimation reflex afferent and efferent limbs
A
aff - opthalmic nerve (v1)
eff - facial nerve (VII)
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
25
typical presentation of epilepsy occuring in the frontal lobe
head/leg movements, posturing, poct-ictal weakness, jacksonian march
26
Typical presentation of epilepsy occuring in the parietal lobe
paraesthesia
27
typical presentation of epilepsy occuring in the occipital lobe
floaters/flashers
28
motor neuron disease
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
29
clues which point towards diagnosis of motor neurone disease
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
30
What is Guillain barre syndrome
immune mediated demyelination of the peripheral nervous system often triggered by an infection
classically campylobacter jejuni
31
Pathogenesis of guillain barre syndrome
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
32
Miller Fisher syndrome
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
33
What does a congruous defect mean
complete or symmetrical visual field loss
34
What does an incongrous defect mean
defect is incomplete or asymmetric
35
Homonymous hemianopia
incongruous defects : lesion of optic tract
congrous defects: lesion of optic radiation or occipital cortex
macula sparing: lesion of occipital cortex
36
Homonymous quadrantanopias
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)
37
Bitemporal hemianopia
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
38
what is thoracic outlet syndrome
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)
39
Risk factors for alzheimers disease
increasing age
FH
5% cases inherited as autosomal dominant trait
Apoprotein E allele E4- encodes a cholesterol transport protein
caucasian ethnicity
Down's syndrome
40
Pathological changes in alzhiemers disease
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
41
Empty sella syndrome overview and features
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
42
Arnold chiari malformation
describes downward displacement or herniation of cerebellar tonsils through the formane magnum
malformations may be congenital or acquired through trauma
43
Features of arnold-chiari malformation
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)
44
Huntington's disease
inherited neurodegenerative condition
progressive and incurable that typically results in death 20 years after initial symptoms develop
45
Genetic components of huntingtons disease
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
46
Features of huntington's disease
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
47
Difference between nystagmus and saccadic eye movements
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.
48
Difference between chorea and dystonia
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.
49
What is phenytoin
used in management of seizures
binds to sodium channels increasing their refractory period
50
Acute adverse effects of phenytoin
dizziness, diplopia, nystagmus, slurred speech, ataxia
confusion, seizure
51
why is phenytoin teratogenic
it is associated with cleft palate and congenital heart disease
52
Cerebral palsy
disorder of movement and posture due to a non-progressive lesion of the motor pathways developing in the brain
53
antenatal causes of cerebral palsy
accounts for 80% cases
cerebral malformation and congenital infection (rubella, toxoplasmosis, CMV)
54
intrapartum causes of cerebral palsy
account for 10% cases
birth asphyxia/trauma
55
post natal causes of cerebral palsy
10 % cases
intraventricular haemorrhage
meningitis
head trauma
56
manifestations of cerebral palsy
abnormal tone early infancy
delayed motor milestones
abnormal gait
feeding difficulties
57
non motor problems in cerebral palsy
learning difficulties
epilepsy
squints
hearing impariment
58
Four classifications of cerebral palsy
spastic
dyskinetic
ataxic
mixed
59
spastic cerebral palsy
subtypes of hemiplegia, diplegia or quadriplegia
increased tone resulting from damage to upper motor neurons
60
dyskinetic cerebral palsy
caused by damage to basal ganglia and the substantia nigra
athetoid movements and oro motor problems
( slow, writhing movements of the distal extremities.)
61
ataxic cerebral palsy
caused by damage with typical cerebellar signs
62
Management of cerebral palsy
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
63
A shaft fracture of the humerus is likely to damage which nerve
the radial nerve
64
what happens if you damage the radial nerve
wrist drop
sensory loss to small area between dorsal aspect of 1st and 2nd metacarpals
65
Wernickes (receptive) aphasia
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
66
Brocas (expressive) aphasia
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
67
Conduction aphasia
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
68
global aphasia
large lesion affecting wernickes, brocas and connection between resulting in severe expressive and receptive aphasia
may still be able to communicate using gestures
69
subtypes of vascular dementia
stroke related VD - multi infarct or single infarct dementia
subcortical VD - caused by small vessel disease
mixed dementia - presence of both VD and alzheimers
70
Risk factors for developing vascular dementia
history of stroke of TIA
AF
HTN
DM
Hyperlipidaemia
Smoking
Obesity
CHD
FH of stroke of CVS disease
71
How do patients present with vascular dementia
several months or several years of history of a sudden or stepwise deterioration of cognitive function
72
Symptoms of vascular dementia
focal neurological abnormalities (visual disturbance, sensory or motor)
Difficulty with attention and concentration
Seizures
memory disturbance
gait disturbance
speech disturbance
emotional disturbance
73
How is a diagnosis for vascular dementia made
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
74
Management of vascular dementia
mainly symptomatic
include - cognitive stimulation programmes, etc.
Consider AChE inhibitors or memantine if they have comorbid Alzheimers, parkinsons, or dementia with Lewy bodies
75
Features of horner's syndrome
miosis (small pupil)
ptosis
enophthalmos (sunken eye)
anhidrosis (loss of sweating on one side)
76
How can apraclonidine eye drops be used to distinguish horners syndrome
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
77
Causes of Horners syndrome
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
78
What is congenital horner's syndrome associated with
heterochromia
difference in colour of the iris on the affected side
79
Parathyroid hormone (PTH) actions on calcium and phosphate
-increase calcium levels and decrease phosphate levels
80
parathyroid hormone actions on bones
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
81
Renal actions of parathyroid hormone
increases renal tubular resorption of calcium
increases synthesis of active form of vit D (1,25(OH)2D)
decreases renal phosphate reabsorption
82
active form of vit d actions on plasma calcium and phosphate
increases plasma calcium and phosphate
83
active form of vit d action on bone and renal system
increases renal tubular reabsorption and gut absorption of calcium
increases renal phosphate reabsorption in the proximal tubule
increases osteoclastic activity
84
calcitonin actions
secreted by C cells of thyroid
inhibits osteoclast activity
inhibits renal tubular absorption of calcium
85
three clinically relevant groups of opioid receptors
Mu receptors
kappa receptors
delta receptors
86
mu opioid receptors
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
87
kappa opioid receptors
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
88
delta opioid receptors
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
89
delta opioid receptors
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
90
examples of weak opioids and their common side effects
codeine or tramadol
constipation, urinary retention , addiction
91
3 examples of strong opioids, administration, common use and effects
morphine, oxycodone, methadone
oral/s/c
postoperative pain, major trauma
sedation, respiratory depression, constipation, addiction
92
2 examples of very strong opioids and effects
fentanyl or dihydrocodeine
oral, Iv, sc, transdermal
intra-operative analgesia. critical care, palliative care
significant sedation, respiratory depression, highly addictive
93
hemiparesis
is weakness or the inability to move on one side of the body
94
how do lacunar strokes present
isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
strong association with HTN
common sites include basal ganglia, thalamus and internal capsule
95
anterior cerebral artery stroke symptoms
contralateral hemiparesis and sensory loss
lower extremity > upper
96
middle cerebral artery stroke symptoms
contralateral hemiparesis and sensory loss
upper limb > lower
contralateral homoymous hemianopia
aphasia
97
posterior cerebral artery stroke symptoms
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
Weber's syndrome symptoms (stroke of posterior cerebral artery that supply the midbrain)
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
posterior inferior cerebellar artery stroke (wallenberg syndrome)
ipsilateral: facial pain and temperature loss
contralateral:limb/torso pain and temperature loss
ataxia and nystagmus
100
anterior inferior cerebellar artery (lateral pontine syndrome) stroke
similar to wallenbergs but ipsilateral facial paralysis and deafness
101
retinal/opthalmic artery stroke
amaurosis fugax (s a temporary loss of vision in one or both eyes due to a lack of blood flow to the retina)
102
basilar artery stroke
locked in syndrome (a rare neurological disorder characterized by complete paralysis of voluntary muscles, except for those that control the eyes.)
103
extradural haematoma
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
Subdural haematoma
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
Subarachnoid haemorrhage
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
Subarachnoid haemorrhage
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
minimum of cerebral perfusion pressure in adults
70mmHg
108
unilaterally dilated pupils with a sluggish or fixed light response means
3rd nerve compression secondary to tentorial herniation
109
bilaterally dilated pupils with a sluggish or fixed light response means
poor CNS perfusion
bilateral 3rd nerve palsy
110
unilaterally dilated pupils or equal with a cross reaction light response means
optic nerve injury
111
bilaterally constricted pupils with difficult to assess light response means
opiates
pontine lesions
metabolic encephalopathy
112
unilaterally constricted pupils with preserved light response means
sympathetic pathway disruption
113
subacute combined degeneration of spinal cord
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
TSH receptor antibodies are present in 90-100% patients with what
Graves disease - thyrotoxicosis
115
anti-TPO antibodies mean
Hashimotos - hypothyroidism
116
Non motor problems in parkinsons
Depression
Memory loss
Pain
Anxiety
Sleep
Balance issues
117
normal intracranial pressure
7-15 mmHg
118
Motor response GCS scoring
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
Verbal response GCS scoring
1. none
2. sounds
3. words
4. confused
5. orientated
120
Eye response GCS scoring
1. none
2. to pain
3. to speech
4. spontaneous
121
Roof of oral cavity formed by
2/3 maxilla bone and 1/3 horizontal plane of palatine bone
122
Anterior nucleus of hypothalamus
cooling by stimulation of parasympathetic nervous system
A/c -> anterior/cooling
123
Lateral nucleus of hypothalamus (stimulation and lesion)
stimulation -> increased appetite
lesions -> anorexia
124
Posterior nucleus of hypothalamus
Heating (conservation and increased production)
Damage results in poikilothermia
stimulates sympathetic nervous system
(posterior - poikillothermia)
125
Septal nucleus of hypothalamus
Regulates sexual desire
(septal = sex)
126
Suprachiasmatic nucleus function in hypothalamus
regulates circadian rhythm
127
Supraoptic nucleus function in hypothalamus
produces ADH
lesions = diabetes insipidus
128
Paraventricular nucleus function in hypothalamus
produces oxytocin and ADH
lesions = diabetes insipidus
129
Ventromedial nucleus function in hypothalamus
Satiety centre
lesions = hyperphagia
130
Dorsomedial nucleus function in hypothalamus
stimulation = savage behaviour
131
Long thoracic nerve derived from
ventral rami c5,c6 and c7
132
Where does long thoracic nerve innervate
tip of serratus anterior muscle
133
What happens in injury to long thoracic nerve
winging of scapula
134
Which cranial nerve has the longest intracranial length
trochlear nerve (CN IV)
135
Parasympathetic stimulation of penis
(Points)
causes erection
136
Sympathetic stimulation of penis
(shoots)
causes ejaculation
137
Wests syndrome
infantile spasms (epilepsy)
brief spasm beginning in the first few months of life
usually secondary to serious neurological abnormality or may be idiopathic
138
Features of Wests syndrome
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
Treatments and prognosis of Wests syndrome
vigabatrin and steroids
has a poor prognosis
140
(petit mal) absence seizures onset and features
onset 4-8years
duration few -30 seconds
no warnings
quick recovery
often many per day
141
Treatment for (petit mal) absence seizures
sodium valproate or ethosuximide
142
Lennox-Gastaut syndrome onset and features and treatment
(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
Benign rolandic epilepsy
most common in childhood, more common in males
features = paraesthesia usually on waking up
144
Juvenile myoclonic epilepsy
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
First line medication for tonic clonic seizures in males
sodium valproate
146
First line medication for generalised tonic clonic seizures in females
lamitrigine or levetiracetam
147
First and second line management for focal seizures
first line: lamotrigine or levetiracetam
second line: carbamazepine, oxcarbazepine or zonisamide
148
What drug might exacerbate absence seizures
carbamezapine
149
First and second line management for absence seizures
first line: ethosuximide
second line:
male: sodium valproate
female: lamotrigine or levetiracetam
150
Management for monoclonic seizures
males: sodium valproate
females: levetiracetam
151
Management for tonic or atonic seizures
males: sodium valproate
females: lamotrigine
152
Guillian Barre syndrome
describes an immune-mediated demyelination of the peripheral nervous system often triggered by an infection (classically Campylobacter jejuni).
153
Characteristic features of Gullian barre syndrome
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
Investigations for Gullian Barre syndrome
LP (Rise in protein with a normal WCC count)
Nerve conduction studies (Decreased motor nerve conduction velocity, prolonged distal motor latency)
155
Another name for motor neurone disease
and describe it
Amyotrophic lateral sclerosis
affects both upper (corticospinal tracts) and lower motor neurons
results in a combination of upper and lower motor neuron signs
156
Spinal tracts affected in Brown-Sequard syndrome (spinal cord hemisection)
1. Lateral corticospinal tract
2. Dorsal columns
3. Lateral spinothalamic tract
157
Clinical findings in Brown-sequard syndrome (spinal cord hemisection)
1. Ipsilateral spastic paresis below lesion
2. Ipsilateral loss of proprioception and vibration sensation
3. Contralateral loss of pain and temperature sensation
158
Clinical findings in Brown-sequard syndrome (spinal cord hemisection)
1. Ipsilateral spastic paresis below lesion
2. Ipsilateral loss of proprioception and vibration sensation
3. Contralateral loss of pain and temperature sensation
159
Spinal tracts affected in Subacute combined degeneration of the spinal cord (vitamin B12 & E deficiency)
1. Lateral corticospinal tracts
2. Dorsal columns
3. Spinocerebellar tracts
160
Clinical findings in subacute combined degeneration of the spinal cord
1. Bilateral spastic paresis
2. Bilateral loss of proprioception and vibration sensation
3. Bilateral limb ataxia
160
Clinical findings in subacute combined degeneration of the spinal cord
1. Bilateral spastic paresis
2. Bilateral loss of proprioception and vibration sensation
3. Bilateral limb ataxia
161
Clinical findings in Friedrich's ataxia
1. Bilateral spastic paresis
2. Bilateral loss of proprioception and vibration sensation
3. Bilateral limb ataxia
4. Cerebellar axtaxia (like an intention tremor)
162
Clinical findings in an anterior spinal artery occlusion
1. Bilateral spastic paresis
2. Bilateral loss of pain and temperature sensation
163
Syringomyelia clinical findings
1. Flacid paresis (typically affecting the intrinsic hand muscles)
2. Loss of pain and temperature sensation
164
Another name for vestibular schwanoma and its classical history
acoustic neuroma
Classical history of vertigo, hearing loss, tinnitus (all CN VIII) and an absent corneal reflex (CN V), facial palsy (VII)
165
Where are bilateral vestibular schwanomas seen
neurofibromatosis type 2
166
Investigation and management of a vestibular schwanoma
MRI of the cerebellopontine angle
surgery, radiotherapy or observation
167
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
levodopa
NOT affecting = dopamine agonist, levodopa or monoamine oxidase B inhibitor
168
some adverse effects that are due to the difficulty in achieving a steady dose of levodopa
(parkinsons)
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
Features of a cluster headache
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
Management of cluster headache
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
Lacunar infarct
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
Myasthenia gravis
Autoimmune disorder resulting in insufficient functioning acetylcholine receptors
More common in women
173
Key features of myasthenia gravis
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
Investigations for myasthenia gravis
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
Management of myasthenia gravis
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
Management of myasthenic crisis
plasmapheresis
intravenous immunoglobulins
177
Migraine criteria
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
arnold chiari malformation
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
Features of arnold chiari malformation
non-communicating hydrocephalus may develop as a result of obstruction of cerebrospinal fluid (CSF) outflow
headache
syringomyelia
180
First line migraine medication
offer combination therapy with an oral triptan and an NSAID, or an oral triptan and paracetamol
181
Prophylaxis of migraines medication
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
Bell's palsy
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
Management of bell's palsy
oral prednisolone within 72 hrs of onset
eye care is important to prevent exposure keratopathy
184
Follow up for Bell's palsy
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
Causes of brain abscesses
extension of sepsis from middle ear or sinuses, trauma or surgery to the scalp, penetrating head injuries and embolic events from endocarditis
186
Symptoms of a brain abscess
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
Management of brain abscess
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
Temporal arteritis
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
Risk factors for idiopathic intracranial hypertension
obesity
female sex
pregnancy
Drugs:
-combined oral contraceptive
-steroids
-tetracyclines
-vitamin A
-lithium
190
Features of idiopathic intracranial hypertension
headache
blurred vision
papilloedema
enlarged blind spot
sixth nerve palsy (maybe)
191
Management of idiopathic intracranial hypertension
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
How does an extradural haematoma appear on imaging
biconvex (or lentiform), hyperdense collection around the surface of the brain
limited by the suture lines of the skull
193
What could happen if you start a combination therapy of sodium valproate and lamotrigine to control generalised epilepsy
serious skin rashes such as steven -johnson syndrome
194
Nerve root for ankle reflex
S1-S2
195
Nerve root for knee reflex
L3-L4
196
Nerve root for biceps reflex
C5-C6
197
Nerve root for triceps reflex
C7-C8
198
Most common presentation of MS
optic neuritis
199
What is malaria spread by
female anopheles mosquitos
200
How is malaria spread
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
Non specific symptoms of malaria
fever, sweat, rigors
malaise
myalgia
headache
vomiting
202
Signs of malaria
pallor due to anaemia
hepatosplenomegaly
Jaundice as bilirubin is released during destruction of RBCs
203
How to diagnose malaria
Blood film
sent on 3 consecutive days to exclude diagnosis (because of 48hr window where the merozoites reproduce)
204
Most dangerous type of malaria
plasmodium falciparum - accounts for 75% of UK cases
205
3 types of antimalarials
Malarone (Proguanil and atovaquone) - best for side effects but most expensive
Mefloquine
doxycycline
206
Should patients with falciparum malaria be admitted
yes always as they can deteriorate rapidly
207
How long to cluster headache attacks last
between 15 mins and 3 hrs
208
What can cluster headache attacks be triggered by
alcohol
strong smells
exercise
209
Acute management for cluster headaches
sumatriptan 6mg s/c
High flow oxygen for 15-20 mins
210
Prophylaxis for cluster headache
verapamil
lithium
prednisolone (short course for 2-3 weeks)
211
Presentation of trigeminal neuralgia
intense facial pain
comes on spontaneously
can last from seconds to hours
attacks often worse over time
212
Triggers of trigeminal neuralgia
cold weather
spicy food
caffeine
Citrus fruits
213
First line treatment for trigmeinal neuralgia
carbamazepine
if it doesnt work surgery can be done to decompress or intentionally damage the trigeminal nerve
214
What is a subarachnoid haemorrhage
Bleeding into the subarachnoid space between the pia mater and the arachnoid membrane. Usually a result of a ruptured cerebral aneurysm
215
Causes of spontaneous subarachnoid haemorrhages
Saccular berry aneurysms (adult polycystic kidney disease, Ehlers danlos syndrome)
AV malformation
Aortic dissection
216
Subarachnoid haemorrhages are more common in?
black patients
female patients
aged 45-70
217
Subarachnoid haemorrhages are associated with what
Neurofibromatosis
Cocaine use
sickle cell anaemia
connective tissue disorders
Autosomal dominant polycystic kidney disease
218
Investigations for subarachnoid haemorrhage
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
Management of subarachnoid haemorrhage
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
What is a subdural haematoma and what is it caused by
occurs between dura mater and arachnoid mater
caused by rupture of bridging veins in the outermost meningeal layer
221
What shape is a subdural haematoma on a head CT
Crescent / banana
222
What is a crescendo TIA
two+ TIAs in one week
carries an increased risk of developing into a stroke
223
RF for stroke
AF
diabetes
Atherosclerosis
HTN
smoking
previous stroke or TIA
vasculitis
thrombophilia
combined oral contraceptive pill
224
What score do you use in ED for stroke
ROSIER
225
Management of stroke
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
Absolute CI to thrombolysis
- 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
Haemorrhagic stroke management
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
Secondary prevention of stroke
- 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
