MRCP2 Flashcards
(340 cards)
1
Q
What are the side effects of 5HT3 antagonists?
A
prolonged QT interval
constipation is common
2
Q
Where does ondansetron act?
A
Medulla oblongata - chemoreceptors
3
Q
What is the other name for petit mal seizure?
A
Abscence
4
Q
EEG: bilateral, symmetrical 3Hz spike and wave pattern~?
A
Abscence seizure ?
5
Q
Features of abscence seizure?
A
absences last a few seconds and are associated with a quick recovery
seizures may be provoked by hyperventilation or stress
the child is usually unaware of the seizure
they may occur many times a day
EEG: bilateral, symmetrical 3Hz spike and wave pattern
6
Q
Management of abscence seizure?
A
Sodium valoprate
Ethuoxomide
7
Q
Risk factors of acute angle closure glaucoma?
A
hypermetropia (long-sightedness)
pupillary dilatation
lens growth associated with age
8
Q
Features of acute angle closure glaucoma?
A
Severe pain: may be ocular or headache
decreased visual acuity
symptoms worse with mydriasis (e.g. watching TV in a dark room)
hard, red-eye
haloes around lights
semi-dilated non-reacting pupil
corneal oedema results in dull or hazy cornea
systemic upset may be seen, such as nausea and vomiting and even abdominal pain
9
Q
Investigations of acvute angle closure glaucoma?
A
- Tonometry
- Gonioscopy - looks at the angle
10
Q
Management of acute angle closure glaucoma?
A
Combination of eye drops:
- Pilocarpine
- Beta blocker
- Alpha 2 agonist
In addition:
- Acetazolamide
11
Q
Definitive management of acute angle closure glaucoma?
A
laser peripheral iridotomy
12
Q
Glaucoma: How does pilocarpine work?
A
Stimulates parasympathetic
13
Q
Glaucoma: How does beta blocker work?
A
Descreases aqueous humour
14
Q
Glaucoma: How does alpha 2 agonist work?
A
Decreases aqueous humour
+
Increases outflow
15
Q
What is acute disseminated myelitis ?
A
autoimmune demyelinating disease of the central nervous system
16
Q
Management of acute sinusitis?
A
- Analgesia
- Intranasal decongestants if present for 10 days
- Phenoxymethapenicillin if very unwell
17
Q
What is double sickening in acute sinusitis?
A
‘double-sickening’ may sometimes be seen, where an initial viral sinusitis worsens due to secondary bacterial infection
18
Q
What is an acute stress reaction?
A
First 4 weeks post traumatic event
19
Q
Features of acute stress reaction?
A
intrusive thoughts e.g. flashbacks, nightmares
dissociation e.g. ‘being in a daze’, time slowing
negative mood
avoidance
arousal e.g. hypervigilance, sleep disturbance
20
Q
Management for acute stress reaction?
A
trauma-focused cognitive-behavioural therapy (CBT)
BZD
21
Q
Features of dry macular degeneraiton?
A
characterised by drusen - yellow round spots in Bruch’s membrane
22
Q
Features of wet macular degeneration?
A
exudative or neovascular macular degeneration
characterised by choroidal neovascularisation
leakage of serous fluid and blood can subsequently result in a rapid loss of vision
carries the worst prognosis
23
Q
Features of macular degeneration?
A
reduction in visual acuity, particularly for near field objects
- gradual in dry ARMD
- subacute in wet ARMD
difficulties in dark adaptation. Worsening night vision
photopsia, (a perception of flickering or flashing lights), and glare around objects
24
Q
Signs of macular degeneration?
A
distortion of line perception may be noted on Amsler grid testing
fundoscopy reveals the presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar.
in wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.
25
Investigations for maccular degneration
1. Slit lamp -- chekc pigments / haemorrhages
2. fluorescein angiography is utilised if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therapy.
3. Ocular coherence tomography is used to visualise the retina in three dimensions because it can reveal areas of disease which aren't visible using microscopy alone.
26
Management of maccular degeneration?
combination of zinc with anti-oxidant vitamins A,C and E reduced progression of the disease by around one third
1. vascular endothelial growth factor (VEGF) (preferred)
2. laser photocoagulation does slow progression of ARMD - but risk of sight loss
27
What is agoraphobia?
Agoraphobia is primarily describes a fear of open spaces but also includes related aspects, e.g. the presence of crowds or the difficulty of escaping to a safe place
28
Alcohol withdrawl symptoms?
symptoms start at 6-12 hours: tremor, sweating, tachycardia, anxiety
peak incidence of seizures at 36 hours
peak incidence of delirium tremens is at 48-72 hours: coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia
29
Management of alcohol withdrawl?
1. Chlordiazepoxide / diazepam
30
WHat BZD is preferred in hepatic dysfunction in alcohol withdrawl?
Lorazepam
31
What antiepileptic can be used in alcohol withdrawl?
Carbamazepine - for siezures
32
What is alcohol hallucinosis?
Alcohol related psychosis - not the same of wernicke's
Features:
1. A psychosis of less than 6 months duration
2. auditory hallucinations, often of persecutory or derogatory nature
3. occurs in clear consciousness
33
What is the other name of iritis?
Anterior uveitis
34
What is inflammaed in anterior uvieitis?
Anterior uvea
Iris and ciliary body.
35
Features of anterior uveitis?
acute onset
ocular discomfort & pain (may increase with use)
pupil may be small +/- irregular due to sphincter muscle contraction
photophobia (often intense)
blurred vision
red eye
lacrimation
ciliary flush: a ring of red spreading outwards
hypopyon; describes pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level
visual acuity initially normal → impaired
36
Association conditions of anterior uveitis?
ankylosing spondylitis
reactive arthritis
ulcerative colitis, Crohn's disease
Behcet's disease
sarcoidosis: bilateral disease may be seen
associated with HLA B 27
37
Management of anterior uveitis?
1. cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate
2. Steroid drops
38
What is anti NMDA encephaltis?
Anti-NMDA receptor encephalitis is a paraneoplastic syndrome, presenting as prominent psychiatric features
39
What cancer is associcated with NMDA encephaltis?
Ovarian teratomas
40
Autoantibody seen in anti NMDA encephalitis?
Ant-MuSK
41
Mechanism of typical antipsychotics?
D2 antagonist
blocking dopaminergic transmission in the mesolimbic pathways
e.g. Haloperidol
Chlopromazine
42
Mechanism of atypical antipsychotics?
Act on a variety of receptors (D2, D3, D4, 5-HT)
43
Side effect of typical vs atypical?
Typical:
Extrapyramidal side-effects and hyperprolactinaemia common
Atypical:
Extrapyramidal side-effects and hyperprolactinaemia less common
Metabolic effects
44
What extrapyramidal side effects are in antipsychotics?
Parkinsonism
Acute dystonia
Akasthsia
Tardive dyskinesia
45
What type of antipsycotic reduces seizure threshold?
Atypicals
46
What antipsychoatic increased QT?
Halperiodl
But a lot of them
47
Where is wernicke's area?
superior temporal gyrus. It is typically supplied by the inferior division of the left MCA
48
Where is the broca area?
"expressive aphasia"
inferior frontal gyrus.
Comprehension not impaired
49
What is wernicke aphasia?
"Receptive aphasia"
Fluent nonsensical speach
Comprehension impaired
50
Where is the lesion in a conductive aphasia
Classically due to a stroke affecting the arcuate fasiculus - the connection between Wernicke's and Broca's area
51
Features of conductive aphasia?
Speech is fluent but repetition is poor. Aware of the errors they are making
Comprehension is normal
52
What is global aphasia?
Large lesion affecting all 3 of the above areas resulting in severe expressive and receptive aphasia
May still be able to communicate using gestures
53
/
54
Small irregular pupil + No response to light + Accomodation relfex intact
Argyl robertson pupil intact
55
Causes of argyl robertson pupil?
Diabetes
Syphilus
56
What is arnold chiari malformation?
downward displacement, or herniation, of the cerebellar tonsils through the foramen magnum
57
Features of arnold chiari malformation?
non-communicating hydrocephalus may develop as a result of obstruction of cerebrospinal fluid (CSF) outflow
headache
syringomyelia
58
Features of ataxia telengectasia?
Telengectasia / spide angioma
IgA deficiencies
Increased leukaemia / lymphomarisk
Onset at 1 year - 5 years
59
Features of Friedrich's ataxia
Trinucleotide nucleotide repeat disorder
Kyphoscliosis
Optic atrophy
HOCM
Diabetes mellituts
Onset 10-15
60
What is the inheritance pattern for friedrichs ataxia and ataxia telengectasia?
Autosmal recessive
61
Adverse effects of atypical antipsychotics/
weight gain
clozapine is associated with agranulocytosis (see below)
hyperprolactinaemia
62
Adverse effects of clozapine?
agranulocytosis (1%), neutropaenia (3%)
reduced seizure threshold - can induce seizures in up to 3% of patients
constipation
myocarditis: a baseline ECG should be taken before starting treatment
hypersalivation
63
What is autnomic dysreflexia?
extreme hypertension, flushing and sweating above the level of the cord lesion, agitation, and in untreated cases severe consequences of extreme hypertension have been reported, e.g. haemorrhagic stroke.
Occurs in indivudals with injury above T6
64
Management of autonomic dysreflexia?
Management of autonomic dysreflexia involves removal/control of the stimulus and treatment of any life-threatening hypertension and/or bradycardia.
65
Features of vertigo?
vertigo triggered by change in head position (e.g. rolling over in bed or gazing upwards)
may be associated with nausea
each episode typically lasts 10-20 seconds
positive Dix-Hallpike manoeuvre, indicated by:
patient experiences vertigo
rotatory nystagmus
66
Management of vertigo?
Epley manoeuvre
Betahistine
67
Mechanism of BZD?
increase number of chloride channels
GABAA drugs
benzodiazipines increase the frequency of chloride channels
barbiturates increase the duration of chloride channel opening
68
Erb's palsy?
damage to C5,6 roots
winged scapula
may be caused by a breech
69
Klumpe's palsy?
damage to T1
loss of intrinsic hand muscles
due to traction
70
Features of brain abscess?
Headache
Fever - not swinging
Focal neurology
71
Management of brain abscess/
Surgery - craniotomy for decompression
IV antibiotics: IV 3rd-generation cephalosporin + metronidazole
intracranial pressure management: e.g. dexamethasone
72
What does subfalcine herniation mean?
Displacement of the cingulate gyrus under the falx cerebri
73
What does central herniation mean?
Downwards displacement of the brain
74
What for transtentorial herniation mean?
Displacement of the uncus of the temporal lobe under the tentorium cerebelli.
Clinical consequences include an ipsilateral fixed, dilated pupil (due to parasympathetic compression of the third cranial nerve) + contralateral paralysis (due to compression of the cerebral peduncle)
75
What does tonsillar herniation mean?
Displacement of the cerebellar tonsils through the foramen magnum. This is called ‘coning’. In raised ICP this causes compression of the cardiorespiratory centre. In Chiari 1 malformation, tonsillar herniation is seen without raised ICP
76
Feature of parietal lobe lesion?
sensory inattention
apraxias
astereognosis (tactile agnosia)
inferior homonymous quadrantanopia
Gerstmann's syndrome (lesion of dominant parietal): alexia, acalculia, finger agnosia and right-left disorientation
77
Feature of occiptal lobe lesion?
homonymous hemianopia (with macula sparing)
cortical blindness
visual agnosia
78
Feature of temporal lobe lesion
Wernicke's aphasia: this area 'forms' the speech before 'sending it' to Brocas area. Lesions result in word substituion, neologisms but speech remains fluent
superior homonymous quadrantanopia
auditory agnosia
prosopagnosia (difficulty recognising faces)
79
feature of frontal love lesion?
expressive (Broca's) aphasia: located on the posterior aspect of the frontal lobe, in the inferior frontal gyrus. Speech is non-fluent, laboured, and halting
disinhibition
perseveration
anosmia
inability to generate a list
80
feature of cerebral lesion?
midline lesions: gait and truncal ataxia
hemisphere lesions: intention tremor, past pointing, dysdiadokinesis, nystagmus
81
Area affected in wernickes / Korsakoff?
Medial thalamus and mammillary bodies of the hypothalamus
82
Area affected in hemibalismis?
Subthalamic nucleus of the basal ganglia
83
Area affected in Huntington disease?
Striatum (caudate nucleus) of the basal ganglia
84
Area affected in Parkinson disease?
Substantia nigra of the basal ganglia
85
Area affected in Kluver-Bucy syndrome
amydala
86
Most common metastasis to the brain?
lung (most common)
breast
bowel
skin (namely melanoma)
kidney
87
Brain tumour: Pleomorphic tumour cells border necrotic areas
Glioblastoma multiformi
88
Treatment for glioblastoma multiform?
Treatment is surgical with postoperative chemotherapy and/or radiotherapy.
Dexamethasone is used to treat the oedema.
89
Brain tumour: central necrosis and a rim that enhances with contrast
Glioblastoma multiforme
90
Most common primary brain tumour?
Glioblastoma multiforme
91
Second most common primary brain tumour?
Meningioma
92
Brain tumour: : Spindle cells in concentric whorls and calcified psammoma bodies
Meningioma
93
What condition is associated with vestibular schwaoma?
Neurofibromatosis type 2 is associated with bilateral vestibular schwannomas.
94
Where is vestibular schwannoma found?
benign tumour arising from the eighth cranial nerve (vestibulocochlear nerve).
Often seen in the cerebellopontine angle
95
Rosenthal fibres (corkscrew eosinophilic bundle)
Pilocytic astrocytoma
96
Small, blue cells. Rosette pattern of cells with many mitotic figures
Medulloblastoma
97
When is ependyma commonly located?
4th ventricle
98
* Histology: perivascular pseudorosettes
Ependymoma
99
Calcifications with 'fried-egg' appearance
Oligodendroma
100
What brain tumour is associated with Hippel-Lindau syndrome
Haemangioblastoma
101
Brain tumour Histology: foam cells and high vascularity
Haemangioblastoma
102
Features of craniopharygioma?
hormonal disturbance, symptoms of hydrocephalus or bitemporal hemianopia.
103
What is capragas syndrome?
Capgras syndrome refers to a disorder in which a person holds a delusion that a friend or partner has been replaced by an identical-looking impostor.
104
Mechanism of carbamazepine?
binds to sodium channels increases their refractory period
105
Features of carbamazepine?
P450 enzyme inducer
dizziness and ataxia
drowsiness
headache
visual disturbances (especially diplopia)
Steven-Johnson syndrome
leucopenia and agranulocytosis
hyponatraemia secondary to syndrome of inappropriate ADH secretion
106
Cataplexy?
sudden and transient loss of muscular tone caused by strong emotion
107
Feature of central retinal artery occlusion?
sudden, painless unilateral visual loss
relative afferent pupillary defect
'cherry red' spot on a pale retina
108
Management of central rental vein occlusion?
macular oedema - intravitreal anti-vascular endothelial growth factor (VEGF) agents
retinal neovascularization - laser photocoagulation
109
Normal pressure in CSF
pressure = 60-150 mm (patient recumbent)
110
Protein in CSF?
protein = 0.2-0.4 g/l
111
Glucose in CSF
glucose = > 2/3 blood glucose
112
CSF + raised lymphocytes?
viral meningitis/encephalitis
TB meningitis
partially treated bacterial meningitis
Lyme disease
Behcet's, SLE
lymphoma, leukaemia
113
Features of Charcot Marie tooth?
There may be a history of frequently sprained ankles
Foot drop
High-arched feet (pes cavus)
Hammer toes
Distal muscle weakness
Distal muscle atrophy
Hyporeflexia
Stork leg deformity
114
Wernicke encephalopathy?
Confusion, gait ataxia, nystagmus + ophthalmoplegia are features of Wernicke's encephalopathy
115
Korsakoff syndrome?
amnesia, deficits in explicit memory, and confabulation.
116
Treatment for central retinal artery occlusion?
Treatment of underlying condition --> intravenous steroids for temporal arteritis
Acute: Intraarterial thrombolysis
117
Features of chronic demyelinating polyneuropathy?
Cause of peripheral neuropathy
Guillain-Barre syndrome (GBS), with motor features predominating
High protein CSF
118
Management of chronic demyelinating polyneuropathy?
Steroids + immunosuppression
119
Features of cluster headache?
-intense sharp, stabbing pain around one eye
pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours
the patient is restless and agitated during an attack due to the severity
clusters typically last 4-12 weeks
accompanied by redness, lacrimation, lid swelling
nasal stuffiness
miosis and ptosis in a minority
120
Management of cluster headache?
acute
100% oxygen (80% response rate within 15 minutes)
subcutaneous triptan (75% response rate within 15 minutes)
121
Prophylaxis in cluster headache?
prophylaxis
verapamil is the drug of choice
there is also some evidence to support a tapering dose of prednisolone
122
Imaging in cluster headache and why?
Can be presenting of tumour
MRI with gadolinium contrast is the investigation of choice
123
Common perineal nerve lesion
weakness of foot dorsiflexion
weakness of foot eversion
weakness of extensor hallucis longus
sensory loss over the dorsum of the foot and the lower lateral part of the leg
wasting of the anterior tibial and peroneal muscles
124
EEG findings in CJD?
EEG: biphasic, high amplitude sharp waves (only in sporadic CJD)
125
CSF in CJD§
Normal
126
MRI findings in CJD?
MRI: hyperintense signals in the basal ganglia and thalamus
127
Features of new variant CJD?
Age. onset - 25
psychological symptoms such as anxiety, withdrawal and dysphonia are the most common presenting features
the 'prion protein' is encoded on chromosome 20 - it's role is not yet understood
methionine homozygosity at codon 129 of the prion protein is a risk factor for developing CJD - all patients who have so far died have had this
median survival = 13 months
128
Main features of CJD?
Myoclonus
Dementia
129
Most common cause of blindness 35-65?
Diabetic retinopathy
130
Mild Non proliferative diabetic retinopathy?
1 or more microaneurysm
131
Moderate nonproliferatie diabetic retinopathy?
microaneurysms
blot haemorrhages
hard exudates
cotton wool spots ('soft exudates' - represent areas of retinal infarction), venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR
132
Severe non proliferative diabetic retinopathy?
blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
IRMA in at least 1 quadrant
133
Features of proliferative diabetic retinopathy?
retinal neovascularisation - may lead to vitrous haemorrhage
fibrous tissue forming anterior to retinal disc
more common in Type I DM, 50% blind in 5 years
134
What is maculopathy (diabetics) ?
based on location rather than severity, anything is potentially serious
hard exudates and other 'background' changes on macula
check visual acuity
more common in Type II DM
135
Management of maculopathy?
Optimise glycaemic control
Maculopathy:
1. Anti-vegf inhibitors
136
Management of non-proliferative retinopathy?
if severe/very severe consider panretinal laser photocoagulation
137
Management of proliferative retinopathy?
Panretinal laser photocoagulation
Anti-VEGF
if severe or vitreous haemorrhage: vitreoretinal surgery
138
What VEGF inhibitor is used in proliferative retinopathy?
ranibizumab
139
Drugs that cause peripheral neuropathy?
amiodarone
isoniazid
vincristine
nitrofurantoin
metronidazole
140
List of patients who cannot drive and must call DVLA?
first unprovoked/isolated seizure: 6 months off - if no cause found then 12 months
established epilepsy or those with multiple unprovoked seizures
- qualify for a driving licence if they have been free from any seizure for 12 months
- no seizures for 5 years (with medication if necessary) a ’til 70 licence is usually restored
If withdrawing from antiepelpetic medication
141
Restricitons in driving for syncope?
simple faint: no restriction
single episode, explained and treated: 4 weeks off
single episode, unexplained: 6 months off
two or more episodes: 12 months off
142
DVLA: Stroke or TIA?
1 month off
143
DVLA: Multiple TIA?
3 months off driving and inform DVLA
144
DVLA: Craniotomy for meningioma
1 year off driving
145
DVLA: craniotomy for pituitary tumour?
6 months
Transphenoidal surgery can drive
146
DVLA: Narcolepsy / catoplexy
Cease driving at diagnosis
147
For all psychiatric DVLA stuff?
may be able to drive but must inform the DVLA
Unless severe anxiety / suicidal: Must not drive
148
Inheritance of the dystrophinopathies?
X linked recessive
- Duchenne
- Beckers
149
Where is the mutation cause dystrophinopathies?
Xp21
150
What is the absolute contrainidcation to ECT?
Raised intracranial pressure
151
Short term side effect of electroconvulsion therapy?
headache
nausea
short term memory impairment
memory loss of events prior to ECT
cardiac arrhythmia
152
What is most likely causative organism of encephalitis?
HSV - 1
153
Management of encephalitis?
intravenous aciclovir should be started in all cases of suspected encephalitis
154
Findings on CSF for encephalitis?
lymphocytosis
elevated protein
PCR for HSV, VZV and enteroviruses
155
EEG: lateralised periodic discharges at 2 Hz
Encephalitis
156
Types of focal seizure?
Focal impaired awareness
FOcal aware
157
Types of generalised seizure?
tonic-clonic (grand mal)
tonic
clonic
typical absence (petit mal)
atonic
158
What is a focal to bilateral seizure?
starts on one side of the brain in a specific area before spreading to both lobes
previously termed secondary generalized seizures
159
Pregnancy + sodium valporate
Neural tube defect
160
Pregnancy + phenytoin?
Cleft lip
161
Are anti-epileptic safe in pregnany ?
Yes - except phenobarbital
162
Generalised tonic clonic management?
Males: Sodium valporate
Females: lamotrigine or levetiracetam
163
Focal seizure management?
Lamotrigene or leveitacetam
164
Abscence seizure management?
first line: ethosuximide
second line:
male: sodium valproate
female: lamotrigine or levetiracetam
165
What treatment may exacerbate abscence seizures?
Carbamazepine
166
Myoclonic seizure management?
males: sodium valproate
females: levetiracetam
167
Tonic or atonic seizure management?
males: sodium valproate
females: lamotrigine
168
What conditions see episcerlitis associated?
IBD
Rheumatoid arthritis
169
Features of episcleritis?
Classically not painful
watering and mild photophobia may be present
170
How to differentiated between scleritis and episcerlitis?
phenylephrine drops
phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels
if the eye redness improves after phenylephrine a diagnosis of episcleritis can be made
171
Inheritance of benign essential tremor ?
autosomal dominant condition
172
Features of benign essential tremor?
postural tremor: worse if arms outstretched
improved by alcohol and rest
most common cause of titubation (head tremor)
173
Management of benign essential tremor?
propranolol is first-line
primidone is sometimes used
174
Causes of bilateral facial nerve palsy?
sarcoidosis
Guillain-Barre syndrome
Lyme disease
bilateral acoustic neuromas (as in neurofibromatosis type 2)
as Bell's palsy is relatively common it accounts for up to 25% of cases f bilateral palsy, but this represents only 1% of total Bell's palsy cases
175
Facial nerve: LMN vs UMN?
upper motor neuron lesion 'spares' upper face i.e. forehead
lower motor neuron lesion affects all facial muscles
176
Supply of facial nerve?
Supply - 'face, ear, taste, tear'
face: muscles of facial expression
ear: nerve to stapedius
taste: supplies anterior two-thirds of tongue
tear: parasympathetic fibres to lacrimal glands, also salivary glands
177
Inheritance of fasciohumeral dystrophy?
Autosomal dominant
it typically affects the face, scapula and upper arms first.
Average onset 20 years
178
Features of fasciohumeral dystrophy?
facial muscles are involved first - difficulty closing eyes, smiling, blowing etc
weakness of the shoulder and upper arm muscles
abnormal prominence of the borders of the shoulder blades - 'winging'
lower limb: hip girdle weakness, foot drop
179
Features of foster keneddy syndrome?
optic atrophy in the ipsilateral eye
papilloedema in the contralateral eye
central scotoma in the ipsilateral eye
anosmia
180
Genetics of friedrick's ataxia?
autosomal recessive, trinucleotide repeat disorder characterised by a GAA repeat in the X25 gene on chromosome 9 (frataxin)
181
Phenotype of friedrick's ataxia?
absent ankle jerks/extensor plantars
cerebellar ataxia
optic atrophy
spinocerebellar tract degeneration
absent ankle jerks/extensor plantars
cerebellar ataxia
optic atrophy
spinocerebellar tract degeneration
182
Management of GAD?
step 1: education about GAD + active monitoring
step 2: low-intensity psychological interventions (individual non-facilitated self-help or individual guided self-help or psychoeducational groups)
step 3: high-intensity psychological interventions (cognitive behavioural therapy or applied relaxation) or drug treatment. See drug treatment below for more information
step 4: highly specialist input e.g. Multi agency teams
183
Drug treatment in GAD?
1. Sertraline
2. Offer an alternative SSRI or a serotonin–noradrenaline reuptake inhibitor (SNRI)
examples of SNRIs include duloxetine and venlafaxine
184
After 12 weeks of treatment with sertraline for GAD - no effect, how to manage?
imipramine or clomipramine should be offered
185
What infection classically trigger guillain barre?
Camplobacter
186
Antibodies in guillain barre?
anti-ganglioside antibody (e.g. anti-GM1)
187
What is miller fisher syndrome?
variant of Guillain-Barre syndrome
associated with ophthalmoplegia, areflexia and ataxia. The eye muscles are typically affected first
usually presents as a descending paralysis rather than ascending as seen in other forms of Guillain-Barre syndrome
anti-GQ1b antibodies are present in 90% of cases
188
What are the features of guillain barre syndrome?
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
189
CSF in guillain barre syndrome?
rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66%
190
Nerve conduction studies for guillain barre?
decreased motor nerve conduction velocity (due to demyelination)
prolonged distal motor latency
increased F wave latency
191
Management of guillain barre
IVIG first line
Plasma exchange
FVC regularly for monitoring respiratory function
192
Where is the bleed in a extradural bleed?
Bleeding into the space between the dura mater and the skull.
Features of increase cranial pressure
Often has lucid level
193
Head injury: fluctuating confusion/consciousness
Subdural
194
Features of migraine?
Recurrent, severe headache which is usually unilateral and throbbing in nature
May be be associated with aura, nausea and photosensitivity
Aggravated by, or causes avoidance of, routine activities of daily living. Patients often describe 'going to bed'.
In women may be associated with menstruation
195
Tension headache?
Recurrent, non-disabling, bilateral headache, often described as a 'tight-band'
Not aggravated by routine activities of daily living
196
Features of cluster headache?
Pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours with clusters typically lasting 4-12 weeks
Intense pain around one eye (recurrent attacks 'always' affect same side)
Patient is restless during an attack
Accompanied by redness, lacrimation, lid swelling
More common in men and smokers
197
Features of 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
198
Features of medication overuse headache?
Present for 15 days or more per month
Developed or worsened whilst taking regular symptomatic medication
Patients using opioids and triptans are at most risk
May be psychiatric co-morbidity
199
Treatment for paroxysmal hemicrania?
Indomethacin
200
Where does HSV1 encephalitis usually affect?
Temporal lobes
201
Features of HSV encephalitis?
meningitis
encephalitis
subarachnoid haemorrhage
head injury
sinusitis
glaucoma (acute closed-angle)
tropical illness e.g. Malaria
202
Investigation findings for HSV encephalitis?
CSF: lymphocytosis, elevated protein
PCR for HSV
CT: medial temporal and inferior frontal changes (e.g. petechial haemorrhages) - normal in one-third of patients
MRI is better
EEG pattern: lateralised periodic discharges at 2 Hz
203
Management of HSV encephalitis?
Aciclovir
204
Features of herpes keratitis?
red, painful eye
photophobia
epiphora
visual acuity may be decreased
fluorescein staining may show an epithelial ulcer
205
Management of herpes keratitis?
immediate referral to an ophthalmologist
topical aciclovir
206
What causes herpes zoster opthalmicus?
Varicella zoster
207
VZ: What is hutchinson sign?
Hutchinson's sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement
208
Management of herpes zoster ophthalmicus?
Oral antivral for 7-10 days
topical antiviral treatment is not given in HZO
209
Complications of herpes zodter ophthalmicus?
ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
ptosis
post-herpetic neuralgia
210
Holms tremor?
Red nucleus
211
What is a holms addie pupil?
dilated pupil
once the pupil has constricted it remains small for an abnormally long time
slowly reactive to accommodation but very poorly (if at all) to light
212
What is holms addie syndrome?
association of Holmes-Adie pupil with absent ankle/knee reflexes
213
Features of horners syndrome?
miosis (small pupil)
ptosis
enophthalmos* (sunken eye)
anhidrosis (loss of sweating one side)
214
Horners syndrome lesion according to anhidrosis?
Central lesion: Anhidrosis of the face, arm and trunk
Preganglionic: Anhidrosis of the face
Post ganglionic: NO anhidrosis
215
Central causes of horners syndrome?
Stroke
Syringomyelia
Multiple sclerosis
Tumour
Encephalitis
216
Preganglionic causes of horner's syndrome?
Stroke
Syringomyelia
Multiple sclerosis
Tumour
Encephalitis
217
Post ganglionic causes of horner's syndromes?
Carotid artery dissection
Carotid aneurysm
Cavernous sinus thrombosis
Cluster headache
218
What is Hereditary sensorimotor neuropathy (HSMN) called?
Charcot marie tooth disease
219
Mechanism of HSMN type 1?
HSMN type I: primarily due to demyelinating pathology
220
Mechanism of HSMN type 2?
HSMN type II: primarily due to axonal pathology
221
Features of HSMN?
autosomal dominant
due to defect in PMP-22 gene (which codes for myelin)
features often start at puberty
motor symptoms predominate
distal muscle wasting, pes cavus, clawed toes
foot drop, leg weakness often first features
222
Features of huntington disease?
chorea
personality changes (e.g. irritability, apathy, depression) and intellectual impairment
dystonia
saccadic eye movements
223
Gene problem in huntington's disease?
Chromome - trinucleotide repeat disorder CAG
224
Stage 1: Hypertensive retinopathy?
Arteriolar narrowing and tortuosity
Increased light reflex - silver wiring
225
Stage 2: Hypertensive retinopathy?
Arteriovenous nipping
226
Stage 3: Hypertensive retinopathy?
Cotton-wool exudates
Flame and blot haemorrhages
These may collect around the fovea resulting in a 'macular star'
227
Stage 4: Hypertensive retinopathy?
Papilloedema
228
Hypotension strokes - causes damage where?
Watershed areas
229
Risk factors of idiopathic cranial hypertension?
obesity
female sex
pregnancy
Drugs
230
What drugs cause idiopathic cranial hypertension ?
obesity
female sex
pregnancy
231
Drug causes of idopathic intracranial hypertension?
combined oral contraceptive pill
steroids
tetracyclines
retinoids (isotretinoin, tretinoin) / vitamin A
lithium
232
Features of idiopathic intracranial hypertension
headache
blurred vision
papilloedema (usually present)
enlarged blind spot
sixth nerve palsy may be present
233
Management of idopathic intracranial hypertension?
Weight loss
diuretics e.g. acetazolamide
topiramate is also used,
repeated lumbar puncture may be used as a temporary measure but is not suitable for longer-term management
surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve.
234
Features of inclusion body myositis?
typically affects older males
can affect both proximal and distal muscles
characteristically affects quadriceps and finger/wrist flexors are usually more severely affected than extensor counterparts
235
cytoplasmic inclusions on muscle biopsy
Inclusion body myositis
236
Goldstand imaging for intracranial venous thrombosis?
MRI venography is the gold standard
CT venography is an alternative
non-contrast CT head is normal in around 70% of patients
D-dimer levels may be elevated
237
Saggital sinus syndrome?
seizures and hemiplegia
parasagittal biparietal or bifrontal haemorrhagic infarctions are sometimes seen
'empty delta sign' seen on venography
238
Cavernous sinus thrombosis?
periorbital oedema
ophthalmoplegia: 6th nerve damage typically occurs before 3rd & 4th
Trigeminal nerve involvement
central retinal vein thrombosis
239
Lateral sinus thrombosis?
6th and 7th cranial nerve palsies
240
What cancer is associated with lambert eaton syndrome?
Small cell lung cancer
Breast
Ovarian
241
Antibody if lambert eaton syndrome?
antibody directed against presynaptic voltage-gated calcium channel in the peripheral nervous system.
242
Features of lambert eaton syndrome?>
repeated muscle contractions lead to increased muscle strength (in contrast to myasthenia gravis)
limb-girdle weakness (affects lower limbs first)
hyporeflexia
autonomic symptoms: dry mouth, impotence, difficulty micturating
ophthalmoplegia and ptosis not commonly a feature (unlike in myasthenia gravis)
243
Treatment for lambert eaton syndrome?
immunosuppression, for example with prednisolone and/or azathioprine
intravenous immunoglobulin therapy and plasma exchange may be beneficial
244
What artery is affected in lateral medullary syndrome?
Posterior inferior cerebellar artery.
245
Features of lateral medullary syndrome?
Cerebellar features
ataxia
nystagmus
Brainstem features
ipsilateral: dysphagia, facial numbness, cranial nerve palsy e.g. Horner's
contralateral: limb sensory loss
246
What is MELAS?
m.3243A>G mutation
Mitochondrial
247
Features of MELAS?
MELAS syndrome (mitochondrial encephalomyopathy, lactic acidosis and stroke-like symptoms)
248
Features of MELAS?
MELAS syndrome (mitochondrial encephalomyopathy, lactic acidosis and stroke-like symptoms)
249
Features of MELAS
Diabetes
Sensorineural hearing loss
Stroke-like symptoms
Retinal dystrophy
Proximal myopathy
Cardiomyopathy, arrhythmias
End stage renal failure - most often FSGS pattern on biopsy
Short stature, low BMI
250
Feature of medication overuse headache?
present for 15 days or more per month
developed or worsened whilst taking regular symptomatic medication
patients using opioids and triptans are at most risk
may be psychiatric co-morbidity
251
Management of medication overuse headache?
simple analgesics and triptans should be withdrawn abruptly (may initially worsen headaches)
opioid analgesics should be gradually withdrawn
252
Features of menieres disease?
recurrent episodes of vertigo, tinnitus and hearing loss (sensorineural). Vertigo is usually the prominent symptom
a sensation of aural fullness or pressure is now recognised as being common
other features include nystagmus and a positive Romberg test
episodes last minutes to hours
typically symptoms are unilateral but bilateral symptoms may develop after a number of years
253
Clinical course of menieres disease ?
symptoms resolve in the majority of patients after 5-10 years
the majority of patients will be left with a degree of hearing loss
psychological distress is common
254
Management of mernieres?
Inform DVLA
acute attacks: buccal or intramuscular prochlorperazine.
prevention: betahistine and vestibular rehabilitation exercises
255
Most common cause of meningitis in adults ?
Strep pneumoniae
may follow on from an episode of otitis media
256
Most common cause of menignits in elderly/ immunocompromised?
Listeria
257
Acute management of migraine?
First-line: offer combination therapy with
an oral triptan and an NSAID, or
an oral triptan and paracetamol
Second line:
offer a non-oral preparation of metoclopramide or prochlorperazine and consider adding a non-oral NSAID or triptan
258
Prophylaxis in migraines?
propranolol
topiramate: should be avoided in women of childbearing age as it may be teratogenic and it can reduce the effectiveness of hormonal
contraceptives
amitriptyline
259
Vitamin advice in migraines?
400mg riboflavin (B2) per day
260
Migraines related to menstruation?
frovatriptan (2.5 mg twice a day) or zolmitriptan (2.5 mg twice or three times a day)
261
Other prophylaxis in migraines not liscenced yet? - but neurology can prescribe?
candesartan: recommended by the British Association for the Study of Headache guidelines
monoclonal antibodies directed against the calcitonin gene-related peptide (CGRP) receptor: examples include erenumab
262
muscle biopsy classically shows 'red, ragged fibres
Mitochondrial
263
Features of mitochondrial disroders?
Leber's optic atrophy
MELAS syndrome: mitochondrial encephalomyopathy lactic acidosis and stroke-like episodes
MERRF syndrome: myoclonus epilepsy with ragged-red fibres
Kearns-Sayre syndrome: onset in patients < 20 years old, external ophthalmoplegia, retinitis pigmentosa. Ptosis may be seen
sensorineural hearing loss
264
Features of motor neurone disease?
asymmetric limb weakness is the most common presentation of ALS
the mixture of lower motor neuron and upper motor neuron signs
wasting of the small hand muscles/tibialis anterior is common
fasciculations
265
What does motor neurone disease not affect?
doesn't affect external ocular muscles
no cerebellar signs
abdominal reflexes are usually preserved and sphincter dysfunction
266
Management of motor neurone disease ?
Riluzole
prevents stimulation of glutamate receptors
used mainly in amyotrophic lateral sclerosis
prolongs life by about 3 months
Respiratory care
non-invasive ventilation (usually BIPAP) is used at night
studies have shown a survival benefit of around 7 months
Nutrition
percutaneous gastrostomy tube (PEG) is the preferred way to support nutrition and has been associated with prolonged survival
267
Neurological weakness + Anti- GM1 ?
Multifocal motor neuropathy
268
Features of multiple sclerosis ?
Visual
optic neuritis: common presenting feature
optic atrophy
Uhthoff's phenomenon: worsening of vision following rise in body temperature
internuclear ophthalmoplegia
Sensory
pins/needles
numbness
trigeminal neuralgia
Lhermitte's syndrome: paraesthesiae in limbs on neck flexion
Motor
spastic weakness: most commonly seen in the legs
Cerebellar
ataxia: more often seen during an acute relapse than as a presenting symptom
tremor
Others
urinary incontinence
sexual dysfunction
intellectual deterioration
269
Investigation fidnings of MS?
MRI:
high signal T2 lesions
periventricular plaques
Dawson fingers: often seen on FLAIR images - hyperintense lesions penpendicular to the corpus callosum
CSF:
oligoclonal bands (and not in serum)
increased intrathecal synthesis of IgG
Visual evoked potentials
delayed, but well preserved waveform
270
Treatment of acute flare MS?
IV Methylprednisolone
271
When to start DMARD therapy in relapsing remitting MS?
relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaided
272
When to start DMARD therapy in secondary progressive disease?
secondary progressive disease + 2 relapses in past 2 years + able to walk 10m (aided or unaided)
273
MS: natalizumab
antagonises alpha-4 beta-1-integrin found on the surface of leucocytes
inhibit migration of leucocytes across the endothelium across the blood-brain barrier
Used first line
274
MS: Ocrelizumab?
humanized anti-CD20 monoclonal antibody
Used first line
275
Management of spastisity in MS?
baclofen and gabapentin are first-line
276
Bladder management in MS>?
if significant residual volume → intermittent self-catheterisation
if no significant residual volume → anticholinergics may improve urinary frequency
277
MS:
Oscillopsia (visual fields appear to oscillate)
gabapentin is first-line
278
Good prognosis MS?
female sex
age: young age of onset (i.e. 20s or 30s)
relapsing-remitting disease
sensory symptoms only
long interval between first two relapses
complete recovery between relapses
the typical patient carries a better prognosis than an atypical presentation
279
Types of multi system atrophy?
1) MSA-P - Predominant Parkinsonian features
2) MSA-C - Predominant Cerebellar features
280
Features of multi system atrophy?
parkinsonism
autonomic disturbance
erectile dysfunction: often an early feature
postural hypotension
atonic bladder
cerebellar signs
281
Types of multi system atrophy?
1) MSA-P - Predominant Parkinsonian features
2) MSA-C - Predominant Cerebellar features
282
Features of myasthenia gravis?
extraocular muscle weakness: diplopia
proximal muscle weakness: face, neck, limb girdle
ptosis
dysphagia
283
Features of myasthenia gravis?
extraocular muscle weakness: diplopia
proximal muscle weakness: face, neck, limb girdle
ptosis
dysphagia
284
Associations of myasthenia gravis?
thymomas in 15%
autoimmune disorders: pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE
thymic hyperplasia in 50-70%
285
Management of myasthenia gravis?
long-acting acetylcholinesterase inhibitors
pyridostigmine is first-line
Additional:
prednisolone initially
azathioprine, cyclosporine, mycophenolate mofetil may also be used
thymectomy
286
Management of myasthenic crisis?
plasmapheresis
intravenous immunoglobulins
287
Features of multi system atrophy?
parkinsonism
autonomic disturbance
erectile dysfunction: often an early feature
postural hypotension
atonic bladder
cerebellar signs
1) MSA-P - Predominant Parkinsonian features
2) MSA-C - Predominant Cerebellar features
288
Exacerbating factors of myasthenia gravis?
penicillamine
quinidine, procainamide
beta-blockers
lithium
phenytoin
antibiotics: gentamicin, macrolides, quinolones, tetracyclines
289
Features of mytonic dystrophy?
myotonic facies (long, 'haggard' appearance)
frontal balding
bilateral ptosis
cataracts
dysarthria
myotonia (tonic spasm of muscle)
weakness of arms and legs (distal initially)
mild mental impairment
diabetes mellitus
testicular atrophy
cardiac involvement: heart block, cardiomyopathy
dysphagia
290
Genetics of myotonic dystrophy?
autosomal dominant
a trinucleotide repeat disorder
DM1 is caused by a CTG repeat at the end of the DMPK (Dystrophia Myotonica-Protein Kinase) gene on chromosome 19
DM2 is caused by a repeat expansion of the ZNF9 gene on chromosome 3
291
Difference between DM1 and DM2 myotonic dystrophy?
DM1:
Distal weakness more common
DM2 :
Proximal weakness more common
292
Features of branchial cyst?
oval, mobile cystic mass that develops between the sternocleidomastoid muscle and the pharynx
failure of obliteration of the second branchial cleft in embryonic development
293
Nerve conduction study: Axonal damage?
normal conduction velocity
reduced amplitude
294
Nerve conduction study: Demyelinating damage?
reduced conduction velocity
normal amplitude
295
Features of NF 1?
Phaecrhomcytoma
Café-au-lait spots (>= 6, 15 mm in diameter)
Axillary/groin freckles
Peripheral neurofibromas
Iris hamatomas (Lisch nodules) in > 90%
Scoliosis
296
Features of NF 2?
Bilateral vestibular schwannomas
Multiple intracranial schwannomas, mengiomas and ependymomas
297
Features of neuromyelitis optica?
Relapsing remitting CNS disorder
1. Spinal cord lesion involving 3 or more spinal levels
2. Initially normal MRI brain
3. Aquaporin 4 positive serum antibody
298
Aquaporin 4 positive serum antibody
Neuromyelitis optica
299
Management of neuromyeltis otpica?
immunosuppressant e.g. with anti-CD20 agent rituximab)
300
Treatment of normal pressure hydrocephalus?
urinary incontinence
dementia and bradyphrenia
gait abnormality (may be similar to Parkinson's disease)
301
Wernicke's is caused by thiamine deficiency
Wernicke is caused by thiamine deficiency
302
Middle cerebral artery lesion?
Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia
303
Anterior cerebral artery lesion?
Contralateral hemiparesis and sensory loss, lower extremity > upper
304
Posterior cerebral artery lesion?
Contralateral homonymous hemianopia with macular sparing
Visual agnosia
305
Weber syndrome?
Posterior cerebral arttery supply to midbrain
Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity
306
Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome) lesion?
Ipsilateral: facial pain and temperature loss
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus
307
Anterior inferior cerebellar artery (lateral pontine syndrome)?
Symptoms are similar to Wallenberg's (see above), but:
Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity
Ipsilateral: facial paralysis and deafness
308
Lyme disease CSF?
results are similar to the 'typical' bacterial picture with low glucose and high protein, however in Lyme disease we would expect a lymphocytic pleocytosis
If see first degree heart block + focal neurological defects think lyme
309
Absolute Contraindications for 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
310
Relative contraindications for thrombolysis?
- Concurrent anticoagulation (INR >1.7)
- Haemorrhagic diathesis
- Active diabetic haemorrhagic retinopathy
- Suspected intracardiac thrombus
- Major surgery / trauma in the preceding 2 weeks
311
Anterior inferior cerebellar artery (lateral pontine syndrome)?
Symptoms are similar to Wallenberg's (see above), but:
Ipsilateral: facial paralysis and deafness`
312
MS and pregnancy?
Relapse is less common in pregnancy
Increase 3-6 months post partum
Then return to normal rates
313
When can candesartan be considered for migraine prophlaxis
If others are contraindicated
314
Management of haemorrhagic transofrmation stroke?
Thrombosis + haemorrhage
Manage with IV heparin
If haemorrhage dose occur, can be as easily reversed as possible
315
Migraine prophylaxis - avoid in young women?
Topiramate
316
Adenoma sebaceum?
Tuberous sclerosis
317
Starting SSRI in young person, when should you review again?
Within one week
318
Maccular star pattern?
Hypertensive retinopathy
319
Continued seizure after lorazepam, and phenobarbitol?
Anaesthesia with thipentate
320
Urgent management acute glaucoma?
IV analgesia and antiemetics, lie patient supine.
Topical beta blockers and steroids.
IV acetazolamide.
After initial treatment, pilocarpine will induce meiosis and open the angle. This is initially ineffective due to pressure induced ischaemic paralysis of the iris.
Iridotomy 24-48 hours after intra-ocular pressure is controlled to prevent recurrence.
321
Headache + St Elevation?
Subarachnoid haemorrhage
322
Increase intracranial pressure + sensory symptoms ?
Think cerebral venous thrombosis
323
IN non-traumatic SAH, what must be done to identify source?
CT angiogram - to look for anneurysm
324
What is malignant MCA syndrome?
occurs in younger patients who have suffered an extensive ischaemic stroke
. After infarction the brain swells. As younger brains are likely to have less atrophy, there is less room for expansion. Subsequently, intracranial hypertension develops. This typically presents 48 hours after onset of stroke with reduced conscious level.
325
How is malignant MCA syndrome managed?
Decompressive carniotomy
326
meningeal enhancement, thickening and shallow subdural haematoma
Features from low pressure headahce
e.g. lumbar puncture headache
327
Grossly abnormal amonia + antiepileptic?
valproate-associated hyperammonaemic encephalopathy (VHE).
328
Management of adenoma sebaceum (angiofibromas):
Sirolimus
329
Features of superficial siderosis?
sensorineural hearing loss
ataxia
dementia
anosmia
anisocoria ( unequal pupils)
330
How to investigate superfical siderosis?
MRI
331
MS + new multiple confluent lesions in the parietooccipital and right motor white matter areas as well as the left occipital area, with no mass effect or enhancement
JC virus serology
Causes PML
332
Difference between paroxysmal hemicrania and cluster headache?
Chronic paroxysmal hemicrania is characterised by multiple (5+) short (5-30 min) headaches centered around the eye. CPH headaches are shorter and more frequent than cluster headaches
Clust headahce last 1-3 hours
333
Basilar migraine?
four episodes of loss of consciousness within the past 4 weeks. She denies palpitations or chest pain but reports sudden onset binocular black dots in visual fields, occasional flashing lights, dysarthria and hearing loss, all of which resolves after about 60 minutes. She is unsure about the relevance of an occipital headache, onset with frequency of about three times per week for the past year. She denies any limb weakness, altered sensation or facial droop. She has no past medical history or family history of epilepsy. Your neurological examination, including fundoscopy is unremarkable. An EEG is unremarkable.
334
Guillain barre + eye stuff ?
Miller Fisher syndrome
Anti GQ1b
335
Falling kidney function + dopamine agonist
Retroperitoneal fibrosis
336
sensory loss in her upper limbs at the level of C5-C7. She has spastic paraparesis, Romberg +ve indicating loss of proprioception in her lower limbs.
Cervical myelopathy
337
Causes of cervical myelopathy?
Cervical cord tumours
ossification of the posterior longitudinal ligament
Trauma
Cervical degenerative changes (spondylosis)
Cervical degenerative disc disease
338
Motor deltoid?
C5, C6
339
Motor bicep
C5 C6
340
Motor serratus anterior
C5, 6, 7
