Neurology Flashcards
spinal cord anatomy
where does it start and end?
foramen magnum to L1
terminates as conus medullaris
what is the cauda equina?
bundle of spinal nerves continuing inferiorly to spinal cord
L2 to L5 nerves, Sacral 1 to 5 and the coccygeal nerves
what suspends the spinal cord in the subarachnoid space?
denticulate ligaments
longitudinal support via filum terminale
Blood supply to spinal cord?
- 3 longitudinal vessels
- 2 posterior spinal arteries: dorsal 1/3
- 1 anterior spinal artery: ventral 2/3
- reinforced by segmental feeder arteries
e. g. artery of Adamkiewicz
Longitudinal veins drain into extradural verterbral plexus
what part of the spinal cord is responsible for fine touch, vibration and proprioception?
Dorsal Columns
fasciulus gracilis
fasciculus cuneatus
where does decussation of the dorsal columns occur?
in medulla forming the medial lemniscus
-> thus, damage below the medial lemniscus means
what part of the spinal cord is responsible for pain and temperature sensation?
lateral spinothalamic tract
where do the lateral spinothalamic tracts decussate?
in cord, at entry level.
This fact aids in determining whether a lesion is in the brain or the spinal cord. With lesions in the brain stem or higher, deficits of pain perception, touch sensation, and proprioception are all contralateral to the lesion. With spinal cord lesions, however, the deficit in pain perception is contralateral to the lesion, whereas the other deficits are ipsilateral.
what part of the spinal cord is responsible for crude touch and firm pressure?
anterior spinothalamic tract
what part of the spinal cord is responsible for motor function?
lateral corticospinal tract
where does decussation of the lateral corticospinal tract occur?
pyramidal decussation in ventral medulla
brain stem lesion -> what is affected??
in terms of pain/ temp, fine touch, motor
in a brain stem or higher lesion,
everything is affected contralateral to the lesion
spinal cord lesion -> what is affected?
in terms of pain/temp, fine touch, motor
fine touch and motor are affected ipsilaterally
while pain/temp is affected contralaterally
what part of the brain is involved with regulation of posture, balance, coordination, movement and speech?
Cerebellum
what area of white matter carries axonal fibres from motor cortex to the pyramids of medulla?
internal capsule
infarcation of the internal capsule -> contralateral hemiparesis
occipital lobe in charge of ?
visual cortex
temporal lobes of brain involved in ?
memory
receptive language (Wernicke’s) in the dominant hemisphere
what function is the parietal lobe involved with?
sensory cortex
body orientation
what functions are the frontal lobe assoc w?
executive function
motor cortex
cognition and memory
dominant hemisphere: expressive speech (Broca’s area)
what is the main neurotransmitter acting across the neuromuscular junction?
acetylcholine
which binds to nicotinic receptors on post-synaptic terminal
What blocks presynaptic choline uptake?
hemicholine
(hemicholinium-3) decreases synthesis of acetylcholine
what blocks acetylcholine vesicle fusion?
botulinum
Lambert-Eaton myasthenic syndrome (antibodies against VGCC decrease ACh release)
what blocks nicotinic ACh receptors at the NMJ?
non-depolarising: atracurium, vecuronium
depolarising: suxamethonium
Sympathetic NS vs Parasympathetic NS
sympathetic: T1-L2
para: CN 3, 7, 9, 10
Sympathetic: preganglionic fibres are myelinated and release ACh whereas postganglionic fibres are unmyelinateed and release NA (except for sweat glands)
Para: both pre and post release ACh
Para has long preganglionic and short postganglionic fibres.
Sympathetic has short preganglionic fibres and long postganglionic fibres
absence of eye movements in caloric tests?
brainstem damage on the side being tested
direction of nystagmus when cold water is used?
and warm?
cold: opposite direction
warm: same side
what happens when warm water is placed in the ear during caloric testing?
warm water increases firing of vestibular nuclei
-> eyes turn to contralateral side with nystagmus to ipsilateral side
UMN vs LMN signs
UMN:
increased tone/ spasticity +/- clonus
hyperreflexia
up going plantars
LMN:
wasting
fasciculation
decreased tone
hyporeflexia
down-going plantars
What is Brown sequard syndrome?
ipsilateral loss of proprioception/ vibration and weakness
w
contralateral loss of pain
Cerebellar Syndrome
what signs?
DANISH
Dysdiadochokinesia + Dysmetria (past-pointing)
Ataxia: limb/ trunkal
Nystagmus: horizontal = ipsilateral hemisphere
Intention tremor
Speech: slurred, staccato, scanning dysarthria
Hypotonia
Common causes of cerebellar syndrome
PASTRIES
Paraneoplastic: e.g. from Ca
Alcohol: thiamine and B12 deficiency
Sclerosis (Multiple)
Trauma
Raised ICP
Infection/ iatrogenic: phenytoin
Endo: Hypothyroidism
Stroke: vertebrobasilar
causes of locked in syndrome
central pontine myelinolysis: rapid correction of hypoNa
ventral pons infarction: basilar artery
features of subclavian steal syndrome?
syncope / presyncope or focal neurology on using the arm
BP difference of > 20mmHg between arms
due to subclavian artery stenosis proximal to origin of verterbral artery -> blood stolen by vertebral artery by retrograde flow
features of Beck’s syndrome/ anterior spinal artery infarct
para/ quadriparesis
impaired pain and temp sensation
preserved touch and proprioception
infarction of spinal cord in distribution of anterior spinal artery: ventral 2/3 of cord
e.g. due to aortic aneurysm dissection
causes of mixed UMN and LMN signs?
MAST
motor neurone disease
ataxia: friedrich’s
Subacute combined degeneration of cord
Taboparesis (tertiary syphilis)
infectious causes of vertigo
ramsay hunt syndrome
labyrinthitis
trauma causing imbalance?
trauma to petrous temporal bone
sudden vertigo provoked by head rotation?
benign positional vertigo
recurrent vertigo,
fluctuating tinnitus,
increasing deafness
feeling of fullness in ear
Meniere’s disease
lesions of nerve causing vertigo?
acoustic neuroma,
vestibular schwannoma
Causes of conductive hearing loss
WIDENING
wax/ foreign body
infection: otitis media
drum perforation
extra: ossicle discontinuity- otosclerosis, trauma
neoplasia
INjury: e.g. barotrauma
Granulomatous: wegeners, sarcoid
features of resting tremor
4-6 Hz, pill-rolling
abolished on voluntary movement
increases with distraction e.g. counting backwards
tx of resting tremor
dopamine agonists
antimuscarinic e.g. procyclidine
features of intention tremor
>6Hz, irregular, large amplitude
worse at end of movement
e.g. past pointing
causes of intention tremor
cerebellar damage
Features of action/ postural tremor
6-12 Hz
absent at rest
worse w outstretched hands or movement
equally bad at all stages of movement
causes of postural / action tremor
BEATS
benign essential tremor
endocrine: thyrotoxicosis, low glucose, phaeo
alcohol withdrawal
Toxins: B agonists, theophylline
Sympathetic: anxiety
autosomal dominant
tremor that occurs w action and worse w anxiety, emotion, caffeine
affects arm, neck, voice
better w alcohol
benign essential tremor
Causes of subarachnoid haemorrhage?
Rupture of berry aneurysm (80%)
Arteriovenous malformations (15%)
RFs of subarachnoid haemorrhage
Smoking, HTN, Alcohol
Bleeding diathesis
Subacute bacterial endocarditis (infected aneurysms)
FH
Where do berry aneurysms most commonly affect?
classically occurs at the point at which a cerebral artery departs from the circle of Willis
e.g. bifurcation of MCA
Berry Aneurysms are assoc w ?
PCKD
Coarctation of aorta
Ehlers Danlos
Features of subarachnoid haemorrhage?
Sudden, severe occipital headache
Collapse
Meningism
Seizures
Drowsiness -> coma
Signs of subarachnoid haemorrhage?
Kernigs
Retinal or subhyaloid haemorrhage
Focal neuro - suggests aneurysm location
Ix of Subarachnoid haemorrhage?
- CT head
LP after 12h if CT -ve and no contraindications-> may show xanthochromia
Mx of subarachnoid haemorrhage?
Frequent neuro obs: GCS, pupils, BP
Maintain Cerebral perfusion pressure: Keep SBP >160
Nimodipine for 3 wks -> decrease cerebral vasospasm
Endovascular coiling
Complications of subarachnoid haemorrhage?
Rebleeding (most common cause of mortality)
Cerebral ischaemia from cerebral vasospasm (most common cause of morbidity)
Hydrocephalus
hypoNa
Causes of stroke?
Ischaemia (80%)
Haemorrhage (20%)
Causes of ischaemic stroke?
Atheroma
Emboli e.g. from AF, endocarditis, MI
Causes of haemorrhagic stroke?
High BP
Trauma
Aneurysm rupture
Anticoagulation
Thrombolysis
When to do endarterectomy in carotid artery stenosis?
If >70% symptomatic stenosis according to ECST criteria
or >50% according to NASCET criteria
recommend if patient has suffered stroke or TIA in the carotid territory and are not severely disabled
Posterior circulation stroke - what part of the circulation is affected?
Vertebrobasilar territory
What would an infarct in the vertebrobasilar territory cause?
Cerebellar syndrome
Brainstem syndrome
Contralateral homonymous hemianopia (macular sparing)
What is a total anterior circulation stroke?
All 3 of
- Contralateral hemiparesis +/- sensory deficit (2 or more in face, arm, leg)
- Contralateral homonymous hemianopia
- Higher cortical dysfunction
- dominant (L usually) lobe: dysphasia
- non dominant: hemispatial neglect
What is a partial anterior circulation stroke?
2/3
Usually
- Contralateral hemiparesis +/- sensory deficit (2 or more in face, arm, leg)
- Higher cortical dysfunction
- dominant (L usually) lobe: dysphasia
- non dominant: hemispatial neglect, constructional apraxia
what would an infarct in the subthalamic nucleus usually present with?
Hemiballismus
what is a lacunar stroke?
most common type of ischaemic stroke
small infarcts around the basal ganglia/ internal capsule/ thalamus / pons
what are the five classical lacunar syndromes?
- pure motor: commonest. causes a hemiparesis. post limb of internal capsule affected
- Pure sensory: affects contralateral side. post thalamus (VPL)
- mixed sensorimotor: internal capsule
- dysarthria/ clumsy hand
- ataxic hemiparesis: cerebellar and motor symptoms on ipsilateral side.
brainstem infarcts in the corticospinal tracts?
presentation
hemi/ quadriparesis
brainstem infarcts in the oculomotor system? presentation
conjugate gaze palsy
brainstem infarct in the CN7 nucleus?
presentation
facial weakness (LMN)
forehead involved
lesion in the CN8 nucleus?
presentation
vertigo, nystagmus
brainstem infarct in the CN9/10 nuclei?
presentation
dysphagia
dysarthria
brainstem infarct in the cerebellar connections?
presentation
ataxia
dysarthria
brainstem infarct in the sympathetic fibres?
presentation
Horner’s syndrome
brainstem infarct in the reticular activating system?
presentation
reduced GCS
occlusion of what artery could cause wallenberg’s syndrome/ lateral medullary syndrome?
Verterbral artery/
posterior inferior cerebellar artery
features of wallenberg’s syndrome/ lateral medullary syndrome?
DANVAH
Dysphagia
Ataxia (ipsilateral)
Nystagmus (ipsilateral)
Vertigo
Anaesthesia
- ipsilateral facial numbness + absent corneal reflex
- contralateral pain loss
Horner’s syndrome (ipsilateral)
what is Millard-Gubler syndrome?
aka ventral pontine syndrome
lesion of the pons
Millard-Gubler syndrome
what parts of the pons are affected?
6th and 7th CN nuclei
corticospinal tracts
Millard-Gubler syndrome
what features?
dipoplia (paralysis of the abducens CN VI)
LMN facial palsy + loss of corneal reflex
contralateral hemiplegia
what is locked in syndrome?
pt aware and cognitively intact but completely paralysed except for the eye muscles
causes of locked in syndrome?
ventral pons infarction: basilar artery
central pontine myelinolysis: rapid correction of hypoNa
acute mx of stroke?
Resus: ABCDE, stabilize patient airway, NBM until swallowing assessed by SALT
Monitor: Glucose levels, BP, Neuro obs
Imaging: urgent CT/ MRI
what imaging modality is most sensitive for acute infarct?
diffusion-weighted MRI
*CT excludes primary haemorrhage
why is CT head used in ix of stroke?
to visualize/ exclude haemorrhage
what medical tx is used in acute stroke?
consider thrombolysis if 18-80 yrs and < 4.5 h since onset of symptoms
e.g. alteplase
then CT head post-thrombolysis 24h to look for haemorrhage
Aspirin 300mg +/- PPI
? modified release dipyridamole / clopidogrel
when is neurosurgery indicated in stroke?
intracranial haemorrhage
decompressive hemicraniectomy for some forms of infarction
coiling of bleeding aneurysms
Primary prevention of stroke?
Control RFs: HTN, high lipids, DM, smoking, cardiac disease
Consider life-long anticoagulation in AF
Carotid endarterectomy if symptomatic- 70% stenosis
Exercise
secondary prevention of stroke?
Risk factor control: statin
Aspirin / Clopi 300mg for 2 wks after stroke then either:
- Clopidogrel 75mg OD
- Aspirin 75 mg OD + dypyridamole MR 200mg BD
*warfarin instead of aspirin/clopi if cardioembolic stroke/ AF. start from 2 wks post-stroke.
Carotid endarterectomy if good recovery + ipsilateral stenosis >70%
Rehab in stroke?
MENDS
MDT: physio, SALT, dietician, OT, specialist nurses, neurologist, family
Eating: Swallowing screen - may need NG/ PEG, supplements if malnourished
Neurorehab: physio and speech therapy
DVT prophylaxis
Sores: avoid bed sores
what drug may be useful to help spasticity seen post-stroke?
botulinum
What does OT post-stroke aim to do?
aims to minimise disability (e.g. can’t write) and abolish handicap (e.g. cant work as accountant)
impairment: e.g. paralysed arm
what is a transient ischaemic attack?
sudden onset focal neurology lasting <24h
due to temporary occlusion of part of the cerebral circulation
(~15% of 1st strokes are preceded by TIAs)
signs of TIA?
brief symptoms
global events e.g. syncope/ dizziness are not typical
signs of causes of TIA?
Carotid bruits
AF
high BP
heart murmur
causes of TIA
atherothromboembolism from carotids
cardioembolism: post-MI, AF, valve disease
Hyperviscosity: polycythaemia, myeloma, Sickle cell
IX of TIA
aim to find cause and define vascular risk
FBC, U+E, ESR, Glucose, Lipids
CXR
ECG
Echo
Carotid doppler +/- angiography
Consider brain imaging: diffusion weighted MRI
Mx of TIA
avoid driving for 1 month
- Antiplatelet therapy/ Anticoagulation:
aspirin/ clopidogrel 300mg for 2 wks then 75mg/d
(add dipyridamole to aspirin)
warfarin if cardiac emboli: AF, MI, MS
- Control cardiac RFs: smoking, BP, lipids, diet, exercise, DM
- Assess risk of subsequent stroke: ABCD2 score
- Specialist referral to TIA clinic
what is the ABCD2 score?
Age ≥ 60
BP ≥ 140/90
Clinical features
a. unilateral weakness (2 pts)
b. speech distrubance w/o weakness
Duration
a. ≥ 1h (2 points)
b. 10-59 min
DM
7 points max
predicts stroke risk following TIA
What is the ABCD2 score used for?
predicts stroke risk following TIA
score ≥ 6 = 8% risk within 2 days. 35% risk within 1 wk
score ≥4 = pt assessment by specialist within 24h
all pts w suspected TIA should be seen by specialist within 7d
What is a subdural haemorrhage?
haematoma between dura and arachnoid
bleeding from bridging veins between cortex and sinuses
often due to minor trauma that occured a long time previously
Risk factors of subdural haemorrhage?
elderly: brain atrophy
falls: epileptics, alcoholics
anticoagulation: increased bleeding risk
symptoms of subdural haemorrhage?
headache
fluctuating GCS, sleepiness
gradual physical/ mental slowing
unsteadiness
signs of subdural haemorrhage?
raised ICP
papilloedema
localising signs occur late
ix of subdural haemorrhage?
CT/ MRI head
crescentic haematoma over one hemisphere
clot goes from white -> grey over time
midline shift
mx of subdural haemorrhage?
1st line: irrigation/ evacuation via burr-hole craniostomy
2nd: craniotomy then suction/ irrigation to remove the clot
extradural haemorrhage usually due to?
fracture over pterion
-> laceration of middle meningeal artery and vein
presentation of extradural haemorrhage?
after head injury, there may be a lucid interval.
deterioration of GCS after head injury that caused no LOC/ following initial improvment in GCS
increased ICP: headache, vomiting, confusion, fits, ipsilateral blown pupil (3rd n palsy) +/- hemiparesis w upgoing plantars and increased reflexes
Brainstem compression
signs of brainstem compression?
deep irregular breathing
cushing response (late): high BP, low HR
death by cardiorespiratory arrest
Ix of extradural haemorrhage?
CT head
- lens shaped haematoma
- skull fracture
subdural vs extradural haemorrhage?
difference between where the blood is
extradural: blood between skull and dura
subdural: blood between dura and arachnoid
mx of extradural haemorrhage?
neuroprotective ventilation (Oxygen)
if raised ICP -> IV mannitol or hypertonic saline
Craniectomy for clot evacuation and vessel ligation.
if small haematoma -> may be treated conservatively but must be observed in case of sudden deterioration
if high ICP, IV mannitol or hypertonic saline?
Hypertonic saline is increasingly considered a safer and more effective alternative.
In the trauma situation it has the advantage of repleting/preserving intravascular volume rather than increasing fluid loss by diuresis.
what is neuroprotective ventilation?
O2>100, CO2 35-40
excessive hypocapnia should be avoided, as it causes cerebral vasoconstriction.
in extradural haemorrhage, what is the cut off for surgical management?
all patients with an EDH volume greater than 30 cm3 should have a surgical evacuation regardless of GCS.
cerebral vein thrombosis
risk factors?
triggered by infections of the ear, face, or neck
oestrogen use (e.g ocp) and pregnancy
inherited and acquired clotting disorders
drugs e.g. tranexamic acid
Sinus thrombosis symptoms?
severe headache (can be of sudden onset/ develops over few days)
nausea, vomiting
blurred vision
serizures, confusion
other neuro symtpoms
symptoms depend on location and extension of clot
sagittal sinus thrombosis symptoms?
Headache, vomiting, seizures, ↓ vision, papilloedema
transverse sinus thrombosis symptoms?
Headache ± mastoid pain, focal neuro, seizures,
papilloedema
symptoms of sigmoid sinus thrombosis
cerebellar signs
lower CN palsies
symptoms of inferior petrosal sinus thrombosis?
5th and 6th CN palsies
(gradenigo’s syndrome)
symptoms of cavernous sinus thrombosis?
headache +/- tearing
painful opthalmoplegia
eyelid oedema
proptosis
fever
Ix of cortical vein thrombosis?
exclude SAH and meningitis
CT/ MRI venography
LP: high pressure, may show RBCs, xanthochromia
Mx of cortical vein thrombosis
LMWH -> warfarin (INR 2-3)
Fibrinolytics e.g. streptokinase
Thrombophilia screen
Features of meningitis
Headache
neck stiffness
- kernig’s +ve
- Brudzinski’s +ve
Photophobia
N+V
reduced GCS
seizures, focal neurology
what is Brudzinski’s sign?
+ve in meningitis
lifting head would cause flexion of legs and thighs
due to neck rigidity
What is Kernig’s sign?
+ve in meningitis
Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.
signs in meningococcal septicaemia
fever
high HR, low BP
high CRT
purpuric non blanching rash
DIC
antibiotic mx of meningitis in the community?
benpen 1.2g IM
antibiotic mx of meningitis in under 50s?
IV Ceftriaxone 2g
or IM BD
antibiotic mx of meningitis in >50s?
Ceftriaxone + Ampicillin
IV
viral meningitis mx?
aciclovir
organisms that cause meningitis
enteroviruses/ HSV2
Meningococcus
Pneumococcus
Listeria
TB
cryptococcus
why is dexamethasone used in acute bacterial meningitis?
Bacterial meningitis is fatal in 5% to 40% of children and 20% to 50% of adults despite treatment with adequate antibiotics.
corticosteroids can reduce the inflammation assoc w infection
CSF findings:
turbid appearance, mainly neutrophils, high WCC, low glucose (<1/2 plasma), high protein
Bacterial meningitis
CSF findings:
clear, lymphocytic, normal glucose, normal protein
viral meningitis
CSF findings:
fibrin web, lymphocytic, low glucose, high protein
TB meningitis
Contraindications to LP?
signs of raised ICP:
reduced GCS, bradycardia/hypotension, focal neuro, abnormal posturing, papilloedema, tense bulging fontanelle
shock
DIC
convulsions until stabilised
coagulation abnormalities
superficial infection at LP site
resp insufficiency
why is LP contraindicated in resp insufficiency?
lumbar puncture is considered to have a high risk of precipitating respiratory failure in the presence of respiratory insufficiency
CT head of encephalitis caused by HSV
- most likely finding?
focal bilateral temporal involvement
Ix of encephalitis?
Bloods: cultures, PCR, malaria film
CT head
LP
mx of encephalitis
aciclovir STAT
supportive measures
phenytoin for seizures
risk factors for cerebral abscess
infection of ear, sinus, dental
skull #
congenital heart disease
endocarditis
bronchiectasis
immunosuppression
signs of cerebral abscess
seizures
fever
signs of raised ICP
localizing signs
signs of infection elsewhere
Ix of Cerebral abscess
CT/MRI head: ring enhancing lesion
raised WCC, ESR
Mx of cerebral abscess
neurosurgical referral
treat raised ICP (mannitol/ hypertonic saline)
Antibiotics e.g. ceftriaxone
what is epilepsy?
recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifest as seizures
causes of non-epileptic / provoked seizures
alcohol/ benzo/ opiate withdrawal
metabolic: Glucose, Na, Ca, urea, NH2
raised ICP: meningitis, encephalitis, HIV, cysticerosis
eclampsia
pseudoseizures
causes of acquired seizures
post-stroke
cortical scarring: trauma, infection
SOL
MS
SLE
sarcoidosis
what is the prodrome of a seizure?
change in mood/ behaviour lasting hrs- days
simple seizure?
awareness intact
complex seizure?
impaired awareness
secondary generalised seizure?
focal -> generalized
e.g. aura -> tonic clonic
what is an aura?
simple partial seizure (usually temporal)
experienced as a strange feeling:
- deja vu/ jamais vu
- automatisms
- smells, lights, sounds
diagnostic features of seizure
aura
specific trigger e.g. flashing lights
lateral tongue biting
typical movements e.g. tonic-clonic
cyanosis
post-ictal phase
features of west syndrome/ infantile spasms?
clusters of head nodding and arm jerks
EEG shows hypsarrhythmia
atonic seizure?
sudden loss of muscle tone -> fall
no LOC
myoclonic seizure?
sudden jerk of limb, face/ trunk
absence seizure features?
Abrupt onset and offset
Short: <10s
Eyes: Glazed, blank stare
Clonus or automatisms may occur
EEG: 3hz spike and wave
stimulated by hyperventilation
localising features of seizures suggesting involvement of occipital lobe?
visual phenomena: spots, lines, flashes
localising features of seizures suggesting involvement of parietal lobe?
sensory disturbance: tingling, numbness
localising features of seizures suggesting frontal lobe involvement?
motor features: jacksonian march, Tood’s palsy, arrest
what is a jacksonian march?
The characteristic features of Jacksonian march are (1) it only occurs on one side of the body; (2) it progresses in a predictable pattern from twitching or a tingling sensation or weakness in a finger, a big toe or the corner of the mouth, then marches over a few seconds to the entire hand, foot or facial muscles.
what is Todd’s paresis?
transient weakness of a hand, arm, or leg after focal seizure activity within that limb. The weakness may range in severity from mild to complete paralysis.
localising features of seizures suggesting temporal lobe involvement?
automaticisms: lip smacking, chewing, fumbling
deja/ jamais vu
abdominal rising/ N+V
emotional disturbance: terror, panic, anger, elation
tastes, smells
delusional behaviour
Pt had a one off seizure while awake and lost consciousness
what advice regarding DVLA and driving?
cannot drive for 6 months (providing no more attacks)
+
DVLA’s medical advisers decide there isnt a high risk pt will have another seizure (ie. normal MRI/ EEG)
If first seizure but abnormal EEG/ MRI
advice regarding DVLA and driving?
cannot drive for 12 months
Seizures only when asleep?
what advice regarding DVLA and driving
cannot drive until past 12 months since first attack
Pt has had epileptic attacks while awake and lost consciousness.
advice re driving and DVLA?
Cannot drive til no attack for at least a year
if a epilepsy pt had a seizure because doctor had changed/ reduced anti-epilepsy medicine
what advice re DVLA and driving?
have to stop driving until seizure > 6m ago
or
back on previous medication for 6 months
seizures that dont affect consciousness or driving?
advice re driving and DVLA
need to contact DVLA.
You may still qualify for a licence if these are the only type of attack you’ve ever had and the first one was 12 months ago.
Bus, coach or lorry license.
advice if pt has had more than one seizure?
cannot drive unless
- no seizure for 10 years
- haven’t taken any anti-epileptic mx for 10 yrs
- <2% risk of another seizure
bus, coach or lorry license.
if pt had a one-off seizure?
no epileptic attack for 5 years
no anti-epileptic mx for 5 years
must have been assessed in the past 12 months by a neurologist
general advice about epilepsy and seizures
diagnosis made by specialist
dont diagnose epilepsy from one seizure
after any seizure, advise against driving, swimming, bath until Dx established
after dx, cannot drive until seizure-free for >1 yr
indications for MRI after a seizure?
developed epilepsy as an adult
any evidence of focal onset
seizures continue despite 1st line tx
1st line tx of absence seizures?
ethosuximide
sodium valproate
1st line mx of focal seizures?
carbamazepine
or
lamotrigine
1st line mx of generalized tonic-clonic seizures
sodium valproate
1st line mx of myoclonic seizures
sodium valproate
1st line mx of atonic/ tonic seizures
sodium valproate
tx of epilepsy in pregnancy
avoid valproate
take lamotrigine/ carbamazepine
5 mg folic acid daily
side effects of lamotrigine?
skin rash-> SJS
rash may be assoc w hypersensitivity -> fever, raised LFTs, DIC
diplopia, blurred vision
levels affected by enzyme inhibitors/ inducers
status epilepticus
mx?
ABC approach
IV lorazepam 2-4 mg IV bolus over 30s
(or buccal midazolam/ rectal diazepam)
can repeat if no response within 2 min
Mx of status epilepticus
after first line tx?
IV Infusion of Phenytoin
monitor ECG and BP
CI: bradycardia or heart block
or IV Diazepam
Call anaesthetic for airway support
mx of cerebral oedema with malignancy?
dexamethasone
primary survey of pt w head injury
A to E approach
A: immobilize C-spine (Hard collar), stabilize airway-> jaw thrust, ?intubation
B: 100% O2, RR
C: IV access, HR, BP
D: GCS, pupils
E: expose pt, look for obvious injuries
Head injury
secondary survey
what would you look for specifically?
lacerations
obvious facial/ skull deformity
CSF leak from nose or ears
Battle’s sign, Racoon eyes
Blood behind Tympanic Membrane
C spine tenderness /deformity
Hx after head injury
GCS after injury
?LOC
headache
fits
vomiting
amnesia
alcohol?
mx of head injury?
neurosurgical opinion if signs of raised ICP, CT evidence of intracranial bleed, significant skull #
Admit if:
- abnormalities on imaging
- CNS signs: vomiting, severe headache
- GCS not returned to 15
- difficult to assess: alcohol, post ictal
Neuro obs half hourly until GCS 15:
GCS, pupils, HR/ BP/ RR/ SpO2/ Temp
Guidelines to intubate after head injury
GCS ≤ 8
PaO2 < 9kPa on air / <13 kPa on O2
or PCO2 > 6 kPa
Spontaneous hyperventilation: PCO2 < 4 KPa
Respiratory irregularity
GCS
Eyes
what is 1-4?
4 - spontaneous eye opening
3 - open to voice
2 - open to pain
1 - no opening
GCS
Verbal
what is 1- 5?
5 - Orientated conversation
4 - confused conversation
3 - inappropriate speech
2 - incomprehensible sounds
1 - no speech
GCS
Motor
what is 1-6?
6: obeys commands
5 - localises pain
4 - withdraws to pain
3 - decorticate posturing to pain (flexor)
2 - decerebrate posturing to pain (extensor)
1 - no movement
After Head injury,
CT head guidelines?
BANGS LOC
Break: open, depressed or base of skull #
Amnesia > 30 min retrograde
Neuro deficit or seizure
GCS: <13 at any time or <15 2h after injury
Sickness: Vomited >1x
LOC or amnesia and any of:
- Age ≥65
- dangerous mechanism: RTA, fall from great height
- coagulopathy (inc warfarin)
risk of intracranial haematoma in adults if confused + skull #?
1:4
risk of intracranial haematoma in adults if fully conscious + skull #?
1:30
risk of intracranial haematoma in adults if confused + no skull #?
1:100
risk of intracranial haematoma in adults if fully conscious + no skull #?
very low.
<1:1000
symptoms of raised ICP
headache: worse on waking, lying down, bending forward, on straining, coughing
Vomiting
reduced consciousness
visual disturbance: transient visual obscurations and visual loss
pulse synchronous tinnitus (pulsatile tinnitus)
(red flag: waking pt up from sleep)
signs of raised ICP
papilloedema
diplopia due to sixth cranial nerve palsy (or other)
reduced GCS
Most common brain tumour is?
secondary metastases: e.g. from breast, lung, melanoma
most common primary brain tumour in adults?
glioblastoma multiforme
presentation of idiopathic intracranial hypertension?
typically obese females
signs and symptoms of raised ICP e.g. headache,
visual disturbances
e.g. blurred vision, 6th CN palsy, enlarged blind spot
causes of idiopathic intracranial HTN?
usually idiopathic
may be secondary to venous sinus thrombosis or drugs
mx of idiopathic intracranial HTN
weight loss if overweight
Acetazolamide: reduces CSF production
loop diuretics
prednisolone - to relieve headaches and reduce the risk of vision loss
regular LPs to drain excess CSF
lumbar-peritoneal shunt may be necessary if drugs fail and visual loss deteriorates
ix of idiopathic intracranial HTN
full neurological examination
assessment of eyes and vision
CT/ MRI head
LP to detect opening pressure
prognosis of idiopathic intracranial HTN?
usually self limiting
permanent visual loss in 10%
types of cerebral oedema
Vasogenic (increased capillary permeability): trauma, tumour, ischaemia, infection
Cytotoxic: e.g. from hypoxia
Interstitial: e.g. obstructive hydrocephalus, low Na+
what are some causes of raised ICP?
haemorrhage
SOL- tumours, abscess
infection
hydrocephalus
cerebral oedema
cerebral venous thrombosis
what is Cushing’s Reflex?
a physiological nervous system response to increased ICP
results in Cushing’s triad of:
raised BP, bradycardia, irregular breathing
usually seen in terminal stages of acute head injury and may indicate imminent brain herniation
what is Cheyne-Stokes respiration?
an abnormal pattern of breathing characterized by progressively deeper, and sometimes faster, breathing followed by a gradual decrease then stop.
pattern repeats with each cycle usually taking 30s - 2 min
acute mx of raised ICP
ABC
Treat seizures and correct hypotension
Elevate bed to 40 degrees
Neuroprotective ventilation:
PaO2>13, PCO2: 4.5, Good sedation +/- NM blockade
Mannitol or hypertonic Saline: may reduce ICP in short-term but may cause rebound raised ICP later
what is tonsillar herniation?
increased pressure in posterior fossa
leading to displacement of cerebellar tonsils through foramen magnum.
-> compression of brainstem and cardiorespiratory centres in medulla
symptoms of tonsillar herniation?
CN6 palsy
upgoing plantars
- > irregular breathing
- > apnoea
Death
what is an uncal hernation?
compression of ipsilateral inferomedial temporal lobe (uncus) against free margin of tentorium cerebelli
uncal herniation symptoms?
ipsilateral CN3 palsy: dilation of pupil then down and out
ipsilateral corticospinal tract: contralateral hemiparesis
may cause compression of contralateral corticospinal tracts -> ipsilateral hemiparesis (Kernohan’s notch)
what is the kernohan’s notch?
a secondary condition caused by a primary injury on the opposite hemisphere of the brain
due to transtentorial (uncal) herniation
-> causes ipsilateral motor weakness/ paralysis
what is a subfalacine herniation?
displacement of cingulate gyrus (medial frontal lobe) under falx cerebri
Symptoms of subfalcine herniation?
compression of ACA -> stroke symptoms
e.g. contralateral motor/sensory loss in legs>arms
abulia (pathological laziness)
Postural instability -> falls
+
speech distrubance (+ dementia)
+
vertical gaze palsy
Dx?
Progressive supranuclear palsy
Autonomic dysfunction: postural hypotension, bladder dysfunction
+
cerebellar + pyramidal signs
+
rigidity > tremor?
Multiple systems atrophy
(shy drager)
parkinsonism + visual hallucinations + fluctuating cognition?
Lewy body dementia
parkinsonism + aphasia, dysarthria, apraxia
+
akinetic rigidity in one limb
+
astereognosis (cortical sensory loss)
+ alien limb phenomenon
Corticobasilar degeneration
what is astereognosis?
Astereognosis (or tactile agnosia if only one hand is affected) is the inability to identify an object by active touch of the hands without other sensory input, such as visual or sensory information.
what is alien hand syndrome?
prevalent in 60% of ppl with corticobasal degeneration
failure of an individual to control the movements of his or her hand, which results from the sensation that the limb is “foreign”
+
The movements of the alien limb are a reaction to external stimuli and do not occur sporadically or without stimulation
other causes of parkinsonism
e.g. infection, vascular, drugs, trauma, genetic
infection: syphilis, HIV, CJD
vascular: multiple infarcts in substantia nigra
drugs: antipsychotics, metoclopramide
trauma: dementia pugilistica
Genetic: wilson’s disease
features of parkinsonism?
tremor: worse at rest, exacerbated by distraction, pill rolling
rigidity: increased tone (lead pipe), rigidity + tremor -> cog wheel rigidity
bradykinesia
gait: decreased arm swing, festinance, freezing
what produces the cog wheel rigidity in parkinsons?
rigidity (increased tone in all muscle groups)
+ tremor
features of bradykinesia of parkinsons?
slow initiation of movement with reduction of amplitude on repetition
expressionless face
monotonous voice
micrografia
how is Parkinson’s disease diagnosed?
Clinical diagnosis
DaTSCAN: Ioflupane has a high binding affinity for presynaptic dopamine transporters (DAT)
on-off effect of motor fluctuations in parkinsons?
refers to a switch between mobility and immobility in levodopa-treated patients, which occurs as an end-of-dose or “wearing off” worsening of motor function or, much less commonly, as sudden and unpredictable motor fluctuations.
Over time: much less ON and more OFF
invasive mx of parkinsons?
deep brain stimulation
Consider deep brain stimulation for people with advanced Parkinson’s disease whose symptoms are not adequately controlled by best medical therapy
Mx of Parkinson’s disease symptoms by MDT?
PD specialist nurses:
point of contact for support, including home visits when appropriate + clinical monitoring and medicines adjustment
Physiotherapy
Occupational Therapy:
help w ADLs
SALT:
to improve speech and communication +
improve the safety and efficiency of swallowing to minimise the risk of aspiration
Dietician:
mx of drooling of saliva in PD pts when SALT has been ineffective?
glycopyrronium bromide
contraindicated (for example, in people with cognitive impairment, hallucinations or delusions, or a history of adverse effects following anticholinergic treatment)
mx of Parkinson’s disease dementia?
anticholinesterase inhibitor e.g. rivastigmine
mx of psychotic symptoms (hallucinations and delusions) in PD pts?
Do not treat hallucinations and delusions if they are well tolerated
or
Reduce the dosage of any Parkinson’s disease medicines that might have triggered hallucinations or delusions, taking into account the severity of symptoms and possible withdrawal effects.
or
Quetiapine
mx of daytime sleepiness in PD pts
advise not to drive
adjust PD medications
consider modafinil
mx of rapid eye movement sleep behaviour disorder in PD pts?
Consider clonazepam or melatonin
if a medicines review has addressed possible pharmacological causes
1st line mx of PD patients whose motor symptoms impact on their quality of life
levodopa
e.g. pts who are biologically frail with comorbidities w lower baseline fitness
1st line mx of PD patients in early stages where motor symptoms do not impact on their quality of life
e.g. pts who are biologically fit
Dopamine agonists e.g. ropinirole, pramipexole
Levodopa
MAO-B inhibitors: rasagiline, selegiline
what is multiple sclerosis?
A chronic inflammatory condition of the CNS characterised by multiple plaques of demyelination disseminated in time and space.
classification of multiple sclerosis?
Relapsing-remitting: 80%
Secondary progressive
Primary progressive: 10%
Progressive relapsing
pathophysiology of multiple sclerosis?
Plaques of demyelination are hallmark
CD4 cell-mediated destruction of oligodendrocytes →demyelination and eventual neuronal death.
what is Lhermitte’s sign?
seen in MS
neck flexion ->
electric shocks traveling down neck -> trunk -> limbs
presentation of MS?
TEAM
tingling (sensory disturbance)
eye: optic neuritis (decreased central vision + pain w eye movement)
ataxia + other cerebellar signs
Motor: usually spastic paraparesis
clinical features of sensory disturbance in MS patients?
paraesthesia
decreased vibration sense
trigeminal neuralgia
clinical features of motor disturbance of MS patients?
spastic weakness
transverse myelitis (inflammation extends across the entire width of the spinal cord)
GI disturbances in MS?
swallowing problems
constipation
Genitourinary problems in MS?
Erectile dysfunction + anorgasmia
urinary retention
incontinence
cerebellar disturbances in MS?
falls
scanning dysarthria
trunk and limb ataxia
eye disturbances in MS?
diplopia
visual phenomena
bilateral conjugate gaze palsy
optic neuritis -> atrophy
what is Uhthoff’s phenomenon?
worsening of neurologic symptoms in multiple sclerosis (or other neurological, demyelinating conditions) when the body gets overheated
e.g. from hot weather, fever, exercise, saunas or hot tubs
presenting complaint of optic neuritis in multiple sclerosis patients?
pain on eye movement
rapidly worsening central vision
uhthoff’s phenomenon: vision worsens with heat (hot meal, bath, exercise)
Findings of optic neuritis on examination?
Decreased visual acuity
decreased colour vision (usually red affected first)
central scotoma
RAPD
what is internuclear ophthalmoplegia?
a disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction
- affected (ipsilateral) eye adducts minimally, if at all
- contralateral eye abducts, with nystagmus
- divergence of the eyes leads to horizontal diplopia
convergence generally preserved
what is the pathology causing internuclear ophthalmoplegia?
multiple sclerosis is often the cause- may cause bilateral INO
caused by injury/ disruption of medial longitudinal fasciculus that allows conjugate eye movement by connecting contralateral (PPRF-abducens) CN6 to ipsilateral (oculomotor) CN3
Ix of Multiple Sclerosis?
MRI Brain + Spine: typically hyper intense plaques
LP: IgG oligoclonal bands
Antibiodies: anti-Myelin basic protein
Evoked potentials: delayed auditory, visual and sensory
Diagnosis of MS?
clinical
demonstration of lesions disseminated in time and space
may use Macdonald Criteria
what is Devic’s syndrome?
loss of vision and spinal cord function.
optic neuritis + spinal cord dysfunction -> muscle weakness, reduced sensation/ loss of bladder or bowel control
similar to Multiple Sclerosis
differentiate between MS and Devic’s syndrome?
Neuromyelitis optica (NMO)- IgG: highly specific for Devic’s syndrome
Devic’s = neuromyelitis optica
MS variant w transverse myelitis and optic atrophy
mx of multiple sclerosis long-term
MDT team: specialist nurse, neurologist, physio, OT
regular follow up in MS clinic
Regular MRI scans (yearly)
mx of Multiple Sclerosis during an acute attack?
methylprednisolone
- decreases duration and severity of attacks
- doesnt influence long-term outcome
e. g. oral methylprednisolone 0.5 g daily for 5 days
what are some disease-modifying agents recommended for use for preventing relapse in MS patients?
Natalizumab: anti-alpha 4 integrin Ab
(decreases relapses by 2/3 in RRMS)
Alemtuzumab: anti-CD52 (2nd line in RRMS)
IFNB
Cladiribine, Dimethyl fumarate, fingolimod, ocrelizumab, teriflunomide
symptomatic medication for MS patients suffering from fatigue?
amantadine
Explain that MS-related fatigue may be precipitated by heat, overexertion and stress or may be related to the time of day.
symptomatic medication for MS patients suffering from depression?
SSRI e.g. citalopram
symptomatic medication for MS patients suffering from pain?
if trigeminal neuralgia: carbamazepine
other neuropathic pain: gabapentin, pregabalin, amitriptyline, duloxetine
symptomatic medication for MS patients suffering from spasticity?
assess and offer treatment for factors that may aggravate spasticity such as constipation, urinary tract or other infections, inappropriately fitted mobility aids, pressure ulcers, posture and pain.
gabapentin/ baclofen
symptomatic management of MS patients suffering from oscillopsia?
gabapentin
symptomatic management of MS patients suffering from urgency/ frequency?
oxybutynin/ tolterodine
symptomatic management of MS patients suffering from emotional lability?
amitriptyline
better vs worse prognostic signs of MS?
better:
female, <25, sensory signs @ onset, long interval between relapses, few MRI lesions
poor:
older, male, motor signs @ onset, many relapses early on, many MRI lesions, axonal loss
The following cranial nerves also carry parasympathetic fibres:
a. oculomotor
b. trigeminal
c. trochlear
d. hypoglossal
e. optic
A
Cranial nerves 3, 7, 10 and S3-5 carry parasympathetic fibres.
what is horner’s syndrome?
lesion of sympathetic supply to the eye
meiosis, ptosis, anhidrosis
what is the visual change assoc with swollen optic discs (papilloedema)?
enlarged blind spot
visual obscurations starting from periphery
features of optic neuritis?
painful on eye movement
reduced visual acuity
loss of red green colour vision
central scotoma
herniation of uncus of the temporal lobe can cause what type of nerve palsy?
third nerve palsy
causes of mononeuropathies?
vasculitides e.g. polyarteritis nodosa
diabetes - causes microvascular infarcts in individual nerves
entrapment and pressure palsies
e.g. Carpal tunnel
homonymous hemianopia
where could the lesion be?
optic tract
optic radiation
occipital lobe
grasp reflex absent
which lobe has pathology?
frontal lobe
what is pseudobulbar palsy?
characterized by the inability to control facial movements (such as chewing and speaking)
condition is usually caused by the bilateral damage to corticobulbar pathways (UMN lesion)
which cranial nerves lie in close proximity to the cerebellopontine angle?
V, VII, VIII cranial nerves
what type of deafness does otosclerosis produce?
conductive deafness
due to reduced compliance in the bony ossicles
how does excess prolonged noise lead to deafness?
damages the cochlear hair cells
-> sensorineural deafness
what is an acoustic neuroma?
develops on the vestibular portion of the VIII th nerve
-> progressive unilateral sensorineural deafness
tx of physiological/ essential tremors?
usually respont to beta blockers
commonest cause of small, poorly reactive pupil?
old age
lesion in midbrain may cause what change to eyes?
enlarged pupil
what is a sixth nerve palsy?
decreased abduction of affected eye
lateral rectus palsy
how does third nerve palsy present?
pupillary dilatation
(third n carries parasympathetic fibres to the constrictor pupillae)
ptosis
(levater palpebrae superioris)
diplopia in all positions of gaze
internuclear ophthalmoplegia
- where is the lesion?
medial longitudinal fasciculus
feature of ramsay-hunt syndrome?
painful vesicles
hyperacusis (nerve to stapedius affected)
loss of taste to anterior 2/3rd of tongue
features of anterior spinal artery occlusion?
loss of pain and sensation
dorsal columns (proprioception and vibration) spared
what causes painful neuropathies?
due to damage of slow unmyelinated fibres in peripheral nerves that carry pain and temp sensation
common causes: alcohol overuse, diabetes
what is cervical spondylosis?
age-related wear and tear affecting the spinal disks in your neck
features of cervical spondylosis?
can cause UMN signs due to compression of cervical spinal cord
+/- LMN signs due to compression of cervical roots
pain often worse at night
secondary headaches are common
what is temporal arteritis assoc with?
polymyalgia rheumatica
features of temporal arteritis?
headache
jaw claudication and scalp tenderness
(due to ischaemia of scalp/ muscles of mastication)
what is the dominant lobe involved with?
the dominant cerebral cortex is on the LEFT in majority of R-handed people and is specifically involved in reading, maths (dyscalculia), writing and langugage.
More subtle functions of the dominant parietal lobe include naming fingers (finger agnosia) and left-right discrimination.
monocular visual loss associated with pain on eye movement
suggests?
Optic neuritis
MS typically presents with?
optic neuritis
what is capgras syndrome seen in?
(patient accusing spouse of being an imposter)
Lewy body dementia
why is thymoma removed in multiple sclerosis?
remove potential risk of malignant transformation and not to improve the underlying disease
features of gerstmann syndrome?
Dysgraphia/agraphia: deficiency in the ability to write
Dyscalculia/acalculia: difficulty in learning or comprehending mathematics
Finger agnosia: inability to distinguish the fingers on the hand
Left-right disorientation
A left homonymous hemianopia may be due to?
lesion on right optic tract/ radiation
or
lesion of right occipital lobe
where is the lesion?
superior quadrantanopia
mnemonic = PITS (Parietal-Inferior, Temporal-Superior)
lesion in temporal lobe
or due to upper optic radiation
where is the lesion?
inferior quadrantanopia
mnemonic = PITS (Parietal-Inferior, Temporal-Superior)
lesion in parietal lobe
or lower optic radiation
what happens when u give folate to a pt with B12 deficiency?
giving folate to a patient deficient in B12 can precipitate subacute combined degeneration of the cord
Always ensure vitamin B12 levels are checked (and replenished) before giving folate for a macrocytic anaemia.
features of subacute combined degeneration of the cord?
Damage to the dorsal columns - loss of proprioception, light touch and vibration sense (sensory ataxia and a positive Romberg’s test).
Damage to lateral columns - spastic weakness and upgoing plantars (UMN signs).
Damage to peripheral nerves - absent ankle and knee jerks (LMN signs).
what is mononeuritis multiplex?
simultaneous or sequential involvement of individual non-contiguous nerve trunks.
acute or subacute loss of sensory and motor function of individual nerves
as the disease progresses, deficit(s) becomes more confluent and symmetrical, making it difficult to differentiate from polyneuropathy.
what psychiatric conditions are common comorbidities of parkinsons?
depression is the most common feature (affects about 40%)
dementia
psychosis
sleep disturbances
acute mx of migraine?
triptan + NSAID or triptan + paracetamol
prophylactic mx of migraine?
topiramate or propranolol ‘according to the person’s preference, comorbidities and risk of adverse events’.
Propranolol should be used in preference to topiramate in women of child bearing age as it may be teratogenic and it can reduce the effectiveness of hormonal contraceptives
what is Hoffman’s sign?
Hoffmann sign was elicited by flicking the nail of the middle finger. Any flexion of the ipsilateral thumb and/or index finger was considered positive.
‘finger flexor reflex’
problem in corticospinal tract (CNS)
what is degenerative cervical myelopathy?
often mistaken for carpal tunnel syndrome
Pain (affecting the neck, upper or lower limbs)
Loss of motor function (loss of digital dexterity, preventing simple tasks such as holding a fork or doing up their shirt buttons, arm or leg weakness/stiffness leading to impaired gait and imbalance
Loss of sensory function causing numbness
Loss of autonomic function (urinary or faecal incontinence and/or impotence) - these can occur and do not necessarily suggest cauda equina syndrome in the absence of other hallmarks of that condition
ix of degenerative cervical myelopathy?
MRI of cervical spine = gold standard test
It may reveal disc degeneration and ligament hypertrophy, with accompanying cord signal change.
mx of degenerative cervical myelopathy?
urgently referred for assessment by specialist spinal services (neurosurgery or orthopaedic spinal surgery).
decompressive surgery
timing of surgery is important, as any existing spinal cord damage can be permanent
Early treatment (within 6 months of diagnosis) offers the best chance of a full recovery
mx of malignancy causing cord compression?
Dexamethasone IV
consider chemo, radiotherapy and decompressive laminectomy
mx of abscess causing cord compression?
abx and surgical decompression
what is the cauda equina?
spinal cord itself ends at L1
horse’s tail
a bundle of spinal nerves and spinal nerve rootlets, L2-5, S1-5 and coccygeal n
cauda equina syndrome?
saddle anaesthesia
back pain
radicular pain down legs
bilateral flaccid arreflexic lower limb weakness
urinary/ faecal incontinence
poor anal tone
neurosurgical emergency
Mx of cauda equina syndrome?
Neurosurgical emergency!
urgent imaging (MRI spine)
surgical decompression
what is the conus medullaris?
the tapered, lower end of the spinal cord.
occurs near lumbar vertebral L1, L2, occasionally lower.
conus medullaris syndrome?
mixed UMN/ LMN weakness
early constipation and retention
back pain
sacral sensory disturbanced
ED
Mx of conus medullaris syndrome?
neurosurgical emergency
urgent Imaging
surgical decompression
What is spondylosis?
degeneration of the spinal column from any cause
usually due to trauma or age related wear and tear
commonly affects verterbral bodies and facet joints
may cause -> spinal cord or nerve root compression
presentation of cervical spondylosis?
usually asympto
neck stiffness +/- crepitus
stabbing/ dull arm pain
upper limb motor and sensory disturbances according to compression level
can -> myelopathy w quadraparesis and sphincter dysfunction
Lhermitte’s sign?
neck flexion -> tingling down spine
seen in MS/ compression of spinal cord
signs of cervical spondylosis?
Lhermitte’s sign: neck flexion -> tingling down spine
Hoffmann’s reflex: flick to middle finger pulp → brief pincer flexion of thumb and index finger (suggests hypertonia)
ix of cervical spondylosis?
MRI c spine
mx of cervical spondylosis?
conservative: stiff collar, analgesia
Medical: transforaminal steroid injection
Surgical: decompression- laminectomy or laminoplasty
presentation of lumbosacral spondylosis?
L5 and S1 roots most commonly compressed by prolapse of L4/5, L5/S1 discs
may present as severe pain on sneezing/ coughing
lower back pain
sciatica - shooting radicular pain down buttock and thigh
signs of lumbosacral spondylosis?
limited spinal flexion
pain on straight leg raise
L5 root compression features?
weak hallux extension +/- foot drop
(in foot drop due to L5 radiculopathy, weak inversion (tib post) helps distinguish from peroneal n palsy)
decreased sensation on inner dorsum of foot
S1 root compression features?
Weak foot plantarflexion and eversion
loss of ankle jerk
calf pain
decreased sensation over sole of foot and back of calf
mx of lumbar spondylosis?
Conservative: rest, analgesia, mobilisation/physio
Medical: transforaminal steroid injection
Surgical: discectomy or laminectomy may be
considered in cauda-equina syndrome, continuing pain or muscle weakness.
what is spinal stenosis?
Developmental predisposition ± facet joint osteoarthritis→ generalized narrowing of lumbar spinal canal.
most often lower back and neck
presentation of spinal stenosis?
spinal claudication
aching or heavy buttock and lower limb pain on walking
rapid onset
parasthesiae/ numbness
pain eased by leaning forward
pain on spine extension
negative straight leg raise
ix of spinal stenosis?
MRI
mx of spinal stenosis?
corsets
NSAIDs
epidural steroid injection
canal decompression surgery
Pathophysiology of bell’s palsy?
inflammatory oedema from entrapment of CNVII in narrow facial canal
usually of viral origin (HSV 1)
75% of facial palsy
features of Bell’s Palsy?
sudden onset e.g. overnight
complete, unilateral facial weakness in 24-72 h
- failure of eye closure -> dryness
- bell’s sign: eyeball rolls up on attempted closure
- drooling, speech difficulty
Numbness or pain around ear
decreased taste
Hyperacusis: stapedius palsy
Ix of Bell’s Palsy?
Serology: Borrelia or VZV abs
MRI: SOL, stroke, MS
LP
Mx of Bell’s Palsy?
prednisolone within 72 h
60mg/d PO for 5/7 followed by tapering
valaciclovir if zoster suspected
protect eye: dark glasses, artificial tears, tape eyes closed at night
complications of Bell’s palsy?
aberrant neural connections
synkinesis: e.g. blinking causes up turning of mouth
crocodile tears: eating stimulates unilateral lacrimation, not salivation
pathophysiology of ramsay hunt syndrome?
reactivation of VZV in geniculate ganglion of CNVII (Facial N)
features of ramsay hunt syndrome?
preceding ear pain or stiff neck
vesicular rash in auditory canal +/- tympanic membrane, pinna, tongue, hard palate
ipsilateral facial weakness, ageusia, hyperacusis
may affect CN8 -> vertigo, tinnitus, deafness
mx of Ramsay Hunt syndrome?
if diagnosis suspected give valaciclovir and prednisolone within first 72h
what is mononeuritis multiplex?
2 or more peripheral nerves affected
usually systemic cause: DM most commonly
median nerve palsy?
sensory: radial 3.5 fingers and palm
tinels and phalens +ve
Thenar wasting
most hand muscles of the anterior forearm -> weakness of wrist and finger flexion + thumb abduction/ flexion/ opposition
ulnar nerve palsy?
sensory loss: ulnar 1.5 fingers
motor: partial claw hand, hypothenar wasting
weakness and wasting of 1st dorsal interosseous
froment’s sign +ve
Radial n palsy?
sensory: dorsal thumb root (snuff box)
motor:
low lesion: finger drop
high: wrist drop
v high: triceps paralysis, wrist drop
tibial n palsy?
sensory loss: sole of foot
motor:
cant plantar flex -> cant stand on tiptoe
weak foot inversion
weak toe flexion
common peroneal n palsy?
sensory loss: below knee laterally
motor: foot drop (cant walk on heels)
weak ankle dorsiflexion, eversion
(inversion intact)
sciatic n palsy?
sensory loss: below knee laterally and foot
motor:
hamstrings
all muscles below knee
phrenic n palsy?
C3-5
orthopnoea + raised hemidiaphragm
lateral cutaneous n of thigh palsy?
meralgia paraesthetica
- anterolateral burning thigh pain
peripheral neuropathy main causes?
DM
B12 deficiency
Alcohol
features of peripheral neuropathy?
glove and stocking distribution
deep tendon reflexes may be decreased/ absent
signs of trauma or joint deformity (charcot’s joints)
diabetic and alcoholic neuropathies are painful
B12 deficiency -> SCDC what fibres are lost first?
dorsal columns
causes of autonomic neuropathy?
DM
HIV
SLE
GBS, LEMS
features of autonomic neuropathy?
postural hypotension
ED, ejaculatory failure
decreased sweating
constipation/ nocturnal diarrhoea
urinary retention
horners
Autonomic function tests?
BP: postural drop > 20/10 mmHg
ECG: variation > 10 bpm w respiration
what is Miller-Fisher syndrome?
variant of guillain-barre
opthalmoplegia + ataxia + areflexia
causes of guillain- barre?
antibodies cross react to gangliosides
may be idiopathic
bacteria: campylobacter jejuni, mycoplasma
Viruses: CMV, EBV, HSV
Vaccines: esp rabies
features of guillain barre?
symmetrical, ascending flaccid weakness/ paralysis
LMN signs: areflexia, fasciculations
progressive phase lasts ≤ 4wks
autonomic neuropathy
**breathing problems
ix of guillain barre syndrome?
serology for anti-ganglioside abs
evidence for infection e.g. stool sample
demyelinating nerve conduction studies: slow conduction velocities
Protein in CSF: protein often > 5.5 g/L, normal WCC
Mx of Guillain Barre Syndrome?
Supportive:
airway/ ventilation: ITU if FVC < 1.5L
analgesia: NSAIDs, gabapentin
autonomic: may need inotropes, catheter
Antithrombotic: TEDS, LMWH
Immunosuppression: IVIG, plasma exchange
Physiotherapy: prevent flexion contractures
what is charcot marie tooth syndrome?
a type of hereditary motor and sensory neuropathy
HMSN1:
commonest form
demyelinating
AD mutation
HMSN2:
second commonest
axonal degeneration
clinical features of charcot marie tooth
onset at puberty
thickened, enlarged nerves esp common peroneal
Motor: foot drop -> high stepping gait
weak ankle dorsiflexion and toe extension
absent ankle jerks
symmetrical muscle atrophy: “champagne bottle” legs due to peroneal muscle wasting, claw hands
Pes cavus (high arched feet)
Sensory: variable loss of sensation in a stocking distribution
neuropathic pain in some
Mx of Charcot Marie Tooth?
Supportive
Physio
Podiatry
Orthoses e.g. ankle braces
Ix of Charcot Marie Tooth?
Genetic Testing: PMP22 gene mutation
Nerve conduction studies: decreased conduction speed in HMSN1
Characteristics of Motor Neuron Disease?
Cluster of degenerative disease characterised by axonal degeneration of neurones in the motor cortex, CN nuclei and anterior horn cells.
UMN and LMN signs
NO sensory loss or sphincter disturbance
dont affect eye movements
Causes of motor neuron disease?
unknown
10% familial: e.g. SOD1 mutation
Ix of motor neuron disease?
Brain/ Cord MRI: exclude structural cause
LP: exclude inflammatory cause
EMG: shows denervation
Diagnosis of motor neuron disease?
Use Revised El Escorial Diagnostic criteria
Mx of motor neuron disease?
MDT: neurologist, physio, OT, specialist nurse, GP, family
Riluzole: antiglutamatergic that prolongs life by ~3 mo
Supportive:
drooling: propantheline or amitriptyline
dysphagia: NG/ PEG feeding
Resp failure: NIV
Pain: analgesia
spasticity: baclofen
prognosis of motor neuron disease?
most die within 3 years
-> from bronchopneumonia and resp failure
worse prognosis: elderly, female, bulbar involvement
types of MND?
Amyotrophic Lateral Sclerosis: 50%
loss of motor neurones in cortex and ant horn -> UMN signs and LMN wasting + fasciculation
Progressive Bulbar Palsy: 10%
only affects CN 9-12 -> bulbar palsy
Progressive muscular atrophy: 10%
anterior horn cell lesion -> LMN signs only
Distal to proximal
Primary lateral sclerosis
loss of Betz cells in motor cortex -> mainly UMN signs
Marked spastic leg weakness and pseudobulbar palsy
no cognitive decline
which type of Motor neuron disease has LMN signs only?
progressive muscular atrophy
-> only anterior horn cell lesions
Features of Bulbar Palsy?
LMN lesions of tongue, talking and swallowing
flaccid, fasciculating tongue
speech: quiet or nasal
normal/ absent jaw jerk
loss of gag reflex
Pseudobulbar Palsy features?
Bilateral lesions above mid pons e.g. corticobulbar tracts -> UMN lesions of swallowing and talking
Spastic tongue
slow tongue movements w slow deliberate speech: hot potato speech
Brisk jaw jerk
Emotional incontinence
Bulbar vs Pseudobulbar palsy?
Bulbar: LMN lesions of tongue, swallowing, speaking
Pseudobulbar: UMN lesions of tongue, swallowing, talking,
features of poliomyelitis?
asymmetric LMN paralysis
No sensory involvement
may be confined to upper or lower limbs or both
resp muscle paralysis can -> death
+ fever, sore throat, myalgia
poliovirus affects anterior horn cells
Pathophysiology of Duchenne’s Muscular Dystrophy?
X-linked recessive, 30% spontaneous -> non functional dystrophin
Dystrophin is important to maintain the muscle fiber’s cell membrane
Presentation of duchenne’s muscular dystrophy?
~4 yo
muscle loss -> weakness
difficulty standing
calf pseudohypertrophy
Gower’s sign +ve
resp failure
Ix of Duchenne’s muscular dystrophy?
creatine kinase levels extremely high
pathophysiology of Becker’s muscular dystrophy?
X linked recessive
partially functioning dystrophin
presents later than duchenne’s, is less severe and has better prognosis
pathophysiology of fascioscapulohumeral muscular dystrophy (landouzy-dejerine)?
autosomal dominant
affects the skeletal muscles of the face (facio), scapula (scapulo) and upper arms (humeral)
presentation of fascioscapulohumeral muscular dystrophy?
onset @ 12-14 yo
weakness of face, shoulders and upper arms (often asymmetric w deltoids spared)
Winging of scapula
foot drop
bilat sensorineural hearing loss
life expectancy threatened by resp insufficiency
pathophysiology of myotonic dystrophy?
autosomal dominant
gradually worsening muscle loss and weakness
muscles often contract and are unable to relax (tonic muscle spasm)
presentation of myotonic dystrophy?
face:
myopathic facies: long, thin, expressionless
wasting of fascial muscles and SCM
bilateral ptosis
dysarthria
hands:
myotonia: slow relaxation
e. g. unable to release hand after shake
wasting and weakness of distal muscles + areflexia -> wrist drop
percussion myotonia: percuss thenar eminance -> involuntary thumb flexion
others:
frontal balding
cataracts
DM
Cardiomyopathy
dysphagia
testicular atrophy
mx of Myotonic dystrophy?
no mx for weakness
phenytoin may improve myotonia
caution w GA: high risk of anaesthetic complications
features of inclusion body myositis?
type of inflammatory myopathy
asymmetric weakness affecting distal and prox muscles
- early involvement of quads, ankle dorsiflexors and wrist/ finger flexors
- > loss of grip strength and decreased dexterity
dysphagia is v common
myalgia is uncommon
what drugs are assoc w idiopathic intracranial HTN?
oral contraceptive pill, steroids, tetracycline, vitamin A, lithium
what antiplatelet regimens are recommended for secondary prevention following acute ischaemic stroke?
Aspirin 300 mg for 2 weeks after stroke then Clopi 75 mg for the long term
Indications for thrombolysis?
administered within 4.5 hours of onset of stroke symptoms
haemorrhage has been definitively excluded (i.e. Imaging has been performed)
what thrombolysis mx is currently recommended?
alteplase
pathophysiology of NF1 vs NF2?
both autosomal dominant
NF1: aka von Recklinghausen’s syndrome. It is caused by a gene mutation on chromosome 17 which encodes neurofibromin
NF2: gene mutation on chromosome 22
Features of NF1?
Café-au-lait spots (>= 6, 15 mm in diameter)
Axillary/groin freckles
Peripheral neurofibromas
Iris hamartomas (Lisch nodules) in > 90%
Scoliosis
Pheochromocytomas
Features of NF2?
Bilateral vestibular schwannomas (SNHL first sign)
Multiple intracranial schwannomas, mengiomas and ependymomas
cafe au lait spots in NF1?
at least how many? and size?
> 6, >15mm across
complications of neurofibromas?
sarcomatous change
compression:
- nerve roots: weakness, pain, paraesthesia
GI: bleeds, obstruction
What are Lisch nodules?
iris hamartomas
seen in NF1
use a slit lamp
mx of NF1?
MDT
Yearly BP and cutaneous review
Excise some neurofibromas
genetic counselling
Juvenile posterior subcapsular lenticular opacity?
form of cataract
bilateral
assoc w NF2
occur before other manifestations and may be useful for screening those @ risk
Mx of NF2?
Hearing tests from puberty in affected families (bilat vestibular schwannomas)
MRI brain if abnormality detected
(look for schwannomas, meningiomas, gliomas)
pathophysiology of myasthenia gravis?
autoimmune disease mediated by antibodies against nicotinic Ach receptors
interferes with neuromuscular transmission via depletion of working post synaptic receptor sites
presentation of myasthenia gravis?
increasing muscular fatigue
- extra-ocular: bilateral ptosis, diplopia
- bulbar: voice deteriorates on counting to 50
- face: myastthenic snarl on attempting to smile
- neck: head droop
- limb: asymmetric proximal weakness
normal tendon reflexes
weakness worsened by pregnancy, infection, emotion, drugs (BB, gent, opiates, tetracyclines)
Ix of myasthenia gravis?
Tensilon Test: IV edrophonium, +ve if power improves within 1 min
Anti-AChR abs increased
EMG: decreased response to a train of impulses
Resp function: decreased FVC
Thymus CT (thymoma may be present)
TFTs
Pathophysiology of Lambert-Eaton Myasthenic Syndrome?
antibodies to VGCC -> decreased influx of calcium during presynaptic excitation -> decreased presynaptic ACh-vesicle fusion
causes of lambert eaton myasthenic syndrome?
autoimmune
paraneoplastic e.g SCLC
presentation of lambert eaton myasthenic syndrome?
Muscle fatigue - movement improves symptoms
leg weakness early (before eyes)
autonomic neuropathy and areflexia
small response to edrophonium
antibodies found in lambert eaton myasthenic syndrome?
Anti-VGCC abs
mx of lambert eaton myasthenic syndrome?
IVIG
Do regular CXRs as symptoms may precede Cancer by 4 years
Myasthenia gravis assoc w ?
<50 yrs: more common in women
assoc with other autoimmune disease (DM, RA, Graves)
thymic hyperplasia
Treatment of myasthenia gravis?
symptom control
- anticholinesterase e.g. pyridostigmine
Immunosuppression:
- tx relapses with prednisolone
Thymectomy:
- consider if young onset and disease not controlled by anticholinesterases
- remission in 25%, benefit in further 50%
Complications of Myasthenia gravis?
myasthenic crisis:
- weakness of respiratory muscles
- monitor FVC -> ventilation support if < 20ml/kg
- plasmapheresis or IVIG
- tx trigger for relapse (e.g. drugs, infection)
pathophysiology of botulism?
Botulinum toxin prevents ACh vesicle release
Presentation of botulism?
Descending flaccid paralysis with no sensory signs
Anti-cholinergic effects: mydriasis, cycloplegia, n/v, dry mouth, constipation
mx of botulism?
benpen + antiserum
cerebellar vermis vs cerebellar hemisphere lesions?
Cerebellar hemisphere lesions cause peripheral (‘finger-nose ataxia’)
Cerebellar vermis lesions cause gait ataxia (locomotion)
Acute vs chronic subdural haematoma on CT?
On CT imaging, acute haematomas appear bright (hyperdense) whereas chronic haematomas appear dark (hypodense).
who is at risk of chronic subdural haematomas?
Elderly and alcoholic patients are particularly at risk of subdural haematomas since they have brain atrophy and therefore fragile or taught bridging veins.
Rupture of the small bridging veins within the subdural space rupture and cause slow bleeding.
Presentation is typically a several week to month progressive history of either confusion, reduced consciousness or neurological deficit.
presentation of intrinsic cord disease?
Painless
Early sphincter / erectile dysfunction
Bilateral motor and sensory disturbance below
lesion
what is brown-sequard syndrome?
Hemi-cord lesion
Ipsilateral loss of proprioception and vibration
sense
Ipsilateral UMN weakness
Contralateral loss of pain sensation (since pain fibres decussate at level of entry)
bilateral acoustic neuromas assoc w?
NF2
Ix of vestibular schwannoma / acoustic neuroma?
MRI cerebellopontine angle
what is syringomyelia?
syrinx: fluid filled cavity formed within the spinal cord
commonly in cervical cord
Symptoms may be static for yrs but then worsen fast
e.g. on coughing, sneezing as ↑ pressure → extension
Syrinx expands ventrally affecting:
- Decussating spinothalamic neurones
- Anterior horn cells
- ant Corticospinal tracts
causes of syringomyelia?
Blocked CSF circulation w decreased flow from posterior fossa
- Arnold-Chiari malformation
- masses
Spina bifida
2o to cord trauma, myelitis, cord tumours, and AVMs
signs of syringomyelia?
Dissociated sensory loss:
- absent pain and temp
- preserved touch, proprioception and vibration
- root distribution reflects syrinx location (usually cape distribution: upper limbs and chest)
Wasting/ weakness of hands +/- claw hand
Loss of reflexes in upper limb
Charcot joints: shoulder and elbow
Horner’s syndrome
syringobulbia: cerebellar and lower CN signs
UMN weakness in lower limbs w upgoing plantars
ix of syringomyelia?
MRI spine
what is friedrich’s ataxia?
auto recessive progressive degeneration of Dorsal root ganglions, spinocerebellar and corticospinal tracts and cerebellar cells
mitochondrial disorder
onset in teenage years
assoc w HOCM and mild dementia
Adult T cell leukaemia/ lymphoma
+
Tropical spastic paraplegia
- slowly progessing spastic paraplegia
- sensory loss and parasthesia
- bladder dysfunction
HTLV- 1
-> HTLV myelopathy
gold standard of venous sinus thrombosis?
MR venogram
mx of cluster headaches?
Acute: 100% Oxygen
triptans e.g. sc sumatriptan
2/52 course of steroids may reduce attack frequency at onset of the cycle
what anaesthetic drug is not as effective in myasthenia gravis pts?
suxamethonium
What kind of diet is an established treatment for children with epilepsy that is hard to control and is generally unresponsive to antiepileptic medications?
Ketogenic diet
high in fat, low in carb, controlled protein
prophylaxis of migraine?
1st line: topiramate or propranolol
presentation of lacunar infarct?
1 of the following:
- unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
- pure sensory stroke.
- ataxic hemiparesis
presentation of Weber’s syndrome?
ipsilateral III palsy
contralateral weakness
CT head
high density fluid (Blood) in the cerebral sulci, sylvian fissure and basal ganglia
-> subarachnoid haemorrhage
usually due to rupture of berry aneurysm
Most common cause of mengitis in adults?
neisseria meningitidis
Pneumococcus
Complications of Meningitis?
deafness (most common)
other neurological: epilepsy, paralysis
infective: sepsis, intracerebral abscess
pressure: brain herniation, hydrocephalus
what triggers pain in trigeminal neuralgia?
light touch, including washing, shaving, smoking, talking, and brushing the teeth
Mx of trigeminal neuralgia?
1st line carbamazepine
Gold standard Ix for Cervical myelopathy?
MRI cervical spine
Mx of cervical myelopathy?
All should be urgently referred for assessment by specialist spinal services (neurosurgery or orthopaedic spinal surgery)
early tx is essential, as any existing spinal cord damage can be permanent
decompressive surgery only effective treatment.
close observation is an option for mild stable disease.
Beware of physio: only initiated by specialist services, as manipulation can cause more damage
Diagnosis of Lewy Body Dementia?
usually clinical
SPECT increasingly used - specificity of 100%
Mx of Lewy Body dementia?
both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s.
Mx of Acute ischaemic stroke which develops into haemorrhagic transformation?
stop aspirin 300mg & control BP (<140)
features of fourth n palsy?
Cant depress eye, look medially
vertical diplopia
classically noticed when reading book or going down stairs
subungual fibromata?
tuberous sclerosis:
ash leaf spots
shagreen patches
adenoma sebaceum
1st line ix for suspected vestibular schwannoma?
audiogram and gadolinium-enhanced MRI head scan (MRI of cerebellopontine angle)
adverse effects of Levodopa?
dyskinesia
‘on-off’ effect
postural hypotension
cardiac arrhythmias
nausea & vomiting
psychosis
reddish discolouration of urine upon standing
levodopa features?
usually combined with a decarboxylase inhibitor (e.g. carbidopa or benserazide) to prevent peripheral metabolism of L-dopa to dopamine
reduced effectiveness with time (usually by 2 years)
no use in neuroleptic induced parkinsonism
features of essential tremor?
Postural tremor: worse if arms outstretched
Improved by alcohol and rest
Titubation (nodding movement of head or body)
Often strong FH
Features of migraine more common in children?
attacks may be shorter-lasting
headache is more commonly bilateral
GI disturbance is more prominent.
What are some typical auras with migraines?
transient hemianopic disturbance or a spreading scintillating scotoma (‘jagged crescent’). Sensory symptoms may also occur
Features of Neuroleptic malignant syndrome?
more common in young male patients
onset usually in first 10 days of treatment or after increasing dose
pyrexia
rigidity
tachycardia
raised CK and WCC
Mx of neuroleptic malignant syndrome?
stop antipsychotic
IV fluids to prevent renal failure
dantrolene* may be useful in selected cases
bromocriptine, dopamine agonist, may also be used
triggers for neuroleptic malignant syndrome?
antipsychotics
dopaminergic drugs (such as levodopa) for Parkinson’s disease, usually when the drug is suddenly stopped or the dose reduced
bilateral sensorineural hearing loss + cafe au lait spots?
NF II
Neurofibromatosis type 2 is associated with bilateral vestibular schwannomas
what cranial nerves pass through the superior orbital fissure?
III, IV, V1, VI
trigeminal nerve palsy causes?
trigeminal neuralgia
loss of corneal reflex (afferent)
loss of facial sensation
paralysis of mastication muscles
deviation of jaw to weak side
Facial n palsy causes?
flaccid paralysis of upper + lower face
loss of corneal reflex (efferent)
loss of taste
hyperacusis
Hypoglossal n palsy?
Tongue deviates towards side of lesion
Accessory n palsy?
Lesions may result in;
weakness turning head to contralateral side
Vagus n palsy causes?
uvula deviates away from site of lesion
loss of gag reflex (efferent)
glossopharyngeal n palsy causes?
hypersensitive carotid sinus reflex
loss of gag reflex (afferent)
Corneal reflex
afferent and efferent?
afferent: V1
Efferent: Facial n
Jaw jerk
afferent and efferent?
afferent: mandibular nerve V3
efferent: Mandibular nerve
gag reflex / carotid sinus
afferent and efferent?
afferent: glossopharyngeal (IX)
Efferent: Vagal (X)
Lacrimation
afferent and efferent?
afferent: ophthalmic V1
efferent: facial n
bitemporal hemianopia
upper quadrant defect > lower quadrant defect?
inferior chiasmal compression, commonly a pituitary tumour
bitemporal hemianopia
lower quadrant defect > upper quadrant defect?
superior chiasmal compression, commonly a craniopharyngioma
ondansetron MOA?
5-HT3 antagonists
used mainly in the management of chemotherapy related nausea
act in the chemoreceptor trigger zone area of the medulla oblongata
SE: constipation is common
A 60 year-old male presents with clumsy hands. He has been dropping cups around the house. His wife complains he doesnt answer his mobile as he struggles to use it. His symptoms have been gradually deteriorating over the preceding months.
Degenerative cervical myelopathy
loss of fine motor function in both upper limbs
in what situation might you consider stopping a pt’s anti epileptic drugs?
if seizure free > 2 yrs
AEDs stopped over 2-3 mo
ix. of degenerative cervical myelopathy?
MRI cspine
may reveal disc degeneration and ligament hypertrophy, with accompanying cord signal change.
features of common peroneal n palsy?
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
prophylaxis of migraine?
topiramate or propranolol
riboflavinn may help
menstrual migraine: frovatriptan
MRC power grading?
Grade 0: No muscle movement
Grade 1: Trace of contraction
Grade 2: Movement at the joint with gravity eliminated
Grade 3: Movement against gravity, but not against added resistance
Grade 4: Movement against an external resistance with reduced strength
Grade 5: Normal strength
recommended screening tool to assess for likelihood of stroke?
ROSIER is an acronym for ‘Recognition Of Stroke In the Emergency Room’
Exclude hypoglycaemia first, then assess
A stroke is likely if > 0
mx of acute cluster headaches?
100% oxygen (80% response rate within 15 minutes)
subcutaneous triptan (75% response rate within 15 minutes)
prophylaxis of cluster headache?
verapamil
some evidence to support a tapering dose of prednisolone
blockage of which artery causes aphasia?
Dominant hemisphere middle cerebral artery strokes cause aphasia
usually L
triad of normal pressure hydrocephalus?
urinary incontinence
dementia and bradyphrenia
gait abnormality (may be similar to Parkinson’s disease)
what is autonomic dysreflexia?
clinical syndrome occurs in patients who have had a spinal cord injury at, or above T6 spinal level
Briefly, afferent signals, most commonly triggered by faecal impaction or urinary retention cause a sympathetic spinal reflex via thoracolumbar outflow. The usual, centrally mediated, parasympathetic response however is prevented by the cord lesion.
-> unbalanced physiological response, characterised by 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.
antiemetic recommended for Parkinsons?
Domperidone
Domperidone does not cross the blood-brain barrier and therefore does not cause extra-pyramidal side-effects
which type of MND carries the worst prognosis?
Progressive bulbar palsy
- palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
mx of fatigue in MS?
once other problems (e.g. anaemia, thyroid or depression) have been excluded NICE recommend a trial of amantadine
CBT/ mindfulness
mx of spasticity in MS?
baclofen and gabapentin are first-line
physio
mx of bladder dysfunction in MS?
guidelines stress the importance of getting an ultrasound first to assess bladder emptying - anticholinergics may worsen symptoms in some patients
if significant residual volume → intermittent self-catheterisation
if no significant residual volume → anticholinergics may improve urinary frequency
Mx of oscillopsia (visual fields appear to oscillate) in MS?
gabapentin is first-line
what anti-emetics are impt in chemotx related nausea?
5-HT3 antagonists
e.g.
ondansetron
granisetron
mainly act in the chemoreceptor trigger zone area of the medulla oblongata.
what is a lacunar stroke?
most common type of ischaemic stroke, and results from the occlusion of small penetrating arteries that provide blood to the brain’s deep structures
5 classic syndromes
- hemiparesis / pure motor
- Ataxic hemiparesis
- dysarthria/ clumsy hand
- Pure sensory
- Mixed sensorimotor
what to give Parkinsons patients if they are unable to take their levodopa orally?
dopamine agonist patch as rescue medication to prevent acute dystonia
viral labyrinthitis vs vestibular neuritis?
vestibular neuritis = only vestibular nerve is involved -> no hearing impairment
Labyrinthitis = both vestibular nerve and labyrinth involved -> vertigo and hearing impairment
symptoms of viral labyrinthitis?
vertigo: not triggered by movement but exacerbated by movement
nausea and vomiting
hearing loss: may be unilateral or bilateral, with varying severity
tinnitus
preceding or concurrent symptoms of upper respiratory tract infection
signs of labyrinthitis?
spontaneous unidirectional horizontal nystagmus towards the unaffected side
sensorineural hearing loss
abnormal head impulse test: signifies an impaired vestibulo-ocular reflex
gait disturbance: the patient may fall towards the affected side
normal skew test
abnormality on inspection of the external ear canal and the tympanic membrane e.g. vesicles in herpes simplex infection
What is intranuclear ophthalmoplegia?
problem in the communication between CN VI (abducens) of the R eye and CN III (occulomotor) of the L eye or vice versa
- cant maintain conjugate gaze -> diplopia
- the side able to abduct will develop compensatory nystagmus
mx of recalcitrant psoriasis (not responsive to conventional treatment)?
topical retinoids
phototherapy
oral drugs e.g. methotrexate, cyclosporin
what hormone can be used to differentiate between true seizure and pseudoseizure?
serum prolactin
what is Hoover’s sign?
differentiates between organic and non-organic lower leg weakness
due to synergistic contraction: examiner would feel the ‘normal’ limb pushing downwards against their hand as the patient tries to lift the ‘weak’ leg.
if -ve: not a true weakness
Features of Lambert-Eaton?
repeated muscle contractions lead to increased muscle strength*
limb girdle weakness (affects lower limbs first)
hyporeflexia
autonomic symptoms: dry mouth, impotence, difficultly micturating
EMG in Lambert Eaton?
incremental response to repetitive electrical stimulation
Mx of Lambert Eaton syndrome?
treatment of underlying cancer (ie. SCLC)
immunosuppression (prednisolone and/or azathioprine)
intravenous immunoglobulin therapy and plasma exchange may be beneficial
causes of lambert eaton syndrome?
autoimmune
malignancy: SCLC, breast, ovarian ca
What blood tests are done to exclude reversible causes of dementia?
FBC, U&E, LFTs, calcium, glucose, TFTs, vitamin B12 and folate levels.
In secondary care, what ix can be done to exclude reversible causes of dementia?
neuroimaging
e.g. subdural, normal pressure hydrocephalus
