Neurology (Z=>F) Flashcards
1
Q
Describe myelin in terms of resistance and capacitance
A
- Increase resistance
- Decrease capacitance (ability to store charge)
2
Q
Is myelin found in cells of CNS or PNS?
A
both!
3
Q
What is myelin sheath made out of ?
A
made of lipid-rich substance (mainly lipoprotein)
4
Q
What is Multiple sclerosis (MS)?
A
Chronic and progressive condition causing demyelination and axonal loss of neurones of the CNS
5
Q
Does MS affect CNS or PNS?
A
Just CNS. PNS not affected.
6
Q
MS Epi?
A
- Young adults (20 - 40)
- more common in women
7
Q
MS pathophysiology/aetiology?
A
Autoimmune process
- Inflammation around myelin and infiltration of immune cells => damage to myelin => affect electrical conduction along the nerve
8
Q
How to patients often present to health services with MS?
A
present with an “attack” (e.g. episode of optic neuritis) and MRI would likely show other lions of demyelination throughout CNS
9
Q
How does early on MS compare to later on?
A
Early disease: demyelination may occur => symptoms resolve
Later: remyelination is incomplete => symptoms gradually become worse
10
Q
What are those buzzwords to describe MS diagnosis? what does it mean?
A
Lesions disseminated in time and space
- lesions change location over time => different nerves are affected => symptoms change over time
11
Q
MS RF? (5)
A
- FHx
- EBV
- Living further away from the equator
- Smoking
- Obesity
12
Q
Signs and symptoms of MS. onset? duration?
A
- Usually progress over >24 hrs
- Symptoms usually last days- weeks
(then improve)
13
Q
What is optic neuritis ?
A
(most common MS presentation)
demyelination of optic nerve => unilateral reduced vision developing over hours-days
14
Q
Optic neuritis symptoms (4)
A
- Pain on eye movement
- Vision loss
- Central scotoma
- Impaired colour vision
(unilateral)
15
Q
Name some MS symptoms
A
Can affect anywhere!
- Central: fatigue, cognitive impairment, depression
- Visual: nystagmus, optic neuritis
- Speech: dysarthria
- Throat: dysphagia
- MSK: weakness, spasms, ataxia
- Sensation: pain, numbness, tingling
- Bowel: incontinence, diarrhoea, constipation
- Urinary: incontinence, frequency, retention
16
Q
What is the first episode of demyelination + neuro signs + symptoms called? why this not MS?
A
Clinically isolated syndrome
- Cannot be diagnosed as MS with just 1 episode
17
Q
Describe relapsing remitting MS disease course. How is it subdivided?
A
(most common)
- episodes of disease followed by recovery
- active/not active
- worsening/ not worsening
18
Q
what does active or no active MS mean?
A
Active: symptoms developing or new lesions appearing on MRI
19
Q
What does worsening or not worsening MS mean?
A
Worsening: overall worsening of disability over time
20
Q
What is secondary progressive MS?
A
initially relapsing-remitting but now progressive worsening of symptoms with incomplete remissions
21
Q
What is primary progressive MS?
A
worsening of disease + neurological symptoms without initial relapses + remissions
22
Q
How do you get MS diagnosis? what criteria?
A
- Based on clinical picture
- McDonald criteria
- Investigations can help
23
Q
What would MRI and LP find in MS?
A
MRI: demyelinating lesions
LP: oligoclonal bands in CSF
24
Q
MS management - 3 general bands and what do they mean?
A
- Disease modification: disease modifying drugs => induce long term remission
- Treating relapses: Steroids (prednisolone)
- Symptomatic treatment: exercise, Neuropathic pain, depression, incontinence, spasticity
25
What is a stroke?
Acute onset of neurological symptoms of presumed vascular origin
26
What causes an ischaemic stroke? + 4 examples
ischaemic + infarction: caused by disruption to blood supply (thrombus, stenosis, shock (reduced BP), vasculitis)
27
What causes haemorrhage stroke?
haemorrhage stroke: caused by vascular rupture => intraparanchymal/SAH/...
28
What is a TIA?
transient ischaemic attack
- Transient neurological dysfunction secondary to ischaemia without infarction
29
Describe presentation of a stroke (5)
- Asymmetrical
- Sudden weakness of limbs
- Sudden weakness of facial muscles
- Sudden onset dysphasia
- Sudden onset visual or sensory loss
30
Stroke RF (8)
- CVD (angina, MI, PVD)
- Prev stroke/TIA
- AF
- Hypertension
- DM
- Smoking
- Vasculitis
- Haemophilia
- COCP
31
What screening tool is used for stroke? what does it stand for?
FAST
- Face
- Arms
- Speech
- Time (act fast and dial 999)
32
What risk score is associated with stroke? tell more - what is it actually used for? what does it stand for?
ABCD2 score: Risk of stoke in next 24 hours
- Age (>60)
- BP (>140/90)
- Clinical features
- Duration
- Diabetes
33
Patient presents with visual defects and perception disorders - what blood vessel effected?
Posterior Cerebral artery
34
Patient presents with sudden onset aphasia. what has likely caused this? be specific
ischaemic stroke
left (or dominant) brain hemisphere - Middle cerebral artery
35
patient presents with weakness and sensory loss of the left sided upper limb. what is this? what affected?
stroke
right ACA/MCA
36
Describe the management of stroke. starting from patient admitted to A&E?
- Admit patient + exclude hypoglycaemia (blood glucose)
- Immediate head CT
- Aspirin 300mg stat (if CT head excludes primary intracerebral haemorrhage). continue aspirin for 2 weeks
- Thrombolysis (alteplase)
- Consider surgical intervention - thrombectomy
37
Management of TIA
- Start aspirin 300mg daily
- ABCD2 score to determine wither seen in 24 hrs or next 7 days
- secondary prevention for CVD (atorvastatin)
38
ongoing management of stroke?
- secondary prevention: clopidogrel (75mg once daily), atorvastatin (80mg), carotid stenting (if carotid US shows stenosis)
- Treat modifiable RF (smoking, hypertension, DM)
39
layers of the meninges (out => in)
Dura => arachnoid => pia
40
What is GCS? min score? categories?
Glasgow Coma Scale
- min score 3/15
- Universal tool to assess consciousness: based on eyes, verbal + motor response
41
What is subdural haemorrhage usually caused by?
rupture of bridging veins (between dura + arachnoid mater)
42
How would subdural haemorrhage look on CT?
- Cresent/banana
- Not limited by cranial sutures
43
Epidemiology for subdural haemorrhage? Why?
elderly + alcoholics
- bridging veins become weaker and more atrophic
44
How does extradural haemorrhage look on CT?
- Biconvex/lemon on CT
- Limited by cranial sutures
45
describe SAH? usually caused by what?
bleeding into subarachnoid space (where CSF is)
- usually caused by ruptured cerebral aneurysm
46
SAH presentation
sudden onset occipital headache (thunderclap) often during strenuous activity (lifting weights, having sex)
47
SAH RF?
- Hypertension, aneurysm, cocaine use, smoking, excessive alcohol
- Cocaine + sickle cell anaemia
48
SAH investigations and what would they show?
CT: bright white bleed
LP: CSF will show raised Red cell count and xanthechromia (yellow colour due to bilirubin)
Angiography (CT or MRI): once SA is confirmed to locate the bleed
49
SAH management? (4)
- Intubation and ventilation
- Surgical intervention, repair vessel to preven re-bleeding
- Nimidipine (CCB) to prevent vasospasm
- LP or shunt insertion to preven hyrdocephalus
50
What is motor neurone disease?
Umbrella term that covers variety of specific diagnosis
- progressive + ultimately fatal condition where motor neurones stop working
51
Describe sensory symtoms in MND
none! no impact on sensory neurones so patient will experience no sensory symptoms
52
MND pathophysiology
progressive degeneration of U + LMN (sensory neurones spared)
- aetiology not fully understood
53
MND presentation? patient speak ?
- Weakness of muscles throughout body affecting limbs, face, trunk, speech
- patient speak: clumsiness, dropping things, tripping over, slurred speech
54
signs of LMN disease? (4)
- muscle wasting
- decreased tone
- fasciculations
- decreased reflexes
55
Signs of UMN disease? (3)
- increased tone/spasticity
- risk (increased) reflexes
- upping plantar reflex
56
how is MND diagnosis made?
clinical presentation + exclude other conditions
57
MND management?
No way to halt or reverse progression of disease
- Riluzole can slow the progression of disease
- Symptomatic + supportive management
58
In general, for neuro syndromes, do signs or symptoms appear first? Which 2 exceptions are there to this rule?
Symptoms appear before signs except for...
- Myelopathy
- Peripheral neuropathy
59
What is a secondary brain problem?
Where the pathological process disrupting brain function is outside the brain
60
How many vital signs are there? what are they?
1) Pulse
2) BP
3) Temp
4) Respiratory rate
5) Oxygen saturation
61
Explain what usually causes a fixed and dilated pupil? go into detail
compression of the parasympathetic fibres on the outside of the third nerve (as it passes over the apex of the patriots part of the temporal bone (McDonalds burger nerve))
- Due to life-threatening brain swelling process
62
What are the 3 sections to the Glasgow Coma Scale? how many points to each one?
- Best motor response (6)
- Best verbal response (5)
- Best eye opening response (4)
63
What do you have to do before performing a lumbar puncture?
ensure prior appropriate cranial imaging (CT head)
64
What do you have to do before scanning (radiology) a patient?
Make sure the patient is stable
- Airway secure, vital signs are normal (resuscitation is complete and respiratory support is appropriate)
65
How many cranial fossa are there
3
- anterior, middle and posterior
66
What separates the anterior and middle cranial fossae?
lesser win of sphenoid
67
What separates the middle and posterior cranial fossae? Name in important structure that runs over this
- petrous part of temporal bone and foramen magnum
- CNIII runs over apex of petrous temporal bone => prone to getting squished (McDonalds burger)
68
Which demential is associated with features of Parkinsonism
Demential with Lewy bodies
69
What is the first line option for most forms of epilepsy? except for which type of seizure?
Name an important SE
Sodium valproate
- First line option for most forms of epilepsy (except focal seizures)
- SE: teratogenic !
70
What medication is first line for focal seizures ? name a SE
Carbamazepine
- SE: agranulocytosis
71
What is status epileptics?
- seizures lasting more than 5 minutes
- or more than 3 seizures in one hour
72
Management of status epileptics in the hospital? think it through
ABCDE approach
- Secure the airway
- Give high-cons oxygen
- Assess cardiac and respiratory function
- Check blood glucose levels
- Gain IV access (insert a cannula)
- IV lorazepam (repeated 10 mins if seizure continues)
- IV phenobarbital if seizure persist
73
What causes neuropathic pain (pathophysiology) ?
Cuased by abnormal functioning of the sensory nerves => delivering abnormal and painful signals to the brain
74
What is Parkinsons disease? caused by?
Progressive reduction of dopamine in the basal ganglia => movement disorders
75
Parkinsons disease triad of symptoms?
- Resting tremor
- Cogwheel rigidity
- Bradykinesia
(classically asymmetrical)
76
Describe (vague) distribution of symptoms in PD:symmetrical or assymtetrical ?
- Asymmetrical (one side is affected worse than the other)
77
What is the role of basal ganglia? explain how this links to PD?
- Basal ganglia responsible for habitual movements (walking, looking around, controlling voluntary movements)
- Substantia nigra produces neurotransmitter called dopamine
- PD: gradual + progressive fall I production of dopamine form substantia nigra
78
Describe the tremor in PD: frequency? symmetry? effect of alcohol?
Pill rolling tremor (4-6 Hz (per second))
- asymmetrical
- No change with alcohol
79
What would cause a PD tremor to improve? to get worse?
- More pronounced when rising, worse if patients is distracted (asked to do task with other hand)
- Improves with voluntary movement
80
Describe the tremor in benign essential tremor: frequency? Symmetry? effect of alcohol?
- Fine tremor:5-8 Hz (faster than PD)
- Symmetrical
- Improves with alcohol
81
What would cause a benign essential tremor to improve? worsen?
- Improves with rest, and alcohol, goes away when asleep
- Worsens with intentional movement, tired/stress/caffeine
82
Describe cogwheel rigidity? associated with what condition?
Associated with parkinsons disease
- Rigidity is resistance to passive movement of a joint
- You would feel the tension in the joint and movement in small increments (like little jerks)
83
What is bradykinsia? how would it present?
Small + slower movements
- Smaller handwriting (micrographia), shuffling gait, difficulty initiating movement, difficulty turning around, reduced facial movements
84
Other than the main triad, name other symptoms of parkinsons disease
- Depressions
- Insomnia
- amnesia (inability to smell)
- Postural instability
- Memory/cognitive problems
85
How is a diagnosis of PD made?
Clinical diagnosis based on symptoms and examination
86
What 2 drugs are the main management for PD? How do they work?
- Levadopa (Synthetic dopamin to boost dopamine levels)
PLUS
- carbidopa (peripheral decarboxylase inhibitor: stops levodopa being broken down before gets to brain)
87
SE of PD drug treatment ? which drug ?
(levodopa SE)
excessive motor activity: dystonia, chorea, athetosis
88
What is a benign essential tremor?
Common condition associated with older age: fine tremor affecting voluntary muscles
89
Differential for a tremor (6)
- Parkinsonism
- MS
- Huntingtons chorea
- Hyperthyroidism
- Fever
- Medications (antipsychotics)
90
features of a benign essential tremor?
- Fien tremor
- Symmetircal
- More prominent on voluntary movement
- Worse when tired/stressed/caffeine
- Improves with alcohol
- nascent during sleep
91
Management of being essential tremor?
no definitive treatment
(lifestyle, caffeine, sleep, stress)
92
What are brain tumours ?
they are abnormal growths in the brain (benign or malignant)
93
How might brain tumours present ? kinda categories of presentation
- Asymptomattic
- Rocal neurological symptoms
- Sign + symptoms of raised ICP
94
What is an ocular sing of raised ICP? explain what causes this ?
papilloedema (swelling of the optic risk) on fundoscopy
- Due to pressure behind optic nerve
95
what surrounds the optic nerve ?
the meninges
96
Causes of raised ICP? (4)
- brain tumour
- IC haemorrhage
- Idiopathic intracranial hypertension
- Abscesses of infection
97
Riased ICP presentation ?
- headache
- other features: change in mental state, confused/drowsy, visual field defects, seizures
98
describe the headache associated with raised ICP? when worse ? (5)
- constant
- Worse at night (nocturnal)
- Worse in morning
- When when coughing/straining/leaning forward
- Vomiting
99
What types of brain tumour are there? (4)
- Secondary metastases
- Glioma (most common primary)
- meningioma
- pituitary tumours
100
what are the most common secondary brain metastasis ? (4)
- Lung
- Breast
- Renal cell carcinoma
- Melanoma
101
what are gliomas ? name some ? which is the most common type ?
tumours of the glial cells
(most common)
- astroglioma
- oligodendroglioma
- ependymoma
(least common)
102
What hormone effects can a pituitary tumour have? name the hormone and the condition associated (4)
- Acromegaly (high GH)
- Hyperprolactinaemia (high prolactin)
- Cushing's disease (high ACTH)
- Thyrotoxicosis (high TSH)
103
treatment of pituitary tumours ?
trans-sphenoidal surgery
104
Management of brain tumours overall ?
depends on type _ grade
- Palliative, chemo, radiotherapy, surgery
105
What is a facial nerve palsy ?
Isolate dysfunction of the facial nerve (CN VII)
106
facial nerve palsy presentation ?
usually present with unilateral facial weakness
107
What is facial nerve function ? (all of them)
- Motor: muscles of expression, stapedius (inner ear)
- Sensory: Tast (anterior 2/3 of tongue)
- Parasympathetic: supply submandibular + sublingual salivary glands + lacrimal gland
108
Why do you need to differentiate between upper and lower motor neurone lesion (facial nerve)? what would general management for each be ?
- UMN: refer urgently with suspected stroke
- LMN: manage in community
109
Describe the facial movements in an UMN lesion ?
forehead will be spare + patient can move forehead as forehead is controlled by UMN from BOTH sides
110
Describe the facial movements in a LMN lesion ?
forehead no spared => patients cannot move forehead on affected side
111
What type of motor neurone involved in a bells palsy ?
LMN
112
what is bells palsy ?
idiopathic, unilateral LMN facial nerve palsy
113
what is recovery from bells palsy like ?
most patients revere in several weeks to a yr (may still have some residual weakness)
114
bells plays management ?
- <72 hrs: prednisolone (50mg for 10 days)
- lubricating eye drops for eye on affected side
115
What is Ramsay-hunt syndrome ? associated with what ?
VZV causing unilateral LMN facial nerve palsy
116
person present with painful + tender vesicular rash in the ear canal and a facial nerve palsy. What is this ?
Ramsay-Hunt syndrome
(VZV shingles of the face - facial nerve)
117
Ramsay hunt syndrome treatment
prednisolone + aciclovir
118
What is neuropathic pain ?
caused by abnormal functioning of the sensory nerves delivering abnormal + painful signals to the brain
119
name some conditions that could cause neuropathic pain ?
- Post-herpetic neuralgia from shingles
- MS
- Diabetic neuralgia
- Trigeminal neuralgia
120
Describe the pain/sensation in neuropathic pain ?
- burning, tingles, pins+needles, electric shocks
121
Management of neuropathic pain ? exception ?
usually amytripyline
- Carbamazepine is recommend for trigeminal neuralgia
122
name the primary headaches ?
- tension
- Migraine
- Cluster
123
differential diagnosis for a headache (12)
- Primary (tension, migraine, cluster)
- sinusitis
- GCA
- Glucoma
- ICH
- SAH
- Hormonal headache
- Drug indiced
- Trigeminal neuralgia
- raised ICP
- Brain tumours
- Encephalitis/meningitis
124
(headache red flag)
Hx of headache +
- fever, photophobia or neck stiffness ? (2)
meningitis or encephalitis
125
(headache red flag)
Hx of headache +
- New neurological symptoms ? (3)
- haemorrhage
- Malignancy
- Stroke
126
(headache red flag)
Hx of headache +
- dizziness (1)
stroke
127
(headache red flag)
Hx of headache +
- visual disturbance ? (2)
- Temporal arteriis
- Glaucoma
128
(headache red flag)
Hx of headache +
- sudden onset occipital headache ? (1)
SAH
129
(headache red flag)
Hx of headache +
- Worse on coughing or straining ? (1)
raised intracranial pressure
130
(headache red flag)
Hx of headache +
- Postural, worse on staining, lying or bending over ? (1)
raised intracranial pressure
131
(head ache red flag)
Hx of headache +
- vomiting (2)
- raised ICP
- Carbon monoxide poisoning
132
(headache red flag)
Hx of headache +
- history of trauma
intracranial haemorhage
133
(headache red flag)
Hx of headache +
- Pregnancy
pre-eclampsia
134
in a patient presenting with a headache, what does fundoscopy look for and what would this indicate ?
- looks for papilloedma
- indicate raised ICP due to being tumour, benign intracranli hypertension, intracranial bleed)
135
Tension headache, describe the:
site, character, severity, associated symptoms, timing ?
- Site: bilateral, bandlike accrsos forehead
- Character: pressing, tightening
- Severity: mild or moderate, not disabling
- Associated symptoms: stress, depression, dehydrated, no N&V, no photophobia
- Timing: 30 min - 7 days
136
What is a secondary headache ?
similar to tension bt with a clear cause
- Underlying medical condition
137
what is sinisutus ?
headache associated with inflammation in ethmoidal/maxillary/frontal/sphenoidal sinuses
- tender over the affected areas
138
What in an analgesic headache ? which drug associated with
caused by long term analgesic use (codeine, tramadol)
139
Analgesic headache Management ?
analgesia withdrawal
140
what is hormonal headache ? what hormone ?
related to (low) oestrogen => generic non-specific tension like headache
141
whe likely to get hormonal headache ?
lower oestrogen
- 2/3 days beofre period
- around menopause
- start of pregnancyhor
142
hormonal headache mangment ?
COCP can improve symptoms
143
what is trigeminal neuralgia ? associated with what ? what type of pain is it ?
unilateral (90%) intense facial pain lasting second - hrs
- electricity-like shooting pain
- associated with MS
- neuropathic pain
144
name the trigeminal branches ?
- V1: opthalmic
- V2: maxillary
- V3: mandibular
145
trigeminal neuralgia treatment ?
carbamazepine
(different to most other neuropathic pain which is treated with amitriptyline)
146
What is a migraine ?
complex neuro condition that causes headache (no pathophysiology found)
147
what are the 4 types of migraine ?
- Migraines without aura
- Migraines with aura
- Silent migraine (aura, no headache)
- Hemiplegic migraine
148
Migraine: describe the site? character? severity? associated features? timing?
- Site: unilateral (often bilateral)
- Character (Pulsating/throbbing)
- Severity: Moderate or severe, disabling (interferes with ability to perform)
- Associated features: Nausea, vomiting, photophobia, photophobia
- Timing: attacks last hours to days (4-72hrs)
149
What is a migraine with aura ? describe
aura: visual changes associated with migraine
- Sparks in vision, blurring, lines, loss of visual fields
150
what is a hemiplegic migraine? symptoms? what is it similar to ?
typical migraine symptoms + hemiplegia, ataxia, changes in consciousness
- Can mimic a stroke so need to exclude this
151
what is hemiplegia ?
unilateral weakness of the limbs
152
Migraine triggers ? (6)
- stress
- bright lights
- strong smells
- Certain foods (cheese, chocolate)
- Dehydration
- Menstruation
153
What are the 5 stages of migraine ? duration of each stage ?
- Prodromal (<3 days)
- Aura (<60 min)
- Headache (4-72 hrs)
- Resolution
- Prostdromal
154
Acute management of a migraine ?
- Acute: paracetamol/NSAIDs, triptans (50mg sumatriptan as soon as headache starts)
155
Long-term management of migraine ?
Prophylaxis: propanolol (first line I think), amitriptyline
156
What is Huntington's chorea ? what inheritance ?
it is an autosomal dominated genetic condition that causes progressive deterioration in the nervous system
157
when do symptoms start in Huntington's chorea ?
usually asymptomatic until symptoms begin around 30-50
158
what type of genetic mutation is huntingtons chorea ? why is this relevant ? what 2 things does this cause ?
trnucleotide repeat disorder => anticipation => earlier age onset + increased severity of disease
159
huntingtons chorea presentation - what comes first ? followed by what ?
progressive worsening of symptoms
- starts with cognitive/psychiatric/mood problems
- followed by movement disorders
160
describe the movement disorders associated with huntingtons disease ? (4)
- Chorea (involuntary abnormal movements)
- Eye movement disorders
- speech difficulties (dysarthria)
- swallowing difficulties (dysphagia)
161
how is huntingtons disease diagnosed ?
genetic testing + pre/post test counselling
162
what is the manamgnet of huntingtons chorea ?
now ay to stop or slow progression
- SLT: for speech + swallowing
- genetic counselling
- advance directives
- End of life management
- Medical
163
what medications could be used to suppress the disordered movements associated with huntingtons disease ? (2) what type of drug
- antipsychotics (olanzipine)
- benzodiazepines (diazepam)
164
what is the prognosis of HD ? let expectancy
life expectancy is 15-20 yrs after onset of symptoms
165
what is often the cause of death in huntingtons disease ? (2)
- Respiratory disease (pneumonia)
- suicide
166
cluster headache: describe the site? character? severity? associated features? and timing?
Site: unilateral
Character: excruciating, stabbing
Severity: very severe
Associated features: red+swollen eye, pupil constriction, lid drooping, lacrimation
Timing: attacks last 15 min - 3hr
167
why are cluster headaches called cluster headaches ?
come in clusters of attacks + then disappear for a while
168
Treatment of cluster headaches: acute (2) and long term (2) ?
- Acute: triptans (sumatriptan), high flow 100% oxygen
- prophylaxis: verapamil, prednisolone (short term to break up cluster of attacks)
169
what is typical person to present with cluster headache ?
30-50 years old male smoker
170
What is myasthenia gravis ? What makes it better/worse ?
autoimmune condition causing muscle weakness that gets progressively worse with activity and improves with rest
171
with what other condition does myasthenia gravis have a strong link with
thyromas (tumours of thymus gland)
172
myasthenia gravis pathophysioloy ?
acytlcholin receptor antibodies (autoantibodies) produce by immune system bind to post-synaptic NMJ receptors => block receptors => prevent EACh from being able to trigger muscle contraction => less effective stimulation of muscle with increased activity
173
myasthenia gravis presentation ? variation throughout the day ? which muscles most affected ?
vary form to mild to life threatening, weakness gets worse with use and improves with rest, worst at end of day
- Mostly affects proximal muscles of head + neck
- diplopia, ptosis, difficulty swallowing, fatigue chewing, slurred speech
174
what could you do to spot myasthenia gravis symptoms on examination ?
reptile exercises to induce fatigue (repetitive blinking)
175
myasthenia gravis diagnosis ? (2)
- test for relevant antibodies: ACh receptor antibodies
- single fibre electromyography
176
myasthenia gravis treatment ? (3) how does each work ?
- Reversible acetylcholinesterase inhimitors (increase amount of ACh in NMJ)
- Immunosuppression (suppress Ab production)
- Thyrectomy
177
complication of myasthenia gravis ? often triggered by what ? and management ?
myasthenia crisis
- Life threatening acute worsening of symptoms (often triggered by RTI) => resp failure
- May require intubation + ventilation, IVIg
178
What is Guillain barre syndrome ? affects CNS or PNS ?
It is an acute paralytic polyneuropathy affecting the PNS
179
what is Guillain barre syndrome usually caused by ? examples (3)
usually triggered by infection
- campylobacter jejuni
- Cytometaloverus
- EBV
180
Guillain barre syndrome pathophysiology ? what is the fancy term for this process
molecular mimicry
- B cells make antibodies agains antigens on pathogen => these also happen to match proteins on myelin sheath or nerve axon => nerve damage (neuropathy)
181
Guillain barre syndrome presentation ?
symmetrical ascending weakness
- Reduced reflexes (as it is a peripheral neuropathy)
- Peripheral loss of sensation of neuropathic pain
182
Guillain barre syndrome diagnosis?
clinical (supported by Brighton criteria
- could do nerve conduction studies of LPw
183
hat would be seen on LP in Guillain barre syndrome
high protein with normal cell count + glucose
184
Guillain barre syndrome management ? (3)
- IVIg
- Supportive care
- VTE prophylaxis (dlateparin)
185
Charcot-marie tooth presentation ? (4)
- peripheral neuorpathy
- high foot acrches
- reduced tendon reglexes
- Inverted champagne bottle legs
186
charcot-marie tooth inheritance pattern ?
autosomal dominant
187
causes of peripheral neuropathy ?
ABCDE
- Alochol
- B12 deficiency
- Charcot-marie tooth
- Diabetes
- Every vasculitis
188
what is neurofibromatosis ?
genetic condition causing neuromas (benign nerve tumours)
- benign but can still cause neurological + structural problems
189
what is the more common type of neurofibromatosis ? what inheritance type is this ?
type 1 - autosomal dominant
190
neurofibromatosis diagnosis
clinical
- CRABBING criteria (2/7 required)
191
neurofibromatosis management ?
no treament
- treat complicaitons
192
neurofibromatosis complications ?
- migraines
- epilepsy
- renal artery stenosis (=> hypertension)
193
patient presents with bilateral acoustic neuromas ? what disease does this indicate ?
neurofibromatosis type 2
(hearing loss, tints, vertigo)
