NEUROLOGY Flashcards
what is Bell’s palsy?
unilateral LOWER motor neuron facial nerve palsy of rapid onset
is the forehead affected in Bell’s palsy? what does this help differentiate it from?
YES
stroke commonly leaves the forehead spared (UMN lesion rather than LMN)
what causes Bell’s palsy?
unknown - could be from inflammation/infection of facial nerve
RFs for Bell’s palsy
- age 15-45
- diabetes
- immunocompromise
- obese
- HTN
- pregnancy
how does Bell’s palsy present?
- rapid onset (<72h)
- unilateral facial weakness/paralysis e.g. loss of forehead and brow movement, inability to close eyes/drooping eyelids, loss of nasolabial folds and drooping lip
- eye probs e.g. dry, painful, excessive tearing
- numbness/tingling of cheek and mouth
- may have ear pain on affected side
will have no other involvement of the body!!! otherwise healthy
investigations for Bell’s palsy. how is it diagnosed?
physical exam - cranial nerves, parotid gland, skin of head and neck, eyes
routine lab tests/imaging not required in primary care for new-onset Bell’s palsy
diagnosis made when no other condition is found to be causing the sx
management of Bell’s palsy
- IF presenting within 72h, can give prednisolone 50mg OD
- self-limiting, will recover within 2-3w
what is an acoustic neuroma?
which cells/nerve is it associated with?
a benign tumour of the Schwann cells arising from the vestibulocochlear nerve innervating the inner ear
what age patients are normally affected by an acoustic neuroma?
what are 3 risk factors?
40-60 years old
RFs
- ionising radiation to head/neck
- neurofibromatosis type 2 (genetic condition)
- family hx
what type of tumour is an acoustic neuroma?
a cerebellopontine angle tumour (occurs in the posterior fossa)
which nerve can get compressed if an acoustic neuroma grows large enough?
facial nerve
signs and symptoms of an acoustic neuroma
GRADUAL ONSET OF…
1. unilateral sensorineural hearing loss
2. unilateral tinnitus
3. dizziness/imbalance
4. sensation of fullness in ear
IF compresses facial nerve > facial nerve palsy (forehead not spared)
clinical hearing tests for an acoustic neuroma and their results
SENSORINEURAL LOSS
1. Rinne’s - air conduction greater than bone conduction bilaterally
2. Weber’s - sound lateralises to unaffected ear
1st line and gold standard investigations for an acoustic neuroma
1st line = audiometry with audiogram
Gold std = MRI head
treatment options for an acoustic neuroma (3)
- conservative + monitoring (if v small, no sx)
- surgery - partial or total removal
- radiotherapy
what pattern of hearing loss will an acoustic neuroma show on an audiogram?
sensorineural hearing loss
what is anterior cord syndrome?
an incomplete spinal cord lesion affecting the anterior 2/3rds of the spine
what can cause ischaemia of the anterior spinal artery, leading to anterior cord syndrome? (think iatrogenic, direct, indirect)
- iatrogenic e.g. cross-clamping of aorta during thoracic/AAA repair
- direct injury/trauma
- crush injury
- burst fracture
- gunshot/knife injury - indirect injury (occlusion/hypoperfrusion of ASA)
- severe hypotension
- atherothrombotic disease
- vasculitis
what causes anterior cord syndrome?
ischaemia within the anterior spinal artery
pathophysiology of anterior cord syndrome…
what tracts are supplied by the ASA?
so what is characteristic of anterior cord syndrome?
- ischaemia within ASA
- ASA supplies blood to anterior 2/3 of spinal cord and to the bilateral SPINOTHALAMIC and CORTICOSPINAL tracts
- these tracts are responsible for pain and temp (spinothalamic) and voluntary movement (corticospinal)
- the dorsal column (fine touch, proprioception, vibration) is spared
so ACS is characterised by a loss of pain and temperature sensation, and loss of motor function
signs and symptoms of anterior cord syndrome
BELOW THE LEVEL OF THE LESION…
1. bilateral loss of pain and temp sensation
2. bilateral loss of motor movement (paralysis)
3. preservation of fine touch, proprioception and vibration
initial and gold std investigations for anterior cord syndrome
initial…
1. bloods - FBC, U&E, clotting, cultures, inflamm markers
- LP and CSF analysis
(to rule out MS, infection or inflamm disease) - echo
(to rule out source of embolism e.g. IE)
GOLD STD…
= MRI
what will be seen on MRI in anterior cord syndrome?
thin, pencil-like hyperintensities of the anterior cord (= ischaemia)
management for anterior cord syndrome
- depends on cause, may need surgery if direct damage or blood thinners e.g. apixaban if atherosclerosis
- MDT including physio
possible causes of secondary epilepsy
- underlying structural lesions - trauma, neoplasms, malformations, stroke
- metabolic - alcohol, electrolyte disorders
- infection e.g. encephalitis
- rare genetic diseases e.g. ion channel mutations
a) what is a partial/focal seizure?
b) what are the two types?
a) a seizure occurring in only one hemisphere/lobe
b) simple partial - pt remains conscious and often remembers
complex partial - pt has impaired/loses consciousness
how does the ICTAL phase of a partial/focal seizure present if the lobe is…
a) temporal
b) frontal
c) parietal
d) occipital
a) think memory, emotion and receptive speech…
auras e.g. deja vu, auditory hallucinations, funny smell,
out of body experience e.g. lip smacking, chewing, fiddling
b) think motor and thought processing…
Jacksonian march - seizure marches up/down homonculus starting in face or thumb
c) sensory disturbance e.g. tingling, numbness
d) visual phenomena e.g. spots, lines, flashes
what is a generalised seizure? who does it more commonly affect and what is ALWAYS impaired?
a seizure affecting BOTH hemispheres of the brain, no localising features
more common in children
consciousness always impaired
what are the 6 seizure types?
- tonic - muscles stiff and flexed, often causes fall (back)
- atonic - muscles relaxed and floppy, loss of tone, often causes fall (forwards)
- clonic - violent muscle contractions/convulsions
- tonic-clonic (gran mal) - tonic phase followed by convulsions
- myoclonic - short muscle twitches
- absence - brief, lost and regain conscious temporarily e.g. stopping mid-sentence, zone out then continue
possible preictal signs/symptoms - how long can this phase last?
- lasting hours/days
- may be change in mood/behaviour
- aura e.g. feeling in gut, flashing lights (implies focal e.g. temporal)
general postictal signs/symptoms
- headache
- confusion
- myalgia/sore tongue
focal lobe specific postictal symptoms
a) temporal
b) frontal
c) parietal
d) occipital
a) emotional disturbance, dysphasia, bizarre associations, hallucinations
b) motor features e.g. pedalling legs, motor arrest, dysphasia, speech arrest, postictal Todd’s palsy (paralysis)
c) sensory disturbance e.g. tingling, numbness, pain
d) visual e.g. spots, lines, flashes
investigations following a seizure
- bloods (FBC, U&Es, LFTs, gluocse) - rule out infection, anaemia, electrolyte abnormalities, metabolic probs, hypoglycaemia
- EEG
- MRI
which antiepileptic drug is contraindicated in pregnancy?
sodium valproate
first-line tx for generalised tonic-clonic seizures in:
a) males
b) females
a) sodium valproate
b) lamotrigine or levetiracetam (if not child-bearing age and not likely to need tx when older, consider SV)
first and second line tx for focal seizures
first = lamotrigine or levetiracetam
second = carbamazepine, oxcarbazepine
first line tx for absence seizures
ethosuximide
how is status epilepticus treated?
a) 1st line
b) 2nd line
c) for kids
d) last line
how to remember this?
I Love to ProD BuMs
1st = IV lorazepam
2nd = PR diazepam
kids = Buccal Medazepam
last = IV phenytoin/levetiracetam
can give 2 doses 5 mins apart
what is an essential tremor? what is it’s heritability pattern?
an autosomal dominant condition affecting both upper limbs
intention vs essential tremor
intention = slower, zig-zag movements evident when intentially moving towards a target e.g. reaching for a mug
essential = bilateral fine tremor without necessarily intentional movement
RFs for an essential tremor (3)
- advancing age
- family hx
- exposure to toxins
signs and symptoms of an essential tremor
a) when does it happen
b) where
c) improves/worsens with what
BILATERAL FINE TREMOR
a) more prominent with voluntary movement e.g. tying shoelaces, but can occur at rest
b) bilaterally in the hands, can also affect head, jaw and vocals
c) improves with alcohol and rest
worsens with stress, fatigue, caffeine and extreme temps
what movement can you ask a pt with an essential tremor to do that will exaggerate their tremor?
worse when patient outstretches arms (called postural tremor)
1st line tx for an essential tremor
what else can you give?
1st line = propranolol
can also give antiepileptic drugs e.g. primidone
where does blood often collect in an EDH? from which artery?
- temporal region
- middle meningeal artery
what is the most common cause of an EDH? who are they common in?
almost always trauma, can be “low-impact” e.g. blow to head or fall
commonly seen in adolescents
what is the classic presentation of a patient with an EDH?
loses consciousness, gains it again and has a LUCID PERIOD, then a second loss of consciousness
signs and symptoms of an EDH
- acute
- headache
- N&V
- drowsy
- lucid interval then rapid neuro deterioration
- hemiparesis
- FIXED DILATED PUPIL
gold std investigation for any haemorrhage
CT head
how will an EDH appear on CT?
- biconvex (lentiform/lemon) hyperdense collection around surface of brain
- limited by suture lines of skull
- may have skull fracture if trauma
definitive tx for an EDH
craniotomy and evacuation of haematoma
other than surgery, how may you manage an EDH?
- IV fluids to maintain circulation/preserve cerebral perfusion
- if raised ICP give IV MANNITOL (osmotic diuretics, reduces cerebral oedema)
what is vasculitis?
inflammation and necrosis of blood vessel walls with subsequent impaired blood flow to end-organs
what is giant cell arteritis (GCA)?
a type of vasculitis affecting medium and large-sized vessel arteries
which disease does GCA commonly overlap with?
polymyalgia rheumatica (50% of pts with GCA will have features of PMR)
main complication of GCA
permanent vision loss
which main artery is often affected by GCA? which branches?
carotid artery - TEMPORAL, OPTHALMIC, FACIAL
patients of what age are typically affected by GCA?
> 60 years old
typical presentation of GCA
rapid onset (< 1 month)…
- headache
- jaw claudication (pain while chewing)
- visual disturbances
- tender, palpable temporal artery
what features of PMR may a patient with GCA present with (alongside typical headache, visual disturbance and jaw claudication)
- aching
- morning stiffness in proximal limb muscles
general nonspecific symptoms of vasculitis (GCA)
- lethargy
- depression
- low grade fever
- night sweats
investigations and findings for GCA
- bloods - inflammatory markers (ESR and CRP) raised
- temporal artery biopsy - may show skip lesions
when should tx for GCA be started?
urgently if suspected - before temporal artery biopsy
management for GCA
- urgent high dose glucocorticoids
- if no visual loss then prednisolone
- if evolving visual loss then IV methylprednisolone before pred - urgent ophthalmology review
- other - bisphosphonates (due to long-term steroids)
define:
a) thrombus
b) embolus
a) a blood clot in a blood vessel aka atherosclerosis
b) clot/fat/air which travels through the blood and lodges elsewhere
what is a stroke?
sudden onset new focal neurological symptoms due to sudden interruption in the vascular supply of the brain
what are the 2 types of stroke? what is their pathophysio? which is most common?
- ischaemic - most common, vascular occlusion/stenosis stops flow
- haemorrhagic - vascular rupture leading to reduction in blood flow
general features of a stroke
- motor weakness
- dysphasia
- swallowing probs
- visual field defects (homonymous hemianopia)
- balance problems
RFs for a stroke
both ischaemic and haemorrhagic:
- age >55
- family hx
- HTN
- T2DM
- smoking
ischaemic:
- Afib
- history of TIA/stroke
- sickle cell disease
Haemorrhagic:
- male
- asian/black
- alcohol
- anticoagulant use
presentation of an anterior cerebral artery stroke
LOWER LIMB contralateral hemiparesis and sensory loss
presentation of a middle cerebral artery stroke
- UPPER LIMB and FACE contralateral sensory loss and paralysis
- contralateral homonymous hemianopia
- aphasia
presentation of a posterior cerebral artery stroke
- contralateral homonymous hemianopia (e.g. cant see out of left of left eye or left of right eye) with macular sparing
- visual agnosia (inability to process sensory info and recognise objects/people/sounds/smells)
presentation of a Weber’s syndrome stroke (branches of posterior artery supplying the midbrain)
- ipsilateral CN III palsy (eye drifting outwards)
- contralateral weakness in upper AND lower body
presentation of a posterior inferior cerebellar artery stroke (Wallenberg syndrome)
- ipsilateral facial pain and temperature loss
- contralateral limb/torso pain and temp loss
- ataxia, nystagmus
presentation of an anterior inferior cerebellar artery stroke (lateral pontine syndrome)
v similar to Wallenberg’s presentation but ipsilateral facial paralysis and deafness
presentation of a retinal/ophthalmic artery stroke
amaurosis fugax
presentation of a basilar artery stroke
‘locked in’ syndrome
investigation for suspected stroke - what needs to be ruled out?
non contrast CT (rule out haemorrhage)
what medication is given following a stroke? which type is it for?
(for THROMBOTIC) - ASPIRIN 300mg daily for 2 weeks
treatment for thrombotic stroke if:
a) presenting within 4.5 hours of onset
b) presenting within 6-24 hours of onset
a) thrombolysis with alteplase
b) thrombectomy
how are the potential causes of a stroke investigated/managed?
- AF - check with ECG
- carotid artery USS - stent if stenosed >50%
- HbA1c - improve diabetic control
- stop smoking and drinking
other than aspirin, what medical tx is given following a thrombotic stroke for preventative measures?
- statins (atorvastatin) - leading cause of thrombotic stroke is atherosclerosis
- clopidogrel 75mg daily
define ischaemia and infarction and use this to explain what a TIA is
ischaemia = lack of blood supply
infarction = tissue damage caused by ischaemia
in a TIA, there is ischaemia to the brain tissue but no infarction (unlike in a stroke)
presentation and timeframe of a TIA
same symptoms as stroke but typically lasts <24 hours
what investigation can be used for a TIA?
diffusion weighted MRI (but may not show evidence)
immediate management of a TIA if patient is NOT currently taking an anticoagulant - when should the pt be referred to a specialist?
- ASPIRIN 300mg
- referral to specialist within 24 hours (OR within 7 days if symptoms were over 7 days ago)
management of a TIA if patient is currently taking an anticoagulant
- urgent non contrast CT head - exclude haemorrhage!
- once ruled out haemorrhage, specialist review within 24 hours
further management of a TIA
a) once reviewed by specialist, for 21 days
b) long-term secondary prevention after 21 days
(after initial 300mg aspirin)
a) aspirin + clopidogrel
b) clopidogrel
3 causes of an SAH. which is most common?
- trauma
- ruptured berry aneurysm (more common)
- AV malformation
what condition is strongly associated with berry anuerysms?
autosomal dominant polycystic kidney disease
RFs for an SAH
- smoking
- HTN
- family hx
- alcohol
- cocaine
classical features of an SAH (location, type of pain, other signs)
- occipital (back of head) thunderclap headache
- meningeal signs - neck stiffness, photophobia, N+V
what 2 signs may be positive in a patient with SAH? why?
Kernig (Knee Extension painful) and Brudzinski (Neck flexion leads to Knee flexion) signs
because SAH sometimes presents with meningism due to bleed pressing on meninges
2 investigation options for an SAH
- CT no contrast head (first line!)
- lumbar puncture
CSF findings from a LP in a patient with SAH (4)
- opening pressure normal/elevated
- blood-tinged CSF (if early on)
- xanthochromia (yellowish CSF)
- normal glucose and protein
medical management for a SAH (5)
- anticoagulant reversal e.g. if on DOAC, apixaban
- manage BP
- pain management
- anti-emetics
- oral nimodipine - prevent vasospasm
surgical management options for SAH and when you would use them (2)
- endovascular coiling - for aneurysm, less invasive but more risk of rebleed
- microsurgical clipping - for big aneurysms in patients suitable for more invasive surgery
what is the most common electrolyte abnormality following SAH?
hyponatraemia (most often due to SIADH -syndrome of inappropriate anti-diuretic hormone)
what is a brain abscess?
a suppurative collection of microbes (bacterial, fungal, parasitic) within a capsule, occurring in the brain parenchyma
can be single or mulitfocal
most common bacterial cause of brain abscesses in adults
streptococcus family
common causes/precipitating events of a brain abscess (4)
- extension of sepsis from middle ear (otitis) or sinuses (sinusitis)
- scalp trauma/surgery
- penetrating head injury
- emboli event from endocarditis
RFs for a brain abscess (there are lots)
- sinusitis, otitis media
- dental procedure/infection
- meningitis
- recent head/neck/neurosurgery
- congenital heart disease
- endocarditis
- diabetes
- HIV/immunocompromise
- IV drug use
- birth prematurity
- haemodialysis
presentation of a brain abscess
similar to tumour!!
- meningism - nuchal rigidity, photophobia, headache
- persistent headache
- cranial nerve palsy e.g. oculomotor or abducens
- +ve Kernig/Brudzinski sign
- fever
- neuro deficit
- raised ICP - papilloedema, nausea, seizures
- in infants - increased head circumference, bulging fontanelle
investigations for a brain abscess - what test helps distinguish it from a tumour?
- BLOODS
- FBC: high WBC (helps rule out tumour)
- ESR and CRP: high (same as above)
- could do cultures - first line imaging = CT scan
management for a brain abscess:
a) what is given before surgery
b) type of surgery
c) medication options
a) give antibiotics
b) craniotomy - abscess cavity debrided
c) IV abx - IV vancomycin + metronidazole + ceftriaxone
if raised ICP - dexamethasone
if seizure - levetiracetam
what is Huntington’s disease?
an autosomal dominant neurodegenerative trinucleotide repeat disorder
what age does Huntington’s typically present?
35-45
what protein is implicated in Huntington’s? on which chromosome?
huntingtin protein on chromosome 4
if one parent has Huntington’s and the other doesn’t, what is the chance of their child having it?
50%
brief pathophysiology of Huntington’s
a) which trinucleotide is involved?
b) how many repeats in a normal human vs Huntington’s?
c) what NT is there too much of?
d) what change occurs in the brain?
- expanded CAG repeat coding for huntingtin protein
- huntingtin gene normally has 10-35 CAG repeats, in HD there are >36
- more repeats = greater risk of disease
- clusters of mutated huntingtin proteins stick in neurons > toxic, neurodegeneration
- too much dopamine and cerebral atrophy
what phenomenon is displayed in Huntington’s? what does this mean?
= anticipation
successive generations have more repeats in the gene, leading to:
- earlier age of onset
- increased disease severity
typical presentation of Huntington’s
- 35yo with fam hx
- non motor = irritability, impulsivity, personality changes
- motor = chorea, twitching, loss of coordination, hyperkinesia, dystonia, saccadic eye movements
how is Huntington’s diagnosed?
clinical diagnosis but can do MRI/CT to confirm
what would be seen on MRI/CT in Huntington’s?
cerebral atrophy
initial management for Huntington’s
counselling for patient and family, carer support
at what age can a child of someone with Huntington’s be tested?
18
management options for Huntington’s
- MDT - physio, SLT
- chorea - tetrabenazine/sulpiride
- mood - SSRIs
- psychosis sx/aggression - risperidone
- advanced directives for disease progression
what are the most common primary tumours that metastasise to the brain? (5)
- lung
- renal cell carcinoma
- melanoma (skin)
- breast
- colorectal
how do primary tumours metastasise to the brain? where do they usually become lodged?
- haematogenous spread via blood vessels
- often lodge at grey matter/white matter junction (where vessels decrease in size)
presentation of brain metastases (7)
may be asymptomatic! (1/3)
- increased ICP
- headache - associated N&V, worse on bending/coughing, worse in morning on awakening
- focal weakness
- altered mental status
- seizures
- ataxia
- stroke
investigations for brain metastases (2)
- neuro exam inc fundoscopy for papilledema
- imaging - CT first-line but contrast-enhanced MRI more sensitive
initial management for a patient presenting with acute brain metastases symptoms (3)
- airway, breathing, circulation
- dexamethasone (manage oedema)
- anti-seizure medication
management options for brain metastases if…
a) large number of mets
b) fewer mets, <3cm
c) simple, easily resectable
d) chemo-sensitive tumour
a) whole-brain radiation therapy
b) stereotactic radiosurgery (precisely focussed beams)
c) surgical resection
d) systemic therapy
what is bulbar palsy? what are the 2 types?
result of disease affecting the lower cranial nerves (VII-XII)
- non-progressive - uncommon, uncertain aetiology
- progressive - more common, type of MN disease
progressive bulbar palsy epidemiology
typically late middle-aged man with an affected relative
causes of bulbar palsy (6)
- MOTOR NEURONE DISEASE
- infection e.g. diphtheria, poliomyelitis
- cerebrovascular event of brainstem
- brainstem tumour
- surgery for acoustic neuroma
- Guillain-Barre syndrome
general signs and symptoms of a bulbar palsy (5)
think LMN signs
1. lips - tremulous
2. tongue - flaccid, fasciculations
3. drooling (dysphagia)
4. dysphonia - quiet, nasal, hoarse speech
5. dysarthria - poor articulation
speech slurred and then indistinct in late stages
specific signs of bulbar palsy if caused by MND (progressive bulbar palsy)
- neuro deficit in limbs e.g. flaccid tone, reduced reflexes, weakness with fasciculations
- clumsiness/dropping things
investigations for bulbar palsy (4)
- assess speech function e.g. with electromagnetic articulography (EMA)
- bloods - rule out other causes
- CT/MRI of brain
- electromyography
how are the symptoms of bulbar palsy managed? (2)
what about specific managements in MN disease?
- for drooling - anticholinergics e.g. oral amitriptyline
- for dysphagia - PEG tube
in MN disease, consider riluzole and resp care e.g. BIPAP at night
what is cerebellar disease? what are some examples?
a group of disorders affecting the cerebellum (controls muscle functions and balance)
e.g. cerebellar degeneration, stroke
causes of cerebellar disease (7)
- neoplastic e.g. cerebellar haemangioma or paraneoplastic e.g. 2nd to lung
- stroke
- alcohol
- MS
- hypothyroidism
- drugs e.g. phenytoin, lead poisoning
- genetic disorders
signs and symptoms of cerebellar disease and the mnemonic for remembering them
DANISH
D - dysdiadochokinesia, dysmetria (past-pointing), appearing Drunk
A - ataxia (loss of muscle control e.g. lack of balance, coordination, slurred, stumbling)
N - nystagmus
I - intention tremor
S - slurred staccato speech, scanning dysarthria
H - hypotonia
investigations for cerebellar disease
- full neurological examination
- MRI head
differential diagnosis for cerebellar disease
acoustic neuroma
examples of managing the various underlying causes of cerebellar disease
- if tumour, surgery/chemo
- if stroke, tx e.g. with aspirin
- if certain meds, stop them
- if MS, optimise tx
what is guillain-barre syndrome?
an acute inflammatory polyneuropathy
which organism is Guillain-Barre syndrome typically caused by?
campylobacter jejuni
presentation of Guillain-Barré syndrome
- 1-4 weeks post infection e.g. GI/resp
- symmetrical ascending muscle weakness/flaccid paralysis
other =
3. absent tendon reflexes
4. paraesthesia distally
3 investigations for Guillain-Barre syndrome
- nerve conduction studies - lack of conduction down bum
- lumbar puncture
- serology - for antibodies against infective pathogen OR anti-ganglioside antibodies
cross reactive antibodies react with which protein in Guillain-Barre syndrome? where?
glycoprotein in neuronal tissue
lumbar puncture result in Guillain-Barre syndrome
isolated elevated protein, normal WCC
1st and 2nd line tx for Guillain-Barre syndrome
1st line = IV immunoglobulins for 5 days
2nd line = plasmapheresis
what is syringomyelia? what congenital malformation is it strongly associated with?
- a collection of CSF within the spinal cord
- strongly associated with congenital Chiari malformation
presentation of syringomyelia
- ‘cape-like’ (neck, shoulders and arms) distribution of loss of sensation to temperature
- spastic weakness (normally lower limbs)
- neuropathic pain
- upgoing plantars
- muscle wasting
- reduced reflexes in upper and lower limbs
what is the most common form of brain tumour in adults?
metastatic brain cancer
which tumours most commonly spread to the brain? which is MOST common?
- lung (most common)
- breast
- skin
- kidney
- bowel
what is Multiple System Atrophy?
a cause of parkinsonism - presents with parkinsonism + unilateral symptoms and severe/early onset autonomic disturbance e.g. postural hypotension, erectile dysfunction
what is the most common complication following meningitis?
sensorineural hearing loss
common reflexes and their nerve roots:
a) ankle
b) knee
c) biceps
d) triceps
a) S1-S2
b) L3-L4
c) C5-C6
d) C7-C8
presentation of a posterior communicating artery aneurysm
- third nerve palsy (down and out, dilated pupil)
- headache (PAIN)
what is the most common cause of peripheral neuropathy?
diabetes
risk factors for diabetic neuropathy/peripheral neuropathy (5)
- poor glucose control
- diabetic hx
- renal disease
- obesity
- smoking
pathophysiology of diabetic neuropathy - which part of the neuron is affected?
axonal degeneration - primary damage in the nerve fibres (axon), nerve fibres then die back from periphery
diabetic neuropathy - presentation of peripheral neuropathy (most common type)
- sensory loss in ‘glove and stocking’ distribution
- lower legs affected first
- pain, numbness, tingling
diabetic neuropathy - presentation of autonomic neuropathy
- hypoglycemia unawareness (erratic sugar control)
- orthostatic hypotension
- GI - N&V, fullness, loss of appetite, GORD
- vision changes
- sweating
- sexual response probs
diabetic neuropathy - presentation of proximal neuropathy
- thighs, hips, buttocks and legs
- severe pain
- weak muscles
- difficulty rising from sitting
- chest wall/abdo pain
diabetic neuropathy - presentation of focal neuropathy
may be…
- foot drop
- numb/tingling hand
- hand weakness e.g. dropping things
- difficulty focussing/diplopia
- unilateral facial paralysis
investigations for diabetic neuropathy
- neurological exam
- bloods
- rule out other causes e.g. B12/thiamine deficiency
- check glucose - consider US, electromyography, nerve conduction studies
diabetic neuropathy management
a) 1st line
b) 2nd line
c) ‘rescue therapy’ for exacerbations
d) for localised pain
a) amitriptyline
b) duloxetine/gabapentin/pregabalin
c) tramadol
d) topical capsaicin
how long must a tension headache be going on for a diagnosis to be made?
> 15 days in one month
exacerbations of a tension headache (6)
- fatigue
- lack of sleep
- poor posture
- anxiety
- stress
- depression
presentation of a tension headache
- episodic
- bilateral
- “band” dull/pressing/non pulsating
- no N&V
how is a tension headache diagnosed?
clinically
exacerbations/causes of a migraine (CHOCOLATE)
Chocolate
Hydration status (dehydrated) and Hormones (menstruation
Orgasm
Caffeine/COCP
Lights
Alcohol
Trauma
Exercise
features of a migraine
- severe, throbbing
- unilateral
- lasting up to 72h
- photophobia/phonophobia
what is a hemiplegic migraine?
rare migraine complication, can get unilateral motor weakness alongside aura
how is a migraine diagnosed?
usually clinically if sx are classical
management of migraines:
a) for pain
b) to take at START of headache
c) antiemetic
d) prevention
a) ibuprofen/aspirin/paracetemol
b) oral triptans e.g. sumatriptan
c) metoclopramide
d) topiramate/propanolol
what advice must women of child-bearing age taking topiramate for a migraine be given?
need to be on v good contraception - topiramate is teratogenic
features of a cluster headache
a) when
b) where
c) type of pain
d) how long for
e) associated sx
a) CYCLICAL e.g. every 6 months have X amount of headaches within X space of time, happens at same time every year
b) unilateral, periorbital or temproral
c) severe, pulsating
d) short attacks
e) autonomic e.g. runny nose, runny eye, partial Horner’s (without anihidrosis)
diagnostic criteria for cluster headaches
5 attacks of severe unilateral orbital/periorbital pain lasting >15 minutes and EITHER/BOTH of…
- autonomic sx
- sensation of restlessness/agitation
management for cluster headaches
a) acute tx
b) prophylaxis
a) intranasal sumatriptan, 100% high flow O2
b) verapamil
a medication headache should be present for > X days or more per month
15 days or more
management for medication overuse headaches
- simple analgesics and triptans withdrawn abruptly
- opioid analgesics withdrawn slowly
what is MS? what is it characterised by?
a chronic degenerative disease of the CNS, characterised by demyelination and axonal degeneration in the brain and spinal cord
what causes MS?
immune-mediated inflammation
epidemiology of MS - age and gender
20-40
more common in females
McDonald Criteria for MS
there must be dissemination in time and space:
- DIT: appearance of new CNS lesions over time
- DIS: presence of lesions in different regions of CNS
investigations for MS
- MRI with contrast
- LP CSF
what will be found in MS on:
a) MRI with contrast
b) CSF analysis
a)
- demyelinating plaques (periventricular)
- plaques also seen in optic nerve, brainstem and spinal cord
b) oligoclonal bands
types of MS (4)
- relapsing-remitting (MOST COMMON)
- secondary progressive
- primary progressive
- progressive-relapsing
describe relapsing-remitting MS
- episodic flare-ups separated by periods of remission
- not fully recovering between flares
- so disability increases over time
what type of MS do 60% of patients with relapsing-remitting develop within 15 years?
secondary progressive - disability becomes constant over time (straight line)
what is often the first presentation of MS?
optic neuritis - unilateral painful eye with impaired vision and colour blindness
MS presentation
a) eyes
b) spinal cord
c) cerebellum
d) CN palsies
e) autonomic dysfunction
f) mental state
FATIGUE, HEADACHE
a) optic neuritis
internuclear ophthalmoplegia - problematic eye cannot look inwards, if the pt tries the contralateral eye will experience nystagmus
b) Lhermitte sign (shooting sensation down spine with neck flexion)
pyramidal tract: UMN weakness, spasticity, hyperreflexia, positive Babinski
DC lesion: loss of vibration, touch, numbness, paraesthesia, sensory ataxia
neuropathic pain
absent abdominal reflex
c) poor postural control, imbalance, gait dysfunction, scanning speech, nystagmus
e) diplopia, trigeminal neuralgia, facial palsy
d) bowel and bladder disorders, impaired sexual function
f) impaired conc and memory, emotional change
MS: what is Uhtoff phenomenon?
worsening of symptoms following increased body temp e.g. in hot shower
MS: acute relapse management
high dose oral/IV methylprednisolone for 5 days
MS: relapse prevention management and sx tx
- IV natalizumab
- ocrelizumab
- fingolimod
- for fatigue: amantadine
- for spasticity: baclofen and gabapentin
MS vs MND signs
MND - mix of UMN and LMN. steady progression.
MS - only UMN signs, sensory, often relapsing-remitting
drugs exacerbating myasthenia gravis (myasthenia crisis) (6)
- penicillamine
- quinidine
- b-blockers e.g. bisoprolol
- lithium
- phenytoin
- abx
which condition is Lambert-Eaton syndrome most commonly associated with?
small cell lung cancer
GCS - what are the 3 components?
motor
verbal response
eye opening
GCS - motor response scoring (6)
- none
- extends to pain
- abnormal flexion to pain
- withdraws from pain
- localises to pain
- obeys command
GCS - verbal response scoring (5)
- none
- sounds
- words
- confused
- orientated
GCS - eye opening scoring (4)
- none
- to pain
- to speech
- spontaneous
what is Lambert-Eaton syndrome?
a rare autoimmune disorder characterised by muscle weakness of the limbs
cause and pathophys of Lambert-Eaton syndrome
autoantibodies against presynaptic voltage gated C-channels > calcium can’t bind to vesicles that release Ach
impaired release of Ach at the NMJ
features of Lambert-Eaton syndrome
- proximal muscle weakness that improves with muscle use (affects lower limbs first)
- waddling gait
- reduced/absent reflexes
- autonomic sx - dry mouth, impotence, difficulty micturating
what sx occurs in MG but not lambert-eaton syndrome?
opthalmoplegia and ptosis
investigations and results for lambert-eaton syndrome
- electrical nerve conduction - increased response to electrical stimulation with muscle use
- bloods - serum anti-VGCC antibodies
consider investigating for underlying malignancy (CXR)
management of lambert-eaton syndrome
- tx underlying cancer
- prednisolone and/or azathioprine (immunosuppression)
- consider IV immunoglobulin therapy and plasma exchange
what is encephalitis?
inflammation of brain
who is most commonly affected by encephalitis?
young children and elderly
non-infective cause of encephalitis
autoimmune
infective causes of encephalitis
what’s most common in:
a) adults and children
b) neonates
mostly VIRAL
a) HSV-1
b) HSV-2
other = ticks, west nile virus, VZV, EBV, mumps, polio, rubella and measles
RFs for encephalitis
- young/old
- travel to certain countries e.g. Asia
- autoimmune conditions
- unvaccinated for polio, mumps, rubella, measles
which lobes are most commonly inflamed in encephalitis?
temporal, inferior frontal
signs and symptoms of encephalitis
- fever
- headache
- altered consciousness
- unusual behaviour
- vomiting
- acute onset focal neuro sx e.g. aphasia
- acute onset seizures
investigations for encephalitis
- LP - PCR testing of CSF
- MRI (after LP)
- EEG
CSF findings in encephalitis
- lymphocytosis
- elevated proteins
when is LP contraindicated? what should be done instead if suspecting encephalitis?
if GCS <9, haemodynamically unstable, active seizures, postictal
CT scan
MRI findings in encephalitis
medial temporal and inferior frontal lobes - petechial haemorrhages
ddx for encephalitis
- meningitis
- stroke
management of encephalitis
- IV aciclovir in ALL pts suspected (treats HSV and VZV)
- repeat LP to ensure successful tx
- FU, support and rehabilitation
which antivirals should be given if CMV is the cause of encephalitis?
IV ganciclovir
what is meniere’s disease?
a progressive disorder of the inner ear of unknown cause
pathophysiology of meniere’s disease
- excessive pressure and progressive dilation of the endolymphatic system (endolymph = fluid in inner ear)
- distorted info travels to brain
- affects balance/sound
epidemiology of Meniere’s disease
mostly affects middle-aged adults
what is the classic triad of meniere’s disease?
- vertigo
- tinnitus
- sensorineural hearing loss
what pattern of symptoms is exhibited in meniere’s disease?
- episodic
- sx all happen at same time
- lasts for minutes/hours then resolves
other sx (besides the classical triad) of meniere’s disease
- sensation of aural fullness/pressure
- nystagmus
what test will be positive in meniere’s disease?
romberg’s test
how is meniere’s disease diagnosed?
ENT assessment
management of meniere’s disease
a) for acute attacks
b) prophylaxis
a) buccal/IM prochlorperazine
b) betahistine (increases blood flow to try and reduce fluid build-up)
driving advice for patients with meniere’s disease
- inform DVLA
- cease driving until control of sx achieved
most common type of MND
amyotrophic lateral sclerosis (ALS)
presentation of MND
MIX OF UMN AND LMN
NO SENSORY
- asymmetric limb weakness
- UMN: increased tone, hyperreflexia, clonus, babinski +ve, muscle atrophy
- LMN: flaccidity, fasciculations, babinski -ve
what is NOT affected in MND?
- external ocular muscles
- cerebellum
how is MND diagnosed?
- by a specialist
- clinical
- nerve conduction studies exclude neuropathy (normal motor conduction)
- MRI to exclude cervical cord compression and myelopathy
management of MND
- RILUZOLE - prolongs life by ab 3 months, mainly for ALS
- resp care - non-invasive (BPAP) at night
- PEG tube
pathophys of MG
autoantibodies against postsynaptic Ach receptors
what disease is MG strongly associated with? what are some other ones?
THYMOMA
other - thymic hyperplasia, autoimmune e.g. RA, SLE, autoimmune thyroid
which gender is myasthenia gravis more common in?
females (2:1)
features of MG
key = muscle FATIGABILITY
- weakness worse throughout day, if you ask to raised arms up they’ll slowly fall down
- improves with rest
- extraocular muscles > diplopia
- ptosis
- face, neck, limb, girdle e.g. raising from chair, dysphagia
which muscles are commonly affected in MG? how does this present?
- extraocular muscles > diplopia, ptsosis
- prox muscles (face, neck, limb girdle) > dysphagia
what clinical test can be used to test for MG?
simpson test - ask pt to look up for 1 minute, eyes will slowly drop down
MG investigations and results (3)
- serum Ach receptors antibody test
- electrical nerve conduction - decreasing response with each stimulation
- chest CT - rule out thymoma
what antibodies may be positive in patients with MG? (2)
- Ach receptor antibodies
- anti-muscle-specific tyrosine kinase antibodies
management of MG (3) - what is 1st line?
- acetylcholinesterase inhibitors - 1st line = pyridostigmine
- immunosuppression - prednisolone initially then azathioprine
- may need thymectomy
what is myasthenic crisis? how does it present?
if myasthenic patient ill/has surgery/gets pregnant/has a certain drug then all sx are exacerbated
muscle weakness, dyspnoea, sweating, urinary/faecal urgency, tachycardia > resp failure
management of myasthenic crisis
- plasmapheresis
- IV immunoglobulins
how to differentiate between idiopathic vs drug-induced parkinson’s
- idiopathic normally asymmetrical sx
- drug-induced normally symmetrical sx
blood test to differentiate between a true epileptic seizure and a psychogenic non-epileptic seizure
serum prolactin - will be raised in true epileptic seizure
which B vitamin is thiamine?
B1
1st line tx for trigeminal neuralgia
carbamazepine
symptoms of trigeminal neuralgia
- severe unilateral pain
- brief, electric-shock like pains
- abrupt in onset and termination
- limited to one/more divisions of trigeminal nerve
- evoked by light touch e.g. washing, shaving, smoking, talking, brushing teeth
what is cerebral palsy?
the permanent neurological problems (disorder of movement and posture) resulting from damage to the brain around the time of birth
what are the 4 types of CP?
- spastic/pyramidal
- dyskinetic
- ataxic
- mixed
spastic/pyramidal CP
a) features
b) damage to where
c) subcategories
a) HYPERTONIA, reduced function
b) resulting from damage to UMNs
c) monoplegia (one limb), hemiplegia (one side of body e.g. one arm, leg), diplegia (symmetrical parts of body e.g. both legs/both arms), quadriplegia (all four limbs)
dyskinetic and ataxic CP
a) features
b) where is the damage?
a) dyskinetic - problems controlling muscle tone > hypertonia and hypotonia
ataxic - problems with coordinated movement
b) dyskinetic - damage to basal ganglia
ataxic - damage to cerebellum
most common cause of major motor impairment in children
cerebral palsy
aetiology of cerebral palsy…
a) antenatal causes
b) intrapartum causes
c) postnatal causes
non-progressive lesion of the motor pathways in the developing brain due to…
a) cerebral malformation, congenital infection e.g. rubella, toxo, CMV
b) birth asphyxia/trauma, preterm
c) intraventricular haemorrhage, meningitis, head trauma
risk factors for CP
- birth problems/trauma
- maternal infection
GENERAL features of CP (6)
- failure to meet milestones
- increased/decreased tone
- hand preference below 18m
- probs with coordination, speech, walking
- feeding/swallowing problems
- learning difficulties
what signs may show in a neurological exam with someone with CP? (gait, UMN, movement, cerebellar exam)
- gait
- hemiplegic/diplegic
- leg extension with plantar flexion of feet/toes (swinging leg in large semi circle when moving leg in front) - UMN signs - increased tone, brisk reflexes
- athetoid movements - involuntary writhing
- poor coordination on cerebellar exam
MDT approach to CP (6)
- physio
- OT for ADLs
- SLT - may need NG/PEG
- dietician
- orthopaedic surgeons - release contractures/lengthen tendons (tenotomy)
- regular FU with paediatrician
medication options for CP (4)
- muscle relaxants - baclofen, diazepam
- antiepileptic drugs
- glycopyyronium bromide (drooling)
- analgesia if required
complications of cerebral palsy (6)
- learning disability
- epilepsy
- kyphoscoliosis
- muscle contractures
- hearing/visual impairment
- GORD
what is parkinsons?
chronic progressive neurological disorder characterised by motor symptoms
epidemiology of parkinsons
- more common in males
- peak onset 55-65
causes of parkinsons (4)
- IDIOPATHIC (most common)
- vascular parkinsonism
- infection e.g. encephalitis, Creutzfeldt-Jacob disease
- toxin/drug-induced
causes of drug-induced parkinsonism (2)
any drugs that block action of dopamine!!
- antipsychotics e.g. haloperidol, chlorpromazine, lithium
- anti-emetics e.g. metoclopramide
brief pathophy of parkinsons
- neurodegenerative loss of dopamine secreting cells from substantia nigra
- thalamus (relays motor info) inhibited
- decrease in movement, eventually dementia
- ALSO depletion of serotonin and noradrenaline > depression
classic triad of parkinsons
- resting tremor
- bradykinesia
- rigidity
are the symptoms of parkinsons classically asymmetrical or symmetrical?
ASYMMETRICAL
how to differentiate between drug-induced parkinsonism and parkinson’s disease
- motor sx rapid onset and BILATERAL
- rigidity and rest tremor less common
describe how the characteristics of bradykinesia, tremor and rigidity featured in parkinsons
BRADYKINESIA
- poverty of movement
- short, shuffling steps
- reduced arm swinging
TREMOR
- mostly at rest
- improves with voluntary movement
- typically ‘pill-rolling’
RIGIDITY
- lead pipe (constant resistance to movement through whole range of movement)
- cogwheel (jerking resistance to movement, resistance stops and starts)
other signs and symptoms of parkinsons (8)
- mask-like facies
- micrographia
- drooling
- depression, dementia, psychosis, sleep disturbance
- fatigue
- autonomic dysfunction e.g. postural hypotension
- stooped posture
- hypophonia
how is parkinsons diagnosed?
clinically by a specialist (would need referral from primary care)
NICE recommended investigation for parkinsons if clinically unclear
dopamine transporter scan (DaTscan) with SPECT - visualises dopamine in brain
parkinsons medical management options and examples
- L-DOPA
- levodopa
- often combined so co-beneldopa or co-careldopa - DOPAMINE AGONISTS
- cabergoline
- ropinirole
- pramipexole
- rotigotine
- bromocriptine - MAO-B INHIBITORS
- selegiline - COMT INHIBITORS
- rasagiline
- entacapone
1st line tx of parkinsons if…
a) motor sx are affecting QOL
b) motor sx are not affecting QOL
a) levodopa
b) dopamine agonist, levodopa or monoamine oxidase B (MAO-B) inhibitor
management of parkinsons if pt continues to have sx despite optimal levodopa tx
add dopamine agonist/MAO-B inhibitor or catechol-methyl transferase (COMT) inhibitor as an adjunct
best anti-emetic tx in parkinsons
domperidone
when are l-dopas used in parkinsons? what with usually?
what are some SEs and how are these dealt with?
most effective but becomes less effective over time so often reserved for when other drugs aren’t working
BUT also used in newly diagnosed pts who’s motor sx are ruining QOL
nearly always combined with carbidopa/benserazide (reduces SEs)
SEs = dyskinesia (excessive motor activity e.g. dystonia, chorea, athetosis), dry mouth, anorexia, palpitations, postural hypotension, psychosis
manage SEs with amantadine
what medication type is combined with levodopa and why?
peripheral dopa-decarboxylase inhibitors e.g. carbidopa
reduces peripheral breakdown of levodopa so a smaller dose can be used, reducing SEs
describe these adverse effects which may occur in pts on levodopa long-term:
a) end-of-dose weaning off
b) on-off phenomenon
a) sx worsen towards end of dosage interval. results in decline of motor activity
b) large variations in motor performance - normal function during ‘on’ period and weakness/restricted mobility during ‘off’ period
when are dopamine agonists typically used in the tx of parkinsons? what are the main SEs?
typically used to delay use of levodopa, then used in combo
main SEs = pulmonary fibrosis, impulse control issues, daytime sleepiness
name 5 atypical forms of PD
- progressive supranuclear palsy
- multiple system atrophy
- lewy body dementia
- corticobasal degeneration
- vascular parkinsonism
presentation of these atypical forms of PD:
a) progressive supranuclear palsy
b) multiple system atrophy
c) corticobasal degen
d) vascular parkinsonism
a) early postural instability, vertical gaze palsy = frequent falls
b) ataxia + autonomic disturbance (incontinence, ED) + dementia. resistant to l-dopa
c) ‘alien limb’
d) v sudden onset. affects those with DM/HTN. minimal tremor and pronounced gait difficulties
presentation of brown-sequard syndrome
CONTRALATERAL loss of pain and temp sensation
IPSILATERAL loss of proprioception, vibration and fine touch, paralysis
what is cauda equina? at which spinal segment?
lumbrosacral nerve roots extending below the spinal cord are compressed (L4/L5 or L5/S1)
most common cause of cauda equina
central disc prolapse at L4/L5 or L5/S1
other causes of cauda equina (4)
- tumour
- infection (abscess, discitis)
- trauma
- haematoma
presentation of cauda equina
- lower back pain
- bilateral sciatica
- reduced sensation/pins & needles in perianal area
- decreased anal tone
- urinary dysfunction
investigation for cauda equina
urgent MRI
where in the spinal cord is a lesion likely to be if…
a) all four limbs affected (quad)
b) only lower limbs affected (di)
c) resp difficulties/diaphragm
a) cervical level
b) thoracic level
c) above C3
management of cauda equina
spinal decompression
what is trigeminal neuralgia?
severe, episodic headache caused by vascular compression of the trigeminal nerve root
which trigeminal branches are typically affected in trigeminal neuralgia?
maxillary and mandibular
describe the headache and triggers in trigeminal neuralgia
SEVERE, EPISODIC FACIAL PAIN
- electric-shock like
- short, up to 2 mins
- unilateral
- recurrent
TRIGGERS
- touching face
- talking
- cold wind
- vibration
- cleaning teeth/brushing hair
investigations for trigeminal neuralgia
clinical diagnosis
management of trigeminal neuralgia
1st line = carbamazepine
what should prompt a referral to neurology for a pt with trigeminal neuralgia?
- failing to respond to tx
- atypical features e.g. <50 years old
red flag symptoms of trigeminal neuralgia (7)
- sensory changes
- deafness
- hx of skin or oral lesions that could spread perineurally
- pain only in opthalmic division (eye socket, forehead and nose) or bilaterally
- optic neuritis
- fam hx of MS
- age onset <40
what causes neuroleptic malignant syndrome?
antipsychotics and dopaminergic drugs e.g. levodopa
when does neuroleptic malignant syndrome happen?
within hours-days of starting antipsychotics
features of neuroleptic malignant syndrome (5)
- pyrexia (fever)
- muscle rigidity
- agitated delirium
- confusion
- HTN, tachycardia, tachypnoea
neuroleptic malignant syndrome
a) creatinine kinase
b) WCC
c) LFTs
d) U&Es
e) metabolic…
a) raised
b) raised
c) deranged
d) deranged
e) metabolic acidosis
management of neuroleptic malignant syndrome (4)
- STOP ANTIPSYCHOTIC
- IV fluids (prevent renal failure)
- if severe - dantrolene
- can use dopamine agonist e.g. bromocriptine (reverses dopamine blockade)
CT results for
a) SDH
b) EDH
c) SAH
a) crescent-shaped haematoma
b) biconvex-shaped haematoma
c) blood mixed in with CSF in basal cisterns and ventricles
presentation of infantile spasms (West’s syndrome)
what will show on EEG?
- brief spasms in first few months of life
- Salaam attacks
- hypsarrhythmia on EEG
name three neuro abnormalities that infantile spasms are often secondary to
- tuberous sclerosis
- encephalitis
- birth asphyxia
what is Lennox-Gastaut syndrome? what are its features?
may be extension of infantile spasms
1-5 years old
- atypical absences, falls, jerks
- 90% moderate-severe mental handicap
presentation of benign rolandic epilepsy
childhood - paraesthesia (unilateral face) usually on waking up
presentation of juvenile myoclonic epilepsy
- typically teens
- infrequent generalised seizures, often in morning e.g. dropping cups of tea
- daytime absences
- sudden myoclonic seizures
tx of juvenile myoclonic epilepsy
sodium valproate
pontine haemorrhage
- presentation
- common cause
- reduced GCS, paralysis, bilateral pin point pupils
- long-standing HTN
define epilepsy
transient occurrence of intermittent, abnormal electrical activity of parts of the brain, manifests as seizures
define aura
part of a seizure, often preceding other manifestations. a disturbance of sensation e.g. strange feeling/smell/taste/flashing lights
metabolic causes of a seizure (5)
- hypoglycemia
- hyponatraemia
- hypocalcemia
- hypernatremia
- uraemia
airway adjunct for pt having a seizure
nasopharyngeal (as mouth may be difficult to open)
what is degenerative cervical myelopathy?
spinal cord compression due to age related changes
RFS for degenerative cervical myelopathy (4)
- older age
- smoking
- occupation e.g. axial loading
- genetics
presentation of degenerative cervical myelopathy (5)
WORSENING…
1. pain (neck, limbs)
2. loss of motor function e.g. shirt buttons, impaired gait/balance
3. loss of sensory function e.g. numbness
4. loss of autonomic function e.g. impotence, incontinence
5. +ve Hoffman’s sign
GS investigation and results for degenerative cervical myelopathy
MRI - disc degeneration, ligament hypertophy, cord signal change
tx of degenerative cervical myelopathy
cord decompression
where does the dorsal column decussate?
medulla
