Neurology Flashcards
What are first line treatments for neuropathic pain? (incl. drug class)
amitriptyline - TCA
duloxetine - SNRI
gabapentin - antiepileptic (blocks Ca2+ channels to inhibit release of glutamate from pain nerve endings)
pregabalin - antiepileptic (-II-)
(monotherapy!)
PAGD - don’t want to get PAGeD about neuropathic pain
What is neuropathic pain?
pain which arises following disruption or damage of the nervous system
what are some causes of neuropathic pain?
diabetic neuropathy
post-herpetic neuralgia
trigeminal neuralgia
prolapsed intervertebral disk
Defective downward gaze and vertical diplopia - which cranial nerve is affected?
CN IV
Between which layers is the bleed in a subdural haemorrhage?
damage to the bridging veins between the cortex and the venous sinuses
Name a diuretic that can cause gynaecomastia and explain how
Spironolactone (spironoLACTone)
It competitively inhibits the binding of dihydrotestosterone (DHT) to androgen receptors
-> leading to a decrease in testosterone levels and an increase in estrogen levels
-> This hormonal imbalance results in the development of breast tissue enlargement in men.
Characteristic presentation of clostridium botulinum infection
IVDU/eating contaminated (canned) food with descending paralysis, diplopia and bulbar palsy
Spreading of reflexes
- this is an abnormal sign that can be seen on neurological examination
- when you elicit a reflex, a different muscle twitches too
Sx of MND
Presentation:
- onset usually age 50-70
- asymmetric weakness in hands/feet
- onset tends to be focal, distal and asymmetrical; progresses in a segmental fashion from one limb to the other.
- initial presentation is highly variable
- atypical/non-specific symptoms at presentation: subtle vocal changes
Life-threatening sx as the condition progresses:
- respiratory impairment
- dysphagia
Age of onset of MND + gender
50-70
more common in males (2:1)
Other names for MND
Amyotrophic lateral sclerosis (ALS) is often used synonymously (although you could also say that ALS is a subtype of MND)
Lou Gehrig’s disease
what does ALS stand for?
amyotrophic lateral sclerosis
prognosis of MND
Most patients die within 3-5 years
30% have a chance of living longer
How is MND diagnosed?
MND is a clinical diagnosis -> hx and clinical examination showing UMN and LMN signs
there is constant disease progression
there may be an element of cognitive impairment
What is the split hand sign and what condition is it seen with?
wasting pattern of the hands in which the muscles of the thenar eminence atrophy due to degeneration of the lateral portion of the anterior horn of the spinal cord.
Muscles of the hypothenar eminence are spared.
-> associated with MND (relatively specific)
-> can also be a lesion of the ulnar nerve (exclude this first)
What form of dementia is associated with MND/ALS?
frontotemporal dementia
Ix in ?MND
- MRI brain and spinal cord to exclude other causes
- EMG supports the diagnosis (shows presence of denervation) - can also see EMG changes of the tongue
- nerve conduction studies are usually normal but can show a reduction in motor nerve conduction amplitudes)
Management of MND
- supportive (there is no cure)
- see in MND specialist clinic
- MDT: includes PT/OT, Psychology, SALT, neurologist - may need noninvasive respiratory support, symptom management (e.g. cramps, spasticity, pain), walking aids, feeding tubes etc.
- consider the carer(s)
Medicines:
- Rilouzole - glutamate receptor antagonist in the CNS, prolongs survival and slows functional decline by about 3 months (-> rilouzole rilly helps Lou Gehrig’s) - check liver enzymes
What is the first line treatment of ocular myasthenia gravis?
long acting ACh esterase inhibitor
e.g. pyridostigmine
What are Broca’s and Wernicke’s areas for? What happens in Broca’s and wernicke’s aphasia?
Broca’s: Producing speech
-> B’s aphasia: Cannot speak fluently, is very effortful and halting; understands speech and can read;
->classically caused by lesions affecting the frontal lobe (think: what you say makes up who you are -> frontal lobe)
Wernicke’s: Understanding & processing speech
-> W Aphasia: speaks, however the content is non-sensical. issues with reading and repeating what was said.
-> Associated with lesions in the posterior superior temporal gyrus
B= broken speech
W= what? struggles understanding
Pyridostigmine MoA and indications
long-acting ACh esterase inhibitor
Used in:
- myasthenia gravis
what is myasthenia gravis?
an autoimmune condition affecting the NMJ
most commonly with antibodies against the ACh R
(but can be other postsynaptic antibodies)
signs and symptoms of myasthenia gravis
- diplopia
- muscle weakness
- ptosis
- blurred vision
- sx worsening after repetition of movements / worse in evening
- difficulty standing from chair/brushing hair/climbing stairs.
- bulbar muscle involvement: difficulty chewing, swallowing, dyspnoea
- often eye muscle movement issues initially, then involvement of larger muscles.
What is a myasthenic crisis and how is it treated?
worsening of muscle weakness resulting in respiratory failure needing intubation and ventilation.
treated with plasmapharesis and IVIG
pathophys of myasthenia gravis
myoid cells in the thymus express AChR -> autoreactive targeting by T-cells -> production of AChR antibodies
How is Myasthenia gravis diagnosed?
Clinically you see:
- weakness (limb weakness is symmetrical)
- eye signs of MG (diplopia, ptosis, blurry vision)
- FATIGUABILITY
Can do the following ix to aid the diagnosis:
- antibody testing for anti-AChR (however a minority of patients can be seronegative)
- EMG
- tensilon test (after injection sx should improve; not used commonly anymore because of risk of cardiac arrythmias;)
- CT chest to screen for thymoma
how is Myasthenia gravis managed?
Medical:
- Pyridostigmine (long acting ACh esterase inhibitor)
- Immunosuppression (initially prednisolone, can also use azathioprine, cyclosporine, MMF)
Surgical:
- thymectomy if the patient has a thymoma
+ CT chest to screen for thymoma
What is classically associated with a pancoast tumour?
Horners syndrome
What is Bell’s palsy?
An idiopathic, unilateral, acute facial nerve (CNVII) paresis/paralysis.
(there are other (secondary) causes of a facial nerve palsy e.g. trauma, infections, brainstem stroke, tumours and metabolic d/o but these are then not called Bell’s.
Signs and symptoms of Bell’s palsy
- decreased or absent movement in the facial muscles
- hyperacusis
- altered taste
- dry eyes and mouth
- decreased lacrimation
- lagophthalmos (inability to close eyes completely)
- sensory disturbances: painful sensation around or behind the ear, impairment of taste in the anterior tongue, hyperacusis.
- can get bell’s phenomenon (eye sign)
Aetiology of Bell’s palsy
idiopathic
?links to HSV infection
Management of Bell’s palsy
- give prednisolone within 72h of onset of palsy (?25 mg BD for 10/7 or 6mg daily for 5/7 followed by 10mg/day for 5/7 more and total 10/7 -> pred increases the chance of complete recovery to 82%
- there is an ongoing debate about the addition of antivirals
- Eye care: advise to make sure eye is closed for sleep and prescribe artificial tears/lubricants; consider taping eye over night.
F/U
- follow up after 3 w
- if not improved after 3 weeks, refer urgently to ENT
- can refer to plastics in long-standing weakness (several months)
Prognosis of Bell’s palsy
- most people make a full recovery after 3-4 months.
- if untreated, around 15% people have permanent moderate to severe weakness.
Metoclopramide MoA
Dopamine antagonist with 5HT3A antagonist activity
-> antiemetic
Why does a CN III palsy cause ptosis?
Due to the impairment of the innervation of the levator palpaebrae superioris?
albumino-cytologic dissociation - what does this mean and what condition is it seen in?
CSF has high protein but normal WCC
seen in Guillian Barre syndrome
What is Ramsay Hunt Syndrome?
Herpes Zoster infection of the facial nerve (CN VII)
What is optic neuritis?
inflammation of the optic nerve
causes of optic neuritis
Most common cause is MS
Can also be due to Infection (TB, syphilis, lyme disease, viral infection)
Toxic: ethambutol/methanol poisoning
sx of optic neuritis
- blurry vision
- sudden vision loss
- colour blindness
- visual field defects (e.g. central scotoma)
- mild pain on eye movement (=retrobulbar pain)
ix findings for optic neuritis
- clinical examination: relative afferent pupillary defect
- neurological examination showing the signs listed above
- ophthalmoscopy: retrobulbar neuritis -> normal findings on ophthalmoscopy usually; papillitis: poorly defined papilla, hyperemia, haemorrhage at the border of the papilla.
- VEP (Visual evoked potential)
- MRI head
management of optic neuritis
steroids!
also manage MS if this is the cause
prognosis of optic neuritis
- visual improvement usually starts after 2/52
- visual acuity is usually good after 1 year
- frequent persistence of deficits in color vision and contrast sensitivity
Definition and aetiology of Wernicke’s
Definition:
An acute reversible presentation caused by thiamine deficiency. Patients present with at least one of 1. confusion, 2, ophthalmoplegia, 3. ataxic gait.
Aetiology:
Due to thiamine deficiency, most commonly in chronic heavy alcohol use.
Thiamine is needed for glucose metabolism. Deficiency causes symmetrical loss of brain function.
Signs, sx and ix in Wernicke’s
Signs/Symptoms:
- Confusion
- Ataxic gait (small steps, wide-based steps), +ve Romberg’s
- Oculomotor dysfunction (diplopia, nystagmus, conjugate gaze palsy
Examination:
- fluctuating mental state/confusion
- Ataxic gait (small steps, wide-based steps), +ve Romberg’
- Oculomotor dysfunction (diplopia, nystagmus, conjugate gaze palsy
- there may be signs of chronic liver disease
Investigations:
- clinical diagnosis!
- thiamine levels in the blood can be used in rare cases where clinical findings alone are insufficient for the diagnosis.
- tests to consider/rule out other diganoses (bloods, urine dip, head imaging)
Management of Wernicke’s
Give Thiamine!!
if the patient also needs glucose:
thiamine should be given before glucose or concurrently.
Do not give glucose before thiamine as this can worsen the symptoms (thiamine is needed for glucose metabolism)
Prognosis of Wernicke’s
Prognosis:
depends on how fast you give thiamine
partial recovery within the day followed by full recovery within weeks is possible if thiamine is started rapidly.
If untreated:
20% mortality rate if untreated
other survivors develop psychosis and Wernicke-korsakoff syndrome which is irreversible.
Acronym for Wernicke’s
Wernicke’s COAT
C - confusion
O - ophthalmoplegia
A - ataxia
T - give THIAMINE
Cerebellar signs of stroke
DANISH
dysdiadokinesia
ataxia
nystagmus
intention tremor
slurred speech
hypotonia
what is nimodipine used for in aneurysmal SAH?
reduce the risk of vasospasm
?vasospasm can lead to stroke?
How long do cluster headaches typically last?
15 min - 3h
Investigations for cluster headache
MRI head with gadolinium contrast
(-> sometimes underlying brain lesions are found even if the clinical sx are typical for a cluster headache)
cluster headache management
100% FiO2 Oxygen
Triptans (subcut triptan in acute episodes)
Prophylaxis:
- verapamil
- tapering dose of prednisolone could be used
seek expert advice from a neurologist if pt develops CH
cluster headache prognosis and complications
Prognosis:
- 25% have a single episode only
- thought to be a lifelong disorder, but there may be less frequent bouts and longer periods of remission between bouts with increasing age
Complications:
- impact QoL
- associated with depression and anxiety
cluster headache - summarise the durations
These headaches last 15 min - 3h, occur 1-2x /day
they occur in ‘clusters’ lasting several weeks (4-12)
clusters occur typically once a year
cluster headache - signs and symtpoms
- unilateral headache (always on the same side) - intense, sharp, stabbing
- headache affecting the periorbital region and forehead (trigeminal innervation area)
- agitation and restlessness during attack
Ipsilateral autonomic sx:
- lacrimation
- rhinorrhoea
- conjunctival injection
- partial Horner’s syndrome
RFs for cluster headache
- smoking
- male gender (3:1)
define cluster headache
A primary headache disorder causing agonising unilateral headaches with symptoms of increased cranial autonomic activity affecting mainly young men in an episodic pattern.
verapamil drug class
CCB
RoA of triptans I acute cluster headache presentation
sc
What is the standard anticoagulation regimen given post stroke?
aspirin 300mg for 2 weeks
followed by 75 mg clopidogrel OD long term
clopidogrel drug class
antiplatelet medication
What is the most appropriate treatments for migraine
propranolol (1st line)
other drug starting with ?T
amitriptyline
candesartan
acupuncture
opening pressure and LP results in bacterial meningiits
high opening pressure (>25 cmCSF)
raised neutrophils
raised protein
reduced glucose
Temporal lobe seizure presentation
palpitations
rising sensation in abdomen
loss of sensation
writhering movement of ?arm
how common are cerebellar seizures?
very rare
frontal lobe seizures signs
screaming
abnormal behaviour
some moevments
ocipital lobe onset seizurecommon prodrome
visual symptoms at onset
Vestibular neuritis - aetiology, sx, and how is it different to labyrinthitis
idiopathic inflammation of the vestibular nerve
aetiology unclear, but commonly occurs after upper airway infections
sx: acute vestibular syndrome with persistent, acute onset vertigo, N&V, gait instability in otherwise healthy patients
when hearing loss is present it is sometimes referred to as labyrinthitis
BPPV timings
recurrent
usually lasts for seconds
dizziness or spinning sensation with a particular positions (e.g turning head or turning in bed)
What does fast phase to one side in nysstagmus suggest?
fast phase to one side suggests peripheral rather than central cause of nystagmus
vestibular migraine timings
comes and goes
duration?
Management of vestibular neuritis
- buccal or intramuscular prochlorperazine is often used to provide rapid relief for severe cases
- a short oral course of prochlorperazine, or an antihistamine (cinnarizine, cyclizine, or promethazine) may be used to alleviate less severe cases
- vestibular rehabilitation exercises are the preferred treatment for patients who experience chronic symptoms
How do lacunar strokes present?
- unilateral motor disturbance affecting the face, arm or leg or all 3
- complete one-sided sensory loss
- ataxia hemiparesis
involves perforating arteries around the internal capsule, thalamus and basal ganglia
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
What first-line drugs are available for migraine prophylaxis?
propranolol (b-blocker)
Topiramate (ideally not in females of childbearing age)
What is amaurosis fugax?
it is a ‘‘stroke’’ of the retinal/ophthalmic artery (which stems from the internal carotid artery)
It causes a painless, transient monocular vision loss. The vision loss is vertical, often described as a curtain closing.
caused by microemboli.
What is an RAPD?
relative afferent pupillary defect
= there is a defect in th pupil that affects the afferent (=sensory) pathway
on swinging light test, you get no constriction (or even paradoxical dilatation) of the pupils when shining light into one eye.
= impaired pupillary constriction due to an afferent defect in the pupillary reflex pathway
in what conditions can you see a RAPD?
MS
optic neuritis
retinal detachment
retinal ischaemia
….
What is bulbar palsy?
Bulbar Palsy vs parabulbar palsy
Timing of LP in ?SAH
To detect a subarachnoid haemorrhage the LP should be done at least 12 hours after the start of the headache
What is the best long term anti-thrombotic for carotid artery stenosis?
a. warfarin
b. clopidogrel
c. aspirin
d. apixaban
e. LMWH
Clopidogrel 75 mg long term
initially can use aspirin 300mg in acute setting.
if pt had AF you would use apixaban (because it would be a cardiembolic cause)
% stenosis considered to be significant and require carotid endartecotmy
> 70 %
(in MDT discussion can consider 50-70%)
What prophylactic medication in pt with carotid artery stenosis and AF to prevent stroke?
DOAC
e.g. apixaban
pharmacological management of stroke/TIA
14 days aspirin 300mg OD
then clopidogrel 75mg OD
List the different causes of stroke
Atherosclerosis
- carotid and vertebral stenosis
- intracranial stenosis
- aortic arch atheroma
- small vessel disease
Cardioembolic
- AF
- cardiac thrombus
Arterial dissection
Inflammatory vascular disorders
- GCA
- vasculitis
Genetic
- CADASIL
- MELAS
Cerebellum stroke - side of signs
ipsilateral signs
- dysdiadokinesia and tremor on the right
- fast phase of nystagmus to the side of the lesion
Brainstem stroke: side of signs
Cross signs:
?lesion would be on the side where the facial signs are?
Stroke management
EMERGENCY
- put out a thrombolysis /stroke call
thrombolysis within 4.5h
thrombectomy:
- needs a large vessel occlusion (=needs imaging)
- 6h timeframe (but sometimes can be extended up to 24h, depending on some imaging modalities)
Causes of SAH
- aneurysm
- traumatic
- AVM
- infectious
- IE -> mycotic aneurysms
- abnormal clotting e.g. warfarin
1st line ix in thunderclap headache
CT head
(if SAH, 98% positive)
if -ve and high suspicion -> LP
LP timeframe for SAH
12 h from onset
Mx of stroke >4.5h
Do you give thrombolysis and aspirin in stroke?
No
not at the same time
if the stroke team give thrombolysis, the aspirin would not be started until the next day.
What is the initial management of status epilepticus?
IV lorazepam is pharmacological mx
- protect airway
- give oxygen
- time
- DEFG - check glucose!
- check if they are on antiepileptics
- contact ITU if no response
(can also give buccal midazolam or rectal diazepam)
What is the definition of status epilepticus?
What is the difference between a seizure and epilepsy?
epilepsy = continuing tendency to have seizures
seizure = area of paradoxical discharge of electrical activity, the episode itself
safety advice for pts with epilepsy
- inform DVLA
- showers > baths
is cauda equina a LMN or UMN lesion?
LMN
What is syringomyelia
A condition where an abnormal, flui-filled cavity develops within the central canal of the spinal cord. The syrinx is a result of disrupted CSF drainage from the central canal, commonly caused by a chiari malformation or previous trauma to the cervical or thoracic spine/
sx include sensory loss in a cape-like distribution.
MRI is used to diagnose.
Mx: supportive therapy like PT, psychotherapy, beclofen for spasticity, analgesia.
Surgical treatment: decompression/removal of tumour if present.
What are causes of both UMN and LMN signs?
- MND
- can also have multiple lesions (MRI brain, nerve conduction studies - to make sure you exclude other causes that can mimic MND)
Ix for GBS
- bloods
- LP (raised protein)
- EMG/NCS
- spirometry (measure FVC as a measure of respiratory muscle function. may need ITU and intubation)
may self resolve, may need IVIG or plasmapheresis
What is a neuropathy?
What are the different types of neuropathies?
Predominantly sensory
- diabetes
- thiamine deficiency
- malignancy
- leprosy
- hereditary sensory neuropathies
- amyloid
- uraemia
Predominantly motor
- Guillian Barre syndrome
- porphyria
- diphtheria
- botulism
- lead
- charcot marie tooth
What L-DOPA side effects can patients get?
MS - location and time
lesions are disseminated in space and time
What part of the tongue does the facial nerve innervate?
anterior 2/3
the Chorda tympani
Which nerves innervate the taste in the tongue?
facial N: anterior 2/3
glossopharyngeal (XI): posterior 1/3
How can you differentiate acute and chronic subdural haematoma on CT head?
There is a crescent shaped bleed in both
in acute: bleed is hyperdense (bright)
in chronic: bleed in hypodense (dark)
What is the key diagnostic test in Guillian Barre syndrome?
LP
shows raised protein with a normal WCC
What are watershed strokes?
Watershed strokes have been described previously as ischemic strokes located in vulnerable border zones between brain tissue supplied by the anterior, posterior, and middle cerebral arteries in the distal junction between two non-anastomotic arterial territories.
Uhthoff phenomenon
temporary, short lived and stereotyped worsening of neurological function among multiple sclerosis patients in response to increases in body core temperature
e.g. due to fever e.g. from UTI, exercising, saunas, hot tubs etc.
Management of acure relapse in MS
high dose steroids (e.g. oral or IV methylprednisolone) may be given for 5 days to shorten the length of an acute relapse
-> shorten the duration but do not alter the degree of recovery i.e. whether the patient returns to their baseline function
features of normal pressure hydrocephalus
dementia
urinary incontinence
gait abnormality
Description of a chronic subdural haematoma on CT
hypodense (dark)
crescenteric collection around the convexity of the brain
not limited to suture lines
contrast or non-contrast MRI for ?MS
contrast MRI of brain and spine
can show acute demyelination
varying degrees of contrast enhancement can also indicate recent vs active demyelination
presentation of HD
middle aged
personality changes
involuntary movements
cognitive decline
Huntington’s disease underlying pathology
CAG repeats (trinucelotide repeat d/o -> anticipation phenomenon may be seen = the more repeats, the earlier onset and more severe the condition )
autosomal dominant
